1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
46
47
48
49
50
51
52
53
54
55
56
57
58
59
60
61
62
63
64
65
66
67
68
69
70
71
72
73
74
75
76
77
78
79
80
81
82
83
84
85
86
87
88
89
90
91
92
93
94
95
96
97
98
99
100
101
102
103
104
105
106
107
108
109
110
111
112
113
114
115
116
117
118
119
120
121
122
123
124
125
126
127
128
129
130
131
132
133
134
135
136
137
138
139
140
141
142
143
144
145
146
147
148
149
150
151
152
153
154
155
156
157
158
159
160
161
162
163
164
165
166
167
168
169
170
171
172
173
174
175
176
177
178
179
180
181
182
183
184
185
186
187
188
189
190
191
192
193
194
195
196
197
198
199
200
201
202
203
204
205
206
207
208
209
210
211
212
213
214
215
216
217
218
219
220
221
222
223
224
225
226
227
228
229
230
231
232
233
234
235
236
237
238
239
240
241
242
243
244
245
246
247
248
249
250
251
252
253
254
255
256
257
258
259
260
261
262
263
264
265
266
267
268
269
270
271
272
273
274
275
276
277
278
279
280
281
282
283
284
285
286
287
288
289
290
291
292
293
294
295
296
297
298
299
300
301
302
303
304
305
306
307
308
309
310
311
312
313
314
315
316
317
318
319
320
321
322
323
324
325
326
327
328
329
330
331
332
333
334
335
336
337
338
339
340
341
342
343
344
345
346
347
348
349
350
351
352
353
354
355
356
357
358
359
360
361
362
363
364
365
366
367
368
369
370
371
372
373
374
375
376
377
378
379
380
381
382
383
384
385
386
387
388
389
390
391
392
393
394
395
396
397
398
399
400
401
402
403
404
405
406
407
408
409
410
411
412
413
414
415
416
417
418
419
420
421
422
423
424
425
426
427
428
429
430
431
432
433
434
435
436
437
438
439
440
441
442
443
444
445
446
447
448
449
450
451
452
453
454
455
456
457
458
459
460
461
462
463
464
465
466
467
468
469
470
471
472
473
474
475
476
477
478
479
480
481
482
483
484
485
486
487
488
489
490
491
492
493
494
495
496
497
498
499
500
501
502
503
504
505
506
507
508
509
510
511
512
513
514
515
516
517
518
519
520
521
522
523
524
525
526
527
528
529
530
531
532
533
534
535
536
537
538
539
540
541
542
543
544
545
546
547
548
549
550
551
552
553
554
555
556
557
558
559
560
561
562
563
564
565
566
567
568
569
570
571
572
573
574
575
576
577
578
579
580
581
582
583
584
585
586
587
588
589
590
591
592
593
594
595
596
597
598
599
600
601
602
603
604
605
606
607
608
609
610
611
612
613
614
615
616
617
618
619
620
621
622
623
624
625
626
627
628
629
630
631
632
633
634
635
636
637
638
639
640
641
642
643
644
645
646
647
648
649
650
651
652
653
654
655
656
657
658
659
660
661
662
663
664
665
666
667
668
669
670
671
672
673
674
675
676
677
678
679
680
681
682
683
684
685
686
687
688
689
690
691
692
693
694
695
696
697
698
699
700
701
702
703
704
705
706
707
708
709
710
711
712
713
714
715
716
717
718
719
720
721
722
723
724
725
726
727
728
729
730
731
732
733
734
735
736
737
738
739
740
741
742
743
744
745
746
747
748
749
750
751
752
753
754
755
756
757
758
759
760
761
762
763
764
765
766
767
768
769
770
771
772
773
774
775
776
777
778
779
780
781
782
783
784
785
786
787
788
789
790
791
792
793
794
795
796
797
798
799
800
801
802
803
804
805
806
807
808
809
810
811
812
813
814
815
816
817
818
819
820
821
822
823
824
825
826
827
828
829
830
831
832
833
834
835
836
837
838
839
840
841
842
843
844
845
846
847
848
849
850
851
852
853
854
855
856
857
858
859
860
861
862
863
864
865
866
867
868
869
870
871
872
873
874
875
876
877
878
879
880
881
882
883
884
885
886
887
888
889
890
891
892
893
894
895
896
897
898
899
900
901
902
903
904
905
906
907
908
909
910
911
912
913
914
915
916
917
918
919
920
921
922
923
924
925
926
927
928
929
930
931
932
933
934
935
936
937
938
939
940
941
942
943
944
945
946
947
948
949
950
951
952
953
954
955
956
957
958
959
960
961
962
963
964
965
966
967
968
969
970
971
972
973
974
975
976
977
978
979
980
981
982
983
984
985
986
987
988
989
990
991
992
993
994
995
996
997
998
999
1000
1001
1002
1003
1004
1005
1006
1007
1008
1009
1010
1011
1012
1013
1014
1015
1016
1017
1018
1019
1020
1021
1022
1023
1024
1025
1026
1027
1028
1029
1030
1031
1032
1033
1034
1035
1036
1037
1038
1039
1040
1041
1042
1043
1044
1045
1046
1047
1048
1049
1050
1051
1052
1053
1054
1055
1056
1057
1058
1059
1060
1061
1062
1063
1064
1065
1066
1067
1068
1069
1070
1071
1072
1073
1074
1075
1076
1077
1078
1079
1080
1081
1082
1083
1084
1085
1086
1087
1088
1089
1090
1091
1092
1093
1094
1095
1096
1097
1098
1099
1100
1101
1102
1103
1104
1105
1106
1107
1108
1109
1110
1111
1112
1113
1114
1115
1116
1117
1118
1119
1120
1121
1122
1123
1124
1125
1126
1127
1128
1129
1130
1131
1132
1133
1134
1135
1136
1137
1138
1139
1140
1141
1142
1143
1144
1145
1146
1147
1148
1149
1150
1151
1152
1153
1154
1155
1156
1157
1158
1159
1160
1161
1162
1163
1164
1165
1166
1167
1168
1169
1170
1171
1172
1173
1174
1175
1176
1177
1178
1179
1180
1181
1182
1183
1184
1185
1186
1187
1188
1189
1190
1191
1192
1193
1194
1195
1196
1197
1198
1199
1200
1201
1202
1203
1204
1205
1206
1207
1208
1209
1210
1211
1212
1213
1214
1215
1216
1217
1218
1219
1220
1221
1222
1223
1224
1225
1226
1227
1228
1229
1230
1231
1232
1233
1234
1235
1236
1237
1238
1239
1240
1241
1242
1243
1244
1245
1246
1247
1248
1249
1250
1251
1252
1253
1254
1255
1256
1257
1258
1259
1260
1261
1262
1263
1264
1265
1266
1267
1268
1269
1270
1271
1272
1273
1274
1275
1276
1277
1278
1279
1280
1281
1282
1283
1284
1285
1286
1287
1288
1289
1290
1291
1292
1293
1294
1295
1296
1297
1298
1299
1300
1301
1302
1303
1304
1305
1306
1307
1308
1309
1310
1311
1312
1313
1314
1315
1316
1317
1318
1319
1320
1321
1322
1323
1324
1325
1326
1327
1328
1329
1330
1331
1332
1333
1334
1335
1336
1337
1338
1339
1340
1341
1342
1343
1344
1345
1346
1347
1348
1349
1350
1351
1352
1353
1354
1355
1356
1357
1358
1359
1360
1361
1362
1363
1364
1365
1366
1367
1368
1369
1370
1371
1372
1373
1374
1375
1376
1377
1378
1379
1380
1381
1382
1383
1384
1385
1386
1387
1388
1389
1390
1391
1392
1393
1394
1395
1396
1397
1398
1399
1400
1401
1402
1403
1404
1405
1406
1407
1408
1409
1410
1411
1412
1413
1414
1415
1416
1417
1418
1419
1420
1421
1422
1423
1424
1425
1426
1427
1428
1429
1430
1431
1432
1433
1434
1435
1436
1437
1438
1439
1440
1441
1442
1443
1444
1445
1446
1447
1448
1449
1450
1451
1452
1453
1454
1455
1456
1457
1458
1459
1460
1461
1462
1463
1464
1465
1466
1467
1468
1469
1470
1471
1472
1473
1474
1475
1476
1477
1478
1479
1480
1481
1482
1483
1484
1485
1486
1487
1488
1489
1490
1491
1492
1493
1494
1495
1496
1497
1498
1499
1500
1501
1502
1503
1504
1505
1506
1507
1508
1509
1510
1511
1512
1513
1514
1515
1516
1517
1518
1519
1520
1521
1522
1523
1524
1525
1526
1527
1528
1529
1530
1531
1532
1533
1534
1535
1536
1537
1538
1539
1540
1541
1542
1543
1544
1545
1546
1547
1548
1549
1550
1551
1552
1553
1554
1555
1556
1557
1558
1559
1560
1561
1562
1563
1564
1565
1566
1567
1568
1569
1570
1571
1572
1573
1574
1575
1576
1577
1578
1579
1580
1581
1582
1583
1584
1585
1586
1587
1588
1589
1590
1591
1592
1593
1594
1595
1596
1597
1598
1599
1600
1601
1602
1603
1604
1605
1606
1607
1608
1609
1610
1611
1612
1613
1614
1615
1616
1617
1618
1619
1620
1621
1622
1623
1624
1625
1626
1627
1628
1629
1630
1631
1632
1633
1634
1635
1636
1637
1638
1639
1640
1641
1642
1643
1644
1645
1646
1647
1648
1649
1650
1651
1652
1653
1654
1655
1656
1657
1658
1659
1660
1661
1662
1663
1664
1665
1666
1667
1668
1669
1670
1671
1672
1673
1674
1675
1676
1677
1678
1679
1680
1681
1682
1683
1684
1685
1686
1687
1688
1689
1690
1691
1692
1693
1694
1695
1696
1697
1698
1699
1700
1701
1702
1703
1704
1705
1706
1707
1708
1709
1710
1711
1712
1713
1714
1715
1716
1717
1718
1719
1720
1721
1722
1723
1724
1725
1726
1727
1728
1729
1730
1731
1732
1733
1734
1735
1736
1737
1738
1739
1740
1741
1742
1743
1744
1745
1746
1747
1748
1749
1750
1751
1752
1753
1754
1755
1756
1757
1758
1759
1760
1761
1762
1763
1764
1765
1766
1767
1768
1769
1770
1771
1772
1773
1774
1775
1776
1777
1778
1779
1780
1781
1782
1783
1784
1785
1786
1787
1788
1789
1790
1791
1792
1793
1794
1795
1796
1797
1798
1799
1800
1801
1802
1803
1804
1805
1806
1807
1808
1809
1810
1811
1812
1813
1814
1815
1816
1817
1818
1819
1820
1821
1822
1823
1824
1825
1826
1827
1828
1829
1830
1831
1832
1833
1834
1835
1836
1837
1838
1839
1840
1841
1842
1843
1844
1845
1846
1847
1848
1849
1850
1851
1852
1853
1854
1855
1856
1857
1858
1859
1860
1861
1862
1863
1864
1865
1866
1867
1868
1869
1870
1871
1872
1873
1874
1875
1876
1877
1878
1879
1880
1881
1882
1883
1884
1885
1886
1887
1888
1889
1890
1891
1892
1893
1894
1895
1896
1897
1898
1899
1900
1901
1902
1903
1904
1905
1906
1907
1908
1909
1910
1911
1912
1913
1914
1915
1916
1917
1918
1919
1920
1921
1922
1923
1924
1925
1926
1927
1928
1929
1930
1931
1932
1933
1934
1935
1936
1937
1938
1939
1940
1941
1942
1943
1944
1945
1946
1947
1948
1949
1950
1951
1952
1953
1954
1955
1956
1957
1958
1959
1960
1961
1962
1963
1964
1965
1966
1967
1968
1969
1970
1971
1972
1973
1974
1975
1976
1977
1978
1979
1980
1981
1982
1983
1984
1985
1986
1987
1988
1989
1990
1991
1992
1993
1994
1995
1996
1997
1998
1999
2000
2001
2002
2003
2004
2005
2006
2007
2008
2009
2010
2011
2012
2013
2014
2015
2016
2017
2018
2019
2020
2021
2022
2023
2024
2025
2026
2027
2028
2029
2030
2031
2032
2033
2034
2035
2036
2037
2038
2039
2040
2041
2042
2043
2044
2045
2046
2047
2048
2049
2050
2051
2052
2053
2054
2055
2056
2057
2058
2059
2060
2061
2062
2063
2064
2065
2066
2067
2068
2069
2070
2071
2072
2073
2074
2075
2076
2077
2078
2079
2080
2081
2082
2083
2084
2085
2086
2087
2088
2089
2090
2091
2092
2093
2094
2095
2096
2097
2098
2099
2100
2101
2102
2103
2104
2105
2106
2107
2108
2109
2110
2111
2112
2113
2114
2115
2116
2117
2118
2119
2120
2121
2122
2123
2124
2125
2126
2127
2128
2129
2130
2131
2132
2133
2134
2135
2136
2137
2138
2139
2140
2141
2142
2143
2144
2145
2146
2147
2148
2149
2150
2151
2152
2153
2154
2155
2156
2157
2158
2159
2160
2161
2162
2163
2164
2165
2166
2167
2168
2169
2170
2171
2172
2173
2174
2175
2176
2177
2178
2179
2180
2181
2182
2183
2184
2185
2186
2187
2188
2189
2190
2191
2192
2193
2194
2195
2196
2197
2198
2199
2200
2201
2202
2203
2204
2205
2206
2207
2208
2209
2210
2211
2212
2213
2214
2215
2216
2217
2218
2219
2220
2221
2222
2223
2224
2225
2226
2227
2228
2229
2230
2231
2232
2233
2234
2235
2236
2237
2238
2239
2240
2241
2242
2243
2244
2245
2246
2247
2248
2249
2250
2251
2252
2253
2254
2255
2256
2257
2258
2259
2260
2261
2262
2263
2264
2265
2266
2267
2268
2269
2270
2271
2272
2273
2274
2275
2276
2277
2278
2279
2280
2281
2282
2283
2284
2285
2286
2287
2288
2289
2290
2291
2292
2293
2294
2295
2296
2297
2298
2299
2300
2301
2302
2303
2304
2305
2306
2307
2308
2309
2310
2311
2312
2313
2314
2315
2316
2317
2318
2319
2320
2321
2322
2323
2324
2325
2326
2327
2328
2329
2330
2331
2332
2333
2334
2335
2336
2337
2338
2339
2340
2341
2342
2343
2344
2345
2346
2347
2348
2349
2350
2351
2352
2353
2354
2355
2356
2357
2358
2359
2360
2361
2362
2363
2364
2365
2366
2367
2368
2369
2370
2371
2372
2373
2374
2375
2376
2377
2378
2379
2380
2381
2382
2383
2384
2385
2386
2387
2388
2389
2390
2391
2392
2393
2394
2395
2396
2397
2398
2399
2400
2401
2402
2403
2404
2405
2406
2407
2408
2409
2410
2411
2412
2413
2414
2415
2416
2417
2418
2419
2420
2421
2422
2423
2424
2425
2426
2427
2428
2429
2430
2431
2432
2433
2434
2435
2436
2437
2438
2439
2440
2441
2442
2443
2444
2445
2446
2447
2448
2449
2450
2451
2452
2453
2454
2455
2456
2457
2458
2459
2460
2461
2462
2463
2464
2465
2466
2467
2468
2469
2470
2471
2472
2473
2474
2475
2476
2477
2478
2479
2480
2481
2482
2483
2484
2485
2486
2487
2488
2489
2490
2491
2492
2493
2494
2495
2496
2497
2498
2499
2500
2501
2502
2503
2504
2505
2506
2507
2508
2509
2510
2511
2512
2513
2514
2515
2516
2517
2518
2519
2520
2521
2522
2523
2524
2525
2526
2527
2528
2529
2530
2531
2532
2533
2534
2535
2536
2537
2538
2539
2540
2541
2542
2543
2544
2545
2546
2547
2548
2549
2550
2551
2552
2553
2554
2555
2556
2557
2558
2559
2560
2561
2562
2563
2564
2565
2566
2567
2568
2569
2570
2571
2572
2573
2574
2575
2576
2577
2578
2579
2580
2581
2582
2583
2584
2585
2586
2587
2588
2589
2590
2591
2592
2593
2594
2595
2596
2597
2598
2599
2600
2601
2602
2603
2604
2605
2606
2607
2608
2609
2610
2611
2612
2613
2614
2615
2616
2617
2618
2619
2620
2621
2622
2623
2624
2625
2626
2627
2628
2629
2630
2631
2632
2633
2634
2635
2636
2637
2638
2639
2640
2641
2642
2643
2644
2645
2646
2647
2648
2649
2650
2651
2652
2653
2654
2655
2656
2657
2658
2659
2660
2661
2662
2663
2664
2665
2666
2667
2668
2669
2670
2671
2672
2673
2674
2675
2676
2677
2678
2679
2680
2681
2682
2683
2684
2685
2686
2687
2688
2689
2690
2691
2692
2693
2694
2695
2696
2697
2698
2699
2700
2701
2702
2703
2704
2705
2706
2707
2708
2709
2710
2711
2712
2713
2714
2715
2716
2717
2718
2719
2720
2721
2722
2723
2724
2725
2726
2727
2728
2729
2730
2731
2732
2733
2734
2735
2736
2737
2738
2739
2740
2741
2742
2743
2744
2745
2746
2747
2748
2749
2750
2751
2752
2753
2754
2755
2756
2757
2758
2759
2760
2761
2762
2763
2764
2765
2766
2767
2768
2769
2770
2771
2772
2773
2774
2775
2776
2777
2778
2779
2780
2781
2782
2783
2784
2785
2786
2787
2788
2789
2790
2791
2792
2793
2794
2795
2796
2797
2798
2799
2800
2801
2802
2803
2804
2805
2806
2807
2808
2809
2810
2811
2812
2813
2814
2815
2816
2817
2818
2819
2820
2821
2822
2823
2824
2825
2826
2827
2828
2829
2830
2831
2832
2833
2834
2835
2836
2837
2838
2839
2840
2841
2842
2843
2844
2845
2846
2847
2848
2849
2850
2851
2852
2853
2854
2855
2856
2857
2858
2859
2860
2861
2862
2863
2864
2865
2866
2867
2868
2869
2870
2871
2872
2873
2874
2875
2876
2877
2878
2879
2880
2881
2882
2883
2884
2885
2886
2887
2888
2889
2890
2891
2892
2893
2894
2895
2896
2897
2898
2899
2900
2901
2902
2903
2904
2905
2906
2907
2908
2909
2910
2911
2912
2913
2914
2915
2916
2917
2918
2919
2920
2921
2922
2923
2924
2925
2926
2927
2928
2929
2930
2931
2932
2933
2934
2935
2936
2937
2938
2939
2940
2941
2942
2943
2944
2945
2946
2947
2948
2949
2950
2951
2952
2953
2954
2955
2956
2957
2958
2959
2960
2961
2962
2963
2964
2965
2966
2967
2968
2969
2970
2971
2972
2973
2974
2975
2976
2977
2978
2979
2980
2981
2982
2983
2984
2985
2986
2987
2988
2989
2990
2991
2992
2993
2994
2995
2996
2997
2998
2999
3000
3001
3002
3003
3004
3005
3006
3007
3008
3009
3010
3011
3012
3013
3014
3015
3016
3017
3018
3019
3020
3021
3022
3023
3024
3025
3026
3027
3028
3029
3030
3031
3032
3033
3034
3035
3036
3037
3038
3039
3040
3041
3042
3043
3044
3045
3046
3047
3048
3049
3050
3051
3052
3053
3054
3055
3056
3057
3058
3059
3060
3061
3062
3063
3064
3065
3066
3067
3068
3069
3070
3071
3072
3073
3074
3075
3076
3077
3078
3079
3080
3081
3082
3083
3084
3085
3086
3087
3088
3089
3090
3091
3092
3093
3094
3095
3096
3097
3098
3099
3100
3101
3102
3103
3104
3105
3106
3107
3108
3109
3110
3111
3112
3113
3114
3115
3116
3117
3118
3119
3120
3121
3122
3123
3124
3125
3126
3127
3128
3129
3130
3131
3132
3133
3134
3135
3136
3137
3138
3139
3140
3141
3142
3143
3144
3145
3146
3147
3148
3149
3150
3151
3152
3153
3154
3155
3156
3157
3158
3159
3160
3161
3162
3163
3164
3165
3166
3167
3168
3169
3170
3171
3172
3173
3174
3175
3176
3177
3178
3179
3180
3181
3182
3183
3184
3185
3186
3187
3188
3189
3190
3191
3192
3193
3194
3195
3196
3197
3198
3199
3200
3201
3202
3203
3204
3205
3206
3207
3208
3209
3210
3211
3212
3213
3214
3215
3216
3217
3218
3219
3220
3221
3222
3223
3224
3225
3226
3227
3228
3229
3230
3231
3232
3233
3234
3235
3236
3237
3238
3239
3240
3241
3242
3243
3244
3245
3246
3247
3248
3249
3250
3251
3252
3253
3254
3255
3256
3257
3258
3259
3260
3261
3262
3263
3264
3265
3266
3267
3268
3269
3270
3271
3272
3273
3274
3275
3276
3277
3278
3279
3280
3281
3282
3283
3284
3285
3286
3287
3288
3289
3290
3291
3292
3293
3294
3295
3296
3297
3298
3299
3300
3301
3302
3303
3304
3305
3306
3307
3308
3309
3310
3311
3312
3313
3314
3315
3316
3317
3318
3319
3320
3321
3322
3323
3324
3325
3326
3327
3328
3329
3330
3331
3332
3333
3334
3335
3336
3337
3338
3339
3340
3341
3342
3343
3344
3345
3346
3347
3348
3349
3350
3351
3352
3353
3354
3355
3356
3357
3358
3359
3360
3361
3362
3363
3364
3365
3366
3367
3368
3369
3370
3371
3372
3373
3374
3375
3376
3377
3378
3379
3380
3381
3382
3383
3384
3385
3386
3387
3388
3389
3390
3391
3392
3393
3394
3395
3396
3397
3398
3399
3400
3401
3402
3403
3404
3405
3406
3407
3408
3409
3410
3411
3412
3413
3414
3415
3416
3417
3418
3419
3420
3421
3422
3423
3424
3425
3426
3427
3428
3429
3430
3431
3432
3433
3434
3435
3436
3437
3438
3439
3440
3441
3442
3443
3444
3445
3446
3447
3448
3449
3450
3451
3452
3453
3454
3455
3456
3457
3458
3459
3460
3461
3462
3463
3464
3465
3466
3467
3468
3469
3470
3471
3472
3473
3474
3475
3476
3477
3478
3479
3480
3481
3482
3483
3484
3485
3486
3487
3488
3489
3490
3491
3492
3493
3494
3495
3496
3497
3498
3499
3500
3501
3502
3503
3504
3505
3506
3507
3508
3509
3510
3511
3512
3513
3514
3515
3516
3517
3518
3519
3520
3521
3522
3523
3524
3525
3526
3527
3528
3529
3530
3531
3532
3533
3534
3535
3536
3537
3538
3539
3540
3541
3542
3543
3544
3545
3546
3547
3548
3549
3550
3551
3552
3553
3554
3555
3556
3557
3558
3559
3560
3561
3562
3563
3564
3565
3566
3567
3568
3569
3570
3571
3572
3573
3574
3575
3576
3577
3578
3579
3580
3581
3582
3583
3584
3585
3586
3587
3588
3589
3590
3591
3592
3593
3594
3595
3596
3597
3598
3599
3600
3601
3602
3603
3604
3605
3606
3607
3608
3609
3610
3611
3612
3613
3614
3615
3616
3617
3618
3619
3620
3621
3622
3623
3624
3625
3626
3627
3628
3629
3630
3631
3632
3633
3634
3635
3636
3637
3638
3639
3640
3641
3642
3643
3644
3645
3646
3647
3648
3649
3650
3651
3652
3653
3654
3655
3656
3657
3658
3659
3660
3661
3662
3663
3664
3665
3666
3667
3668
3669
3670
3671
3672
3673
3674
3675
3676
3677
3678
3679
3680
3681
3682
3683
3684
3685
3686
3687
3688
3689
3690
3691
3692
3693
3694
3695
3696
3697
3698
3699
3700
3701
3702
3703
3704
3705
3706
3707
3708
3709
3710
3711
3712
3713
3714
3715
3716
3717
3718
3719
3720
3721
3722
3723
3724
3725
3726
3727
3728
3729
3730
3731
3732
3733
3734
3735
3736
3737
3738
3739
3740
3741
3742
3743
3744
3745
3746
3747
3748
3749
3750
3751
3752
3753
3754
3755
3756
3757
3758
3759
3760
3761
3762
3763
3764
3765
3766
3767
3768
3769
3770
3771
3772
3773
3774
3775
3776
3777
3778
3779
3780
3781
3782
3783
3784
3785
3786
3787
3788
3789
3790
3791
3792
3793
3794
3795
3796
3797
3798
3799
3800
3801
3802
3803
3804
3805
3806
3807
3808
3809
3810
3811
3812
3813
3814
3815
3816
3817
3818
3819
3820
3821
3822
3823
3824
3825
3826
3827
3828
3829
3830
3831
3832
3833
3834
3835
3836
3837
3838
3839
3840
3841
3842
3843
3844
3845
3846
3847
3848
3849
3850
3851
3852
3853
3854
3855
3856
3857
3858
3859
3860
3861
3862
3863
3864
3865
3866
3867
3868
3869
3870
3871
3872
3873
3874
3875
3876
3877
3878
3879
3880
3881
3882
3883
3884
3885
3886
3887
3888
3889
3890
3891
3892
3893
3894
3895
3896
3897
3898
3899
3900
3901
3902
3903
3904
3905
3906
3907
3908
3909
3910
3911
3912
3913
3914
3915
3916
3917
3918
3919
3920
3921
3922
3923
3924
3925
3926
3927
3928
3929
3930
3931
3932
3933
3934
3935
3936
3937
3938
3939
3940
3941
3942
3943
3944
3945
3946
3947
3948
3949
3950
3951
3952
3953
3954
3955
3956
3957
3958
3959
3960
3961
3962
3963
3964
3965
3966
3967
3968
3969
3970
3971
3972
3973
3974
3975
3976
3977
3978
3979
3980
3981
3982
3983
3984
3985
3986
3987
3988
3989
3990
3991
3992
3993
3994
3995
3996
3997
3998
3999
4000
4001
4002
4003
4004
4005
4006
4007
4008
4009
4010
4011
4012
4013
4014
4015
4016
4017
4018
4019
4020
4021
4022
4023
4024
4025
4026
4027
4028
4029
4030
4031
4032
4033
4034
4035
4036
4037
4038
4039
4040
4041
4042
4043
4044
4045
4046
4047
4048
4049
4050
4051
4052
4053
4054
4055
4056
4057
4058
4059
4060
4061
4062
4063
4064
4065
4066
4067
4068
4069
4070
4071
4072
4073
4074
4075
4076
4077
4078
4079
4080
4081
4082
4083
4084
4085
4086
4087
4088
4089
4090
4091
4092
4093
4094
4095
4096
4097
4098
4099
4100
4101
4102
4103
4104
4105
4106
4107
4108
4109
4110
4111
4112
4113
4114
4115
4116
4117
4118
4119
4120
4121
4122
4123
4124
4125
4126
4127
4128
4129
4130
4131
4132
4133
4134
4135
4136
4137
4138
4139
4140
4141
4142
4143
4144
4145
4146
4147
4148
4149
4150
4151
4152
4153
4154
4155
4156
4157
4158
4159
4160
4161
4162
4163
4164
4165
4166
4167
4168
4169
4170
4171
4172
4173
4174
4175
4176
4177
4178
4179
4180
4181
4182
4183
4184
4185
4186
4187
4188
4189
4190
4191
4192
4193
4194
4195
4196
4197
4198
4199
4200
4201
4202
4203
4204
4205
4206
4207
4208
4209
4210
4211
4212
4213
4214
4215
4216
4217
4218
4219
4220
4221
4222
4223
4224
4225
4226
4227
4228
4229
4230
4231
4232
4233
4234
4235
4236
4237
4238
4239
4240
4241
4242
4243
4244
4245
4246
4247
4248
4249
4250
4251
4252
4253
4254
4255
4256
4257
4258
4259
4260
4261
4262
4263
4264
4265
4266
4267
4268
4269
4270
4271
4272
4273
4274
4275
4276
4277
4278
4279
4280
4281
4282
4283
4284
4285
4286
4287
4288
4289
4290
4291
4292
4293
4294
4295
4296
4297
4298
4299
4300
4301
4302
4303
4304
4305
4306
4307
4308
4309
4310
4311
4312
4313
4314
4315
4316
4317
4318
4319
4320
4321
4322
4323
4324
4325
4326
4327
4328
4329
4330
4331
4332
4333
4334
4335
4336
4337
4338
4339
4340
4341
4342
4343
4344
4345
4346
4347
4348
4349
4350
4351
4352
4353
4354
4355
4356
4357
4358
4359
4360
4361
4362
4363
4364
4365
4366
4367
4368
4369
4370
4371
4372
4373
4374
4375
4376
4377
4378
4379
4380
4381
4382
4383
4384
4385
4386
4387
4388
4389
4390
4391
4392
4393
4394
4395
4396
4397
4398
4399
4400
4401
4402
4403
4404
4405
4406
4407
4408
4409
4410
4411
4412
4413
4414
4415
4416
4417
4418
4419
4420
4421
4422
4423
4424
4425
4426
4427
4428
4429
4430
4431
4432
4433
4434
4435
4436
4437
4438
4439
4440
4441
4442
4443
4444
4445
4446
4447
4448
4449
4450
4451
4452
4453
4454
4455
4456
4457
4458
4459
4460
4461
4462
4463
4464
4465
4466
4467
4468
4469
4470
4471
4472
4473
4474
4475
4476
4477
4478
4479
4480
4481
4482
4483
4484
4485
4486
4487
4488
4489
4490
4491
4492
4493
4494
4495
4496
4497
4498
4499
4500
4501
4502
4503
4504
4505
4506
4507
4508
4509
4510
4511
4512
4513
4514
4515
4516
4517
4518
4519
4520
4521
4522
4523
4524
4525
4526
4527
4528
4529
4530
4531
4532
4533
4534
4535
4536
4537
4538
4539
4540
4541
4542
4543
4544
4545
4546
4547
4548
4549
4550
4551
4552
4553
4554
4555
4556
4557
4558
4559
4560
4561
4562
4563
4564
4565
4566
4567
4568
4569
4570
4571
4572
4573
4574
4575
4576
4577
4578
4579
4580
4581
4582
4583
4584
4585
4586
4587
4588
4589
4590
4591
4592
4593
4594
4595
4596
4597
4598
4599
4600
4601
4602
4603
4604
4605
4606
4607
4608
4609
4610
4611
4612
4613
4614
4615
4616
4617
4618
4619
4620
4621
4622
4623
4624
4625
4626
4627
4628
4629
4630
4631
4632
4633
4634
4635
4636
4637
4638
4639
4640
4641
4642
4643
4644
4645
4646
4647
4648
4649
4650
4651
4652
4653
4654
4655
4656
4657
4658
4659
4660
4661
4662
4663
4664
4665
4666
4667
4668
4669
4670
4671
4672
4673
4674
4675
4676
4677
4678
4679
4680
4681
4682
4683
4684
4685
4686
4687
4688
4689
4690
4691
4692
4693
4694
4695
4696
4697
4698
4699
4700
4701
4702
4703
4704
4705
4706
4707
4708
4709
4710
4711
4712
4713
4714
4715
4716
4717
4718
4719
4720
4721
4722
4723
4724
4725
4726
4727
4728
4729
4730
4731
4732
4733
4734
4735
4736
4737
4738
4739
4740
4741
4742
4743
4744
4745
4746
4747
4748
4749
4750
4751
4752
4753
4754
4755
4756
4757
4758
4759
4760
4761
4762
4763
4764
4765
4766
4767
4768
4769
4770
4771
4772
4773
4774
4775
4776
4777
4778
4779
4780
4781
4782
4783
4784
4785
4786
4787
4788
4789
4790
4791
4792
4793
4794
4795
4796
4797
4798
4799
4800
4801
4802
4803
4804
4805
4806
4807
4808
4809
4810
4811
4812
4813
4814
4815
4816
4817
4818
4819
4820
4821
4822
4823
4824
4825
4826
4827
4828
4829
4830
4831
4832
4833
4834
4835
4836
4837
4838
4839
4840
4841
4842
4843
4844
4845
4846
4847
4848
4849
4850
4851
4852
4853
4854
4855
4856
4857
4858
4859
4860
4861
4862
4863
4864
4865
4866
4867
4868
4869
4870
4871
4872
4873
4874
4875
4876
4877
4878
4879
4880
4881
4882
4883
4884
4885
4886
4887
4888
4889
4890
4891
4892
4893
4894
4895
4896
4897
4898
4899
4900
4901
4902
4903
4904
4905
4906
4907
4908
4909
4910
4911
4912
4913
4914
4915
4916
4917
4918
4919
4920
4921
4922
4923
4924
4925
4926
4927
4928
4929
4930
4931
4932
4933
4934
4935
4936
4937
4938
4939
4940
4941
4942
4943
4944
4945
4946
4947
4948
4949
4950
4951
4952
4953
4954
4955
4956
4957
4958
4959
4960
4961
4962
4963
4964
4965
4966
4967
4968
4969
4970
4971
4972
4973
4974
4975
4976
4977
4978
4979
4980
4981
4982
4983
4984
4985
4986
4987
4988
4989
4990
4991
4992
4993
4994
4995
4996
4997
4998
4999
5000
5001
5002
5003
5004
5005
5006
5007
5008
5009
5010
5011
5012
5013
5014
5015
5016
5017
5018
5019
5020
5021
5022
5023
5024
5025
5026
5027
5028
5029
5030
5031
5032
5033
5034
5035
5036
5037
5038
5039
5040
5041
5042
5043
5044
5045
5046
5047
5048
5049
5050
5051
5052
5053
5054
5055
5056
5057
5058
5059
5060
5061
5062
5063
5064
5065
5066
5067
5068
5069
5070
5071
5072
5073
5074
5075
5076
5077
5078
5079
5080
5081
5082
5083
5084
5085
5086
5087
5088
5089
5090
5091
5092
5093
5094
5095
5096
5097
5098
5099
5100
5101
5102
5103
5104
5105
5106
5107
5108
5109
5110
5111
5112
5113
5114
5115
5116
5117
5118
5119
5120
5121
5122
5123
5124
5125
5126
5127
5128
5129
5130
5131
5132
5133
5134
5135
5136
5137
5138
5139
5140
5141
5142
5143
5144
5145
5146
5147
5148
5149
5150
5151
5152
5153
5154
5155
5156
5157
5158
5159
5160
5161
5162
5163
5164
5165
5166
5167
5168
5169
5170
5171
5172
5173
5174
5175
5176
5177
5178
5179
5180
5181
5182
5183
5184
5185
5186
5187
5188
5189
5190
5191
5192
5193
5194
5195
5196
5197
5198
5199
5200
5201
5202
5203
5204
5205
5206
5207
5208
5209
5210
5211
5212
5213
5214
5215
5216
5217
5218
5219
5220
5221
5222
5223
5224
5225
5226
5227
5228
5229
5230
5231
5232
5233
5234
5235
5236
5237
5238
5239
5240
5241
5242
5243
5244
5245
5246
5247
5248
5249
5250
5251
5252
5253
5254
5255
5256
5257
5258
5259
5260
5261
5262
5263
5264
5265
5266
5267
5268
5269
5270
5271
5272
5273
5274
5275
5276
5277
5278
5279
5280
5281
5282
5283
5284
5285
5286
5287
5288
5289
5290
5291
5292
5293
5294
5295
5296
5297
5298
5299
5300
5301
5302
5303
5304
5305
5306
5307
5308
5309
5310
5311
5312
5313
5314
5315
5316
5317
5318
5319
5320
5321
5322
5323
5324
5325
5326
5327
5328
5329
5330
5331
5332
5333
5334
5335
5336
5337
5338
5339
5340
5341
5342
5343
5344
5345
5346
5347
5348
5349
5350
5351
5352
5353
5354
5355
5356
5357
5358
5359
5360
5361
5362
5363
5364
5365
5366
5367
5368
5369
5370
5371
5372
5373
5374
5375
5376
5377
5378
5379
5380
5381
5382
5383
5384
5385
5386
5387
5388
5389
5390
5391
5392
5393
5394
5395
5396
5397
5398
5399
5400
5401
5402
5403
5404
5405
5406
5407
5408
5409
5410
5411
5412
5413
5414
5415
5416
5417
5418
5419
5420
5421
5422
5423
5424
5425
5426
5427
5428
5429
5430
5431
5432
5433
5434
5435
5436
5437
5438
5439
5440
5441
5442
5443
5444
5445
5446
5447
5448
5449
5450
5451
5452
5453
5454
5455
5456
5457
5458
5459
5460
5461
5462
5463
5464
5465
5466
5467
5468
5469
5470
5471
5472
5473
5474
5475
5476
5477
5478
5479
5480
5481
5482
5483
5484
5485
5486
5487
5488
5489
5490
5491
5492
5493
5494
5495
5496
5497
5498
5499
5500
5501
5502
5503
5504
5505
5506
5507
5508
5509
5510
5511
5512
5513
5514
5515
5516
5517
5518
5519
5520
5521
5522
5523
5524
5525
5526
5527
5528
5529
5530
5531
5532
5533
5534
5535
5536
5537
5538
5539
5540
5541
5542
5543
5544
5545
5546
5547
5548
5549
5550
5551
5552
5553
5554
5555
5556
5557
5558
5559
5560
5561
5562
5563
5564
5565
5566
5567
5568
5569
5570
5571
5572
5573
5574
5575
5576
5577
5578
5579
5580
5581
5582
5583
5584
5585
5586
5587
5588
5589
5590
5591
5592
5593
5594
5595
5596
5597
5598
5599
5600
5601
5602
5603
5604
5605
5606
5607
5608
5609
5610
5611
5612
5613
5614
5615
5616
5617
5618
5619
5620
5621
5622
5623
5624
5625
5626
5627
5628
5629
5630
5631
5632
5633
5634
5635
5636
5637
5638
5639
5640
5641
5642
5643
5644
5645
5646
5647
5648
5649
5650
5651
5652
5653
5654
5655
5656
5657
5658
5659
5660
5661
5662
5663
5664
5665
5666
5667
5668
5669
5670
5671
5672
5673
5674
5675
5676
5677
5678
5679
5680
5681
5682
5683
5684
5685
5686
5687
5688
5689
5690
5691
5692
5693
5694
5695
5696
5697
5698
5699
5700
5701
5702
5703
5704
5705
5706
5707
5708
5709
5710
5711
5712
5713
5714
5715
5716
5717
5718
5719
5720
5721
5722
5723
5724
5725
5726
5727
5728
5729
5730
5731
5732
5733
5734
5735
5736
5737
5738
5739
5740
5741
5742
5743
5744
5745
5746
5747
5748
5749
5750
5751
5752
5753
5754
5755
5756
5757
5758
5759
5760
5761
5762
5763
5764
5765
5766
5767
5768
5769
5770
5771
5772
5773
5774
5775
5776
5777
5778
5779
5780
5781
5782
5783
5784
5785
5786
5787
5788
5789
5790
5791
5792
5793
5794
5795
5796
5797
5798
5799
5800
5801
5802
5803
5804
5805
5806
5807
5808
5809
5810
5811
5812
5813
5814
5815
5816
5817
5818
5819
5820
5821
5822
5823
5824
5825
5826
5827
5828
5829
5830
5831
5832
5833
5834
5835
5836
5837
5838
5839
5840
5841
5842
5843
5844
5845
5846
5847
5848
5849
5850
5851
5852
5853
5854
5855
5856
5857
5858
5859
5860
5861
5862
5863
5864
5865
5866
5867
5868
5869
5870
5871
5872
5873
5874
5875
5876
5877
5878
5879
5880
5881
5882
5883
5884
5885
5886
5887
5888
5889
5890
5891
5892
5893
5894
5895
5896
5897
5898
5899
5900
5901
5902
5903
5904
5905
5906
5907
5908
5909
5910
5911
5912
5913
5914
5915
5916
5917
5918
5919
5920
5921
5922
5923
5924
5925
5926
5927
5928
5929
5930
5931
5932
5933
5934
5935
5936
5937
5938
5939
5940
5941
5942
5943
5944
5945
5946
5947
5948
5949
5950
5951
5952
5953
5954
5955
5956
5957
5958
5959
5960
5961
5962
5963
5964
5965
5966
5967
5968
5969
5970
5971
5972
5973
5974
5975
5976
5977
5978
5979
5980
5981
5982
5983
5984
5985
5986
5987
5988
5989
5990
5991
5992
5993
5994
5995
5996
5997
5998
5999
6000
6001
6002
6003
6004
6005
6006
6007
6008
6009
6010
6011
6012
6013
6014
6015
6016
6017
6018
6019
6020
6021
6022
6023
6024
6025
6026
6027
6028
6029
6030
6031
6032
6033
6034
6035
6036
6037
6038
6039
6040
6041
6042
6043
6044
6045
6046
6047
6048
6049
6050
6051
6052
6053
6054
6055
6056
6057
6058
6059
6060
6061
6062
6063
6064
6065
6066
6067
6068
6069
6070
6071
6072
6073
6074
6075
6076
6077
6078
6079
6080
6081
6082
6083
6084
6085
6086
6087
6088
6089
6090
6091
6092
6093
6094
6095
6096
6097
6098
6099
6100
6101
6102
6103
6104
6105
6106
6107
6108
6109
6110
6111
6112
6113
6114
6115
6116
6117
6118
6119
6120
6121
6122
6123
6124
6125
6126
6127
6128
6129
6130
6131
6132
6133
6134
6135
6136
6137
6138
6139
6140
6141
6142
6143
6144
6145
6146
6147
6148
6149
6150
6151
6152
6153
6154
6155
6156
6157
6158
6159
6160
6161
6162
6163
6164
6165
6166
6167
6168
6169
6170
6171
6172
6173
6174
6175
6176
6177
6178
6179
6180
6181
6182
6183
6184
6185
6186
6187
6188
6189
6190
6191
6192
6193
6194
6195
6196
6197
6198
6199
6200
6201
6202
6203
6204
6205
6206
6207
6208
6209
6210
6211
6212
6213
6214
6215
6216
6217
6218
6219
6220
6221
6222
6223
6224
6225
6226
6227
6228
6229
6230
6231
6232
6233
6234
6235
6236
6237
6238
6239
6240
6241
6242
6243
6244
6245
6246
6247
6248
6249
6250
6251
6252
6253
6254
6255
6256
6257
6258
6259
6260
6261
6262
6263
6264
6265
6266
6267
6268
6269
6270
6271
6272
6273
6274
6275
6276
6277
6278
6279
6280
6281
6282
6283
6284
6285
6286
6287
6288
6289
6290
6291
6292
6293
6294
6295
6296
6297
6298
6299
6300
6301
6302
6303
6304
6305
6306
6307
6308
6309
6310
6311
6312
6313
6314
6315
6316
6317
6318
6319
6320
6321
6322
6323
6324
6325
6326
6327
6328
6329
6330
6331
6332
6333
6334
6335
6336
6337
6338
6339
6340
6341
6342
6343
6344
6345
6346
6347
6348
6349
6350
6351
6352
6353
6354
6355
6356
6357
6358
6359
6360
6361
6362
6363
6364
6365
6366
6367
6368
6369
6370
6371
6372
6373
6374
6375
6376
6377
6378
6379
6380
6381
6382
6383
6384
6385
6386
6387
6388
6389
6390
6391
6392
6393
6394
6395
6396
6397
6398
6399
6400
6401
6402
6403
6404
6405
6406
6407
6408
6409
6410
6411
6412
6413
6414
6415
6416
6417
6418
6419
6420
6421
6422
6423
6424
6425
6426
6427
6428
6429
6430
6431
6432
6433
6434
6435
6436
6437
6438
6439
6440
6441
6442
6443
6444
6445
6446
6447
6448
6449
6450
6451
6452
6453
6454
6455
6456
6457
6458
6459
6460
6461
6462
6463
6464
6465
6466
6467
6468
6469
6470
6471
6472
6473
6474
6475
6476
6477
6478
6479
6480
6481
6482
6483
6484
6485
6486
6487
6488
6489
6490
6491
6492
6493
6494
6495
6496
6497
6498
6499
6500
6501
6502
6503
6504
6505
6506
6507
6508
6509
6510
6511
6512
6513
6514
6515
6516
6517
6518
6519
6520
6521
6522
6523
6524
6525
6526
6527
6528
6529
6530
6531
6532
6533
6534
6535
6536
6537
6538
6539
6540
6541
6542
6543
6544
6545
6546
6547
6548
6549
6550
6551
6552
6553
6554
6555
6556
6557
6558
6559
6560
6561
6562
6563
6564
6565
6566
6567
6568
6569
6570
6571
6572
6573
6574
6575
6576
6577
6578
6579
6580
6581
6582
6583
6584
6585
6586
6587
6588
6589
6590
6591
6592
6593
6594
6595
6596
6597
6598
6599
6600
6601
6602
6603
6604
6605
6606
6607
6608
6609
6610
6611
6612
6613
6614
6615
6616
6617
6618
6619
6620
6621
6622
6623
6624
6625
6626
6627
6628
6629
6630
6631
6632
6633
6634
6635
6636
6637
6638
6639
6640
6641
6642
6643
6644
6645
6646
6647
6648
6649
6650
6651
6652
6653
6654
6655
6656
6657
6658
6659
6660
6661
6662
6663
6664
6665
6666
6667
6668
6669
6670
6671
6672
6673
6674
6675
6676
6677
6678
6679
6680
6681
6682
6683
6684
6685
6686
6687
6688
6689
6690
6691
6692
6693
6694
6695
6696
6697
6698
6699
6700
6701
6702
6703
6704
6705
6706
6707
6708
6709
6710
6711
6712
6713
6714
6715
6716
6717
6718
6719
6720
6721
6722
6723
6724
6725
6726
6727
6728
6729
6730
6731
6732
6733
6734
6735
6736
6737
6738
6739
6740
6741
6742
6743
6744
6745
6746
6747
6748
6749
6750
6751
6752
6753
6754
6755
6756
6757
6758
6759
6760
6761
6762
6763
6764
6765
6766
6767
6768
6769
6770
6771
6772
6773
6774
6775
6776
6777
6778
6779
6780
6781
6782
6783
6784
6785
6786
6787
6788
6789
6790
6791
6792
6793
6794
6795
6796
6797
6798
6799
6800
6801
6802
6803
6804
6805
6806
6807
6808
6809
6810
6811
6812
6813
6814
6815
6816
6817
6818
6819
6820
6821
6822
6823
6824
6825
6826
6827
6828
6829
6830
6831
6832
6833
6834
6835
6836
6837
6838
6839
6840
6841
6842
6843
6844
6845
6846
6847
6848
6849
6850
6851
6852
6853
6854
6855
6856
6857
6858
6859
6860
6861
6862
6863
6864
6865
6866
6867
6868
6869
6870
6871
6872
6873
6874
6875
6876
6877
6878
6879
6880
6881
6882
6883
6884
6885
6886
6887
6888
6889
6890
6891
6892
6893
6894
6895
6896
6897
6898
6899
6900
6901
6902
6903
6904
6905
6906
6907
6908
6909
6910
6911
6912
6913
6914
6915
6916
6917
6918
6919
6920
6921
6922
6923
6924
6925
6926
6927
6928
6929
6930
6931
6932
6933
6934
6935
6936
6937
6938
6939
6940
6941
6942
6943
6944
6945
6946
6947
6948
6949
6950
6951
6952
6953
6954
6955
6956
6957
6958
6959
6960
6961
6962
6963
6964
6965
6966
6967
6968
6969
6970
6971
6972
6973
6974
6975
6976
6977
6978
6979
6980
6981
6982
6983
6984
6985
6986
6987
6988
6989
6990
6991
6992
6993
6994
6995
6996
6997
6998
6999
7000
7001
7002
7003
7004
7005
7006
7007
7008
7009
7010
7011
7012
7013
7014
7015
7016
7017
7018
7019
7020
7021
7022
7023
7024
7025
7026
7027
7028
7029
7030
7031
7032
7033
7034
7035
7036
7037
7038
7039
7040
7041
7042
7043
7044
7045
7046
7047
7048
7049
7050
7051
7052
7053
7054
7055
7056
7057
7058
7059
7060
7061
7062
7063
7064
7065
7066
7067
7068
7069
7070
7071
7072
7073
7074
7075
7076
7077
7078
7079
7080
7081
7082
7083
7084
7085
7086
7087
7088
7089
7090
7091
7092
7093
7094
7095
7096
7097
7098
7099
7100
7101
7102
7103
7104
7105
7106
7107
7108
7109
7110
7111
7112
7113
7114
7115
7116
7117
7118
7119
7120
7121
7122
7123
7124
7125
7126
7127
7128
7129
7130
7131
7132
7133
7134
7135
7136
7137
7138
7139
7140
7141
7142
7143
7144
7145
7146
7147
7148
7149
7150
7151
7152
7153
7154
7155
7156
7157
7158
7159
7160
7161
7162
7163
7164
7165
7166
7167
7168
7169
7170
7171
7172
7173
7174
7175
7176
7177
7178
7179
7180
7181
7182
7183
7184
7185
7186
7187
7188
7189
7190
7191
7192
7193
7194
7195
7196
7197
7198
7199
7200
7201
7202
7203
7204
7205
7206
7207
7208
7209
7210
7211
7212
7213
7214
7215
7216
7217
7218
7219
7220
7221
7222
7223
7224
7225
7226
7227
7228
7229
7230
7231
7232
7233
7234
7235
7236
7237
7238
7239
7240
7241
7242
7243
7244
7245
7246
7247
7248
7249
7250
7251
7252
7253
7254
7255
7256
7257
7258
7259
7260
7261
7262
7263
7264
7265
7266
7267
7268
7269
7270
7271
7272
7273
7274
7275
7276
7277
7278
7279
7280
7281
7282
7283
7284
7285
7286
7287
7288
7289
7290
7291
7292
7293
7294
7295
7296
7297
7298
7299
7300
7301
7302
7303
7304
7305
7306
7307
7308
7309
7310
7311
7312
7313
7314
7315
7316
7317
7318
7319
7320
7321
7322
7323
7324
7325
7326
7327
7328
7329
7330
7331
7332
7333
7334
7335
7336
7337
7338
7339
7340
7341
7342
7343
7344
7345
7346
7347
7348
7349
7350
7351
7352
7353
7354
7355
7356
7357
7358
7359
7360
7361
7362
7363
7364
7365
7366
7367
7368
7369
7370
7371
7372
7373
7374
7375
7376
7377
7378
7379
7380
7381
7382
7383
7384
7385
7386
7387
7388
7389
7390
7391
7392
7393
7394
7395
7396
7397
7398
7399
7400
7401
7402
7403
7404
7405
7406
7407
7408
7409
7410
7411
7412
7413
7414
7415
7416
7417
7418
7419
7420
7421
7422
7423
7424
7425
7426
7427
7428
7429
7430
7431
7432
7433
7434
7435
7436
7437
7438
7439
7440
7441
7442
7443
7444
7445
7446
7447
7448
7449
7450
7451
7452
7453
7454
7455
7456
7457
7458
7459
7460
7461
7462
7463
7464
7465
7466
7467
7468
7469
7470
7471
7472
7473
7474
7475
7476
7477
7478
7479
7480
7481
7482
7483
7484
7485
7486
7487
7488
7489
7490
7491
7492
7493
7494
7495
7496
7497
7498
7499
7500
7501
7502
7503
7504
7505
7506
7507
7508
7509
7510
7511
7512
7513
7514
7515
7516
7517
7518
7519
7520
7521
7522
7523
7524
7525
7526
7527
7528
7529
7530
7531
7532
7533
7534
7535
7536
7537
7538
7539
7540
7541
7542
7543
7544
7545
7546
7547
7548
7549
7550
7551
7552
7553
7554
7555
7556
7557
7558
7559
7560
7561
7562
7563
7564
7565
7566
7567
7568
7569
7570
7571
7572
7573
7574
7575
7576
7577
7578
7579
7580
7581
7582
7583
7584
7585
7586
7587
7588
7589
7590
7591
7592
7593
7594
7595
7596
7597
7598
7599
7600
7601
7602
7603
7604
7605
7606
7607
7608
7609
7610
7611
7612
7613
7614
7615
7616
7617
7618
7619
7620
7621
7622
7623
7624
7625
7626
7627
7628
7629
7630
7631
7632
7633
7634
7635
7636
7637
7638
7639
7640
7641
7642
7643
7644
7645
7646
7647
7648
7649
7650
7651
7652
7653
7654
7655
7656
7657
7658
7659
7660
7661
7662
7663
7664
7665
7666
7667
7668
7669
7670
7671
7672
7673
7674
7675
7676
7677
7678
7679
7680
7681
7682
7683
7684
7685
7686
7687
7688
7689
7690
7691
7692
7693
7694
7695
7696
7697
7698
7699
7700
7701
7702
7703
7704
7705
7706
7707
7708
7709
7710
7711
7712
7713
7714
7715
7716
7717
7718
7719
7720
7721
7722
7723
7724
7725
7726
7727
7728
7729
7730
7731
7732
7733
7734
7735
7736
7737
7738
7739
7740
7741
7742
7743
7744
7745
7746
7747
7748
7749
7750
7751
7752
7753
7754
7755
7756
7757
7758
7759
7760
7761
7762
7763
7764
7765
7766
7767
7768
7769
7770
7771
7772
7773
7774
7775
7776
7777
7778
7779
7780
7781
7782
7783
7784
7785
7786
7787
7788
7789
7790
7791
7792
7793
7794
7795
7796
7797
7798
7799
7800
7801
7802
7803
7804
7805
7806
7807
7808
7809
7810
7811
7812
7813
7814
7815
7816
7817
7818
7819
7820
7821
7822
7823
7824
7825
7826
7827
7828
7829
7830
7831
7832
7833
7834
7835
7836
7837
7838
7839
7840
7841
7842
7843
7844
7845
7846
7847
7848
7849
7850
7851
7852
7853
7854
7855
7856
7857
7858
7859
7860
7861
7862
7863
7864
7865
7866
7867
7868
7869
7870
7871
7872
7873
7874
7875
7876
7877
7878
7879
7880
7881
7882
7883
7884
7885
7886
7887
7888
7889
7890
7891
7892
7893
7894
7895
7896
7897
7898
7899
7900
7901
7902
7903
7904
7905
7906
7907
7908
7909
7910
7911
7912
7913
7914
7915
7916
7917
7918
7919
7920
7921
7922
7923
7924
7925
7926
7927
7928
7929
7930
7931
7932
7933
7934
7935
7936
7937
7938
7939
7940
7941
7942
7943
7944
7945
7946
7947
7948
7949
7950
7951
7952
7953
7954
7955
7956
7957
7958
7959
7960
7961
7962
7963
7964
7965
7966
7967
7968
7969
7970
7971
7972
7973
7974
7975
7976
7977
7978
7979
7980
7981
7982
7983
7984
7985
7986
7987
7988
7989
7990
7991
7992
7993
7994
7995
7996
7997
7998
7999
8000
8001
8002
8003
8004
8005
8006
8007
8008
8009
8010
8011
8012
8013
8014
8015
8016
8017
8018
8019
8020
8021
8022
8023
8024
8025
8026
8027
8028
8029
8030
8031
8032
8033
8034
8035
8036
8037
8038
8039
8040
8041
8042
8043
8044
8045
8046
8047
8048
8049
8050
8051
8052
8053
8054
8055
8056
8057
8058
8059
8060
8061
8062
8063
8064
8065
8066
8067
8068
8069
8070
8071
8072
8073
8074
8075
8076
8077
8078
8079
8080
8081
8082
8083
8084
8085
8086
8087
8088
8089
8090
8091
8092
8093
8094
8095
8096
8097
8098
8099
8100
8101
8102
8103
8104
8105
8106
8107
8108
8109
8110
8111
8112
8113
8114
8115
8116
8117
8118
8119
8120
8121
8122
8123
8124
8125
8126
8127
8128
8129
8130
8131
8132
8133
8134
8135
8136
8137
8138
8139
8140
8141
8142
8143
8144
8145
8146
8147
8148
8149
8150
8151
8152
8153
8154
8155
8156
8157
8158
8159
8160
8161
8162
8163
8164
8165
8166
8167
8168
8169
8170
8171
8172
8173
8174
8175
8176
8177
8178
8179
8180
8181
8182
8183
8184
8185
8186
8187
8188
8189
8190
8191
8192
8193
8194
8195
8196
8197
8198
8199
8200
8201
8202
8203
8204
8205
8206
8207
8208
8209
8210
8211
8212
8213
8214
8215
8216
8217
8218
8219
8220
8221
8222
8223
8224
8225
8226
8227
8228
8229
8230
8231
8232
8233
8234
8235
8236
8237
8238
8239
8240
8241
8242
8243
8244
8245
8246
8247
8248
8249
8250
8251
8252
8253
8254
8255
8256
8257
8258
8259
8260
8261
8262
8263
8264
8265
8266
8267
8268
8269
8270
8271
8272
8273
8274
8275
8276
8277
8278
8279
8280
8281
8282
8283
8284
8285
8286
8287
8288
8289
8290
8291
8292
8293
8294
8295
8296
8297
8298
8299
8300
8301
8302
8303
8304
8305
8306
8307
8308
8309
8310
8311
8312
8313
8314
8315
8316
8317
8318
8319
8320
8321
8322
8323
8324
8325
8326
8327
8328
8329
8330
8331
8332
8333
8334
8335
8336
8337
8338
8339
8340
8341
8342
8343
8344
8345
8346
8347
8348
8349
8350
8351
8352
8353
8354
8355
8356
8357
8358
8359
8360
8361
8362
8363
8364
8365
8366
8367
8368
8369
8370
8371
8372
8373
8374
8375
8376
8377
8378
8379
8380
8381
8382
8383
8384
8385
8386
8387
8388
8389
8390
8391
8392
8393
8394
8395
8396
8397
8398
8399
8400
8401
8402
8403
8404
8405
8406
8407
8408
8409
8410
8411
8412
8413
8414
8415
8416
8417
8418
8419
8420
8421
8422
8423
8424
8425
8426
8427
8428
8429
8430
8431
8432
8433
8434
8435
8436
8437
8438
8439
8440
8441
8442
8443
8444
8445
8446
8447
8448
8449
8450
8451
8452
8453
8454
8455
8456
8457
8458
8459
8460
8461
8462
8463
8464
8465
8466
8467
8468
8469
8470
8471
8472
8473
8474
8475
8476
8477
8478
8479
8480
8481
8482
8483
8484
8485
8486
8487
8488
8489
8490
8491
8492
8493
8494
8495
8496
8497
8498
8499
8500
8501
8502
8503
8504
8505
8506
8507
8508
8509
8510
8511
8512
8513
8514
8515
8516
8517
8518
8519
8520
8521
8522
8523
8524
8525
8526
8527
8528
8529
8530
8531
8532
8533
8534
8535
8536
8537
8538
8539
8540
8541
8542
8543
8544
8545
8546
8547
8548
8549
8550
8551
8552
8553
8554
8555
8556
8557
8558
8559
8560
8561
8562
8563
8564
8565
8566
8567
8568
8569
8570
8571
8572
8573
8574
8575
8576
8577
8578
8579
8580
8581
8582
8583
8584
8585
8586
8587
8588
8589
8590
8591
8592
8593
8594
8595
8596
8597
8598
8599
8600
8601
8602
8603
8604
8605
8606
8607
8608
8609
8610
8611
8612
8613
8614
8615
8616
8617
8618
8619
8620
8621
8622
8623
8624
8625
8626
8627
8628
8629
8630
8631
8632
8633
8634
8635
8636
8637
8638
8639
8640
8641
8642
8643
8644
8645
8646
8647
8648
8649
8650
8651
8652
8653
8654
8655
8656
8657
8658
8659
8660
8661
8662
8663
8664
8665
8666
8667
8668
8669
8670
8671
8672
8673
8674
8675
8676
8677
8678
8679
8680
8681
8682
8683
8684
8685
8686
8687
8688
8689
8690
8691
8692
8693
8694
8695
8696
8697
8698
8699
8700
8701
8702
8703
8704
8705
8706
8707
8708
8709
8710
8711
8712
8713
8714
8715
8716
8717
8718
8719
8720
8721
8722
8723
8724
8725
8726
8727
8728
8729
8730
8731
8732
8733
8734
8735
8736
8737
8738
8739
8740
8741
8742
8743
8744
8745
8746
8747
8748
8749
8750
8751
8752
8753
8754
8755
8756
8757
8758
8759
8760
8761
8762
8763
8764
8765
8766
8767
8768
8769
8770
8771
8772
8773
8774
8775
8776
8777
8778
8779
8780
8781
8782
8783
8784
8785
8786
8787
8788
8789
8790
8791
8792
8793
8794
8795
8796
8797
8798
8799
8800
8801
8802
8803
8804
8805
8806
8807
8808
8809
8810
8811
8812
8813
8814
8815
8816
8817
8818
8819
8820
8821
8822
8823
8824
8825
8826
8827
8828
8829
8830
8831
8832
8833
8834
8835
8836
8837
8838
8839
8840
8841
8842
8843
8844
8845
8846
8847
8848
8849
8850
8851
8852
8853
8854
8855
8856
8857
8858
8859
8860
8861
8862
8863
8864
8865
8866
8867
8868
8869
8870
8871
8872
8873
8874
8875
8876
8877
8878
8879
8880
8881
8882
8883
8884
8885
8886
8887
8888
8889
8890
8891
8892
8893
8894
8895
8896
8897
8898
8899
8900
8901
8902
8903
8904
8905
8906
8907
8908
8909
8910
8911
8912
8913
8914
8915
8916
8917
8918
8919
8920
8921
8922
8923
8924
8925
8926
8927
8928
8929
8930
8931
8932
8933
8934
8935
8936
8937
8938
8939
8940
8941
8942
8943
8944
8945
8946
8947
8948
8949
8950
8951
8952
8953
8954
8955
8956
8957
8958
8959
8960
8961
8962
8963
8964
8965
8966
8967
8968
8969
8970
8971
8972
8973
8974
8975
8976
8977
8978
8979
8980
8981
8982
8983
8984
8985
8986
8987
8988
8989
8990
8991
8992
8993
8994
8995
8996
8997
8998
8999
9000
9001
9002
9003
9004
9005
9006
9007
9008
9009
9010
9011
9012
9013
9014
9015
9016
9017
9018
9019
9020
9021
9022
9023
9024
9025
9026
9027
9028
9029
9030
9031
9032
9033
9034
9035
9036
9037
9038
9039
9040
9041
9042
9043
9044
9045
9046
9047
9048
9049
9050
9051
9052
9053
9054
9055
9056
9057
9058
9059
9060
9061
9062
9063
9064
9065
9066
9067
9068
9069
9070
9071
9072
9073
9074
9075
9076
9077
9078
9079
9080
9081
9082
9083
9084
9085
9086
9087
9088
9089
9090
9091
9092
9093
9094
9095
9096
9097
9098
9099
9100
9101
9102
9103
9104
9105
9106
9107
9108
9109
9110
9111
9112
9113
9114
9115
9116
9117
9118
9119
9120
9121
9122
9123
9124
9125
9126
9127
9128
9129
9130
9131
9132
9133
9134
9135
9136
9137
9138
9139
9140
9141
9142
9143
9144
9145
9146
9147
9148
9149
9150
9151
9152
9153
9154
9155
9156
9157
9158
9159
9160
9161
9162
9163
9164
9165
9166
9167
9168
9169
9170
9171
9172
9173
9174
9175
9176
9177
9178
9179
9180
9181
9182
9183
9184
9185
9186
9187
9188
9189
9190
9191
9192
9193
9194
9195
9196
9197
9198
9199
9200
9201
9202
9203
9204
9205
9206
9207
9208
9209
9210
9211
9212
9213
9214
9215
9216
9217
9218
9219
9220
9221
9222
9223
9224
9225
9226
9227
9228
9229
9230
9231
9232
9233
9234
9235
9236
9237
9238
9239
9240
9241
9242
9243
9244
9245
9246
9247
9248
9249
9250
9251
9252
9253
9254
9255
9256
9257
9258
9259
9260
9261
9262
9263
9264
9265
9266
9267
9268
9269
9270
9271
9272
9273
9274
9275
9276
9277
9278
9279
9280
9281
9282
9283
9284
9285
9286
9287
9288
9289
9290
9291
9292
9293
9294
9295
9296
9297
9298
9299
9300
9301
9302
9303
9304
9305
9306
9307
9308
9309
9310
9311
9312
9313
9314
9315
9316
9317
9318
9319
9320
9321
9322
9323
9324
9325
9326
9327
9328
9329
9330
9331
9332
9333
9334
9335
9336
9337
9338
9339
9340
9341
9342
9343
9344
9345
9346
9347
9348
9349
9350
9351
9352
9353
9354
9355
9356
9357
9358
9359
9360
9361
9362
9363
9364
9365
9366
9367
9368
9369
9370
9371
9372
9373
9374
9375
9376
9377
9378
9379
9380
9381
9382
9383
9384
9385
9386
9387
9388
9389
9390
9391
9392
9393
9394
9395
9396
9397
9398
9399
9400
9401
9402
9403
9404
9405
9406
9407
9408
9409
9410
9411
9412
9413
9414
9415
9416
9417
9418
9419
9420
9421
9422
9423
9424
9425
9426
9427
9428
9429
9430
9431
9432
9433
9434
9435
9436
9437
9438
9439
9440
9441
9442
9443
9444
9445
9446
9447
9448
9449
9450
9451
9452
9453
9454
9455
9456
9457
9458
9459
9460
9461
9462
9463
9464
9465
9466
9467
9468
9469
9470
9471
9472
9473
9474
9475
9476
9477
9478
9479
9480
9481
9482
9483
9484
9485
9486
9487
9488
9489
9490
9491
9492
9493
9494
9495
9496
9497
9498
9499
9500
9501
9502
9503
9504
9505
9506
9507
9508
9509
9510
9511
9512
9513
9514
9515
9516
9517
9518
9519
9520
9521
9522
9523
9524
9525
9526
9527
9528
9529
9530
9531
9532
9533
9534
9535
9536
9537
9538
9539
9540
9541
9542
9543
9544
9545
9546
9547
9548
9549
9550
9551
9552
9553
9554
9555
9556
9557
9558
9559
9560
9561
9562
9563
9564
9565
9566
9567
9568
9569
9570
9571
9572
9573
9574
9575
9576
9577
9578
9579
9580
9581
9582
9583
9584
9585
9586
9587
9588
9589
9590
9591
9592
9593
9594
9595
9596
9597
9598
9599
9600
9601
9602
9603
9604
9605
9606
9607
9608
9609
9610
9611
9612
9613
9614
9615
9616
9617
9618
9619
9620
9621
9622
9623
9624
9625
9626
9627
9628
9629
9630
9631
9632
9633
9634
9635
9636
9637
9638
9639
9640
9641
9642
9643
9644
9645
9646
9647
9648
9649
9650
9651
9652
9653
9654
9655
9656
9657
9658
9659
9660
9661
9662
9663
9664
9665
9666
9667
9668
9669
9670
9671
9672
9673
9674
9675
9676
9677
9678
9679
9680
9681
9682
9683
9684
9685
9686
9687
9688
9689
9690
9691
9692
9693
9694
9695
9696
9697
9698
9699
9700
9701
9702
9703
9704
9705
9706
9707
9708
9709
9710
9711
9712
9713
9714
9715
9716
9717
9718
9719
9720
9721
9722
9723
9724
9725
9726
9727
9728
9729
9730
9731
9732
9733
9734
9735
9736
9737
9738
9739
9740
9741
9742
9743
9744
9745
9746
9747
9748
9749
9750
9751
9752
9753
9754
9755
9756
9757
9758
9759
9760
9761
9762
9763
9764
9765
9766
9767
9768
9769
9770
9771
9772
9773
9774
9775
9776
9777
9778
9779
9780
9781
9782
9783
9784
9785
9786
9787
9788
9789
9790
9791
9792
9793
9794
9795
9796
9797
9798
9799
9800
9801
9802
9803
9804
9805
9806
9807
9808
9809
9810
9811
9812
9813
9814
9815
9816
9817
9818
9819
9820
9821
9822
9823
9824
9825
9826
9827
9828
9829
9830
9831
9832
9833
9834
9835
9836
9837
9838
9839
9840
9841
9842
9843
9844
9845
9846
9847
9848
9849
9850
9851
9852
9853
9854
9855
9856
9857
9858
9859
9860
9861
9862
9863
9864
9865
9866
9867
9868
9869
9870
9871
9872
9873
9874
9875
9876
9877
9878
9879
9880
9881
9882
9883
9884
9885
9886
9887
9888
9889
9890
9891
9892
9893
9894
9895
9896
9897
9898
9899
9900
9901
9902
9903
9904
9905
9906
9907
9908
9909
9910
9911
9912
9913
9914
9915
9916
9917
9918
9919
9920
9921
9922
9923
9924
9925
9926
9927
9928
9929
9930
9931
9932
9933
9934
9935
9936
9937
9938
9939
9940
9941
9942
9943
9944
9945
9946
9947
9948
9949
9950
9951
9952
9953
9954
9955
9956
9957
9958
9959
9960
9961
9962
9963
9964
9965
9966
9967
9968
9969
9970
9971
9972
9973
9974
9975
9976
9977
9978
9979
9980
9981
9982
9983
9984
9985
9986
9987
9988
9989
9990
9991
9992
9993
9994
9995
9996
9997
9998
9999
10000
10001
10002
10003
10004
10005
10006
10007
10008
10009
10010
10011
10012
10013
10014
10015
10016
10017
10018
10019
10020
10021
10022
10023
10024
10025
10026
10027
10028
10029
10030
10031
10032
10033
10034
10035
10036
10037
10038
10039
10040
10041
10042
10043
10044
10045
10046
10047
10048
10049
10050
10051
10052
10053
10054
10055
10056
10057
10058
10059
10060
10061
10062
10063
10064
10065
10066
10067
10068
10069
10070
10071
10072
10073
10074
10075
10076
10077
10078
10079
10080
10081
10082
10083
10084
10085
10086
10087
10088
10089
10090
10091
10092
10093
10094
10095
10096
10097
10098
10099
10100
10101
10102
10103
10104
10105
10106
10107
10108
10109
10110
10111
10112
10113
10114
10115
10116
10117
10118
10119
10120
10121
10122
10123
10124
10125
10126
10127
10128
10129
10130
10131
10132
10133
10134
10135
10136
10137
10138
10139
10140
10141
10142
10143
10144
10145
10146
10147
10148
10149
10150
10151
10152
10153
10154
10155
10156
10157
10158
10159
10160
10161
10162
10163
10164
10165
10166
10167
10168
10169
10170
10171
10172
10173
10174
10175
10176
10177
10178
10179
10180
10181
10182
10183
10184
10185
10186
10187
10188
10189
10190
10191
10192
10193
10194
10195
10196
10197
10198
10199
10200
10201
10202
10203
10204
10205
10206
10207
10208
10209
10210
10211
10212
10213
10214
10215
10216
10217
10218
10219
10220
10221
10222
10223
10224
10225
10226
10227
10228
10229
10230
10231
10232
10233
10234
10235
10236
10237
10238
10239
10240
10241
10242
10243
10244
10245
10246
10247
10248
10249
10250
10251
10252
10253
10254
10255
10256
10257
10258
10259
10260
10261
10262
10263
10264
10265
10266
10267
10268
10269
10270
10271
10272
10273
10274
10275
10276
10277
10278
10279
10280
10281
10282
10283
10284
10285
10286
10287
10288
10289
10290
10291
10292
10293
10294
10295
10296
10297
10298
10299
10300
10301
10302
10303
10304
10305
10306
10307
10308
10309
10310
10311
10312
10313
10314
10315
10316
10317
10318
10319
10320
10321
10322
10323
10324
10325
10326
10327
10328
10329
10330
10331
10332
10333
10334
10335
10336
10337
10338
10339
10340
10341
10342
10343
10344
10345
10346
10347
10348
10349
10350
10351
10352
10353
10354
10355
10356
10357
10358
10359
10360
10361
10362
10363
10364
10365
10366
10367
10368
10369
10370
10371
10372
10373
10374
10375
10376
10377
10378
10379
10380
10381
10382
10383
10384
10385
10386
10387
10388
10389
10390
10391
10392
10393
10394
10395
10396
10397
10398
10399
10400
10401
10402
10403
10404
10405
10406
10407
10408
10409
10410
10411
10412
10413
10414
10415
10416
10417
10418
10419
10420
10421
10422
10423
10424
10425
10426
10427
10428
10429
10430
10431
10432
10433
10434
10435
10436
10437
10438
10439
10440
10441
10442
10443
10444
10445
10446
10447
10448
10449
10450
10451
10452
10453
10454
10455
10456
10457
10458
10459
10460
10461
10462
10463
10464
10465
10466
10467
10468
10469
10470
10471
10472
10473
10474
10475
10476
10477
10478
10479
10480
10481
10482
10483
10484
10485
10486
10487
10488
10489
10490
10491
10492
10493
10494
10495
10496
10497
10498
10499
10500
10501
10502
10503
10504
10505
10506
10507
10508
10509
10510
10511
10512
10513
10514
10515
10516
10517
10518
10519
10520
10521
10522
10523
10524
10525
10526
10527
10528
10529
10530
10531
10532
10533
10534
10535
10536
10537
10538
10539
10540
10541
10542
10543
10544
10545
10546
10547
10548
10549
10550
10551
10552
10553
10554
10555
10556
10557
10558
10559
10560
10561
10562
10563
10564
10565
10566
10567
10568
10569
10570
10571
10572
10573
10574
10575
10576
10577
10578
10579
10580
10581
10582
10583
10584
10585
10586
10587
10588
10589
10590
10591
10592
10593
10594
10595
10596
10597
10598
10599
|
<!DOCTYPE html PUBLIC "-//W3C//DTD XHTML 1.0 Strict//EN"
"http://www.w3.org/TR/xhtml1/DTD/xhtml1-strict.dtd">
<html xmlns="http://www.w3.org/1999/xhtml" xml:lang="en" lang="en">
<head>
<meta http-equiv="Content-Type" content="text/html;charset=iso-8859-1" />
<meta http-equiv="Content-Style-Type" content="text/css" />
<title>
The Project Gutenberg eBook of Arteriosclerosis and Hypertension with Chapters on Blood Pressure, by Louis M. Warfield.
</title>
<style type="text/css">
body {
margin-left: 10%;
margin-right: 10%;
}
h1,h2,h3,h4 {
text-align: center; /* all headings centered */
clear: both;
}
p {
margin-top: .75em;
text-align: justify;
margin-bottom: .75em;
}
.hanging {margin-left: 2em; text-indent: -2em;}
hr {
margin: 3em auto 3em auto;
height: 0px;
border-width: 1px 0 0 0;
border-style: solid;
border-color: #dcdcdc;
width: 500px;
clear: both;
}
hr.hr2 {
width: 250px;
margin: 3em auto 3em auto;
}
.toc {
margin: 0 25% auto 25%;
padding: 0;
}
p.toc {
font-size: 60%;
margin-bottom: 0;
padding-bottom: 0;
}
.toc li {
list-style-type: none;
}
.toc li p {
margin-top: 0;
padding-top: 0;
text-indent: -1em;
text-align: justify; padding-right: 2em;
}
.toc .num {
position: absolute;
right: 25%;
top: auto;
text-indent: 0;
}
.tocdesc {
padding-right: 2.2em;
}
.pgnum-contents {
position: absolute;
left: 90%;
text-align: right;
}
.pagenum { /* uncomment the next line for invisible page numbers */
/* visibility: hidden; */
position: absolute;
left: 92%;
font-size: smaller;
text-align: right;
color: #999;
} /* page numbers */
.blockquot {
margin-left: 5%;
margin-right: 10%;
}
.bbox {border: solid 2px;}
.center {text-align: center;}
.smcap {font-variant: small-caps;}
.u {text-decoration: underline;}
.caption {font-weight: bold;}
.gap { margin-top: 1em; }
table {
width: auto;
border-collapse: collapse;
margin-left: auto;
margin-right: auto
}
table.leftside {
margin-left: 2em;
margin-right: auto
}
td {
padding-bottom: 0em;
padding-left: 1em;
padding-right: 1em;
padding-top: 0em
}
th {
padding-bottom: 0em;
padding-left: 1em;
padding-right: 1em;
padding-top: 0em
}
.tdouble {
border-bottom: black;
border-left: black;
border-top: black double;
border-right: black
}
.bdouble {
border-bottom: black double;
border-left: black;
border-top: black;
border-right: black
}
.bb {
border-bottom: black 2px solid
}
.bl {
border-left: black 1px solid
}
.bt {
border-top: black 2px solid
}
.br {
border-right: black 1px solid
}
ol.upper-roman {
list-style-type: upper-roman
}
ol.upper-alpha {
list-style-type: upper-alpha
}
ol.lower-alpha {
list-style-type: lower-alpha
}
ol.decimal {
list-style-type: decimal
}
ol.none {
list-style-type: none
}
ul {
list-style-type: none
}
li.pad {
padding-top: 3%
}
/* Images */
.figcenter {
margin: auto;
text-align: center;
}
.bord img {
padding: 1px;
border: 1px solid black;
}
p.caption {
margin-top: 0;
font-size: 70%;
text-align: left;
}
/* Transcriber Notes */
div.tn {
background-color: #EEE;
border: dashed 1px;
color: #000;
margin-left: 20%;
margin-right: 20%;
margin-top: 5em;
margin-bottom: 5em;
padding: 1em;
}
/* Footnotes */
div.fn {
background-color: #EEE;
border: dashed 1px;
color: #000;
margin-left: 20%;
margin-right: 20%;
margin-top: 5em;
margin-bottom: 5em;
padding: 1em;
}
.footnote {
margin-left: 10%;
margin-right: 10%;
font-size: 0.9em;
}
.footnote .label {
position: absolute;
right: 84%;
text-align: right;
}
.fnanchor {
vertical-align: super;
font-size: .8em;
text-decoration: none;
}
.signature {
text-align: right;
margin-right: 5%;
}
/* INDEX */
ul.index { list-style-type: none;
width: 20em;
margin: 2em auto;
}
ul.index2 { list-style-type: none; }
li.pad { padding-top: 2.0%; }
</style>
</head>
<body>
<pre>
The Project Gutenberg EBook of Arteriosclerosis and Hypertension:, by
Louis Marshall Warfield
This eBook is for the use of anyone anywhere at no cost and with
almost no restrictions whatsoever. You may copy it, give it away or
re-use it under the terms of the Project Gutenberg License included
with this eBook or online at www.gutenberg.org
Title: Arteriosclerosis and Hypertension:
with Chapters on Blood Pressure, 3rd Edition.
Author: Louis Marshall Warfield
Release Date: October 12, 2011 [EBook #37675]
Language: English
Character set encoding: ISO-8859-1
*** START OF THIS PROJECT GUTENBERG EBOOK ARTERIOSCLEROSIS AND HYPERTENSION: ***
Produced by Bryan Ness, Julia Neufeld and the Online
Distributed Proofreading Team at http://www.pgdp.net (This
file was produced from images generously made available
by The Internet Archive/American Libraries.)
</pre>
<h4><span class="smcap">Erratum</span></h4>
<p>Page 75, Figure shown is not the Brown sphygmomanometer
described in the text, but the Baumanometer
manufactured by W. A. Baum Co., Inc.,
New York. It is claimed that the Baumanometer
is made with particular care and hence the readings
are said to be more accurate than other mercury
instruments. It is apparently a good instrument.
The author has had no personal experience with it.<br /><br /></p>
<hr style="width: 45%;" />
<h1>
ARTERIOSCLEROSIS<br />
<br />
AND<br />
<br />
HYPERTENSION</h1>
<h3>
With Chapters on Blood Pressure<br />
<br />
BY<br />
</h3>
<h2>LOUIS M. WARFIELD, A.B., M.D., (Johns Hopkins),<br />
F.A.C.P.</h2>
<div class="center"><br />
<br />
FORMERLY PROFESSOR OF CLINICAL MEDICINE, MARQUETTE UNIVERSITY MEDICAL<br />
SCHOOL; CHIEF PHYSICIAN TO MILWAUKEE COUNTY HOSPITAL; ASSOCIATE<br />
MEMBER ASSOCIATION AMERICAN PHYSICIANS; MEMBER AMERICAN<br />
ASSOCIATION PATHOLOGISTS AND BACTERIOLOGISTS;<br />
AMERICAN MEDICAL ASSOCIATION, ETC., FELLOW<br />
AMERICAN COLLEGE OF PHYSICIANS<br />
<br /><br />
<i>THIRD EDITION</i><br />
<br /><br />
ST. LOUIS<br />
<br />
C. V. MOSBY COMPANY<br />
<br />
1920<br />
<br />
</div>
<hr style="width: 45%;" />
<div class="center"><span class="smcap">Copyright, 1912, 1920, by C. V. Mosby Company</span><br />
<br />
<i>Press of<br />
C. V. Mosby Company<br />
St. Louis</i><br />
<br />
</div>
<hr style="width: 65%;" />
<div class="center">TO<br />
<br />
MY MOTHER<br />
<br />
THIS VOLUME IS AFFECTIONATELY<br />
<br />
DEDICATED<br />
</div>
<hr style="width: 65%;" />
<p><span class="pagenum"><a name="Page_15" id="Page_15">[15]</a></span></p>
<h2>PREFACE TO THIRD EDITION</h2>
<p>Several years have elapsed since the appearance of the
second edition of this book. During this time there has
been considerable experimentation and much writing on
arteriosclerosis. The total of all work has not been to add
very much to our knowledge of the etiology of arterial degeneration.
Points of view and opinions change from time
to time. It is so with arteriosclerosis. In this edition arteriosclerosis
is not regarded as a disease with a definite
etiologic factor. Rather it is looked upon as a degenerative
process affecting the arteries following a variety of causes
more or less ill defined. It is not considered a true disease.
Possibly syphilitic arteritis may be viewed as an entity, the
cause is known and the lesions are characteristic.</p>
<p>Much new material and many new figures have been
added to this edition. Some rearranging has been done.
The chapter on Blood Pressure has been much expanded
and some original observations have been included. The
literature has been selected rather than indiscriminately
quoted. Much that is written on the subject is of little
value.</p>
<p>It has always seemed to the author that there is not
enough of the personal element in medical writings. At the
risk of being severely criticized, he has attempted to make
this book represent largely his own ideas, only here and
there quoting from the literature.</p>
<p>New chapters on Cardiac Irregularities Associated with
Arteriosclerosis, and Blood Pressure in Its Clinical Application
have been added.</p>
<p>The fact that the book has passed through two editions is
very gratifying and seems to show that it has met with favor.
The author takes this opportunity of thanking those
who have loaned him illustrations. Wherever figures are
borrowed due credit is given.</p>
<p><span class="pagenum"><a name="Page_16" id="Page_16">[16]</a></span>It is hoped that the kind of reception accorded to the first
and second editions will also not be withheld from this present
edition.</p>
<div class="signature"><span class="smcap">Louis M. Warfield.</span></div>
<p>
Milwaukee, Wisc.
</p>
<hr style="width: 65%;" />
<h2>PREFACE TO THE SECOND EDITION</h2>
<p>In this second edition so many changes and additions
have been made that the book is practically a new one. All
the chapters which were in the previous edition have been
carefully revised. Two chapters, "Pathology" and "Physiology,"
have been completely rewritten and brought up to
date. It was thought best to add some references for those
who had interest enough to pursue the subject further.
These references have been selected on account of the readiness
with which they may be procured in any library, public
or private. Two new chapters have been added—one on
"The Physical Examination of the Heart and Arteries,"
the other on "Arteriosclerosis in Its Relation to Life Insurance,"
and it is hoped that these will add to the practical
value of the book.</p>
<p>Arteriosclerosis can scarcely be considered apart from
blood pressure, and in the view expressed within, with
which some may not concur, high tension is considered to be
a large factor in the production of arteriosclerosis. As the
data on blood pressure have increased, the importance of it
has become more evident. The chapter on "Blood Pressure"
has been wholly rewritten, expanded so as to give
a comprehensive grasp of the essential features, and several
illustrations have been added in order to elucidate the text
more fully. The chief objects in view were to make clear
to the physician the technique and the necessity for estimating
both systolic and diastolic pressures.</p>
<p>The author is grateful for the kindly reception accorded
the first edition. No one is more keenly aware of the imperfections<span class="pagenum"><a name="Page_17" id="Page_17">[17]</a></span>
than he. The necessity for a second edition is
taken to mean that the book has found a place for itself
and has been of use to some.</p>
<p>The author hopes that this new edition will fulfill adequately
the purpose for which he prepared the book—namely,
as a practical guide to the knowledge and appreciation
of a most important and exceedingly common
disease.</p>
<div class="signature"><span class="smcap">Louis M. Warfield.</span></div>
<p>Milwaukee, May, 1912.<br />
</p>
<hr style="width: 65%;" />
<h2>PREFACE TO THE FIRST EDITION</h2>
<p>It is hoped that this small volume may fill a want in the
already crowded field of medical monographs. The author
has endeavored to give to the general practitioner a
readable, authoritative essay on a disease which is especially
an outcome of modern civilization. To that end all
the available literature has been freely consulted, and the
newest results of experimental research and the recent
ideas of leading clinicians have been summarized. The author
has supplemented these with results from his own
experience, but has thought it best not to burden the contents
with case histories.</p>
<p>The stress and strain of our daily life has, as one of
its consequences, early arterial degeneration. There can
be no doubt that arterial disease in the comparatively
young is more frequent than it was twenty-five years ago,
and that the mortality from diseases directly dependent
on arteriosclerotic changes is increasing. Fortunately, the
almost universal habit of getting out of doors whenever
possible, and the revival of interest in athletics for persons
of all ages, have to some extent counteracted the tendency
to early decay. Nevertheless, the actual average prolongation
of life is more probably due to the very great
reduction in infant mortality and in deaths from infectious
and communicable diseases.</p>
<p><span class="pagenum"><a name="Page_18" id="Page_18">[18]</a></span>The wear and tear on the human organism in our modern
way of living is excessive. Hard work, worry, and
high living all predispose to degenerative changes in the
arteries, and so bring on premature old age. The author
has tried to emphasize this by laying stress on the prevention
of arteriosclerosis rather than on the treatment of the
fully developed disease.</p>
<p>No bibliography is given, as this is not intended as a
reference book, but rather as a guide to a better appreciation
and understanding of a most important subject. It
has been difficult to keep from wandering off into full discussions
of conditions incident to and accompanied by
arteriosclerosis, but, in order to be clear in his statements
and complete in his descriptions, the author has to invade
the fields of heart disease, kidney disease, brain disease,
etc. It is hoped, however, that these excursions will serve
to show how intimately disease of the arteries is bound
up with diseases of all the organs and tissues of the body.</p>
<p>Some authors have been named when their opinions
have been given. Thanks are extended also to many others
to whom the writer is indebted, but of whom no individual
mention has been made.</p>
<p>The author also takes this opportunity of expressing
his appreciation of the kindness of Dr. D. L. Harris, who
took the microphotographs, and to the publishers for their
unfailing courtesy and consideration.</p>
<div class="signature">
<span class="smcap">Louis M. Warfield.</span></div>
<p>St. Louis, August, 1908.<br />
</p>
<hr style="width: 65%;" />
<p><span class="pagenum"><a name="Page_19" id="Page_19">[19]</a></span></p>
<h2>CONTENTS</h2>
<blockquote>
<p><span class="pgnum-contents"><span class="smcap">page</span></span></p>
<h3><a href="#CHAPTER_I">CHAPTER I.</a></h3>
<p><span class="smcap">Anatomy</span><span class="pgnum-contents">25</span></p>
<p class="hanging">Introduction, 25; Definition, 26; General Structure of the Arteries,
27; Arteries, 29; Veins, 30; Capillaries, 31.</p>
<h3><a href="#CHAPTER_II">CHAPTER II.</a></h3>
<p><span class="smcap">Pathology</span><span class="pgnum-contents">32</span></p>
<p class="hanging">Syphilitic Aortitis, 44; Experimental Arteriosclerosis, 50; Arteriosclerosis
of the Pulmonary Arteries, 63; Sclerosis of the Veins, 64.</p>
<h3><a href="#CHAPTER_III">CHAPTER III.</a></h3>
<p><span class="smcap">Physiology of the Circulation</span><span class="pgnum-contents">65</span></p>
<p class="hanging">Blood Pressure, 68; Blood Pressure Instruments, 70; Technic, 80;
Arterial Pressure, 85; Normal Pressure Variations, 88; The Auscultatory
Blood Pressure Phenomenon, 90; The Maximum and Minimum
Pressures, 94; Relative Importance of the Systolic and Diastolic
Pressures, 97; Pulse Pressure, 100; Blood Pressure Variations,
102; Hypertension, 106; Hypotension, 117; The Pulse, 123; The
Venous Pulse, 123; The Electrocardiogram, 126.</p>
<h3><a href="#CHAPTER_IV">CHAPTER IV.</a></h3>
<p><span class="smcap">Important Cardiac Irregularities Associated With Arteriosclerosis</span> <span class="pgnum-contents">13</span></p>
<p class="hanging">Auricular Flutter, 131; Auricular Fibrillation, 133; Ventricular
Fibrillation, 138; Extrasystole, 138; Heart Block, 140.</p>
<h3><a href="#CHAPTER_V">CHAPTER V.</a></h3>
<p><span class="smcap">Blood Pressure in Its Clinical Applications</span><span class="pgnum-contents">147</span></p>
<p class="hanging">Blood Pressure in Surgery, 147; Head Injuries, 148; Shock and
Hemorrhage, 148; Blood Pressure in Obstetrics, 152; Infectious
Diseases, 153; Valvular Heart Disease, 155; Kidney Disease, 155;
Other Diseases, Liver, Spleen, Abdomen, etc., 156.</p>
<h3><a href="#CHAPTER_VI">CHAPTER VI.</a></h3>
<p><span class="smcap">Etiology</span><span class="pgnum-contents">157</span></p>
<p class="hanging">Congenital Form, 157; Acquired Form, 159; Hypertension, 159;
Age, Sex, Race, 161; Occupation, 162; Food Poisons, 163; Infectious
Diseases, 163; Syphilis, 165; Chronic Drug Intoxications, 166;
Overeating, 167; Mental Strain, 168; Muscular Overwork, 169;
Renal Disease, 169; Ductless Glands, 171.</p>
<p><span class="pagenum"><a name="Page_20" id="Page_20">[20]</a></span></p>
<h3><a href="#CHAPTER_VII">CHAPTER VII.</a></h3>
<p><span class="smcap">The Physical Examination of the Heart and Arteries</span><span class="pgnum-contents">172</span></p>
<p class="hanging">Heart Boundaries, 172; Percussion, 174; Auscultation, 176; The
Examination of the Arteries, 177; Estimation of Blood Pressure,
179; Palpation, 180; Precautions When Estimating Blood Pressure,
181; The Value of Blood Pressure, 181.</p>
<h3><a href="#CHAPTER_VIII">CHAPTER VIII.</a></h3>
<p><span class="smcap">Symptoms and Physical Signs</span><span class="pgnum-contents">183</span></p>
<p class="hanging">General, 183; Hypertension, 185; The Heart, 188; Palpable Arteries,
189; Ocular Signs and Symptoms, 190; Nervous Symptoms, 191.</p>
<h3><a href="#CHAPTER_IX">CHAPTER IX.</a></h3>
<p><span class="smcap">Symptoms and Physical Signs</span><span class="pgnum-contents">194</span></p>
<p class="hanging">Special, 194; Cardiac, 195; Renal, 199; Abdominal or Visceral, 201;
Cerebral, 203; Spinal, 205; Local or Peripheral, 207; Pulmonary
Artery, 209.</p>
<h3><a href="#CHAPTER_X">CHAPTER X.</a></h3>
<p><span class="smcap">Diagnosis</span><span class="pgnum-contents">210</span></p>
<p class="hanging">Early Diagnosis, 210; Differential Diagnosis, 215; Diseases in Which
Arteriosclerosis is Commonly Found, 216.</p>
<h3><a href="#CHAPTER_XI">CHAPTER XI.</a></h3>
<p><span class="smcap">Prognosis</span><span class="pgnum-contents">218</span></p>
<h3><a href="#CHAPTER_XII">CHAPTER XII.</a></h3>
<p><span class="smcap">Prophylaxis</span><span class="pgnum-contents">224</span></p>
<h3><a href="#CHAPTER_XIII">CHAPTER XIII.</a></h3>
<p><span class="smcap">Treatment</span><span class="pgnum-contents">229</span></p>
<p class="hanging">Hygienic Treatment, 230; Balneotherapy, 233; Personal Habits,
234; Dietetic Treatment, 235; Medicinal, 238; Symptomatic Treatment,
245.</p>
<h3><a href="#CHAPTER_XIV">CHAPTER XIV.</a></h3>
<p><span class="smcap">Arteriosclerosis in Its Relation to Life Insurance</span><span class="pgnum-contents">249</span></p>
<h3><a href="#CHAPTER_XV">CHAPTER XV.</a></h3>
<p><span class="smcap">Practical Suggestions</span><span class="pgnum-contents">256</span></p>
</blockquote>
<hr style="width: 65%;" />
<p><span class="pagenum"><a name="Page_21" id="Page_21">[21]</a></span></p>
<h2>ILLUSTRATIONS</h2>
<div class="center">
<table border="0" cellpadding="4" cellspacing="0" summary="LIST OF ILLUSTRATIONS">
<tr><td align="left">FIG.</td><td><span class="smcap">page</span></td></tr>
<tr><td align="left"><a href="#Cross_section_of_a_large_artery">1. Cross section of a large artery</a></td><td align="right">28</td></tr>
<tr><td align="left"><a href="#Cross_section_of_a_coronary_artery">2. Cross section of a coronary artery</a></td><td align="right">36</td></tr>
<tr><td align="left"><a href="#Arteriosclerosis_of_the_thoracic_and_abdominal_aorta">3. Arteriosclerosis of the thoracic and abdominal aorta</a></td><td align="right">39</td></tr>
<tr><td align="left"><a href="#Arteriosclerosis_of_the_arch_of_the_aorta">4. Arteriosclerosis of the arch of the aorta</a></td><td align="right">40</td></tr>
<tr><td align="left"><a href="#Normal_Aorta">5. Normal Aorta</a></td><td align="right">41</td></tr>
<tr><td align="left"><a href="#Radiogram_showing_calcification_of_both_radial_and_ulnar_arteries">6. Radiogram showing calcification of both radial and ulnar arteries</a></td><td align="right">42</td></tr>
<tr><td align="left"><a href="#Syphilitic_aortitis_of_long_standing">7. Syphilitic aortitis of long standing</a></td><td align="right">44</td></tr>
<tr><td align="left"><a href="#Diagrammatic_representation_of_strain_hypertrophy">8. Diagrammatic representation of strain hypertrophy</a></td><td align="right">48</td></tr>
<tr><td align="left"><a href="#Strain_hypertrophy">9. Strain hypertrophy</a></td><td align="right">49</td></tr>
<tr><td align="left"><a href="#Cross_section_of_small_artery_in_the_mesentery">10. Cross section of small artery in the mesentery</a></td><td align="right">56</td></tr>
<tr><td align="left"><a href="#Enormous_hypertrophy_of_left_ventricle">11. Enormous hypertrophy of left ventricle</a></td><td align="right">58</td></tr>
<tr><td align="left"><a href="#Aortic_incompetence_with_hypertrophy_and_dilatation_of_left_ventricle">12. Aortic incompetence with hypertrophy and dilatation of left ventricle</a></td><td align="right">61</td></tr>
<tr><td align="left"><a href="#Cooks_modification_of_Riva-Roccis_blood_pressure_instrument">13. Cooks modification of Riva-Roccis blood pressure instrument</a></td><td align="right">72</td></tr>
<tr><td align="left"><a href="#Stantons_sphygmomanometer">14. Stanton's sphygmomanometer</a></td><td align="right">73</td></tr>
<tr><td align="left"><a href="#The_Erlanger_sphygmomanometer_with_the_Hirschfelder_attachments">15. The Erlanger sphygmomanometer with the Hirschfelder attachments</a></td><td align="right">74</td></tr>
<tr><td align="left"><a href="#Desk_model_Baumanometer">16. Desk model Baumanometer</a></td><td align="right">75</td></tr>
<tr><td align="left"><a href="#Faught_blood_pressure_instrument">17. Faught blood pressure instrument</a></td><td align="right">76</td></tr>
<tr><td align="left"><a href="#Rogers_Tycos_dial_sphygmomanometer">18. Rogers' "Tycos" dial sphygmomanometer</a></td><td align="right">77</td></tr>
<tr><td align="left"><a href="#Detail_of_the_dial_in_the_Tycos_instrument">19. Detail of the dial in the "Tycos" instrument</a></td><td align="right">78</td></tr>
<tr><td align="left"><a href="#Faught_dial_instrument">20. Faught dial instrument</a></td><td align="right">79</td></tr>
<tr><td align="left"><a href="#Detail_of_the_dial_of_the_Faught_instrument">21. Detail of the dial of the Faught instrument</a></td><td align="right">79</td></tr>
<tr><td align="left"><a href="#The_Sanborn_instrument">22. The Sanborn instrument</a></td><td align="right">80</td></tr>
<tr><td align="left"><a href="#Method_of_taking_blood_pressure_with_a_patient_in_sitting_position">23. Method of taking blood pressure with a patient in sitting position</a></td><td align="right">81</td></tr>
<tr><td align="left"><a href="#Method_of_taking_blood_pressure_with_patient_lying_down">24. Method of taking blood pressure with patient lying down</a></td><td align="right">82</td></tr>
<tr><td align="left"><a href="#Observation_by_the_auscultatory_method_and_a_mercury_instrument">25. Observation by the auscultatory method and a mercury instrument</a></td><td align="right">84</td></tr>
<tr><td align="left"><a href="#Observation_by_the_auscultatory_method_and_a_dial_instrument">26. Observation by the auscultatory method and a dial instrument</a></td><td align="right">85</td></tr>
<tr><td align="left"><a href="#Schema_to_illustrate_decrease_in_pressure">27. Schema to illustrate decrease in pressure</a></td><td align="right">86</td></tr>
<tr><td align="left"><a href="#Chart_showing_the_normal_limits_of_variation_in_systolic_blood_pressure">28. Chart showing the normal limits of variation in systolic blood pressure</a></td><td align="right">89</td></tr>
<tr><td align="left"><a href="#Tracing_of_auscultatory_phenomena">29. Tracing of auscultatory phenomena</a></td><td align="right">94</td></tr>
<tr><td align="left"><a href="#Tracings_of_auscultatory_phenomena">30. Tracings of auscultatory phenomena</a></td><td align="right">95</td></tr>
<tr><td align="left"><a href="#Clinical_determination_of_diastolic_pressure_fast_drum">31. Clinical determination of diastolic pressure fast drum</a></td><td align="right">96</td></tr>
<tr><td align="left"><a href="#Clinical_determination_of_diastolic_pressure_slow_drum">32. Clinical determination of diastolic pressure slow drum</a></td><td align="right">96</td></tr>
<tr><td align="left"><a href="#Venous_blood_pressure_instrument">33. Venous blood pressure instrument</a></td><td align="right">121</td></tr>
<tr><td align="left"><a href="#New_venous_pressure_instrument">34. New venous pressure instrument</a></td><td align="right">122</td></tr>
<tr><td align="left"><a href="#Events_in_the_cardiac_cycle">35. Events in the cardiac cycle</a></td><td align="right">124</td></tr>
<tr><td align="left"><a href="#Simultaneous_tracings_of_the_jugular_and_carotid_pulses">36. Simultaneous tracings of the jugular and carotid pulses</a></td><td align="right">125</td></tr>
<tr><td align="left"><a href="#Jugular_and_carotid_tracings">37. Jugular and carotid tracings</a></td><td align="right">125</td></tr>
<tr><td align="left"><a href="#Right_side_of_the_heart_showing_distribution_of_the_two_vagus_nerves">38. Right side of the heart showing distribution of the two vagus nerves</a></td><td align="right">127</td></tr>
<tr><td align="left"><a href="#Normal_electrocardiogram">39. Normal electrocardiogram</a></td><td align="right">128</td></tr>
<tr><td align="left"><a href="#Auricular_flutter">40. Auricular flutter</a></td><td align="right">132</td></tr>
<tr><td align="left"><a href="#Auricular_fibrillation">41. Auricular fibrillation</a></td><td align="right">134</td></tr>
<tr><td align="left"><span class="pagenum"><a name="Page_22" id="Page_22">[22]</a></span></td></tr>
<tr><td align="left"><a href="#Auricular_fibrillations">42. Auricular fibrillation</a></td><td align="right">134</td></tr>
<tr><td align="left"><a href="#Pulse_deficit">43. Pulse deficit</a></td><td align="right">135</td></tr>
<tr><td align="left"><a href="#Ventricular_fibrillation">44. Ventricular fibrillation</a></td><td align="right">137</td></tr>
<tr><td align="left"><a href="#Auricular_extrasystoles">45. Auricular extrasystoles</a></td><td align="right">139</td></tr>
<tr><td align="left"><a href="#Ventricular_extrasystole">46. Ventricular extrasystole</a></td><td align="right">139</td></tr>
<tr><td align="left"><a href="#Delayed_conduction">47. Delayed conduction</a></td><td align="right">141</td></tr>
<tr><td align="left"><a href="#Partial_heart_block">48. Partial heart block</a></td><td align="right">141</td></tr>
<tr><td align="left"><a href="#Complete_heart_block">49. Complete heart block</a></td><td align="right">142</td></tr>
<tr><td align="left"><a href="#Alternating_periods_of_sinus_rhythm_and_auriculoventricular_rhythm">50. Alternating periods of sinus rhythm and auriculoventricular rhythm</a></td><td align="right">144</td></tr>
<tr><td align="left"><a href="#Auriculoventricular_or_nodal_rhythm">51. Auriculoventricular or "nodal" rhythm</a></td><td align="right">144</td></tr>
<tr><td align="left"><a href="#Influence_of_mechanical_pressure_on_the_right_vagus_nerve">52. Influence of mechanical pressure on the right vagus nerve</a></td><td align="right">144</td></tr>
<tr><td align="left"><a href="#Schematic_distribution_of_right_and_left_vagus">53. Schematic distribution of right and left vagus</a></td><td align="right">145</td></tr>
<tr><td align="left"><a href="#Blood_pressure_record_from_a_normal_reaction_to_ether">54. Blood pressure record from a normal reaction to ether</a></td><td align="right">149</td></tr>
<tr><td align="left"><a href="#Chart_showing_the_method_of_recording_blood_pressure_during_an">55. Chart showing the method of recording blood pressure during an</a></td></tr>
<tr><td align="left">operation</td><td align="right">150</td></tr>
<tr><td align="left"><a href="#Method_of_using_blood_pressure_instrument_during_operation">56. Method of using blood pressure instrument during operation</a></td><td align="right">151</td></tr>
<tr><td align="left"><a href="#Finger-tip_palpation_of_the_radial_artery">57. Finger-tip palpation of the radial artery</a></td><td align="right">178</td></tr>
<tr><td align="left"><a href="#Finger-tip_palpations_of_the_radial_artery">58. Finger-tip palpation of the radial artery</a></td><td align="right">178</td></tr>
<tr><td align="left"><a href="#Aneurysm_of_the_heart_wall">59. Aneurysm of the heart wall</a></td><td align="right">196</td></tr>
<tr><td align="left"><a href="#Large_aneurysm_of_the_aorta_eroding_the_sternum">60. Large aneurysm of the aorta eroding the sternum</a></td><td align="right">198</td></tr>
</table></div>
<p><span class="pagenum"><a name="Page_24" id="Page_24"></a></span><span class="pagenum"><a name="Page_23" id="Page_23"></a></span></p>
<hr style="width: 65%;" />
<p><span class="pagenum"><a name="Page_25" id="Page_25">[25]</a></span></p>
<h2>ARTERIOSCLEROSIS AND HYPERTENSION</h2>
<hr style="width: 65%;" />
<h2><a name="CHAPTER_I" id="CHAPTER_I"></a>CHAPTER I.</h2>
<h3>ANATOMY</h3>
<p>With the increased complexity of our modern life comes
increased wear and tear on the human organism. "A man
is as old as his arteries" is an old dictum, and, like many
proverbs, the application to mankind today is, if anything,
more pertinent than it was when the saying was
first uttered. Notwithstanding the fact that the average
age of mankind at death has been materially lengthened—the
increase in years amounting to fourteen in the past
one hundred years of history—clinicians and pathologists
are agreed that the arterial degeneration known as arteriosclerosis
is present to an alarming extent in persons over
forty years of age. Figures in all vital statistics have shown
us that all affections of the circulatory and renal systems
are definitely on the increase. "Arterial diseases of various
kinds, atheroma, aneurysm, etc., caused 15,685 deaths
in 1915, or 23.3 per 100,000. This rate, although somewhat
lower than the corresponding ones for 1912 and 1913, is
higher than that for 1914, and is very much higher than
that for 1900, which was 6.1."</p>
<p>The great group of cases of which cardiac incompetence,
aneurysm, cerebral apoplexy, chronic nephritis, emphysema,
and chronic bronchitis are the most frequent and important
appear as terminal events in which arteriosclerosis has
probably played an important part.</p>
<p>Thus, in the sense in which we speak of tuberculosis or
pneumonia as a distinct disease, we can not so designate the
diseased condition of the arteries.</p>
<p>Arteriosclerosis is not a disease <b>sui generis</b>. It is best<span class="pagenum"><a name="Page_26" id="Page_26">[26]</a></span>
viewed as a degeneration of the coats of the arteries, both
large and small resulting in several different more or less
distinct types.</p>
<p>These types blend one into the other and in the same patient
all types may be found. Thus the sclerosis of the
arteries is the result of a variety of causes, none of which
is definitely known in the sense of a bacterial disease. As
we shall see later, one type of arteriosclerosis has a special
pathology and etiology, the syphilitic arterial changes.</p>
<p>Bearing in mind that arteriosclerosis (called by some
"arteriocapillary fibrosis," by others "atherosclerosis")
is not a true disease, it may, for convenience be defined as a
chronic disease of the arteries and arterioles, characterized
anatomically by increase or decrease of the thickness of the
walls of the blood vessels, the initial lesion being a weakening
of the middle layer caused by various toxic or mechanical
agencies. This weakness of the media leads to
secondary effects, which include hypertrophy or atrophy
of the inner layer—and not infrequently hypertrophy of
the outer layer—connective tissue formation and calcification
in the vessels, and the formation of minute aneurysms
along them. The term arteriocapillary fibrosis has
a broader meaning, but is a cumbersome phrase, and conveys
the idea that the capillary changes are an essential
feature of the process, whereas these are for the most part
secondary to the changes in the arteries. The veins do
not always escape in the general morbid process, and when
these are affected the whole condition is sometimes called
vascular sclerosis or angiosclerosis.</p>
<p>Upon the anatomical structure of the arteries depends,
as a rule, the character and extent of the arteriosclerotic
lesions. For the clear comprehension of the process, it is
necessary to keep in mind the essential histological differences
between the aorta and the larger and smaller
branches of the arterial tree.</p>
<p>The vascular system is often likened to a central pump,
from which emanates a closed system of tubes, beginning<span class="pagenum"><a name="Page_27" id="Page_27">[27]</a></span>
with one large distributing pipe, which gives rise to a series
of tubes, whose number is constantly increasing at the
same time that their caliber is decreasing in size. From
the smallest of these tubes, larger and larger vessels collect
the flowing blood, until, at the pump, two large trunks
of approximately the same area as the one large distributing
trunk empty the blood into the heart, thus completing
the circle. This is but a rough illustration, and, while possibly
useful, takes into account none of the vital forces
which are constantly controlling every part of the distributing
system.</p>
<h4>General Structure of the Arteries</h4>
<p>The aorta and its branches are highly elastic tubes, having
a smooth, glistening inner surface. When the arteries
are cut open, they present a yellowish appearance, due to
the large quantity of elastic tissue contained in the walls.
The elasticity is practically perfect, being both longitudinal
and transverse. The essential portion of any blood vessel
is the endothelial tube, composed of flat cells cemented together
by intercellular substance and having no stomata
between the cells. This tube is reinforced in different
ways by connective tissue, smooth muscle fibers, and fibroelastic
tissue. Although the gradations from the larger to
the smaller arteries and from these to the capillaries and
veins are almost insensible, yet particular arteries present
structural characters sufficiently marked to admit of
histological differentiation.</p>
<p>The whole vascular system, including the heart, has an endothelial
lining, which may constitute a distinct inner coat,
the tunica intima, or may be without coverings, as in the
case of the capillaries. The intima (Fig. 1) consists typically
of endothelium, reinforced by a variable amount of fibroelastic
tissue, in which the elastic fibers predominate. The
tunica media is composed of intermingled bundles of elastic
tissue, smooth muscle fibers, and some fibrous tissue.
The adventitia or outer coat is exceedingly tough. It is<span class="pagenum"><a name="Page_28" id="Page_28">[28]</a></span>
usually thinner than the media, and is composed of fibroelastic
tissue. This division into three coats is, however,
somewhat arbitrary, as in the larger arteries particularly
it is difficult to discover any distinct separation into layers.</p>
<div class="figcenter bord" style="width: 415px;"><a name="Cross_section_of_a_large_artery" id="Cross_section_of_a_large_artery"></a>
<img src="images/fig_001.png" width="415" height="500" alt="Fig. 1.—Cross section of a large artery showing the division into the three coats; intima,
media, adventitia. The intima is a thin line composed of endothelial cells. The
wavy elastic lamina is well seen. The thick middle coat is composed of muscle fibers
and fibroelastic tissue. The loose tissue on the outer (lower portion of cut) side of the
media is the adventitia. (Microphotograph, highly magnified.)" title="Fig. 1.—Cross section of a large artery showing the division into the three coats; intima,
media, adventitia... (Microphotograph, highly magnified.)" />
<span class="caption">Fig. 1.—Cross section of a large artery showing the division into the three coats; intima,
media, adventitia. The intima is a thin line composed of endothelial cells. The
wavy elastic lamina is well seen. The thick middle coat is composed of muscle fibers
and fibroelastic tissue. The loose tissue on the outer (lower portion of cut) side of the
media is the adventitia. (Microphotograph, highly magnified.)</span>
</div>
<p>The muscular layer varies from single scattered cells, in
the arterioles, to bands of fibers making up the body of the
vessel in the medium-sized arteries and veins.</p>
<p>There is elastic tissue in all but the smallest arteries,
and it is also found in some veins. It varies in amount
from a loose network to dense membranes. In the intima
of the larger arteries the elastic tissue occurs as sheets,
which under the microscope appear perforated and pitted,
the so-called fenestrated membrane of Henle.</p>
<p>The nutrient vessels of the arteries and veins, the vasa
vasorum, are present in all the vessels except those less<span class="pagenum"><a name="Page_29" id="Page_29">[29]</a></span>
than one millimeter in diameter. The vasa vasorum course
in the external coat and send capillaries into the media,
supplying the outer portion of the coat and the externa
with nutritive material. The nutrition of the intima and
inner portion of the media is obtained from the blood circulating
through the vessel. Lymphatics and nerves are
also present in the middle and outer layers of the vessels.</p>
<h4>Arteries</h4>
<p>The structure of the arteries varies notably, depending
upon the size of the vessel. A cross section of the thoracic
aorta reveals a dense network of elastic fibers, occupying
practically all of the space between the single layer of
endothelial cells and the loose elastic and connective tissue
network of the outer layer. Smooth muscle fibers are
seen in the middle coat, but, in comparison with the mass
of elastic tissue, they appear to have only a limited function.</p>
<p>In a cross section of the radial artery one sees a wavy
outline of intima, caused by the endothelium following the
corrugations of the elastica. The endothelium is seen as
a delicate line, in which a few nuclei are visible. The
media is comparatively thick, and is composed of muscle
cells, arranged in flat bundles, and plates of elastic tissue.
Between the media and the externa the elastic tissue is
somewhat condensed to form the external elastic membrane.
The adventitia varies much in thickness, being better
developed in the medium-sized than in the large arteries.
It is composed of fibrous tissue mixed with elastic
fibers.</p>
<p>"Followed toward the capillaries, the coats of the artery
gradually diminish in thickness, the endothelium resting
directly upon the internal elastic membrane so long as the
latter persists, and afterward on the rapidly attenuating
media. The elastica becomes progressively reduced until
it entirely disappears from the middle coat, which then becomes
a purely muscular tunic, and, before the capillary is
reached, is reduced to a single layer of muscle cells. In<span class="pagenum"><a name="Page_30" id="Page_30">[30]</a></span>
the precapillary arterioles the muscle no longer forms a
continuous layer, but is represented by groups of fiber cells
that partially wrap around the vessel, and at last are replaced
by isolated elements. After the disappearance of
the muscle cells the blood vessel has become a true capillary.
The adventitia shares in the general reduction, and
gradually diminishes in thickness until, in the smallest arteries,
it consists of only a few fibroelastic strands outside
the muscle cells." (Piersol's Anatomy.)</p>
<p>The large arteries differ from those of medium size
mainly in the fact that there is no sharp line of demarcation
between the intima and the media. There is also much
more elastic tissue distributed in firm bundles throughout
the media, and there are fewer muscle fibers, giving a
more compact appearance to the artery as seen in cross
section. The predominance of elastic tissue permits of
great distention by the blood forced into the artery at
every heartbeat, the caliber of the tube being less markedly
under the control of the vasomotor nerves than is the case
in the small arteries, where the muscle tissue is relatively
more developed. The adventitia of the large arteries is
strong and firm, and is made up of interlacing fibroelastic
tissue, of which some of the bundles are arranged longitudinally.</p>
<h4>Veins</h4>
<p>The walls of the veins are thinner than those of the arteries;
they contain much less elastic and muscular tissue,
and are, therefore, more flaccid and less contractile. Many
veins, particularly those of the extremities, are provided
with cup-like valves opening toward the heart. These
valves, when closed, prevent the return of the blood to the
periphery and distribute the static pressure of the blood
column. The bulgings caused by the valves may be seen
in the superficial veins of the arm and leg. There are no
valves in the veins of the neck, where there is no necessity
for such a protective mechanism, gravity sufficing to drain
the venous blood from the cranial cavity.</p>
<p><span class="pagenum"><a name="Page_31" id="Page_31">[31]</a></span></p>
<h4>Capillaries</h4>
<p>These are endothelial tubes in the substance of the organs,
the tissue of the organ giving them the necessary
support. They are the final subdivisions of the blood vessels,
and the vast capillary area offers the greatest amount
of resistance to the blood flow, thus serving to slow the
blood stream and allowing time for nutritive substances
or waste products to pass from and to the blood. Usually
the capillaries are arranged in the form of a network,
the channels in any one tissue being of nearly uniform size,
and the closeness of the mesh depending upon the organ.</p>
<p>As far back as 1865, Stricker observed contraction of the
capillaries. This observation was apparently forgotten until
revived again by Krogh recently. The latter finds that
the capillaries are formed of cells which are arranged in
strands encircling the vessel. The capillaries are rarely
longer than 1 mm., and, according to Krogh, are capable of
enormous dilatation.</p>
<p>The rate of flow through any capillary area is very inconstant,
and the usual explanation has been that the capillaries
were endothelial tubes the blood flow of which was dependent
upon the contraction or dilatation of the terminal
arterioles. The actual fact that in an observed capillary
area some capillaries are empty renders the above explanation
untenable. The color of a tissue depends upon the state
of filling of the capillaries with blood.</p>
<p>It would seem that all the evidence now leads us to believe
that the capillaries themselves are contractile and it
is even possible that they may be under vasomotor control.
If the anatomic structure as stated above, is correct, it
would take but a slight contraction of the encircling cell to
shut off completely the capillary. When the enormous capillary
bed is considered, it is not inconceivable that circulating
poisons may act on large areas and produce a true
capillary resistance to the onflow of blood which might
express itself, if long continued, in actual hypertrophy of
the heart.</p>
<hr style="width: 65%;" />
<p><span class="pagenum"><a name="Page_32" id="Page_32">[32]</a></span></p>
<h2><a name="CHAPTER_II" id="CHAPTER_II"></a>CHAPTER II.</h2>
<h3>PATHOLOGY</h3>
<p>The whole subject of the pathology of arteriosclerosis has
been much enriched by the study of the experimental lesions
produced by various drugs and microorganisms upon the
aortas of rabbits. Simple atheroma must not be confused
with the lesions of arteriosclerosis. The small whitish or
yellowish plaques so frequently seen on the aorta and its
main branches, may occur at any age, and have seemingly
no great significance. Such plaques may grow to the size
of a dime or larger, and even become eroded. They represent
fatty degeneration of the intima which, at times, has
no demonstrable cause; at times follows in the course of
various diseases, and undoubtedly is due to disturbances of
nutrition in the intima. Except for the remote danger of
clot formation on the uneven or eroded spot, these places
are of no special significance, and are not to be confused
with the atheroma of nodular sclerosis.</p>
<p>The lesions of arteriosclerosis are of a different character.
It has been customary to differentiate three types:
(1) nodular; (2) diffuse; (3) senile. It must be understood
that this is not a classification of distinct types. As a rule
in advanced arteriosclerosis, lesions representing all types
and all grades are found. The nodular type, however, may
occur in the aorta alone, the branches remaining free. This
is most often found in syphilitic sclerosis where the lesion is
confined to the ascending portion of the arch of the aorta.</p>
<p>The retrogressive changes of advancing years can not
be rightly termed disease, yet it becomes necessary to regard
them as such, for the senile changes, as we shall see,
may be but the advanced stages of true arteriosclerosis.
Much depends on the nature of the arterial tissue and much<span class="pagenum"><a name="Page_33" id="Page_33">[33]</a></span>
on the factors at work tending to injure the tissue. A man
of forty years may therefore have the calcified, pipe stem
arteries of a man of eighty. Our parents determine, to
great extent, the kind of tissue with which we start life.
The arteries are elastic tubes capable of much stretching
and abuse. In the aorta and large branches there is much
elastic tissue and relatively little muscle. When the vessels
have reached the organs, they are found to be structurally
changed in that there is in them a relatively small amount
of elastic tissue but a great deal of smooth muscle. This
is a provision of nature to increase or decrease the supply
of blood at any point or points.</p>
<p>The aorta and the large branches are distributing tubes
only. It is after all in the arterioles and smaller arteries
that the lesions of arteriosclerosis do the most damage. A
point to be emphasized is that the whole arterial system is
rarely, if ever, attacked uniformly. That is, there may be
a marked degree of sclerosis in the aorta and coronary
arteries with very little, if any, change in the radials. On
the contrary, a few peripheral arteries only may be the seat
of disease. A case in point was seen at autopsy in which
the aorta in its entirety and all the large peripheral
branches were absolutely smooth. In the brain, however,
the arteries were tortuous, hard, and were studded with
miliary aneurysms. It is not possible to judge accurately
the state of the whole arterial system by the stage of the
lesion in any one artery; but on the whole one may say that
an undue thickening of the radial artery indicates analogous
changes in the mesenteric arteries and in the aorta.</p>
<p>So far as the anatomical lesions in the aorta and
branches are concerned, there is much uniformity even
though the etiologic factors have been diverse. The only
difference is one of extent. To Thoma we owe the first
careful work on arteriosclerosis. He regarded the lesion
in arteriosclerosis as one situated primarily in the media;
there is a lack of resistance in this coat. His views are<span class="pagenum"><a name="Page_34" id="Page_34">[34]</a></span>
now chiefly of historical interest. As the author understands
him, he considered a rupture in the media to be the
cause of a local widening and consequently the blood could
not be distributed evenly to the organ which was supplied
by the diseased artery or arteries. Moreover, there was
danger of a rupture at the weak spot unless this were
strengthened. It was essential for the even distribution of
blood that the lumen be restored to its former size. Nature's
method of repair was a hypertrophy of the subintimal
connective tissue and the formation of a nodule at
that point. The thickening was compensatory, resulting
in the establishment of the normal caliber of the vessel.
Thoma showed that by injecting an aorta in the subject of
such changes, with paraffin at a pressure of 160 mm. of mercury,
these projections disappeared and the muscle bulged
externally. He recognized the fact that the character of
the artery changed as the years passed, and to this form
he gave the name, primary arteriosclerosis. To the group
of cases caused by various poisonous agents, or following
high peripheral resistance and consequent high pressure,
he gave the name, secondary arteriosclerosis. This is a
useful but not essential division, as the changes which age
and high tension produce may not be different from those
produced in much younger persons by some circulating
poison. And most important to bear in mind, octogenarians
may have soft, elastic arteries.</p>
<p>As the body ages, certain changes usually take place in
the arteries leading to thickening and inelasticity of their
walls. This is a normal change, and in estimating the palpable
thickening of an artery, such as the radial, the age
of the individual must always be considered.</p>
<p>Thayer and Fabyan, in an examination of the radial
artery from birth to old age, found that, in general, the
artery strengthens itself, as more strain is thrown upon it,
by new elastica in the intima and connective tissue in the
media and adventitia. Up to the third decade there is only<span class="pagenum"><a name="Page_35" id="Page_35">[35]</a></span>
a strengthening of the media and adventitia. During the
third and fourth decades there is also distinct connective
tissue thickening in the intima. "In other words, the strain
has begun to tell upon the vessel wall, and the yielding tube
fortifies itself by the connective tissue thickening of the
intima and to a lesser extent of the media." By the fifth
decade the connective tissue deposits in the intima are
marked, there is an increase of fibrous tissue upon the
medial side of the intima and, in lesser degree, throughout
the media. "Finally, in these sclerotic vessels degenerative
changes set in, which are somewhat different from those
seen in the larger arteries, consisting, as they do, of local
areas of coagulation necrosis with calcification, especially
marked in the deep layers of the connective tissue thickenings
of the intima, and in the muscle fibers of the media,
particularly opposite these points. These changes may ... go
on to actual bone formation." The mesenteric
artery differs in some respects from the radial, but in the
main, the changes brought about by age are the same.
Thayer and Fabyan note two striking points of difference:
"(1) calcification is apparently much less frequent than in
the radials; (2) in several cases plaques were seen with
fatty softening of the deeper layers of the intima and superficial
proliferation—a picture which we have never seen in
the radial." (See Fig. 2.)</p>
<div class="figcenter bord" style="width: 434px;">
<a name="Cross_section_of_a_coronary_artery" id="Cross_section_of_a_coronary_artery"></a>
<img src="images/fig_002.png" width="434" height="500" alt="Fig. 2.—Cross section of a coronary artery, ×50, showing nodular sclerosis. Note the
heaping up of cells in the intima, the fracture of the elastica, and the destruction of the
media beneath the nodule. The primary lesion evidently was in the media. The thickened
intima is the effort on the part of nature to heal the breach. At such places as
shown here aneurysms may form. (Microphotograph.)" title="Fig. 2.—Cross section of a coronary artery, ×50, showing nodular sclerosis. Note the
heaping up of cells in the intima, the fracture of the elastica, and the destruction of the
media beneath the nodule.... (Microphotograph.)" />
<span class="caption">Fig. 2.—Cross section of a coronary artery, ×50, showing nodular sclerosis. Note the
heaping up of cells in the intima, the fracture of the elastica, and the destruction of the
media beneath the nodule. The primary lesion evidently was in the media. The thickened
intima is the effort on the part of nature to heal the breach. At such places as
shown here aneurysms may form. (Microphotograph.)</span>
</div>
<p>Aschoff's studies of the aorta show that, "in infancy the
elastic laminæ of the media stand out sharply defined, well
separated from each other by the muscle layers, which are
well developed.... From childhood there is to be observed
a slowly progressive increase in the elastic elements of the
media. Not only do the individual lamellæ seen in cross-sections
become thicker, but also they afford an increasing
number of fine secondary filaments feathering off from these
and crossing the muscle layer, so that now they are no
longer sharply defined, but more ragged upon cross-section.
This progressive increase attains its maximum at or about<span class="pagenum"><a name="Page_36" id="Page_36">[36]</a></span>
the age of thirty-five, and from now on for the next fifteen
years the condition is relatively stationary. After fifty
there is to be observed a slowly progressive atrophy of
the elastica. The media becomes obviously thinner and
presumably weaker." (Adami.) It has also been found
(Klotz) that after the age of thirty-five, the muscle of the
media begins to exhibit fatty degeneration which after fifty
years is well marked. The fatty degeneration may then
give place to a calcareous infiltration or the fibers may undergo
complete absorption. It would appear that the thinning
of the aortic media is due not so much to the atrophy
of the elastic tissue as to that of the muscle tissue. The
elastic tissue does lose its specific property and the artery
thus becomes practically a connective tissue tube.</p>
<p><span class="pagenum"><a name="Page_37" id="Page_37">[37]</a></span>Scheel has made very careful measurements of the
ascending, the thoracic, and the abdominal aorta, and the
pulmonary artery. He found that from birth to sixty
years, the aorta became progressively wider and lost its
elasticity. The pulmonary changed little, if at all, after
thirty to forty years, and where before it was wider than
the aorta, it now was found to be smaller. In chronic
nephritis both were widened. The continuous increase of
width and length of the aorta stands in reverse relationship
to the elasticity of its walls.</p>
<p>Although the division of the lesions into nodular, diffuse,
and senile has been the usual one, it is better to separate
three groups into (1) nodular, (2) diffuse or senile, and (3)
syphilitic. There is more known about the histology of
the syphilitic form and the lesions which consist of puckerings
and scars seen on opening an aorta just above the
valves, and on the ascending portion of the arch are characteristic.
A macroscopic examination suffices in most cases
for a definite diagnosis.</p>
<p>In the nodular form the lesions are found on the aorta
and large branches particularly at or near the orifices of
branching vessels. These nodules may increase in size,
forming rather large, slightly raised plaques of yellowish-white
color. They are, as a rule, irregularly scattered
throughout the aorta and branches and tend to be more
numerous and larger in the abdominal aorta. The initial
lesion is in the media, consisting of an actual dissolution of
this coat with rupture of the elastic fibers and infiltration
with small round cells. There is thus a weak spot in the
artery. Hypertrophy of the intimal cells takes place,
layer upon layer being added in an attempt to strengthen
the vessel at the injured place. Coincidently with this,
there is thickening by a connective tissue growth in the
adventitia. The process begins, at least in syphilis, around
the terminals of the vasa vasorum. It will be recalled that
the blood supply of the inner portion of the media comes<span class="pagenum"><a name="Page_38" id="Page_38">[38]</a></span>
from within the vessel itself. As the intimal growth increases,
the blood supply is cut off. The inevitable result
is softening of the portion farthest from the lumen of the
vessel. As a rule there has been a sufficient growth of connective
tissue in the media and adventitia to repair the
damage done to the media. This softening and dissolution
gives rise to a granular debris composed of degenerated
cells and fat. This is the so-called atheromatous abscess.
There are no leucocytes as in ordinary pus. These "abscesses"
are frequent and in rupturing leave open ulcers
with smooth bases, the atheromatous ulcer. A further
change which often takes place is calcification of the bases
of the ulcers and calcification of the softened spots before
rupture takes place. This only occurs in advanced cases.
(See Fig. 3.)</p>
<div class="figcenter bord" style="width: 201px;"><a name="Arteriosclerosis_of_the_thoracic_and_abdominal_aorta" id="Arteriosclerosis_of_the_thoracic_and_abdominal_aorta"></a>
<img src="images/fig_003.png" width="201" height="500" alt="Fig. 3.—Arteriosclerosis of the thoracic and abdominal aorta, showing irregular
nodules, atheromatous plaques, denudation of the intima, thin plates of bone scattered
throughout with spicules extending into the lumen of the vessel. Note the contraction
of the openings of the large branches, the rough appearance of the aorta and the greater
degree of sclerosis of the upper two-thirds, i. e., of the aorta above the diaphragm.
This aorta in the recent state was much thickened and almost inelastic." title="Fig. 3.—Arteriosclerosis of the thoracic and abdominal aorta, showing irregular
nodules, atheromatous plaques, denudation of the intima, thin plates of bone scattered
throughout with spicules extending into the lumen of the vessel...." />
<span class="caption">Fig. 3.—Arteriosclerosis of the thoracic and abdominal aorta, showing irregular
nodules, atheromatous plaques, denudation of the intima, thin plates of bone scattered
throughout with spicules extending into the lumen of the vessel. Note the contraction
of the openings of the large branches, the rough appearance of the aorta and the greater
degree of sclerosis of the upper two-thirds, i. e., of the aorta above the diaphragm.
This aorta in the recent state was much thickened and almost inelastic.</span>
</div>
<div class="figcenter" style="width: 359px;">
<a name="Arteriosclerosis_of_the_arch_of_the_aorta" id="Arteriosclerosis_of_the_arch_of_the_aorta"></a>
<img src="images/fig_004.png" width="359" height="500" alt="Fig. 4.—Arteriosclerosis of the arch of the aorta. Numerous calcified plaques,
thickening and curling of the aortic valves, giving rise to insufficiency of the aortic
valves. The aortic ring is rigid and not much dilated. (Milwaukee County Hospital.)" title="Fig. 4.—Arteriosclerosis of the arch of the aorta.... (Milwaukee County Hospital.)" />
<span class="caption">Fig. 4.—Arteriosclerosis of the arch of the aorta. Numerous calcified plaques,
thickening and curling of the aortic valves, giving rise to insufficiency of the aortic
valves. The aortic ring is rigid and not much dilated. (Milwaukee County Hospital.)</span>
</div>
<div class="figcenter bord" style="width: 200px;">
<a name="Normal_Aorta" id="Normal_Aorta"></a>
<img src="images/fig_005.png" width="200" height="500" alt="Fig. 5.—Normal aorta. Compare with Fig. 3. Note the perfectly smooth, glossy appearance
of the intima. The openings of all the intercostal arteries are distinctly seen.
In the recent state this artery was highly elastic, capable of much stretching both
transversely and longitudinally." title="Fig. 5.—Normal aorta. Compare with Fig. 3. Note the perfectly smooth, glossy appearance
of the intima. The openings of all the intercostal arteries are distinctly seen...." />
<span class="caption">Fig. 5.—Normal aorta. Compare with Fig. 3. Note the perfectly smooth, glossy appearance
of the intima. The openings of all the intercostal arteries are distinctly seen.
In the recent state this artery was highly elastic, capable of much stretching both
transversely and longitudinally.</span>
</div>
<p>Rather contrary to what one would expect, there are no
new capillaries advancing from the media to the intima in
the nodular form of arteriosclerosis, consequently there is
no granulation tissue to heal and leave scars. It must be
borne in mind that these changes rarely, if ever, are the
only ones found throughout the arterial system. Nevertheless,
the manifold changes, as will be shown within, appear
to be but stages of one primary process.</p>
<p>The character of the changes which are known as diffuse
arteriosclerosis seems to have, at first sight, little in common
with those of the nodular sclerosis. The aorta may
or may not have plaques of nodular sclerosis, while the
arteries, such as the radial or temporal, may be beaded or
pipe stem in hardness. In spite of these far advanced
peripheral lesions the aorta may appear smooth but it is
markedly dilated, particularly the thoracic portion, it is
noticeably thinned even on macroscopic examination, it
has elongated as evidenced by its slight tortuosity, and it
has lost the greater part of its elasticity. The abdominal
aorta is not so extensively affected, although this, too, shows
some elongation and slight thinning. This is considered by<span class="pagenum"><a name="Page_39" id="Page_39">[39]</a></span>
some pathologists to be the uncomplicated form of the so-called
senile arteriosclerosis. It is more of the nature of a
degenerative change, it is true, but, as will be shown later,
it has its beginnings, at times, in comparatively young persons<span class="pagenum"><a name="Page_40" id="Page_40">[40]</a></span>
and its etiology is not simple. This type has been
studied most carefully by Moenckeberg, who showed that on
the large branches of the aorta there were depressions due
to a degeneration of the middle coat. These depressions
encircled the vessel to a greater or lesser extent, causing<span class="pagenum"><a name="Page_41" id="Page_41">[41]</a></span>
small bulgings at such places and giving to the vessel a
beaded appearance. On viewing such an artery held to the
light, the sacculated spots are seen to be much thinner than
the contiguous normal artery. Associated with such
changes in the aorta and large branches is marked sclerosis
of the smaller arteries. Intimal fibrosis is common, together
with hypertrophy and fibrosis of the middle coat. Not infrequently
periarterial thickening is also seen. Calcification<span class="pagenum"><a name="Page_43" id="Page_43">[43]</a></span><span class="pagenum"><a name="Page_42" id="Page_42"></a></span>
of the media is found and is said to be preceded by hypertrophy
of the middle coat.</p>
<p>Pure cases of this, the so-called Moenckeberg type, are
seen but seldom. Most commonly there are nodules and
plaques in the aorta and large branches together with thinning
and sacculation of other portions of the vessels' walls.
While the two processes appear at a glance to be so different
from each other, it is possible for them to have a
common origin. The initial lesion is in the media but the
resulting sclerotic changes depend upon the kind of vessel,
the strength of the coats, the pressure in the vessel, and
other causes.</p>
<p>Thus the sclerosis of the radials of such an extent that
these arteries are easily palpable, appears to be a different
process from that of the sclerosis in the aorta, yet fundamentally
it is the same. The difference lies in the anatomic
structure of the two vessels, and possibly also in the
degree of stretching and strain to which the vessels are
subjected at every heart beat. In the radial artery the
media as usual is affected first. The muscle cells undergo
degeneration and either marked thickening takes place or
sacculation results, depending upon the severity of the exciting
cause. Calcification of the media is common. This
occasionally takes the form of rings encircling the vessel,
and gives to the examining finger the sensation of feeling
a string of fine beads. There may be calcification of the
subintimal tissue without deposits of lime salts in the media,
but this is more commonly found in the larger arteries.
When the calcification occurs in plates through the media,
the well known pipe stem vessel is produced. (Fig. 6.)</p>
<div class="figcenter bord" style="width: 290px;">
<a name="Radiogram_showing_calcification_of_both_radial_and_ulnar_arteries" id="Radiogram_showing_calcification_of_both_radial_and_ulnar_arteries"></a>
<img src="images/fig_006.png" width="290" height="500" alt="Fig. 6.—Radiogram of a man aged seventy-five, showing calcification of both radial and
ulnar arteries." title="Fig. 6.—Radiogram of a man aged seventy-five, showing calcification of both radial and
ulnar arteries." />
<span class="caption">Fig. 6.—Radiogram of a man aged seventy-five, showing calcification of both radial and
ulnar arteries.</span>
</div>
<p>The senile sclerosis found in old people is usually a combination
of the Moenckeberg type in the large and medium-sized
arteries, and the nodular type in the aorta, leading
eventually to calcareous intimal deposits, and widened,
elongated, inelastic aorta.</p>
<p><span class="pagenum"><a name="Page_44" id="Page_44">[44]</a></span></p>
<h4>Syphilitic Aortitis</h4>
<div class="figcenter" style="width: 375px;">
<a name="Syphilitic_aortitis_of_long_standing" id="Syphilitic_aortitis_of_long_standing"></a>
<img src="images/fig_007.png" width="375" height="500" alt="Fig. 7.—Syphilitic aortitis of long standing. The aortic valves are curled and
thickened, the heart is enlarged and the cavity of the left ventricle is dilated. (Milwaukee
County Hospital.)" title="Fig. 7.—Syphilitic aortitis of long standing. The aortic valves are curled and
thickened, the heart is enlarged and the cavity of the left ventricle is dilated. (Milwaukee
County Hospital.)" />
<span class="caption">Fig. 7.—Syphilitic aortitis of long standing. The aortic valves are curled and
thickened, the heart is enlarged and the cavity of the left ventricle is dilated. (Milwaukee
County Hospital.)</span>
</div>
<p>The seat of election of the syphilitic poison is in the aorta
just above the aortic valves, Fig. 7, and in the ascending
portion of the arch. There are semitranslucent, hyaline-like
plaques which have a tendency to form into groups and,<span class="pagenum"><a name="Page_45" id="Page_45">[45]</a></span>
instead of undergoing an atheromatous change as in the ordinary
nodular form of arteriosclerosis, they are prone to
scar formation with puckering, so that macroscopically the
nature of the process may, as a rule, be readily diagnosed.
Microscopically the process is found to be a subacute inflammation
of the media, which has been called a mesaortitis.
There is marked small celled infiltration around some
of the branches of the vasa vasorum and there appears to be
actual absorption of the tissue elements of the middle coat.
This is accompanied by hypertrophy of the intimal tissue.
There follows degeneration in the deeper portions of this
new tissue and new capillaries are formed which have their
origin in the inflammatory area in the media. As is everywhere
the case throughout the body, granulation tissue in
the process of healing contracts and forms scars. This explains
the scar formation in the aorta. When the process
is more acute, instead of there being a reparative attempt
on the part of the intima, there is actual stretching of the
wall at the weakened spot and there results an aneurysmal
dilatation. <b>Spirochetæ pallidæ</b> have been found in the degenerated
media and in small gummata which were situated
beneath the intima. Within the past years it has been
found that a large percentage of patients with cardiovascular
disease give the Wassermann reaction. In cases of
aortic insufficiency, the reaction is present in almost every
case. This is in marked contrast to the cases of diffuse endocarditis
where the reaction is rarely present.</p>
<p>According to Adami the effects of syphilis upon the aorta
are the following: (1) the primary disturbance is a granulomatous,
inflammatory degeneration of the media; (2) this
leads to a local giving way of the aorta; (3) if this be
moderate it results in a strain hypertrophy of the intima
and of the adventitia, with the development of a nodose intimal
sclerosis; (4) if it be extreme, there results, on the
contrary, an overstrain atrophy of the intima and aneurysm
formation; (5) the intimal nodosities are here not of an<span class="pagenum"><a name="Page_46" id="Page_46">[46]</a></span>
inflammatory type and are nonvascular, although, with the
progressive laying down of layer upon layer of connective
tissue on the more intimal aspect of the intima, the earlier
and deeper-placed layers of new tissue gain less and less
nourishment, and so are liable to exhibit fatty degeneration
and necrosis; (6) these products of necrosis exert a chemotactic
influence upon the nearby vessels of the medial granulation
tissue, with, as a result, (a) a secondary and late
entrance of new vessels into the early and deeply-placed
atheromatous area, (b) absorption of the necrotic products,
(c) replacement by granulation tissue, (d) contraction of
the granulation tissue, and (e) depression and scarring of
the sclerotic nodules so characteristic of syphilitic sclerosis.</p>
<p>In the smaller arteries and arterioles the arteriosclerotic
process appears on superficial examination to be a different
process from that in the aorta and large arteries, but the
difference is only apparent. It will be recalled that there
is relatively much more muscle tissue in the arterioles than
in the large arteries. The size, of course, is much less.
Large nodular plaques are not possible. The atheromatous
degeneration is not marked. In the smaller muscular
arteries is seen the intimal proliferation, the stretching of
the Moenckeberg type, and the calcification of the media
rather than the intima. The media is thinned beneath the
marked intimal proliferation so that the artery exhibits
translucent areas when held to the light. Again, there is
seen degeneration of the muscle and replacement by connective
tissue with or without hypertrophy of the intima.
In the arterioles three kinds of changes occur: a muscular
hypertrophy; a fibrosis of all the coats; or a marked proliferation
of the intimal endothelium. The last two are
probably the same process, the connective tissue having its
origin in the proliferated endothelial cells. Such a deposition
of layer upon layer of cells in an arteriole and the resulting
fibrosis leads to the condition of disappearance of
the lumen of the vessel, endarteritis obliterans. This obliterating<span class="pagenum"><a name="Page_47" id="Page_47">[47]</a></span>
endarteritis is not, of course, due alone to
syphilis. Syphilis is only a type of poison which produces
such changes as have been described above. It is in the
organs such as the kidney, liver, spleen, and intestines that
one sees the most perfect examples of this obliterating
endarteritis. Endarteritis deformans is a term applied to
the condition of the arteries as a result of irregular thickenings
and deposits of lime salts in the walls. These
changes give rise to marked tortuosity of the vessels.</p>
<p>Occasionally such an obliterating process takes place in
a larger artery. A thrombus forms and by a process of
central softening, new channels permeate the thrombus,
thus restoring to some extent the function of the vessel.</p>
<p>That the same process leads at one time to thinning and
at another time to thickening of the arterial walls has been
noted above. Prof. Adami holds that the regular development
of layer upon layer of new connective tissue is non-inflammatory.
He calls it a "strain hypertrophy." It is
analogous to the localized hypertrophy of bone where the
muscle tendons are attached, as is so frequently seen in
athletes. The increased tension on connective tissue, provided
that it is not overstrained, leads to its overgrowth,
but only when there is sufficient nourishment. Such conditions
are adequately fulfilled in the arteries. When a
local giving way under pressure occurs in the media, the
intima is put on the stretch (see Fig. 8), and there results
a hypertrophy of the intima until the volume of the new
tissue and the resistance which this affords to the mean distending
force, balances the loss sustained by the weakened
media. When the balance is struck, the hypertrophy is
arrested. The youngest tissue is thus found directly beneath
the endothelium. Now should this local weakening of
the media have an acute origin, instead of a stimulus to
growth there is overstrain, and there is, in consequence, not
hypertrophy but atrophy. The beginning process is here
a mesaortitis, but the acuteness of the poison, and the pressure<span class="pagenum"><a name="Page_48" id="Page_48">[48]</a></span>
from within the artery so stretches the artery that
there is no compensatory hypertrophy, but a thinning, and
the ground is prepared for aneurysmal dilatation or pouching.</p>
<div class="figcenter" style="width: 308px;">
<a name="Diagrammatic_representation_of_strain_hypertrophy" id="Diagrammatic_representation_of_strain_hypertrophy"></a>
<img src="images/fig_008.png" width="308" height="500" alt="Fig. 8.—I, media weakened at M' with overgrowth of intima filling in the depression.
II, with postmortem rigor and contraction of the muscles of the media and removal
of the blood pressure from within, the stretched media at M'' contracts; the intimal
thickening thus projects into the arterial lumen. (After Adami.)" title="Fig. 8.—I, media weakened at M' with overgrowth of intima filling in the depression.
II, with postmortem rigor and contraction of the muscles of the media and removal
of the blood pressure from within, the stretched media at M'' contracts; the intimal
thickening thus projects into the arterial lumen. (After Adami.)" />
<span class="caption">Fig. 8.—I, media weakened at M' with overgrowth of intima filling in the depression.
II, with postmortem rigor and contraction of the muscles of the media and removal
of the blood pressure from within, the stretched media at M'' contracts; the intimal
thickening thus projects into the arterial lumen. (After Adami.)</span>
</div>
<p>Again, one not infrequently encounters intimal nodosities
when the underlying media appears of normal thickness.
The explanation of this apparent exception is that the media
in the living aorta is actually thinned, but the layers of
subintimal tissue deposited over the weak spot due to strain
hypertrophy become bulged inward when the pressure is
relieved, as at postmortem. The media has not lost all of
its elasticity (see Fig. 9), hence it contracts and there is
the appearance of a nodule on the intima beneath which is a
media equal in thickness to that of the healthy surrounding
media.</p>
<div class="figcenter" style="width: 171px;">
<a name="Strain_hypertrophy" id="Strain_hypertrophy"></a>
<img src="images/fig_009.png" width="171" height="500" alt="Fig. 9.—Schematic representation of the increased strain brought to bear upon the
cells of the intima, Int., when the media, Med., undergoes a localized expansion through
relative weakness. (After Adami.)" title="Fig. 9.—Schematic representation of the increased strain brought to bear upon the
cells of the intima, Int., when the media, Med., undergoes a localized expansion through
relative weakness. (After Adami.)" />
<span class="caption">Fig. 9.—Schematic representation of the increased strain brought to bear upon the
cells of the intima, Int., when the media, Med., undergoes a localized expansion through
relative weakness. (After Adami.)</span>
</div>
<p>The essential lesion in arteriosclerosis of the aorta and
large arteries is a degeneration in the middle coat. This
may be brought about by a variety of poisons circulating in
the body. In syphilis, for example, the initial lesion has<span class="pagenum"><a name="Page_49" id="Page_49">[49]</a></span>
been shown to be a mesaortitis. The media seems to be dissolved,
the artery is consequently thinned, there is actual
depression along the level of the vessel. The elastic fibers
disappear and small-celled infiltration takes its place. The
intima hypertrophies, layer upon layer being added in an
attempt to restore the strength of the vessel. There is also,
as a rule, rather pronounced hypertrophy of the adventitia.</p>
<p><span class="pagenum"><a name="Page_50" id="Page_50">[50]</a></span></p>
<h4>Experimental Arteriosclerosis</h4>
<p>Within the past few years many workers have attempted
by various means, to produce arterial lesions in animals,
chiefly rabbits and dogs. The present status is somewhat
chaotic, some affirming and some denying that arterial
changes follow the various methods employed. Following
the injection of small, repeated doses of adrenalin over a
certain period of time, changes occur in the arteries of
rabbits which are arteriosclerotic in type, the essential
lesion being a degeneration of the muscular and elastic tissue
of the media with the consequent production of aneurysm
in the vessel. This is said by some to be quite like
the type of arteriosclerosis in man which has been so well
described by Moenckeberg. The degenerations in the arteries
following the experimental lesions are of the nature
of a fatty metamorphosis, and later proceed to calcification.
Barium chloride, digitalin, physostigmin, nicotin and other
substances, as well as adrenalin, have been found to exert
a selective toxic action on the muscle cells of the middle
coat of the aorta. The infundibular portion of the pituitary
body, the portion which is developed from the infundibulum
of the brain, possesses an internal secretion, which, injected
intravenously, causes a marked rise of blood pressure and
slowing of the heart beat. So far as I know, this active
principle of the gland has not been used in an attempt to
produce experimentally the lesions of arteriosclerosis.</p>
<p>Wacker and Hueck succeeded in producing aortic disease
in rabbits which they considered to be in many points
quite like human arteriosclerosis. They injected the rabbits
intravenously with cholesterin. They feel that this is
of great importance in view of the fact that exercise (muscle
metabolism) dyspnea, certain poisons, as well as adrenalin,
and even adrenal extirpation occasion a high cholesterin
content of the blood. Anitschow's experiments are
confirmatory. He fed rabbits on large amounts of cholesterin-containing substances<span class="pagenum"><a name="Page_51" id="Page_51">[51]</a></span>
(yolk of egg, brain tissue) and
pure cholesterin and found changes in the intima and inner
portion of the media consisting of fatty infiltration between
the muscle and elastic fibres, advent of small round cells
and large phagocytic cells containing fat droplets of cholesterin
esters. The elastic fibres were dissolved, broken up
into fibrillæ and these seemed to be absorbed. The internal
elastic lamina as such disappeared and the inner layer of
the aorta fused with the middle coat. He considers these
changes to be quite analogous to those found in human
aortas.</p>
<p>Oswald Loeb produced changes in the arteries of rabbits
by feeding them sodium lactate (lactic acid). His controls
fed on other acids became cachectic, but showed no arterial
changes. He further found that in 100 gm. of human blood
there was normally from 15 to 30 mg. of lactic acid. After
heavy work, he found as much as 150 gm. He considers
that after adrenalin or nicotin injections, the function of the
liver is so disturbed that lactic acid is not bound. The arteriosclerosis
is actually due to the presence of free lactic
acid in the circulation. He succeeded, also, in producing
lesions of the intima in a dog fed for a long time on protein
poor diet, plus lactic acid and sodium lactate.</p>
<p>Another investigator, Steinbiss, fed rabbits on animal
proteins only, a diet totally foreign to their natural habits.
He succeeded, however, in keeping some alive for three
months. He also tried various substances and in the general
conclusions says that no aortic changes could be produced
in animals kept in natural living conditions by any mechanical
means, increase of blood pressure, digital compression,
hanging by hind legs, etc. In infectious diseases, especially
septic, widespread sclerotic changes occurred in the aorta.
A most suggestive conclusion in this "the most important
result of feeding rabbits with animal proteins is, along with
a constant glycosuria, disease of the aorta and peripheral
arteries which is identical with changes in the aorta produced<span class="pagenum"><a name="Page_52" id="Page_52">[52]</a></span>
by injections of adrenalin. The degree of disease of
the circulatory system increases with the duration of the
experiment."</p>
<p>By a small addition of vegetable to the protein diet, the
lives of the animals were prolonged at will. With this
modification of the experiment, the findings in the vessel
walls were noticeably altered. The changes affected chiefly
the intima, to less degree the media, and histologically were
very much like human intimal disease.</p>
<p>I have been unable to produce the slightest arterial lesions
in rabbits by intravenous injections of lead. Frothingham
had no success feeding animals with lead. In a
study of autopsy material from persons up to 40 years, who
died of infectious disease, he found changes in the arteries
of those who had succumbed to infection with the pus cocci
or to very severe infectious disease. These changes were,
however, localized, and were not like those of the general
diffuse arteriosclerosis.</p>
<p>Adler has recently reported experiments on dogs, to
which he fed or injected intravenously various substances
supposed to induce arteriosclerotic changes. He was unable
to find any arterial lesions comparable to human arteriosclerosis.</p>
<p>The difficulty experienced by experimenters is not surprising
when the character of the changes is considered.
Arteriosclerosis is not an acute process. In its very nature,
it is of months' or years' standing, the specific changes are
of slow growth, and more in the nature of degeneration. It
would seem that a very careful study of the histories of
those with arteriosclerosis and a final examination upon the
actual tissue might eventually give us data for the etiology.</p>
<p>The most frequent site of disease in these experimental
lesions is the thoracic aorta, and it is there also that the
most severe changes are seen. While the toxic action is felt
in the vessels all over the body, the lesions are, as a rule,
scattered and small. The thoracic aorta stands the brunt<span class="pagenum"><a name="Page_53" id="Page_53">[53]</a></span>
of the high pressure, and this combined with the poisonous
action of the drug or drugs, results in the formation of a
fusiform aneurysmal dilatation which stops at the diaphragmatic
opening. The aortic opening in the diaphragm
seems to act as a flood gate, allowing only a certain amount
of blood to flow through, and thus the abdominal aorta is
protected to a great extent from the deleterious effects of
increased pressure. Focal degenerative lesions are, however,
found in the abdominal aorta.</p>
<p>Changes somewhat analogous to those found in the human
aorta as the result of intimal proliferations, are produced
in animals by the toxins of the typhoid bacillus and the
Streptococcus pyogenes. Clinically, Thayer and Brush
have found that the arteries of those who have recovered
from an attack of typhoid fever are more palpable than the
arteries of average individuals of equal age who have never
had the disease.</p>
<p>Experimentally, the changes caused by the toxins above
noted are proliferations of cells in the intima and subintimal
tissues, and a breaking up of the internal elastic laminæ
into several parallel layers which stretch themselves among
the proliferating cells. The diphtheria toxin, on the contrary,
produces a lesion more like that caused by adrenalin.
All pathologists are not agreed as to whether the experimental
lesions produced by blood pressure raising drugs
are similar to the arteriosclerotic changes in the arteries
of man.</p>
<p>Some of the work on rabbits has been discredited for the
reason that arteriosclerosis appears spontaneously in about
fifteen per cent of all laboratory rabbits. Furthermore,
comparatively young rabbits have been found with arteriosclerosis.
O. Loeb, however, denies this. He has examined
in the course of eight years 483 healthy rabbits and never
found arterial changes. The spontaneous lesions can not
be distinguished histologically from those due to adrenalin.<span class="pagenum"><a name="Page_54" id="Page_54">[54]</a></span>
They differ macroscopically in that the lesion is usually
limited to a few foci near the origin of the aorta.</p>
<p>Lesions produced by the drugs enumerated above represent
one type of experimental arteriosclerosis. More interesting
and important are the experiments which seem to
show that high tension alone is capable of producing lesions
in arteries which in all respects correspond to Adami's
strain hypertrophy and overstrain theory. It has been
shown that when a portion of vein is placed under conditions
of high arterial pressure, as in a transplantation of a
portion of vein into a carotid artery, the vein undergoes
marked connective tissue hypertrophy which includes all
the coats. This is evidently strain hypertrophy. Again, it
has been demonstrated that by suspending a previously
healthy rabbit by the hind legs for three minutes daily over
a period of three to four months, there results hypertrophy
of the heart with thinning and dilatation of the arch and the
upper part of the thoracic aorta. No change was found in
the abdominal aorta. The carotids, however, were larger
than normal and they showed typical intimal sclerosis with
connective tissue thickening.</p>
<p>Neither I nor others have been able to confirm this experiment,
so it is very doubtful whether mechanical pressure
alone can produce true arteriosclerosis. Some evidence
is adduced to bear on this point, however, in the fact
that sclerosis of the pulmonary artery follows often upon
mitral stenosis. Yet we do not know but that factors other
than pressure alone produce the arteriosclerotic change in
such cases, so we are forced back on our conclusion expressed
above; viz., that experiments on animals fail to
sustain the purely mechanical origin of arteriosclerosis.</p>
<p>The changes in the intima constitute the effort on the
part of nature to repair a defect in the vessel wall which is
to compensate for the weakened media and the widened
lumen. This applies only to true arteriosclerosis, not to<span class="pagenum"><a name="Page_55" id="Page_55">[55]</a></span>
the condition produced experimentally by the toxin of the
typhoid bacillus, for example.</p>
<p>When an artery loses its elasticity and begins to have
connective tissue deposited in its walls, the pressure of the
blood stretches the vessel which is now no longer capable of
retracting when the pulse wave has passed, and, in consequence,
the artery is actually lengthened. This necessarily
causes a tortuosity of the vessel which can be easily seen in
such arteries as the temporals, brachials, radials, and other
arteries near the surface of the skin.</p>
<p>The exact mechanism of increase of blood pressure is not
satisfactorily explained. The smaller arteries all over the
body are supplied with vasoconstrictor and vasodilator
nerve fibers from the sympathetic nervous system. Normally
when an organ is actively functionating the vessels
are widely dilated and the flow of blood is rapid. Among
the many factors which influence blood pressure and blood
supply must be reckoned the psychic.</p>
<p>We know that normally there is a certain resistance
offered to the propulsion of blood through the arteries by
the contraction of the heart. This tonus is essential to the
maintenance of an equalized circulation. The muscular
arterioles throughout the body by their tonus serve to keep
up the normal blood pressure and to distribute the blood
evenly to the various organs. Contraction of a large area
of arterioles increases the blood pressure and, strangely
enough, the arteries respond to increased arterial pressure,
not by dilatation, but by contraction. It would appear that
rise of blood pressure tends to throw increased work upon
the musculature of the arterioles. This may be sufficient
only to cause them to hypertrophy, but further strain may
easily lead to exhaustion and to dilatation. "As a result
strain hypertrophy of the intima shows itself with thickening,
and it may also be of the adventitia, resulting in chronic
periarteritis. And now with continued degeneration of the
medial muscle in those muscular arteries, fibrosis of the<span class="pagenum"><a name="Page_56" id="Page_56">[56]</a></span>
media may also show itself. I would thus regard muscular
hypertrophy of the arteries and fibrosis of the different
coats as different stages in one and the same process.
Whether these peripheral changes are the more marked, or
the central, depends upon the relative resisting power of
the elastic and muscular arteries of the individual respectively."
(Adami.)</p>
<div class="figcenter bord" style="width: 417px;">
<a name="Cross_section_of_small_artery_in_the_mesentery" id="Cross_section_of_small_artery_in_the_mesentery"></a>
<img src="images/fig_010.png" width="417" height="500" alt="Fig. 10.—Cross-section of a small artery in the mesentery. Note that the vessel appears
capable of being much widened. The internal elastic lamina is thrown into folds
somewhat resembling the convolutions of the brain. Note also that the middle coat
of the artery is composed almost entirely of muscle. The enormous number of such
vessels in the mesentery and intestines explains the ability of the splanchnic area to
accommodate the greater part of the blood in the body. Universal constriction of these
vessels would naturally render the intestines anemic. The vasomotor control of these
vessels plays an important rôle in the distribution of the blood. Small arteries in the
skin and in other organs, possibly the brain, have a similar function. (Microphotograph,
highly magnified".)" title="Fig. 10.—Cross-section of a small artery in the mesentery... (Microphotograph,
highly magnified.)" />
<span class="caption">Fig. 10.—Cross-section of a small artery in the mesentery. Note that the vessel appears
capable of being much widened. The internal elastic lamina is thrown into folds
somewhat resembling the convolutions of the brain. Note also that the middle coat
of the artery is composed almost entirely of muscle. The enormous number of such
vessels in the mesentery and intestines explains the ability of the splanchnic area to
accommodate the greater part of the blood in the body. Universal constriction of these
vessels would naturally render the intestines anemic. The vasomotor control of these
vessels plays an important rôle in the distribution of the blood. Small arteries in the
skin and in other organs, possibly the brain, have a similar function. (Microphotograph,
highly magnified.)</span>
</div>
<p>It is conceivable that in one section of the body the vessels<span class="pagenum"><a name="Page_57" id="Page_57">[57]</a></span>
may be markedly contracted, but if there is dilatation in
some other part there will be no increased work on the part
of the heart, and theoretically, there should be no rise of
blood pressure. The vascular system, however, while likened
to a system of rubber tubes, must be regarded as a
very live system, every subsystem having the property of
separate control.</p>
<p>For blood tension to be raised all over the body, conditions
must favor the generalized contraction of a large area
of arterioles. Some authors consider that the so-called
viscosity of the blood also is a factor in the causation of
increased tension. The usual cause for the high tension is
probably the presence in the blood of some poisonous substance.</p>
<p>It is held by some authors that the great splanchnic area
is capable of holding all the blood in the body and in respect
of its liability to arteriosclerosis, it is second only to the
aorta and coronary arteries. The enormous area of the
skin vessels could probably contain most of the blood.
The tone of the vasoconstrictor center controls the distribution
of blood throughout the body. The fact that the vessels
in the splanchnic area are frequently attacked by
sclerotic changes means, as a rule, increase of work for
the heart.<a name="FNanchor_1_1" id="FNanchor_1_1"></a><a href="#Footnote_1_1" class="fnanchor">[1]</a> The resistance offered to the passage of the
blood must be great and signifies that, for blood to travel at
the same rate that it did before the resistance set in, more
power must be expended in its propulsion. In other words,
the heart must gradually become accustomed to the changed
conditions, and, as a result of increased work, the muscle
hypertrophies. (See Fig. 11.)</p>
<div class="figcenter" style="width: 500px;">
<a name="Enormous_hypertrophy_of_left_ventricle" id="Enormous_hypertrophy_of_left_ventricle"></a>
<img src="images/fig_011.png" width="500" height="357" alt="Fig. 11.—Enormous hypertrophy of left ventricle probably due to prolonged increased
peripheral resistance. Note that the whole anterior surface of the heart is occupied
by the left ventricle. The right ventricle does not appear to be much affected.
× ⅔." title="Fig. 11.—Enormous hypertrophy of left ventricle probably due to prolonged increased
peripheral resistance. Note that the whole anterior surface of the heart is occupied
by the left ventricle. The right ventricle does not appear to be much affected.
× ⅔." />
<span class="caption">Fig. 11.—Enormous hypertrophy of left ventricle probably due to prolonged increased
peripheral resistance. Note that the whole anterior surface of the heart is occupied
by the left ventricle. The right ventricle does not appear to be much affected.
× ⅔.</span>
</div>
<p>In diffuse arteriosclerosis accompanied by chronic nephritis
the heart is always hypertrophied. This is a result, not<span class="pagenum"><a name="Page_58" id="Page_58">[58]</a></span>
a cause of the condition. In the pure type, there is hypertrophy
only of the left ventricle without dilatation of the
chamber. The muscle fibers are increased in number and in
size, and there are frequently areas of fibrous myocarditis
due to necrosis caused by insufficient nutrition of parts of
the muscle. In these cases the coronary arteries share in
the generalized arteriosclerotic process. The openings of
the arteries behind the semilunar valves may be very small.
There is often thickening and puckering of the aortic valves
and of the anterior leaflet of the mitral valve leading, at
times, to actual insufficiency of the orifice. Later, when the
heart begins to weaken, there is dilatation of the chambers
and loud murmurs result, caused by the inability of the nondistensible
valves to close the dilated orifices. Until the
compensation is established, it is impossible to say whether
or not true insufficiency is present.</p>
<p><span class="pagenum"><a name="Page_59" id="Page_59">[59]</a></span>In senile arteriosclerosis there is the physiologic atrophy
of the media to be reckoned with. This change has already
been referred to. When such degeneration has taken place,
the normal blood pressure may be sufficient to cause stretching
of the already weakened media with or without hypertrophy
of the intima. The arteries may be so lined with
deposits of calcareous matter that they appear as pipe
stems. More frequently there are rings of calcified material
placed closely together or irregular beading, giving to the
palpating finger the impression of feeling a string of very
fine beads. The arteries are often tortuous, hard, and are
absolutely nondistensible. At times no pulse wave can be
felt.</p>
<p>The larger arteries such as the brachials and femorals
are most affected. The walls become thinned and show
cracks, and areas apparently, but not actually denuded of
intima. Yellowish-white, irregular, raised plaques are scattered
here and there. Interspersed among these areas are
irregularly shaped clean-cut ulcers having as a rule a
smooth base, and frequently on the base is a thin plate of
calcified matter. The color of these denuded areas is usually
brownish red or reddish brown. White thrombi may
be deposited on these areas. The danger of an embolus
plugging one of the smaller arteries is great and probably
happens more often than we think. The collateral circulation
is able to supply the thrombosed area. Should the
thrombus be on the carotid arteries, hemiplegia may result
from cerebral embolism. On microscopic examination of
the arteries there is seen extreme degeneration of all the
coats, the degeneration of the media leading almost to an
obliteration of that coat. On seeing such arteries as these
one wonders how the circulation could have been maintained
and the organs nourished. Senile atrophy of the
internal organs naturally goes hand in hand with such
arterial changes.</p>
<p>There is, as a rule, no increase in arterial tension; on the<span class="pagenum"><a name="Page_60" id="Page_60">[60]</a></span>
contrary, the pressure is apt to be low. This is readily
understood when the heart is seen. This organ is small,
the muscle is much thinned, it is flabby and of a brownish
tint, the so-called "brown atrophy." Microscopically,
there is seen to be much fragmentation of the fibers with
a marked increase of the brown pigment granules which
surround the cell nuclei. Cases are seen, however, in which
blood pressure increases as the patient grows older. The
hearts in such cases are more or less hypertrophied and
show extensive areas of fibroid myocarditis.</p>
<p>From what has been said, it follows that hypertension
alone may be the cause of arteriosclerosis; that certain
poisons in the blood which attack the media and cause it
to degenerate and weaken cause arteriosclerosis without
increased blood pressure; that the normal blood pressure
may be, for the artery which is physiologically weakened in
an individual over fifty, really hypertension, and arteriosclerosis
may result. Our observations lead us to believe
that the process is at bottom one and the same. The different
types noted clinically depend upon the nature of the
etiologic factors and the kind of arterial tissue with which
the individual is endowed. This view at least brings some
order out of previous chaos, and corresponds well with our
present knowledge of the disease.</p>
<p>There are many cases of arteriosclerosis which lead to
definite interference with the closure of the valves of the
heart, particularly the aortic and the mitral. It has been
said that puckerings of the valves frequently occur (Fig.
12). This arteriosclerotic endocarditis at times leads to
very definite heart lesions, chiefly aortic or mitral insufficiency,
or both with, at times, murmurs of a stenotic character
at the base. There is rarely true aortic stenosis,
however. The murmur is caused by the passage of the
blood over the roughened valves and into the dilated aorta.
Aortic stenosis is one of the rarest of the valvular lesions
affecting the valves of the left heart, and should be diagnosed<span class="pagenum"><a name="Page_61" id="Page_61">[61]</a></span>
only when all factors, including the typical pulse
tracings, are taken into consideration.</p>
<div class="figcenter" style="width: 500px;">
<a name="Aortic_incompetence_with_hypertrophy_and_dilatation_of_left_ventricle" id="Aortic_incompetence_with_hypertrophy_and_dilatation_of_left_ventricle"></a>
<img src="images/fig_012.png" width="500" height="451" alt="Fig. 12.—Aortic incompetence with hypertrophy and dilatation of left ventricle, the
result of arteriosclerosis affecting the aortic valves. Note how the valves have been curled,
thickened, and shortened, the edges of valves being a half inch below the upper points
of attachment. The anterior coronary artery is shown, the lumen narrowed. (Reduced
one-half.)" title="Fig. 12.—Aortic incompetence with hypertrophy and dilatation of left ventricle, the
result of arteriosclerosis affecting the aortic valves.... (Reduced
one-half.)" />
<span class="caption">Fig. 12.—Aortic incompetence with hypertrophy and dilatation of left ventricle, the
result of arteriosclerosis affecting the aortic valves. Note how the valves have been curled,
thickened, and shortened, the edges of valves being a half inch below the upper points
of attachment. The anterior coronary artery is shown, the lumen narrowed. (Reduced
one-half.)</span>
</div>
<p>The kidneys, as a rule, show extensive sclerosis. They
are small, firm, and contracted and not always to be differentiated
from the contracted kidneys of chronic inflammation.
The lesions of the arteriosclerotic kidney are due
to narrowing and eventual obstruction of the afferent vessels.
The organs are usually bright red or grayish red in
color. At times there is marked fatty degeneration of
cortex and medulla, giving to them a yellowish streaking.
The capsule is here and there adherent, the cortex is much
thinned and irregular. The surface presents a roughly<span class="pagenum"><a name="Page_62" id="Page_62">[62]</a></span>
granular appearance. The glomeruli stand out as whitish
dots and the sclerosed arteries are easily recognized, as
their walls are much thickened. The process does not, as
a rule, affect the whole kidney equally, but rather affects
those portions corresponding to the interlobular arteries.
The replacement of the normal kidney tissue by connective
tissue and the resulting contraction of this latter tissue
leads to the formation of scars. As the process is not regular,
the scarring is deeper in some places than in others,
with the result that localized rather sharply depressed
areas appear on the surface. The pelvis is relatively large
and is filled with fat. The renal artery is often markedly
sclerosed and the whole process may be due to localized
thickening of the artery, or as part of a general arteriosclerosis.
The latter is the more frequent. Microscopically,
it is seen that the tubules are atrophied, the Bowman's
capsules are, as a rule, thickened, and the glomeruli are
shrunken or have been replaced by fibrous tissue. In places
they have fallen out of the section. There is marked proliferation
of connective tissue in cortex and medulla. The
arterioles are thickened, the sclerosis being either of the
intima or media or of both. There is even occlusion of
many arterioles.</p>
<p>Changes in other organs as the result of arteriosclerosis
of their afferent vessels occur, but are not so characteristic
as in the kidney. In the brain the result of gradual thickening
of the arterioles is a diminished blood supply, softening
of the portion supplied by the artery, and later a connective
tissue deposit. The occurrence of thrombi is favored
and, now and again, a thrombus plugs an artery
which supplies an important and even vital part of the
brain. The arteries of the brain are end arteries, hence
there is no chance for collateral circulation. It is therefore
evident how serious a result may follow the disturbance
in or actual deprivation of blood supply to any of the
brain centers or to the internal capsule.</p>
<p><span class="pagenum"><a name="Page_63" id="Page_63">[63]</a></span></p>
<h4>Arteriosclerosis of the Pulmonary Arteries</h4>
<p>There have been a number of cases of sclerosis of the
pulmonary arteries, either alone, or associated with general
systemic arteriosclerosis.</p>
<p>A primary and a secondary form are recognized, the former
in conjunction with congenital malformations of the
heart, the latter as the result of severe infection or of mitral
stenosis. These two causes seem to be the most important
in the production of the arterial changes. The cases
thus far described have revealed widespread thickening
of the pulmonary arteries. If one may judge by the description
of the pathologic changes, the condition is quite
similar to that produced in a vein by transplantation along
the course of an artery. The diffuse form with connective
tissue thickening of all coats has been generally described.
There is also obliterating endarteritis of the smaller vessels.
In the etiology of the condition severe infection seems
to play a prominent rôle. The constant presence of right
ventricular hypertrophy is interesting, the heart dullness
extends, as a rule, far to the right of the sternum. In some
of the cases no demonstrable changes were observed in the
bronchial arteries or in the pulmonary veins.</p>
<p>Sanders has described a case of primary pulmonary arteriosclerosis
with hypertrophy of the right ventricle.</p>
<p>Recently Warthin<a name="FNanchor_2_2" id="FNanchor_2_2"></a><a href="#Footnote_2_2" class="fnanchor">[2]</a> has reported a case of syphilitic
sclerosis of the pulmonary artery which places the lesion
in exactly the same category as that of syphilis in the systemic
arteries. There was also aneurysm of the left upper
division present and, to settle the etiologic nature of the
process, Spirochete pallida were found in the wall of the
aneurysm sac and in that of the pulmonary artery. The
microscopic picture in the pulmonary artery could not be
told from that in a syphilitic aorta.</p>
<p><span class="pagenum"><a name="Page_64" id="Page_64">[64]</a></span></p>
<h4>Sclerosis of the Veins</h4>
<p>Phlebosclerosis not infrequently occurs with arteriosclerosis.
It is seen in those cases characterized by high blood
pressure. Such increased pressure in the veins is due, for
example, to cirrhosis of the liver which affects the portal
circulation, or to mitral stenosis which affects the pulmonary
veins. The affected vessels are usually dilated. The
intima shows compensatory thickening especially where the
media is thinned. As a rule all the coats are involved in the
connective tissue thickening. Occasionally hyaline degeneration
or calcification of the new-formed tissue is seen.
"Without existing arteriosclerosis the peripheral veins
may be sclerotic usually in conditions of debility, but not infrequently
in young persons." (Osler.)</p>
<p>In many cases of arteriosclerosis, the pathologic changes
are not confined to the arteries, but are found in the veins
as well as in the capillaries. Such cases could be called
angiosclerosis.</p>
<hr style="width: 65%;" />
<p><span class="pagenum"><a name="Page_65" id="Page_65">[65]</a></span></p>
<h2><a name="CHAPTER_III" id="CHAPTER_III"></a>CHAPTER III.</h2>
<h3>PHYSIOLOGY OF THE CIRCULATION</h3>
<p>No attempt will be made to cover the entire subject of
the physiology of the circulation. Only in so far as it relates
to arteriosclerosis and blood pressure and has a bearing
on the probable explanation of blood pressure phenomena
will it be discussed.</p>
<p>"The heart and the blood vessels form a closed vascular
system, containing a certain amount of blood. This blood
is kept in endless circulation mainly by the force of the
muscular contractions of the heart; but the bed through
which it flows varies greatly in width at different parts of
the circuit, and the resistance offered to the moving blood
is very much greater in the capillaries than in the large
vessels. It follows, from the irregularities in size of the
channels through which it flows, that the blood stream is
not uniform in character throughout the entire circuit—indeed,
just the opposite is true. From point to point in
the branching system of vessels the blood varies in regard
to its velocity, its head of pressure, etc. These variations
are connected in part with the fixed structure of the system
and in part are dependent upon the changing properties of
the living matter of which the system is composed." (W.
H. Howell.)</p>
<p>If the vascular system were composed of a central pump,
projecting at every stroke a given amount of liquid into
a series of rigid tubes, the aggregate cross sections of which
were equal to the cross section of the main pipe, then the
velocity at the openings would be the same as at the source
(making allowances for friction). The problem would then
be a simple one. In the circulation of the blood no such
simple condition obtains. The capillary beds is an enormous<span class="pagenum"><a name="Page_66" id="Page_66">[66]</a></span>
area through which the blood flows slowly. From the
time the blood is thrown into the aorta the velocity begins
to diminish until it reaches its minimum in the capillaries.
In no two persons is the initial velocity at the heart the
same, nor in the same person is it the same at all times of
day. The size of the heart, the actual strength of the
muscle, the amount of blood ejected at every beat, and the
size and elasticity of the aorta are some of the factors which
determine the velocity of blood at the aortic orifice. When
to these factors are added the differences in arterial tissue,
the activity or resting stage of the various organs, etc., the
question becomes exceedingly complicated. In spite of
these many disturbing elements, attempts more or less successful
have been made to estimate the velocity of the blood
in animals. Thus, in the carotid of the horse the velocity
was found to be 300 mm. per second (Volkman) and 297
mm. (Chauveau); in the carotid of the dog, 260 mm.
(Vierordt). In the jugular vein of the dog Vierordt found
the velocity to be 225 mm. per second. These figures do
not represent the actual velocity of the blood in all horses
or all dogs, but they do give us some general idea of the
rate of flow of the blood. For man it has been calculated
that the velocity in the aorta is about 320 mm. per second.
The velocity is not uniform in the large arteries, where at
every heart beat there is a sudden increase followed by a
decrease as the heart goes into diastole. The farther away
from the heart the measurements are made the more even
is the flow.</p>
<p>Observations by W. H. Luedde with the Zeiss binocular
corneal microscope on the rate of flow in the conjunctival
capillaries must modify somewhat our former conceptions.
He finds that "The rate varies in the different arteries,
capillaries, and veins from a barely perceptible motion to
a little more than 1 mm. per second. Further, some parts
of the capillary network are ordinarily supplied with blood
elements only occasionally. This is shown by the passage<span class="pagenum"><a name="Page_67" id="Page_67">[67]</a></span>
of a column of corpuscles along a certain line, followed
after an interval of seconds, during which no corpuscles
pass, by another column in the same line as before."</p>
<p>The vessels of the conjunctiva probably are quite like
superficial vessels in the skin and mucous membranes.
Therefore, we must be free to admit that the circulation
in them is not absolutely steady. Luedde found further that
in syphilitics there were tortuosities, irregularities, minute
aneurysmal dilatations and even obliterations of capillaries.
Some of the changes occurred as early as one month after
infection.</p>
<p>The rate in the capillaries of man is estimated to be between
0.5 mm. and 0.9 mm. per second. As the blood is
collected into the veins and the bed becomes smaller, the
velocity increases until at the heart it is almost the same
as in the aorta. That the velocity could not be exactly the
same is evident from the fact that the cross section of the
veins, which return the blood to the right auricle, is greater
than is the cross section of the aorta.</p>
<p>The volume of the bed is subject to rapid and wide
fluctuations, which are dependent on many causes, both
physiologic and pathologic. The call of an actively functionating
organ or group of organs causes a widening
of a more or less extensive area, and the velocity necessarily
varies. In states of great relaxation of the vessels there
may be a capillary pulse. In order to force blood at the
same rate through dilated vessels as through normal vessels,
there must be more blood or there must be a more
rapid contraction of the central pump. What actually
happens, as a rule, is an increase in the rate of the heart
beat. There are conditions—such, for example, as aortic
insufficiency—where actually more blood is thrown into
the circulation at every beat, so that the rate is not
changed.</p>
<p>It has been calculated that the average amount of blood
thrown into the aorta at every systole of the heart is from<span class="pagenum"><a name="Page_68" id="Page_68">[68]</a></span>
50 to 100 c.c. This is forcibly ejected into a vessel already
filled (apparently) with blood. In order to accommodate
this sudden accession of fluid, the aorta must expand. The
aortic valves close, and during diastole the blood is forced
through the vascular system by the forcible, steady contraction
of the highly elastic aorta. Other large vessels which
branch from the aorta also have a part in this steady propulsion
of blood. From seventy to eighty times a minute
the aorta is normally forcibly expanded to accommodate
the charge of the ventricle. It is not difficult to understand
the great frequency of patches of sclerosis in the arch
when these facts are borne in mind.</p>
<p>What relationship the viscosity of the blood has to the
rate and volume of flow is not fully understood. As yet
there is not much known about the subject, and no one has
devised a satisfactory means of measuring the viscosity.
It is thought by some that an increased viscosity assists in
producing an increased amount of work for the heart.</p>
<h4>Blood Pressure</h4>
<p>Blood pressure is the expression used for a series of
phenomena resulting from the action of the heart. As every
heart beat is actual work done by the heart in overcoming
resistance to the outflow of blood, this force is approximately
measurable in a large artery such as the brachial.
It has been determined that the pressure in the brachial
artery is almost equal to the intraventricular pressure in
the left ventricle. In animals it is easy to attach manometers
to the carotid artery and to measure the blood pressure
accurately. Formerly the method consisted in attaching
a tube and allowing the blood to rise in the tube. The
height to which the blood rose measured the maximum pressure.
This is a crude method and has been replaced by
the U-tube of mercury with connection made to the artery
by saline or Ringer's solution. This apparatus is familiar
to all physiologists.</p>
<p><span class="pagenum"><a name="Page_69" id="Page_69">[69]</a></span>In man the measurement is most conveniently made from
the brachial artery. There is some difference in the pressure
in the femoral and the brachial and some use both
arteries. However, the difficulty of adjusting instruments
to the upper leg, the great force which must be used to compress
the femoral artery and the relative inaccessibility of
the leg as compared to the arm, make the leg an inconvenient
part for use in blood pressure determinations. It is
not to be recommended.</p>
<p>Blood pressure is a valuable aid in diagnosis and of material
help in many cases in prognosis, but it is not infallible
neither can it be used alone to diagnose a case. Blood
pressure is only one of many links in a chain of evidence
leading to diagnosis. It has been badly used and much
abused. It has been condemned unjustly when it did not
furnish <i>all</i> the evidence. It has been made a fetish and
worshipped by both doctors and patients. A sane conception
of blood pressure must be widely disseminated lest
we find it being discarded altogether.</p>
<p>Blood pressure consists of more than the estimation of
the systolic pressure. The blood pressure picture consists
of (1) the systolic pressure, (2) the diastolic pressure, (3)
the pulse pressure which is the difference between the
systolic and diastolic pressure, (4) the pulse rate. Expressed
in the literature it should read thus: 120-80-40; 72.
That tells the whole story in a brief, accurate form. This
is recommended in history reporting. It must be ever kept
in mind that a blood pressure reading represents the work
of the heart at the <i>moment when it was taken</i>. Within a
few minutes the pressure may vary up or down. There is
no normal pressure as such, but an average pressure for
any group of people of the same age living under similar
conditions. The habit of speaking of any systolic figure as
normal should be broken. A pressure picture may be normal
but a systolic reading, whatever it may be, is not accurately
designated as normal. This distinction is worth
insisting upon.</p>
<p><span class="pagenum"><a name="Page_70" id="Page_70">[70]</a></span></p>
<h4>Blood Pressure Instruments</h4>
<p>There are several instruments which are in common use
for the purpose of recording blood pressure in man.</p>
<p>Historically, the determination of blood pressure for man
began with the attempt of K. Vierordt in 1855 to measure
the blood pressure by placing weights on the radial pulse
until this was obliterated. The first useful instrument,
however, was devised by Marcy in 1876. He placed the
hand in a closed vessel containing water connected by tubing
with a bottle for raising the pressure and by another
tube with a tambour and lever for recording the size of the
pulse waves. He maintained that when pressure on the
hand was made, the point where oscillations of the lever
ceased was the maximal pressure, the point where the oscillations
of the recording lever was largest, was the minimal
pressure.</p>
<p>This pioneer work was practically forgotten for twenty-five
years. It was not until 1887 that V. Basch devised an
instrument which was used to some extent. This instrument
recorded only maximum pressure. It consisted of a
small rubber bulb filled with water communicating with a
mercury manometer. The bulb was pressed on the radial
artery until the pulse below it was obliterated and the
pressure then read off on the column of mercury. V. Basch
later substituted a spring manometer for the mercury
column. Potain modified the apparatus by using air in the
bulb with an aneroid barometer for recording the pressure.
These instruments are necessarily grossly inaccurate.
Moreover, they do not record the diastolic pressure.</p>
<p>In 1896 and 1897 further attempts were made to record
blood pressure by the introduction of a flat rubber bag
encased in some nonyielding material, which was placed
around the upper arm. Riva-Rocci used silk, while Hill
and Barnard used leather. The latter used a bulb or
Davidson syringe to force air into the cuff around the arm<span class="pagenum"><a name="Page_71" id="Page_71">[71]</a></span>
and palpated the radial artery at the wrist, noting the point
of return of the pulse after compression of the upper arm,
and reading the pressure on a column of mercury in a tube.</p>
<p>Except that the width of the cuff has been increased from
5 cm. to 12 cm., this is the general principle upon which all
the blood pressure instruments now in use are based.
Most of the apparatuses make use of a column of mercury
in a U-tube to record the millimeters of pressure. As the
mercury is depressed in one arm to the same extent as it
is raised in the other arm the scale where readings are made
is .5 cm. and the divisions represent 2 mm. of mercury but
are actually 1 mm. apart.</p>
<p>The cuff was made 12 cm. in diameter because it was
shown (v. Recklinghausen) that with narrow cuffs much
pressure was dissipated in squeezing the tissues. Janeway
has shown that with the use of the 12 cm. cuff
accurate values are obtained independently of the amount
of muscle and fat around the brachial artery. In other
words if an actual systolic blood pressure of 140 mm. is
present in two individuals, the one with a thin arm, the
other with a thick arm, the instrument will record these
pressures the same where a 12 cm. arm band is used. We
need have no fear of obtaining too high a reading when
we are taking pressure in a stout or very muscular individual.
Janeway also was the first to call attention to the fact
that the diastolic or minimal pressure was at the point
where the greatest oscillation of the mercury took place.
This is difficult to estimate in many cases as the eye can
not follow slight changes in the oscillation when the pressure
in the cuff is gradually reduced. Practically this is
the case in small pulses.</p>
<p>The Riva-Rocci instrument was modified by Cook. (See
Fig. 13.) He used a glass bulb containing mercury into
which a glass tube projected. The bulb was connected by
outlet and tubing to the cuff and syringe. The glass tube
was marked off in centimeters and millimeters and for convenience<span class="pagenum"><a name="Page_72" id="Page_72">[72]</a></span>
was jointed half way in its length. The instrument
could be carried in a box of convenient size. This
instrument is fragile and more cumbersome, although
lighter in weight, than others and is very little used at
present.</p>
<div class="figcenter" style="width: 500px;">
<a name="Cooks_modification_of_Riva-Roccis_blood_pressure_instrument" id="Cooks_modification_of_Riva-Roccis_blood_pressure_instrument"></a>
<img src="images/fig_013.png" width="500" height="386" alt="Fig. 13.—Cook's modification of Riva-Rocci's blood pressure instrument." title="Fig. 13.—Cook's modification of Riva-Rocci's blood pressure instrument." />
<span class="caption">Fig. 13.—Cook's modification of Riva-Rocci's blood pressure instrument.</span>
</div>
<p>Stanton's instrument (Fig. 14) is practically Cook's
made more rigid in every way but without the jointed tube.
The cuff has a leather casing, the pressure bulb is of heavy
rubber, the glass tube in which the mercury rises is fixed
against a piece of flat metal and there are stopcocks in a
metal chamber introduced between the bulb and mercury
with which to regulate the in- and out-flow of air. The
pressure can be gradually lowered conveniently without removing
the pressure bulb.</p>
<div class="figcenter" style="width: 386px;">
<a name="Stantons_sphygmomanometer" id="Stantons_sphygmomanometer"></a>
<img src="images/fig_014.png" width="386" height="500" alt="Fig. 14.—Stanton's sphygmomanometer." title="Fig. 14.—Stanton's sphygmomanometer." />
<span class="caption">Fig. 14.—Stanton's sphygmomanometer.</span>
</div>
<p>The most accurate mercury manometer is that of Erlanger.
(Fig. 15.) The instrument is bulky and is not
practicable for the physician in practice. The principle is
that used by Riva-Rocci. There is an extra T-tube introduced<span class="pagenum"><a name="Page_73" id="Page_73">[73]</a></span>
between the manometer and air bulb connecting with
a rubber bulb in a glass chamber. The oscillations of this
are communicated to a Marey tambour and recorded on
smoked paper revolving on a drum. There is a complicated
valve which enables the operator to reduce the pressure
with varying degrees of slowness. The mercury is
placed in a U-tube with a scale alongside it. The instrument
is expensive and not as easy to manipulate as its
advocates would have us believe. Hirschfelder has added
to the usefulness (as well as to the complexity) of the Erlanger
instrument, by placing two recording tambours for
the simultaneous registering of the carotid and venous
pulses. In spite of its complexity and necessary bulkiness,
very valuable data are obtained concerning the auricular
contractions.</p>
<p><span class="pagenum"><a name="Page_74" id="Page_74">[74]</a></span></p>
<div class="figcenter" style="width: 362px;">
<a name="The_Erlanger_sphygmomanometer_with_the_Hirschfelder_attachments" id="The_Erlanger_sphygmomanometer_with_the_Hirschfelder_attachments"></a>
<img src="images/fig_015.png" width="362" height="500" alt="Fig. 15.—The Erlanger sphygmomanometer with the Hirschfelder attachments by
means of which simultaneous tracings can be obtained from the brachial, carotid, and
venous pulses." title="Fig. 15.—The Erlanger sphygmomanometer with the Hirschfelder attachments by
means of which simultaneous tracings can be obtained from the brachial, carotid, and
venous pulses." />
<span class="caption">Fig. 15.—The Erlanger sphygmomanometer with the Hirschfelder attachments by
means of which simultaneous tracings can be obtained from the brachial, carotid, and
venous pulses.</span>
</div>
<p>One of the best of the mercury instruments is the Brown
sphygmomanometer. In this (Fig. 16) the mercury is in
a closed, all-glass tube so that it can not spill under any<span class="pagenum"><a name="Page_75" id="Page_75">[75]</a></span>
sort of manipulation. It is in this sense "fool-proof." The
cuff, however, is poorly constructed. It is too short and
there are strings to tie it around the arm. I have found
that this causes undue pressure in a narrow circle and renders
the reading inaccurate. In the clinic we use this mercury
instrument with a long cuff like that provided by the
Tycos instrument.</p>
<div class="figcenter" style="width: 271px;">
<a name="Desk_model_Baumanometer" id="Desk_model_Baumanometer"></a>
<img src="images/fig_016.png" width="271" height="500" alt="Fig. 16.—Desk model Baumanometer." title="Fig. 16.—Desk model Baumanometer." />
<span class="caption">Fig. 16.—Desk model Baumanometer.</span>
</div>
<p>The Faught instrument (Fig. 17) is larger than the
Brown, but is less easily broken and is not too cumbersome<span class="pagenum"><a name="Page_76" id="Page_76">[76]</a></span>
to carry around. The substitution of a metal air pump for
the rubber makes the apparatus more durable.</p>
<div class="figcenter" style="width: 483px;">
<a name="Faught_blood_pressure_instrument" id="Faught_blood_pressure_instrument"></a>
<img src="images/fig_017.png" width="483" height="500" alt="Fig. 17.—The Faught blood pressure instrument. An excellent instrument which is
quite easily carried about and is not easily broken." title="Fig. 17.—The Faught blood pressure instrument. An excellent instrument which is
quite easily carried about and is not easily broken." />
<span class="caption">Fig. 17.—The Faught blood pressure instrument. An excellent instrument which is
quite easily carried about and is not easily broken.</span>
</div>
<p>The v. Recklinghausen instrument is not employed to
any extent in this country. It is both expensive and cumbersome,
and has no advantages over the other instruments.</p>
<p>Several other instruments have been devised and new ones
are constantly being added to the already large list. With
those employing mercury the principle is the same. The
aim is to make an instrument which is easily carried, durable,
and accurate.</p>
<p>In all the mercury instruments the diameter of the tube
is 2 mm. One would suppose that there would be noticeable
differences in the readings of the different mercury
instruments depending upon the amount of mercury used
in the tube. By actual weight there is from 35 to 45 gms.
of mercury in the several instruments. After many trials,
no noticeable differences in blood pressure readings can be
made out between a column weighing 35 gm. and one weighing
45 gm.</p>
<p>There is, however, the inertia of the mercury to be overcome,<span class="pagenum"><a name="Page_77" id="Page_77">[77]</a></span>
friction between the tube and the mercury, and vapor
tension. The mercury is therefore not as sensitive to rapid
changes of pressure in the cuff as a lighter fluid would be.
The mercury must be clean and the tube dry so that there
is no more friction than what is inherent between the mercury
and glass. In making readings on a rapid pulse the
oscillations of the mercury column are apt to be irregular
or to cease now and then, due to the fact that the downward
oscillation coincides with a pulse wave, or an upward oscillation
receives the impact of two pulse waves transmitted
through the cuff. Instruments have been devised to obviate
this difficulty, but they have not come into favor. They are
usually too complicated and at present can not be recommended.</p>
<div class="figcenter" style="width: 500px;">
<a name="Rogers_Tycos_dial_sphygmomanometer" id="Rogers_Tycos_dial_sphygmomanometer"></a>
<img src="images/fig_018.png" width="500" height="341" alt="Fig. 18.—Rogers' "Tycos" dial sphygmomanometer." title="Fig. 18.—Rogers' "Tycos" dial sphygmomanometer." />
<span class="caption">Fig. 18.—Rogers' "Tycos" dial sphygmomanometer.</span>
</div>
<p>An instrument devised by Dr. Rogers (the "Tycos")
has met with considerable popularity. (Fig. 18.) This is
not an instrument which operates with a spring and lever.
The instrument is composed essentially of two metal discs
carefully ground and attached at their circumferences to
the metal casing below the dial. There is an air chamber
between these discs through the center of which air is
forced by the syringe bulb. When air is forced into the
space between these two discs, they are forced apart to a
very slight extent, with the highest pressures only 2-3 mm.
of bulging occurs. From data gathered after extensive use<span class="pagenum"><a name="Page_78" id="Page_78">[78]</a></span>
for five years these discs were not found to have sprung.
A lever attached to a cog which in turn is attached to the
dial needle magnifies to an enormous extent the slightest
expansion of the discs. Every dial is handmade and every
division is actually determined by using a U. S. government
mercury manometer of standard type. No two dials
therefore are alike in the spacing of the divisions of the
scale but every one is calibrated as an individual instrument.
There is no doubt in the author's mind that for the
general practitioner the instrument has some advantages
over the mercury instruments. It reveals the slightest
irregularity in force of the heart beat. The oscillation of
the dial needle is more accurately followed by the eye than
is that of the column of mercury. The needle passes directly
over the divisions of the scale, while with usual mercury<span class="pagenum"><a name="Page_79" id="Page_79">[79]</a></span>
instruments the scale is an appreciable distance (sometimes
.5 cm.) from the column of mercury at the side. (Fig.
19.) The diastolic pressure is more easily read on the<span class="pagenum"><a name="Page_80" id="Page_80">[80]</a></span>
"Tycos." It is where the maximum oscillation of the needle
occurs as the pressure is slowly released from the cuff.
Although it does not appear that this instrument, if properly
made and standardized, could become inaccurate,
nevertheless it is advisable to check it every few months
against a known accurate mercury manometer instrument.</p>
<div class="figcenter" style="width: 297px;">
<a name="Detail_of_the_dial_in_the_Tycos_instrument" id="Detail_of_the_dial_in_the_Tycos_instrument"></a>
<img src="images/fig_019.png" width="297" height="500" alt="Fig. 19.—Detail of the dial in the "Tycos" instrument." title="Fig. 19.—Detail of the dial in the "Tycos" instrument." />
<span class="caption">Fig. 19.—Detail of the dial in the "Tycos" instrument.</span>
</div>
<div class="figcenter" style="width: 500px;">
<a name="Faught_dial_instrument" id="Faught_dial_instrument"></a>
<img src="images/fig_020.png" width="500" height="323" alt="Fig. 20.—Faught dial instrument." title="Fig. 20.—Faught dial instrument." />
<span class="caption">Fig. 20.—Faught dial instrument.</span>
</div>
<div class="figcenter" style="width: 282px;">
<a name="Detail_of_the_dial_of_the_Faught_instrument" id="Detail_of_the_dial_of_the_Faught_instrument"></a>
<img src="images/fig_021.png" width="282" height="500" alt="Fig. 21.—Detail of the dial of the Faught instrument." title="Fig. 21.—Detail of the dial of the Faught instrument." />
<span class="caption">Fig. 21.—Detail of the dial of the Faught instrument.</span>
</div>
<p>Another perfectly satisfactory dial instrument is the
Faught (Figs. 20 and 21). The general plan of this differs
in some minor points from the "Tycos." I have compared
the two and have found no difference in the readings. Both
can be recommended.</p>
<div class="figcenter bord" style="width: 500px;">
<a name="The_Sanborn_instrument" id="The_Sanborn_instrument"></a>
<img src="images/fig_022.png" width="500" height="246" alt="Fig. 22.—The Sanborn instrument." title="Fig. 22.—The Sanborn instrument." />
<span class="caption">Fig. 22.—The Sanborn instrument.</span>
</div>
<p>One or two other cheaper dial instruments are on the
market. The Sanborn seems to be quite satisfactory. (Fig.
22.) It is cheaper than the other dial instruments. There
is this much to be said, no instrument using a spring as resistance
to measure pressure can be recommended.</p>
<h4>Technic</h4>
<p>The same technic applies to all the mercury instruments.
The patient sits or lies down comfortably. The right or left
arm is bared to the shoulder, the cuff is then slipped over
the hand to the upper arm. (See Fig. 23.) At least an inch
of bare arm should show between the lower end of the cuff
and the bend of the elbow. The rubber is adjusted so that
the actual pressure from the bag is against the inner side<span class="pagenum"><a name="Page_81" id="Page_81">[81]</a></span>
of the arm. The straps are tightened, care being taken not
to compress the veins. The upper part of the cuff should
fit more snugly than the lower part. The part of the instrument
carrying the mercury column is now placed on a
level surface; the two arms of the mercury in the tube must
be even, and at <i>0</i> on the scale. With the fingers of one hand
on the radial pulse, the bag is compressed until the pulse
is no longer felt. (See Fig. 24.) One should raise the pressure
from 10-12 mm. above this, and close the stopcock
between the bulb and the mercury tube. In a good instrument
the column should not fall. If it does there is a leak
of air in the system of tubing and arm bag. Now with the
finger on the pulse, or where the pulse was last felt, gradually
allow air to escape by turning the stopcock so that
the column of mercury falls about 2 mm. (one division on
the scale) for every heart beat or two. One must not allow
the column of mercury to descend too slowly as it is uncomfortable<span class="pagenum"><a name="Page_82" id="Page_82">[82]</a></span>
for the patient and introduces a psychic element
of annoyance which affects the blood pressure. On the
other hand, the pressure must not be released too rapidly,
else one runs over the points of systolic and diastolic pressure
and the readings are grossly inaccurate. It is impossible
to say how rapidly the mercury must fall. Every operator
must find that out for himself by practice. The first perceptible
pulse wave felt beneath the palpating finger at the
wrist, represents on the scale the systolic pressure. This
can be seen to correspond to a sudden increase in the magnitude
of the oscillation of the mercury column. The systolic
pressure, thus obtained, is from 5-10 mm. lower than the
real systolic pressure. The more sensitive the palpating
finger, the more nearly does the systolic pressure reading
approach that found by using such an instrument as Erlanger's,
where the first pulse wave is magnified by the
lever of the tambour.</p>
<div class="figcenter bord" style="width: 500px;">
<a name="Method_of_taking_blood_pressure_with_a_patient_in_sitting_position" id="Method_of_taking_blood_pressure_with_a_patient_in_sitting_position"></a>
<img src="images/fig_023.png" width="500" height="417" alt="Fig. 23.—Method of taking blood pressure with a patient in sitting position." title="Fig. 23.—Method of taking blood pressure with a patient in sitting position." />
<span class="caption">Fig. 23.—Method of taking blood pressure with a patient in sitting position.</span>
</div>
<div class="figcenter bord" style="width: 500px;">
<a name="Method_of_taking_blood_pressure_with_patient_lying_down" id="Method_of_taking_blood_pressure_with_patient_lying_down"></a>
<img src="images/fig_024.png" width="500" height="349" alt="Fig. 24.—Method of taking blood pressure with patient lying down." title="Fig. 24.—Method of taking blood pressure with patient lying down." />
<span class="caption">Fig. 24.—Method of taking blood pressure with patient lying down.</span>
</div>
<p>The pressure is now allowed to fall, until the palpating<span class="pagenum"><a name="Page_83" id="Page_83">[83]</a></span>
finger feels the largest possible pulse wave, which is coincident
with the greatest oscillation of the mercury. This is
the diastolic pressure. Beyond this point there is no oscillation
of the mercury column. The difference between the
two is the pulse pressure. Thus the pulse is felt after compression
at 120 on the scale, and the maximum oscillation
occurs at 80. The systolic pressure is 120 mm., the diastolic
is 80 mm., and the pulse pressure is 40 mm.</p>
<p>With the "Tycos" or Faught the arm band is snugly
wound around the arm, the bag next to the skin and the end
tucked in, so that the whole band will not loosen when air
is forced into the bag. The cuff is blown up until the pulse
is no longer felt. One should raise the pressure not more
than 10 mm. above the point of obliteration of the pulse.
The valve is then carefully opened so that the needle gradually
turns toward zero. At the first return of the pulse
wave felt at the wrist, the needle is sure to give a sudden
jump. This is the systolic pressure and is read off on the
scale. The needle is now carefully watched until it shows
the maximum oscillation. This is the diastolic pressure.
The difference between the two is, as above, the pulse pressure.</p>
<p>In taking pressure one should take the average of several,
three or four. Moreover, one must not take consecutive
readings too quickly and one must be sure that between
every two readings all the air is out of the cuff and that the
mercury or dial is at zero. <i>It has been repeatedly shown
that in a cyanosed arm the systolic pressure is raised so
that even slight cyanosis between readings must be carefully
avoided.</i></p>
<p>The only accurate method of determining both the systolic
and diastolic pressure, but especially the diastolic, is
by the so-called auscultatory method. (See Fig. 25.) The
cuff is adjusted in the usual way and one places the bell
of a binaural stethoscope over the brachial artery from
one to two centimeters below the lower edge of the<span class="pagenum"><a name="Page_84" id="Page_84">[84]</a></span>
cuff.<a name="FNanchor_3_3" id="FNanchor_3_3"></a><a href="#Footnote_3_3" class="fnanchor">[3]</a> Care must be taken that the bell is not pressed too
firmly against the arm and that the edge of the bell nearest
the cuff is not pressed more firmly than the opposite end.
For this purpose, one can not use the ordinary Bowles
stethoscope or any of the other much lauded stethoscopes,
because the surface of the bell is too large. The
diameter of the bell must not be more than twenty-five millimeters,
twenty is still better. It is advisable before beginning
the observation to locate with the finger the pulse
in the brachial artery just above the elbow, so that the
stethoscope may be placed over the course of the artery.
(Fig. 26.) The first wave which comes through is heard as
a click, and occurs at a point on the manometer or dial scale
from 5-10 mm. higher than can usually be palpated at the
radial artery. This is the true systolic pressure. By keeping<span class="pagenum"><a name="Page_85" id="Page_85">[85]</a></span>
the bell of the stethoscope over the brachial artery
while the pressure is falling, one comes to a point when all
sound suddenly ceases. This is said to be the diastolic pressure.
This is incorrect as will be shown later.</p>
<div class="figcenter bord" style="width: 500px;">
<a name="Observation_by_the_auscultatory_method_and_a_mercury_instrument" id="Observation_by_the_auscultatory_method_and_a_mercury_instrument"></a>
<img src="images/fig_025.png" width="500" height="484" alt="Fig. 25.—Observation by the auscultatory method and a mercury instrument. One hand
regulates the stop cock which releases air gradually." title="Fig. 25.—Observation by the auscultatory method and a mercury instrument. One hand
regulates the stop cock which releases air gradually." />
<span class="caption">Fig. 25.—Observation by the auscultatory method and a mercury instrument. One hand
regulates the stop cock which releases air gradually.</span>
</div>
<div class="figcenter bord" style="width: 500px;">
<a name="Observation_by_the_auscultatory_method_and_a_dial_instrument" id="Observation_by_the_auscultatory_method_and_a_dial_instrument"></a>
<img src="images/fig_026.png" width="500" height="485" alt="Fig. 26.—Observation by the auscultatory method and a dial instrument. The right
hand holds the bulb and regulates the air valve." title="Fig. 26.—Observation by the auscultatory method and a dial instrument. The right
hand holds the bulb and regulates the air valve." />
<span class="caption">Fig. 26.—Observation by the auscultatory method and a dial instrument. The right
hand holds the bulb and regulates the air valve.</span>
</div>
<h4>Arterial Pressure</h4>
<p>The arterial pressure in the large arteries undergoes extensive
fluctuations with every heart beat. The maximum
pressure produced by the systole of the left ventricle of the
heart is known as the <b>maximum</b> or <b>systolic pressure</b>. It
practically equals the intraventricular pressure. The minimum
pressure in the artery, the pressure at the end of diastole,
is called the <b>diastolic pressure</b>. The difference between
the systolic and diastolic pressures is known as the
<b>pulse pressure</b>. There is yet another term known as the
<b>mean pressure</b>. For convenience, this may be said to be the<span class="pagenum"><a name="Page_86" id="Page_86">[86]</a></span>
arithmetical mean of the systolic and diastolic pressures.
Actually, however, this can not be the case, owing to the
form of the pulse wave, which is not a uniform rise and fall—the
upstroke being a straight line, but the downstroke being
broken usually by two notches. We do not make use of
the mean pressure in recording results. It is of experimental
interest and needs only to be mentioned here.</p>
<div class="figcenter" style="width: 500px;">
<a name="Schema_to_illustrate_decrease_in_pressure" id="Schema_to_illustrate_decrease_in_pressure"></a>
<img src="images/fig_027.png" width="500" height="193" alt="Fig. 27.—Schema to illustrate the gradual decrease in pressure from the heart to the
vena cava: (a), arteries; (c), capillaries; (v), veins; (A), aorta, pressure 150 mm.;
(B), brachial artery, pressure 130 mm.; (F), femoral vein, 20 mm.; (IVC), inferior
vena cava, 3 mm. (Modified from Howell.)" title="Fig. 27.—Schema to illustrate the gradual decrease in pressure from the heart to the
vena cava: (a), arteries; (c), capillaries; (v), veins; (A), aorta, pressure 150 mm.;
(B), brachial artery, pressure 130 mm.; (F), femoral vein, 20 mm.; (IVC), inferior
vena cava, 3 mm. (Modified from Howell.)" />
<span class="caption">Fig. 27.—Schema to illustrate the gradual decrease in pressure from the heart to the
vena cava: (a), arteries; (c), capillaries; (v), veins; (A), aorta, pressure 150 mm.;
(B), brachial artery, pressure 130 mm.; (F), femoral vein, 20 mm.; (IVC), inferior
vena cava, 3 mm. (Modified from Howell.)</span>
</div>
<p>It has been shown that the mean pressure is quite constant
throughout the whole arterial system. The maximum
pressure necessarily falls as the periphery of the vascular
system is approached. In general it may be said that
the minimal pressure is quite constant. Too little attention
is paid to minimal and pulse pressure. The minimal pressure
is important, for it gives us valuable data as to the
actual propulsive force driving the blood forward to the
periphery at the end of diastole.</p>
<p>It is readily understood how the maximum pressure falls
as the periphery is approached, until in the arterioles the
maximum and minimum pressures are about equal. The
pressure then in these arterioles is practically the same as
the diastolic pressure. Actually it is a few millimeters
less. The diastolic blood pressure would, therefore, measure
the peripheral resistance and, as the maximum for
systolic pressure represents approximately the intraventricular<span class="pagenum"><a name="Page_87" id="Page_87">[87]</a></span>
pressure, the difference between the two, the pulse
pressure, actually represents the force which is driving the
blood onward from the heart to the periphery. It is hence
very evident that the mere estimation of the systolic pressure
gives us but a portion of the information we are
seeking.</p>
<p>The pulse pressure is subject to wide fluctuations but as
a rule for any one normal heart it remains fairly constant
as the rate varies. In a rapidly beating heart the diastole
is short and the diastolic pressure rises. If the systolic
pressure does not also rise, as in a normal heart following
exercise, we will say, the pulse pressure falls. We know
that when the pulse rate is constant, vasodilatation causes a
fall in diastolic pressure and a rise in pulse pressure. On
the contrary, vasoconstriction causes a rise in diastolic
pressure and a fall in pulse pressure.</p>
<p>It is very probably the case that with two individuals of
equal age and equal pulse rate, and equal systolic pressure
of 160 mm., the one with a diastolic pressure of 110 mm.
and, therefore, a pulse pressure of 50 mm. is much worse
off than the other with a diastolic pressure of 90 mm. and a
pulse pressure of 70 mm. The latter may be normal for the
age of the person especially when certain forms of fibrous
arteriosclerosis accompanied by enlarged heart are present.</p>
<p>The former is not normal for any age. Low pulse pressure
usually means a weak vasomotor control and is only
found in failing circulation or in markedly run down states,
such as after serious illness or in tuberculosis. Therefore,
it is most important to estimate accurately the diastolic
pressure as well as the systolic pressure, for only in this
way can we obtain any data of value regarding the driving
power of the heart and the condition of the vasomotor system.
A high systolic pressure does not necessarily mean
that a great deal of blood is forced into the capillaries. Actually
it may mean that very little blood enters the periphery.
The heart wastes its strength in dilating constricted<span class="pagenum"><a name="Page_88" id="Page_88">[88]</a></span>
vessels without actually carrying on the circulation adequately.</p>
<h4>Normal Pressure Variations</h4>
<p>The systolic pressure varies considerably under conditions
which are by no means abnormal. Thus, the average
for men at all ages is about 127 mm. Hg. (All measurements
are taken from the brachial artery, with the individuals
in the sitting posture.) For women the average is
somewhat lower, 120 mm. Hg. The pressure is lowest in
children. In children from 6-12 years the average systolic
pressure is 112 mm. Normally, there is a gradual increase
as age comes on, due, as will be shown in the succeeding
chapter, to physiologic changes which take place in the
arteries from birth to old age. In the chart here appended
is graphically shown the normal variations in the blood
pressure at different ages compiled from observations made
on one thousand presumably normal persons. (Fig. 28.)</p>
<div class="figcenter" style="width: 441px;">
<a name="Chart_showing_the_normal_limits_of_variation_in_systolic_blood_pressure" id="Chart_showing_the_normal_limits_of_variation_in_systolic_blood_pressure"></a>
<img src="images/fig_028.png" width="441" height="500" alt="Fig. 28.—Chart showing the normal limits of variation in systolic blood pressure. (After
Woley.)" title="Fig. 28.—Chart showing the normal limits of variation in systolic blood pressure. (After
Woley.)" />
<span class="caption">Fig. 28.—Chart showing the normal limits of variation in systolic blood pressure. (After
Woley.)</span>
</div>
<p>The diastolic pressure has been estimated to be about 35
to 45 mm. Hg lower than the systolic pressure, and consequently
these figures represent the pulse pressure in the
brachial artery of man. This is equivalent to saying that
every systole of the left ventricle distends this artery by a
sudden increase in pressure equal to the weight of a column
of mercury 2 mm. in diameter and 35 to 45 mm. high. Naturally,
at the heart the pressure is highest. As the blood
goes toward the capillary area the pressure gradually decreases
until, at the openings of the great veins into the
heart, the pressure is least. At the aorta (A) the pressure
(systolic) is approximately 150 mm. Hg, at the brachial
artery (B) it is 130 mm., in the capillary system (C) it is
30 mm., in the femoral vein (F) it is 20 mm., at the opening
of the inferior vena cava (I) it is 3 mm.</p>
<p>Attention has been called to the normal systolic pressure
at different ages. This is not the only cause for variations
in the blood pressure. Normally, it is greater when in the<span class="pagenum"><a name="Page_89" id="Page_89">[89]</a></span>
erect position than when seated, and greater when seated
than when lying down. During the day there are well-recognized
changes. The pressure is lowest during the
early morning hours, when the person is asleep. In women
there are variations due to menstruation. Muscular exercise
raises the blood pressure markedly. The effect of a
full meal is to raise the blood pressure. The explanation
is that during and following a meal there is dilatation of
the abdominal vessels. This takes blood from other parts
of the body, provided that the other factors in the circulation<span class="pagenum"><a name="Page_90" id="Page_90">[90]</a></span>
remain constant. A fall of pressure would necessarily
occur in the aorta. To compensate for this, there is increased
work on the part of the heart, which reveals itself
as increased pressure and pulse pressure. It is well known
that the interest in the process taken by an individual upon
whom the blood pressure is estimated for the first time tends
to increase the rate of the heart and to raise the blood pressure.
For this reason the first few readings on the instrument
must be discarded, and not until the patient looks
upon the procedure calmly can the true blood pressure be
obtained. As a corollary to this statement, mental excitement,
of whatever kind, has a marked influence on the
pressure. The patient must remain absolutely quiet. Raising the head or
the free arm causes the pressure to rise.
Another important physiologic variation is produced by
concentrated mental activity. This tends to hurry the heart
and increase the force of the beat. In short, it may be
stated as a general rule that any active functioning of a
part of the body which naturally requires a great excess of
blood tends to elevate the blood pressure. At rest the pressure
is constant. Variations caused by the factors mentioned
act only transitorily, and the pressure shortly returns
to normal.</p>
<h4>The Auscultatory Blood Pressure Phenomenon</h4>
<p>Since the first description of the auscultatory blood pressure
sounds by Korotkov in 1905, this method has been more
and more employed until today it is the standard, recognized
method of determining the points in the blood pressure
reading. When one applies the 12 cm. arm band over
the brachial artery and listens with the bell of the stethoscope
about one cm. below the cuff directly over the brachial
artery near the bend of the elbow, one hears an interesting
series of sounds when the air in the cuff is gradually
reduced. The cuff is blown up above the maximum pressure.
As the air pressure around the arm gradually is<span class="pagenum"><a name="Page_91" id="Page_91">[91]</a></span>
lowered, the series of sounds begins with a rather low-pitched,
clear, clicking sound. This is the first phase. This
only lasts through a few millimeters fall when a murmur
is added and the tone becomes louder. This click and murmur
phase is the second phase. A few millimeters more of
drop in pressure and a clear, sharp, loud tone is audible.
Usually this tone lasts through a greater drop than any of
the other tones. This is the third phase. Rather suddenly
the loud, clear tone gives place to a dull muffled tone. In
general the transition is quite sharp and distinct. This is
the fourth phase. The tone gradually or quickly ceases
until no tone is heard. This is the fifth phase (Ettinger.)</p>
<p>The first phase is due to the sudden expansion of the
collapsed portion of the artery below the cuff and to the
rapidity of the blood flow. This causes the first sharp
clicking sound which measures the systolic pressure.</p>
<p>The second, or murmur and sound phase, is due to the
whorls in the blood stream as the pressure is further released
and the part of the artery below the cuff begins to
fill with blood.</p>
<p>The third tone phase is due to the greater expansion of
the artery and to the lowered velocity in the artery. A
loud tone may be produced by a stiff artery and a slow
stream or by an elastic artery and a rapid stream. This
tone is clear cut and in general is louder than the first
phase.</p>
<p>The fourth phase is a transition from the third and becomes
duller in sound as the artery approaches the normal
size.</p>
<p>The fifth phase, no sound phase, occurs when the pressure
in the cuff exerts no compression on the artery and the
vessel is full throughout its length.</p>
<p>It is generally conceded that the sounds heard are produced
in the artery itself and not at the heart.</p>
<p>The tones vary greatly in different hearts. A very
strong third tone phase or prolongation of this phase usually<span class="pagenum"><a name="Page_92" id="Page_92">[92]</a></span>
means that the heart which produces the tone is a
strongly acting one, although allowances must be made for
a sclerosed artery in which there is a tendency to the production
of a sharp third phase.</p>
<p>Weakness of the third phase, as a rule, indicates weakness
of the heart and this dulling of the third phase may be
so excessive that no sound is produced. Goodman and
Howell have carried this method further by measuring the
individual phases and calculating the percentage of each
phase to the pulse pressure. Thus, if in a normal individual
the systolic pressure is 130 mm., the diastolic 85 mm.,
and the pulse pressure 45 mm., the first phase lasts from
130 to 116 or 14 mm., the second from 116 to 96, or 20 mm.,
the third from 96 to 91 or 5 mm., the fourth from 91 to 85, or
6 mm. The first phase would then be 31.1 per cent of the
total pulse pressure, the second phase 44.4 per cent, the
third phase 11.1 per cent, and the fourth phase 13.3 per
cent. They consider that the second and third phases represent
cardiac strength (C. S.) and the first and fourth represent
cardiac weakness (C. W.). They believe that C. S.
should normally be greater than C. W. In the example
above C. S.:C. W. = 55.5:44.4. In weak hearts, especially in
uncompensated hearts, the conditions are reversed and C.
W. > C. S. This is often the case. As a heart improves
C. S. again tends to become greater than C. W. They think
that the phases should be studied in respect to the sounds
and also to the encroachment of one sound upon another.</p>
<p>These observations are interesting but we have not found
the division into phases as helpful as it was thought to be.
We spent a great deal of time on this question. All that
can be said, in my opinion, is that a loud, long third phase
is usually evidence of cardiac strength.</p>
<p>A further interesting feature which can be heard in all
irregular hearts is a great difference in intensity of the individual
sounds. Goodman and Howell call this phenomenon
tonal arrhythmia. Irregularities can be made out by<span class="pagenum"><a name="Page_93" id="Page_93">[93]</a></span>
the auscultatory method which can not be heard at the
heart.</p>
<p>In anemia the sounds are very loud and clear and do not
seem to represent the actual strength of the heart.</p>
<p>The general lack of vasomotor tone in the blood vessels
together with some atrophy and flabbiness of the coats
probably explains the loud sounds.</p>
<p>In polycythemia the sounds have a curious, dull, sticky
character and can not be differentiated accurately into
phases, a condition which was predicted from the knowledge
of the sharp sounds in anemia.</p>
<p>In not all cases can all phases be made out. It is usually
the fourth phase which fails to be heard.</p>
<p>In such cases the loud third tone almost immediately
passes to the fifth phase or no sound phase. The importance
of this will later be taken up.</p>
<p>"In arteriosclerosis, with hardening and loss of elasticity
of the vessel walls, the auscultatory phenomena, according
to Krylow, are apt to be more pronounced, since the back
pressure at the cuff probably causes some dilatation of the
vessel above it, while the lumen of the vessel is smaller
than normal. Both of these factors cause an increased
rapidity in the transmission of the blood wave when pressure
in the cuff is released, which in time favors the vibration
of the vessel walls.</p>
<p>"In high grade thickening of the arterial walls, however,
especially where calcification had occurred, Fischer
found that the sounds were distinctly less loud than normal,
the more so in the arm, which showed the greater
degree of hardening. According to Ettinger's experience,
the rapidity of the flow distinctly increases the auscultatory
phenomenon." (Gittings.)</p>
<p>The sounds depend upon the resonating character of the
cuff, upon the size and accessibility of the vessel, upon the
force of the heart beat, and upon the velocity of the blood.</p>
<p><span class="pagenum"><a name="Page_94" id="Page_94">[94]</a></span></p>
<h4>The Maximum and Minimum Pressures</h4>
<p>The maximum (systolic) pressure is read at the point
where the first audible click is heard after the cuff is blown
up and the pressure gradually reduced by means of the
needle valve in the hand bulb or on the upright of the
glass containing the mercury. All are agreed upon this
point. There has been some dispute as to the place where
the diastolic pressure should be read. Korotkov considered
that the diastolic pressure should be read at the fourth
phase when the loud tone suddenly becomes dulled. Others
held that the diastolic pressure should be read at the fifth
phase, the absence of all sound. Experiments carried out
to determine this point were made by me with the assistance
of Prof. Eyster and Dr. Meek at the Physiological
Laboratory of the University of Wisconsin. We arranged
apparatus making it possible to hold the pressure in the
carotid artery of dogs at maximum or minimum. A femoral<span class="pagenum"><a name="Page_95" id="Page_95">[95]</a></span>
artery was then dissected and an instrument devised to
compress the artery with a water jacket. The whole was
connected up with a kymograph. A time marker was put
in so as to record the place where changes in sound were
heard while listening below the cuff around the femoral
artery. Two sets of records were taken. One with pressure
greater than minimum pressure and a falling pressure
over the femoral artery (Fig. 29), the other with
pressure at zero and gradually raised to minimum pressure
(Fig. 30). Both sets of records showed the same result;
viz., that at a point corresponding to the sudden
change of tone the pressure on the artery corresponded to
the minimum pressure. It was therefore concluded that
experimentally in dogs the point where diastolic pressure
should be read is at the tone change from clear to dull,
not at the point where all sound disappears.</p>
<div class="figcenter bord" style="width: 500px;">
<a name="Tracing_of_auscultatory_phenomena" id="Tracing_of_auscultatory_phenomena"></a>
<img src="images/fig_029.png" width="500" height="479" alt="Fig. 29.—Tracing of auscultatory phenomena. (See explanation in legend of Fig. 30.)" title="Fig. 29.—Tracing of auscultatory phenomena. (See explanation in legend of Fig. 30.)" />
<span class="caption">Fig. 29.—Tracing of auscultatory phenomena. (See explanation in legend of Fig. 30.)</span>
</div>
<div class="figcenter" style="width: 500px;">
<a name="Tracings_of_auscultatory_phenomena" id="Tracings_of_auscultatory_phenomena"></a>
<img src="images/fig_030.png" width="500" height="260" alt="Fig. 30.—Figures are to be read from left to right. The top line records the points
where sounds were heard, the figures above the short vertical lines refer to tones (see
text). Mx. B. P., maximum blood-pressure. M. B. P., minimum blood-pressure. P. B.,
pressure bulb recorder. It was impossible to lower and raise this bulb by hand without
obtaining the great irregular oscillations of the attached lever above the mercury manometer.
B. L., base line." title="Fig. 30.—Figures are to be read from left to right. The top line records the points
where sounds were heard, the figures above the short vertical lines refer to tones (see
text)...." />
<span class="caption">Fig. 30.—Figures are to be read from left to right. The top line records the points
where sounds were heard, the figures above the short vertical lines refer to tones (see
text). Mx. B. P., maximum blood-pressure. M. B. P., minimum blood-pressure. P. B.,
pressure bulb recorder. It was impossible to lower and raise this bulb by hand without
obtaining the great irregular oscillations of the attached lever above the mercury manometer.
B. L., base line.</span>
</div>
<p>Erlanger showed some years ago, that with his instrument,
the point at which diastolic pressure should be read
was at the instant when the maximum oscillation of the<span class="pagenum"><a name="Page_96" id="Page_96">[96]</a></span>
lever suddenly became smaller. While checking up the
graphic with the auscultatory method using Erlanger's instrument,
it was noticed that the disappearance of all sound
did not correspond with the sudden diminution of the oscillation
of the lever connected with the brachial artery. A
series of records were carefully made on patients. It was
seen that during the period of the third tone phase the oscillations
of the lever on the drum reached a maximum
(Fig. 31) and remained at approximately the same height
for some millimeters while the pressure was gradually falling.
At a point at which the third tone, clear and distinct,
became dull, there was an appreciable decrease in the height
of the pulse wave. From this point to the disappearance
of all sound there was a gradual diminution of the size of
the pulse waves.<span class="pagenum"><a name="Page_97" id="Page_97">[97]</a></span></p>
<div class="figcenter" style="width: 500px;">
<a name="Clinical_determination_of_diastolic_pressure_fast_drum" id="Clinical_determination_of_diastolic_pressure_fast_drum"></a>
<img src="images/fig_031.png" width="500" height="83" alt="Fig. 31.—Fast drum. Sudden decrease in size of pulse wave at 4, marking the change
from clear sharp tone to dull tone." title="Fig. 31.—Fast drum. Sudden decrease in size of pulse wave at 4, marking the change
from clear sharp tone to dull tone." />
<span class="caption">Fig. 31.—Fast drum. Sudden decrease in size of pulse wave at 4, marking the change
from clear sharp tone to dull tone.</span>
</div>
<div class="figcenter" style="width: 500px;">
<a name="Clinical_determination_of_diastolic_pressure_slow_drum" id="Clinical_determination_of_diastolic_pressure_slow_drum"></a>
<img src="images/fig_032.png" width="500" height="315" alt="Fig. 32.—Slow drum. Sudden decrease in amplitude at 4." title="Fig. 32.—Slow drum. Sudden decrease in amplitude at 4." />
<span class="caption">Fig. 32.—Slow drum. Sudden decrease in amplitude at 4.</span>
</div>
<p>For normal pressures the difference between the fourth
(dull) tone and the fifth (disappearance of all tone) phase,
amounted to 4 to 10 mm. Occasionally the difference was
so little, the change from sharp third tone through fourth
dull tone to disappearance of all sound was so abrupt, that
one could take the disappearance of all sound as the diastolic
pressure, with an error of not more than 2 to 4 mm.
This is within the limits of normal error and practically
may be used by those who have difficulty in noting the
change from third to fourth phase. For high pressures,
however, the difference between fourth and fifth phases was
never less than 8 mm., and was found as much as 16 mm.
The diastolic, therefore, should always be taken at the
fourth phase if possible.</p>
<p>It was found that with the dial instrument the greatest
fling of the lever corresponded to the third phase and the
sudden lessened amplitude of the oscillation was at the
fourth phase and was coincident with the change of tone
from sharp to dull. Thus the diastolic pressure may be
read off on the dial scale by watching the fling of the hand
and with some practice one might acquire considerable accuracy.
It is better, simpler, and, for most observers, more
accurate to use the stethoscope and hear the change of
sound.</p>
<h4>The Relative Importance of the Systolic and Diastolic Pressures</h4>
<p>The systolic pressure represents the maximum force of
the heart. It is measured by noting the first sound audible
over the brachial artery using the auscultatory method.
It is the summation of two factors largely; the force expended
in opening the aortic valves (potential) and the
force expended from that point to the end of systole, the
force which is actually driving the blood to the periphery
(kinetic). To start the blood in motion, the heart must
overcome a dead weight equal to the sum of all the forces<span class="pagenum"><a name="Page_98" id="Page_98">[98]</a></span>
holding the aortic valves closed. This sum of factors,
called the peripheral resistance, must be reached and passed
by the force of the ventricular beat before one drop of
blood is set in motion along the aorta. This factor of resistance
assumes a great importance.</p>
<p>The systolic pressure is always fluctuating as it depends
upon so many conditions, and the calls of the body except
during sleep are many and various. In a study of diurnal
variations in arterial blood pressure it has been found that—(1)
A rise of maximum pressure averaging 8 mm. of Hg.
occurs immediately on the ingestion of food. A gradual
fall then takes place until the beginning of the next meal.
There is also a slight general rise of the maximum pressure
during the day. (2) The range of maximum pressure
varies considerably in different individuals, but the highest
and lowest maximum pressures are practically equidistant
from the average pressure of any one individual.<a name="FNanchor_4_4" id="FNanchor_4_4"></a><a href="#Footnote_4_4" class="fnanchor">[4]</a></p>
<p>The pressure is lowest during sleep and gradually rises
near the end of sleep, so that on awakening the pressure
was the same as before sleep.</p>
<p>Physiologically there are many conditions which modify
the systolic pressure. Sleep, position, meals, exercise, emotional
states cause often wide fluctuations which may be
very sudden. It should be constantly borne in mind, that
the systolic pressure reading which is made, is the maximum
effort of the heart at that moment only.</p>
<p>The diastolic pressure measures the peripheral resistance.
It measures the work of the heart, the potential energy, up
to the moment of the opening of the aortic valves. It is
the actual pressure in the aorta. The diastolic pressure is
not very variable; it is not subject to the same influences
which disturb the systolic pressure. It fluctuates as a rule,
within a small range. It is not affected by diet, by mental
excitement, by subconscious psychic influences, to anything
like the extent to which the systolic pressure is affected by<span class="pagenum"><a name="Page_99" id="Page_99">[99]</a></span>
the action of these factors. The diastolic pressure is determined
by the tone in the arterioles and is under the control
of the vasomotor sympathetic system. Any agent
which causes chronic irritation of the whole vasomotor system
produces increase in the peripheral resistance with consequent
rise in the diastolic pressure. Any agent which
acts to produce thickening of the walls of the arterioles,
narrowing their lumina, produces the same effect.</p>
<p>Such states naturally result in increased work on the
part of the heart, which as a result, hypertrophies in the
left ventricle. The increase in size and strength is a compensatory
process in order to keep the tissues supplied
with their requisite quota of blood. Conversely, paralysis
of the vasomotor system produces fall of diastolic pressure
which, if long continued, results in death.</p>
<p>The diastolic pressure then is of importance for the following
reasons:</p>
<p>1. It measures peripheral resistance.</p>
<p>2. It is the measure of the tonus of the vasomotor system.</p>
<p>3. It is one of the points to determine pulse pressure.</p>
<p>4. Pulse pressure measures the actual driving force, the
kinetic energy of the heart.</p>
<p>5. It enables us to judge of the volume output, for pulse
pressure which is only determined by measuring both systolic
and diastolic pressure, is such an index.</p>
<p>6. It is more stable than the systolic pressure, subject to
fewer more or less unknown influences.</p>
<p>7. It is increased by exercise.</p>
<p>8. It is increased by conditions which increase peripheral
resistance.</p>
<p>9. The gradual increase of diastolic pressure means
harder work for the heart to supply the parts of the body
with blood.</p>
<p>10. Increased diastolic pressure is always accompanied
by increased pulse pressure, and increased size of the left
ventricle, temporarily (exercise) or permanently.</p>
<p><span class="pagenum"><a name="Page_100" id="Page_100">[100]</a></span>11. Decreased diastolic pressure goes hand in hand with
vasomotor relaxation, as in fevers, etc.</p>
<p>12. Low diastolic pressure is frequently pathognomonic
of aortic insufficiency.</p>
<p>13. When the systolic and diastolic pressures approach,
heart failure is imminent either when pressure picture is
high or low.</p>
<p>When all these factors are taken into consideration, it
becomes apparent that the diastolic pressure is most important,
if not the most important part of the pressure
picture.</p>
<p>Up to within a very brief time all the statistical evidence
of blood pressure was based on systolic readings alone.
This data is most valuable and much has been learned as
to diagnosis and prognosis, but it is a mass of data based
on a one-sided picture and can not be as valuable as the
statistics which will undoubtedly be published later when
all the pressure picture figures can be analyzed.</p>
<h4>Pulse Pressure</h4>
<p>The pulse pressure is the actual head of pressure which
is forcing the blood to the periphery. At every systole a
certain amount of blood 75-90 c.c. (Howell) is thrown violently
into an already comfortably filled aorta. The sudden
ejection of this blood instigates a wave which rapidly
passes down the arteries as the pulse wave. The elastic
recoil of the aorta and large arteries near the heart contract
upon the blood and keep it moving during diastole.
Normally the blood-vessels are highly elastic tubes with
an almost perfect coefficient of elasticity. The pulse pressure
varies under normal conditions from 30 to 50 mm. Hg.
There is a very definite relationship between the velocity
of blood and the pulse pressure which is expressed thus;
velocity = pulse rate × pulse pressure.<a name="FNanchor_5_5" id="FNanchor_5_5"></a><a href="#Footnote_5_5" class="fnanchor">[5]</a></p>
<p><span class="pagenum"><a name="Page_101" id="Page_101">[101]</a></span></p>
<p>Further it has been demonstrated that under normal conditions
and during various procedures—the pulse pressure
is a reliable index of the systolic output.<a name="FNanchor_6_6" id="FNanchor_6_6"></a><a href="#Footnote_6_6" class="fnanchor">[6]</a></p>
<p>Increased pulse pressure therefore goes hand in hand
with greater systolic output. Physiologically this is most
ideally seen during exercise. Following exercise the pulse
rate increases, the systolic pressure rises greatly, the diastolic
slightly or not at all. The pulse pressure therefore is
increased. The velocity also is much increased. The call
comes for more blood and the heart responds. In the chronic
high pulse pressures there are four correlated conditions
which, so far as I have studied them, are always present.
These are: (1) An increase in size of the cavity of the left
ventricle. The ventricle actually by measurement contains
more blood than normal, and therefore throws out more
blood at every systole. The volume output is greater per
unit of time. (2) There is actual permanent increase in
diameter of the arch of the aorta. This is a compensating
process to accommodate the increased charge from the left
ventricle. (3) There are on careful auscultation over the
manubrium, particularly the lower half, breath sounds
which vary from bronchial to intensely tubular, depending
upon the anatomic placing of the aorta, the shape of the
chest, and the degree of dilatation. Often there is very
slight impairment of the percussion note as well. (4)
There is increase in size of all the large distributing arteries,
carotids, brachials, femorals, renals, celiac axis, etc.,
with fibrous changes in the media, loss of some elasticity,
and increase in size of the pulse wave. Increased pulse
pressure means increased volume output, but does not always
mean increased velocity. The proper distribution of
blood to the various organs of the body is regulated by the
vasomotor system acting upon the small arteries which contain
considerable unstriated muscle. When fibrous arteriosclerosis
is present there is loss of elasticity in the distributing<span class="pagenum"><a name="Page_102" id="Page_102">[102]</a></span>
arteries and a greater volume of blood must be
thrown out by the ventricle at every systole in order that
every organ shall have its full quota of blood. A force
which is sufficient to send blood through elastic normal distributing
tubes becomes totally insufficient to send the same
amount of blood through tortuous and more or less inelastic
tubes.</p>
<p>It is evident then that pulse pressure is exceedingly important.
It can only be determined by measuring both the
<i>systolic</i> and <i>diastolic</i> pressure. The pulse rate must also
be known in order to compute the velocity. It is essential
to have the whole pressure picture for all cases if correct
conclusions are to be drawn.</p>
<p>In an irregular heart, especially in the cases due to myocardial
disease, it is quite impossible to determine the true
diastolic pressure. One can only approximate it and say
that the pulse pressure is low or high. As a matter of fact
the real systolic pressure can not be determined. For this
figure the place on the scale where most of the beats are
heard may be taken for the average systolic pressure. No
one can seriously maintain that he can measure the diastolic
pressure under all circumstances.</p>
<p>By means of the auscultatory method of measuring blood
pressure we are able to determine irregularities of force in
the heart beats more easily than by listening to the heart
sounds. A pulsus alternans is readily made out. The irregular
tones heard over the brachial artery in cases of irregular
heart action have been called "tonal arrhythmias."</p>
<h4>Blood Pressure Variations</h4>
<p>A recent study of diurnal variations in blood pressure has
shown that while the maximum pressure rises after the ingestion
of food and steadily rises slightly throughout the
day, the minimum blood pressure is very uniform throughout
the day, and is little affected by the ingestion and digestion
of meals. When it is affected, a rise or a fall may<span class="pagenum"><a name="Page_103" id="Page_103">[103]</a></span>
take place. Throughout the day, it tends to become slightly
lower. The pulse pressure then is greater towards evening.</p>
<p>Weysse and Lutz in a study of this question draw the following
conclusions:</p>
<p>1. A rise of maximum pressure averaging 8 mm. of Hg
occurs immediately on the ingestion of food. A gradual
fall then takes place until the beginning of the next meal.
There is also a slight general rise of the maximum pressure
during the day.</p>
<p>2. The average maximum blood pressure for healthy
young men in the neighborhood of 20 years of age is 120
mm. of Hg. This pressure obtains commonly one hour
after meals. The higher maximum pressures occur immediately
after meals, and the lower, as a rule, immediately
before meals.</p>
<p>3. The range of maximum pressure varies considerably in
different individuals, but the highest and lowest maximum
pressures are practically equidistant from the average pressure
of any one individual.</p>
<p>4. The minimum blood pressure is very uniform throughout
the day, and is little affected by the ingestion and digestion
of meals. When it is affected a rise or fall may take
place. There is a tendency for a slight general lowering
of the minimum pressure throughout the day.</p>
<p>5. The average minimum blood pressure for healthy
young men in the neighborhood of 20 years of age is 85 mm.
of Hg. Thus we get an average pulse pressure of 35 mm.
of Hg.</p>
<p>6. Pulse pressure, pulse rate, and the relative velocity
of the blood flow are increased immediately upon the ingestion
of meals. They attain the maximum, as a rule, in
half an hour, and then decline slowly until the next meal.
There is a general increase in each throughout the day.</p>
<p>These measurements were made upon persons at rest.
Almost any form of exercise would have made the variations
much greater. No account is taken of the psychic
variations which for the physician are the most important
to bear in mind. Neglect to take this variation into account
will inevitably lead to false conclusions.</p>
<div class="center"><span class="smcap">The Average Diurnal Blood Pressure Record of the Ten Subjects</span></div>
<table summary="Diurnal blood Pressure">
<tr>
<th class="tdouble">TIME</th>
<th class="tdouble">MAXIMUM</th>
<th class="tdouble">MINIMUM</th>
<th class="tdouble">MEAN</th>
<th class="tdouble">PULSE</th>
<th class="tdouble">PULSE</th>
<th class="tdouble">PP x PR</th>
<th class="tdouble">NOTES</th></tr>
<tr>
<th class="bdouble bb"> </th>
<th class="bdouble bb"> </th>
<th class="bdouble bb"> </th>
<th class="bdouble bb"> </th>
<th class="bdouble bb">PRESSURE</th>
<th class="bdouble bb">RATE</th>
<th class="bdouble bb"> </th>
<th class="bdouble bb"> </th>
</tr>
<tr><td align="left"> </td><td align="left"><i>mm.</i>Hg</td><td align="left"><i>mm.</i>Hg</td><td align="left"><i>mm.</i>Hg</td><td align="left"><i>mm.</i>Hg</td></tr>
<tr><td align="left">4:30 p.m.</td><td align="left">119.5</td><td align="left">84.1</td><td align="left">101.8</td><td align="left">35.4</td><td align="left">72.0</td><td align="left">2549</td></tr>
<tr><td align="left">5:00 p.m.</td><td align="left">117.7</td><td align="left">83.5</td><td align="left">100.6</td><td align="left">34.2</td><td align="left">71.1</td><td align="left">2432</td></tr>
<tr><td align="left">6:00 p.m.</td><td align="left">118.0</td><td align="left">84.0</td><td align="left">101.0</td><td align="left">34.0</td><td align="left">74.9</td><td align="left">2547</td><td align="left">Before dinner</td></tr>
<tr><td align="left">6:45 p.m.</td><td align="left">127.2</td><td align="left">88.2</td><td align="left">107.7</td><td align="left">39.0</td><td align="left">78.1</td><td align="left">3046</td><td align="left">After dinner</td></tr>
<tr><td align="left">7:00 p.m.</td><td align="left">124.7</td><td align="left">87.7</td><td align="left">106.2</td><td align="left">37.0</td><td align="left">76.0</td><td align="left">2812</td></tr>
<tr><td align="left">7:30 p.m.</td><td align="left">122.0</td><td align="left">83.4</td><td align="left">102.7</td><td align="left">38.6</td><td align="left">76.0</td><td align="left">2934</td></tr>
<tr><td align="left">8:00 p.m.</td><td align="left">122.4</td><td align="left">85.5</td><td align="left">103.4</td><td align="left">36.9</td><td align="left">71.2</td><td align="left">2527</td></tr>
<tr><td align="left">8:30 p.m.</td><td align="left">120.0</td><td align="left">85.0</td><td align="left">102.5</td><td align="left">35.0</td><td align="left">69.7</td><td align="left">2439</td></tr>
<tr><td align="left">9:00 p.m.</td><td align="left">120.5</td><td align="left">84.7</td><td align="left">102.5</td><td align="left">35.8</td><td align="left">65.2</td><td align="left">2334</td></tr>
<tr><td align="left">9:30 p.m.</td><td align="left">118.2</td><td align="left">84.4</td><td align="left">101.6</td><td align="left">33.8</td><td align="left">64.4</td><td align="left">2177</td></tr>
<tr><td align="left">7:30 a.m.</td><td align="left">118.4</td><td align="left">87.6</td><td align="left">103.0</td><td align="left">30.8</td><td align="left">70.3</td><td align="left">2165</td></tr>
<tr><td align="left">8:00 a.m.</td><td align="left">116.4</td><td align="left">86.4</td><td align="left">101.4</td><td align="left">30.0</td><td align="left">69.8</td><td align="left">2094</td><td align="left">Before breakfast</td></tr>
<tr><td align="left">8:30 a.m.</td><td align="left">124.2</td><td align="left">85.4</td><td align="left">104.8</td><td align="left">38.8</td><td align="left">79.4</td><td align="left">3081</td><td align="left">After breakfast</td></tr>
<tr><td align="left">9:00 a.m.</td><td align="left">123.8</td><td align="left">84.4</td><td align="left">104.1</td><td align="left">39.4</td><td align="left">84.1</td><td align="left">3313</td></tr>
<tr><td align="left">10:00 a.m.</td><td align="left">118.2</td><td align="left">83.6</td><td align="left">100.9</td><td align="left">34.6</td><td align="left">70.7</td><td align="left">2446</td></tr>
<tr><td align="left">11:00 a.m.</td><td align="left">116.2</td><td align="left">84.8</td><td align="left">100.5</td><td align="left">31.4</td><td align="left">67.7</td><td align="left">2126</td></tr>
<tr><td align="left">12:00 m</td><td align="left">114.4</td><td align="left">83.2</td><td align="left">98.8</td><td align="left">31.2</td><td align="left">66.2</td><td align="left">2065</td><td align="left">Before luncheon</td></tr>
<tr><td align="left">12:30 p.m.</td><td align="left">122.8</td><td align="left">83.2</td><td align="left">103.0</td><td align="left">39.6</td><td align="left">70.9</td><td align="left">2808</td><td align="left">After luncheon</td></tr>
<tr><td align="left">1:00 p.m.</td><td align="left">122.3</td><td align="left">82.0</td><td align="left">102.1</td><td align="left">40.3</td><td align="left">79.7</td><td align="left">3212</td></tr>
<tr><td align="left">2:00 p.m.</td><td align="left">118.4</td><td align="left">81.4</td><td align="left">99.9</td><td align="left">37.0</td><td align="left">77.6</td><td align="left">2871</td></tr>
<tr><td align="left">3:00 p.m.</td><td align="left">118.8</td><td align="left">82.6</td><td align="left">100.7</td><td align="left">36.2</td><td align="left">75.1</td><td align="left">2719</td></tr>
<tr><td align="left">4:00 p.m.</td><td align="left">115.8</td><td align="left">82.0</td><td align="left">98.9</td><td align="left">33.8</td><td align="left">71.9</td><td align="left">2420</td></tr>
<tr><td align="left">5:00 p.m.</td><td align="left">117.2</td><td align="left">83.4</td><td align="left">100.3</td><td align="left">33.8</td><td align="left">69.6</td><td align="left">2352</td></tr>
<tr><td align="left">6:00 p.m.</td><td align="left">117.4</td><td align="left">84.4</td><td align="left">100.9</td><td align="left">33.0</td><td align="left">72.8</td><td align="left">2402</td><td align="left">Before dinner</td></tr>
<tr><td align="left">6:45 p.m.</td><td align="left">124.6</td><td align="left">83.1</td><td align="left">103.8</td><td align="left">41.5</td><td align="left">80.4</td><td align="left">3337</td><td align="left">After dinner</td></tr>
<tr><td align="left">7:00 p.m.</td><td align="left">125.2</td><td align="left">84.2</td><td align="left">104.7</td><td align="left">41.0</td><td align="left">76.1</td><td align="left">3120</td></tr>
<tr><td align="left">7:30 p.m.</td><td align="left">122.0</td><td align="left">84.0</td><td align="left">103.0</td><td align="left">38.0</td><td align="left">73.7</td><td align="left">2801</td></tr>
<tr><td align="left">8:00 p.m.</td><td align="left">119.6</td><td align="left">85.0</td><td align="left">102.3</td><td align="left">34.6</td><td align="left">72.3</td><td align="left">2502</td></tr>
<tr><td align="left">8:30 p.m.</td><td align="left">119.7</td><td align="left">84.0</td><td align="left">101.3</td><td align="left">34.7</td><td align="left">69.0</td><td align="left">2394</td></tr>
<tr><td align="left">9:00 p.m.</td><td align="left">120.0</td><td align="left">86.2</td><td align="left">103.1</td><td align="left">33.8</td><td align="left">68.0</td><td align="left">2298</td></tr>
<tr><td align="left">Average</td><td align="left">120.0</td><td align="left">85.0</td><td align="left">102.5</td><td align="left">35.0</td><td align="left">72.0</td><td align="left">2550</td></tr>
</table>
<div class="center">(Taken from Weysse and Lutz.)</div>
<p>In some experiments to determine the changes upon the
blood pressure induced by hot and cold applications on and
within the abdomen, Hammett, Tice and Larson found that
heat applied to the outside of the abdomen raises the blood
pressure. The application of cold produces no change. Either
hot or cold saline introduced within the abdomen
causes a fall in blood pressure.</p>
<p><span class="pagenum"><a name="Page_105" id="Page_105">[105]</a></span>Experimentally, certain drugs such as adrenalin, barium
chloride, nicotine, digitalis, strophanthus and the infundibular
portion of the pituitary body known as pituitrin raise
the maximum pressure. In the clinic it is difficult to conclude
always whether the drug alone is responsible for rise
in maximum pressure. Adrenalin given intravenously will
raise the pressure. So will digitalis and strophanthus. I
have watched the maximum pressure rise within three minutes
following an intravenous injection of gr. <sup>1</sup>⁄<sub>100</sub> (0.0006
gm.) strophanthin 20 mm. of Hg: I have seen the subcutaneous
injection of 10 minims of adrenalin repeated several
times daily for six months fail to have the least effect
on the blood pressure picture.</p>
<p>Elevation of the foot of the bed about nine inches proved
so efficacious in steadying failing hearts in acute infectious
diseases, particularly typhoid, that a study was made of
the effect upon blood pressure. Many observations were
made, but no instrumental proof of rise in blood pressure
could be adduced.</p>
<p>Exercise always raises blood pressure, the maximum
much more than the minimum. In athletes the minimum
pressure may actually fall, the maximum rise so that a
greater volume output results from the greater pulse pressure.</p>
<p>Shock and hemorrhage lower it. Hemorrhage lowers
also the pulse pressure, and it may be possible to prognosticate
internal hemorrhage by frequent estimations of the
systolic and diastolic pressures (Wiggers). Compression
of the superior mesenteric artery or the celiac axis in dogs
raises the blood pressure measured in the carotid artery
for a period of at least an hour. This seems to be dependent
on purely mechanical causes, and is not a reflex vasomotor
phenomenon. (Longcope and McClintock.)</p>
<p>Experimentally blood pressure can be increased by direct
compression of the brain as Cushing has shown. It was
thought at one time that in man the same effect would result<span class="pagenum"><a name="Page_106" id="Page_106">[106]</a></span>
from tumor of the brain or especially from subdural
or extradural hemorrhage following head injuries. This,
however, is not the case. No information of great value
can be obtained by the measurement of blood pressure in
these states. We do know that too high and too prolonged
compression of the medulla brings about exhaustion of the
cardiac center accompanied with rapid pulse, low pressure
and eventual death.</p>
<h4>Hypertension</h4>
<p>All the conflict during the past few years over the subject
of blood pressure has revolved around this much overworked
word. Hypertension means high pressure, and yet
it carries with it a suggestion of high pressure which is
harmful to the individual. As a matter of fact hypertension
is a compensatory process, it is often a saving process
in spite of the fact that it carries possibilities of harm in
its possessor. It has been made a fetish, a god to fall down
before and worship and it has been the means of holding a
torch of fear over a patient which has not been lost on the
charlatans. Popularization of blood pressure has brought
its crop of evils, no one of which has been as fruitful in
dollars to unprincipled quacks as hypertension.</p>
<p>Hypertension is the expression on the part of the circulation
to meet new conditions in the tissues so that all tissues
will be nourished and all will be enabled to function.
Looked at from that point of view it is a conservative process
and in many cases it is. It is not an average normal
state, but it is normal state for the man who has it in
chronic form. Hypertension should be viewed rationally
and its proper place in the whole make-up of the patient determined.
Hypertension is a relative term. What might
be high pressure in a man of sedentary habits who reaches
the age of fifty, might not be high pressure in a full blooded
formerly athletic man of the same age. Temporary hypertension
due to excitement, exercise, etc., must be kept in<span class="pagenum"><a name="Page_107" id="Page_107">[107]</a></span>
mind. It is not intended to convey the impression that
hypertension is of no moment. It is a matter for investigation,
but not a matter to worship as the all-in-all.</p>
<p>Hypertension is, after all, a physiologic response on the
part of the organism in order to maintain the circulation in
equilibrium in the face of conditions which tend to produce
vasoconstriction in large areas and, therefore tend to deprive
these areas of blood. That there must be some substance
in the blood stream which causes this constriction
seems certain. What it is, is not at present known. Recently,
Voegtlin and Macht<a name="FNanchor_7_7" id="FNanchor_7_7"></a><a href="#Footnote_7_7" class="fnanchor">[7]</a> have isolated a crystalline substance
from the blood of man and other mammals which
they regard as a lipoid and closely related to cholesterin.
This substance was recovered by them from the cortex of
the adrenal gland. This becomes of added interest in the
light of observations made by Gubar (quoted by Voegtlin
and Macht). He noted "that the vasoconstricting properties
of blood serum vary in different pathologic conditions,
being increased in nephritis, for instance, and diminished
in others." In some experiments made in the summer of
1913, we found there was no marked difference in the anaphylactic
shock produced in half-grown rabbits by the injection
of normal and uremic blood serum. As lipoids do
not cause anaphylaxis, there should be no difference in the
reaction of normal and uremic sera unless in one there was
some form of protein not in the other. This does not seem
to be the case. The presence of something in the circulation,
therefore, produces constriction of vessels. This calls
for more force in contraction on the part of the heart. This
substance may be of lipoid nature. The continued presence
of this hypothetical substance naturally would lead to hypertrophy
of the heart.</p>
<p>What makes hypertension of significance is not the hypertension
itself, but the fact that it is the expression of<span class="pagenum"><a name="Page_108" id="Page_108">[108]</a></span>
processes going on in the body which demand exhaustive
investigation. To attach a blood pressure cuff to the arm,
find the pressure, and diagnose hypertension is like putting
a thermometer under the tongue, noting a rise in the mercury,
and diagnosing fever. What causes the hypertension?
Can the causes be removed? Those are the really
vital questions after the symptom hypertension has been
discovered.</p>
<p>All states of hypertension are accompanied by more or
less increase of pulse pressure. In other words the systolic
pressure is always increased to greater degree than the diastolic
pressure. In studies carried out in the wards and
Pathological Laboratory of the Milwaukee County Hospital,
Milwaukee, we found that in all of the cases of chronic
high blood pressure with resulting high pulse pressure four
correlated factors were found. If any one of these factors
is present, the other three are found.</p>
<p>1. In all high pulse pressure cases there is increase in the
size of the cavity of the left ventricle. The ventricle actually
contains more blood when it is full, and throws out,
therefore, more blood at each systole. The actual volume
output is greater per unit of time. Such hearts always
show increase in thickness of the ventricular wall. I quite
agree with Stone,<a name="FNanchor_8_8" id="FNanchor_8_8"></a><a href="#Footnote_8_8" class="fnanchor">[8]</a> who says, "It is merely to be emphasized
that when the pulse pressure persistently equals the
diastolic pressure (high pressure pulse, in other words)
with a resulting 50 per cent, <i>overload</i>, which means the expenditure
of double the normal amount of kinetic energy on
the part of the heart muscle, cardiac hypertrophy has occurred."
They are found in aortic insufficiency, in chronic
nephritis, in the diffuse fibrous type of arteriosclerosis, and
in some cases of exophthalmic goiter. Such a condition
occurs temporarily after exercise.</p>
<p><span class="pagenum"><a name="Page_109" id="Page_109">[109]</a></span></p>
<p>2. In all high pulse pressure cases there is actual permanent
increase in diameter of the arch of the aorta. This
is a compensating process to accommodate the increased
charge from the left ventricle. Smith and Kilgore<a name="FNanchor_9_9" id="FNanchor_9_9"></a><a href="#Footnote_9_9" class="fnanchor">[9]</a> have
shown this to be true in cases of chronic nephritis with hypertension.
Their research confirms my own observations.
They found dilatation of the arch in (1) syphilis (that is,
aortitis); (2) age over 50 (that is, probable factor of arteriosclerosis);
(3) other serious cardiac enlargement, and
(4) hypertension (with more or less hypertrophy, as in
chronic nephritis).</p>
<p>In ten cases showing arches at the upper limit of normal
(that is, 6 cm. in diameter) and hypertrophy of the heart,
three were chronic mitral endocarditis; one was chronic
aortic endocarditis; three were chronic mitral and aortic
endocarditis, and there was one each of hyperthyroidism,
pericarditis and adherent pericardium.</p>
<p>In fourteen cases of hypertension (highest systolic 270
mm., average systolic, 215 mm.), all showed cardiac hypertrophy.
"All but three of these cases had great vessels
whose transverse diameters measured over the normal
limit of 6 cm., and in one of those measuring 6 cm. the
Roentgen-ray diagnosis was 'slight dilatation' of the
arch." Smith and Kilgore are at a loss to explain the three
exceptions. They did not give diastolic pressures, so pulse
pressures are not known. Possibly the three exceptions
were cases of high diastolic pressure in which the pulse
pressure possible was not over 60 mm. Such cases might
show "slight dilatation of the arch," but not marked dilatation,
such as was found in the other, evidently high pulse
pressure cases.</p>
<p>We have found that only the high pulse pressure cases
show dilatation of the arch. Certain high tension cases
which have had a very high diastolic pressure do not reveal
any accurately measurable dilatation of the aortic<span class="pagenum"><a name="Page_110" id="Page_110">[110]</a></span>
arch. An empty aorta after death is quite different from a
functionating aorta during life. Hence the dilatation
which is found postmortem must have been considerable
during life. And conversely, a dilatation which was present
during life might not be looked on as such after death.</p>
<p>3. In all high pulse pressure cases one will find on careful
auscultation over the manubrium, particularly its lower
half, breath sounds which vary from bronchial to intensely
tubular. At times the percussion note will be slightly impaired,
as McCrae<a name="FNanchor_10_10" id="FNanchor_10_10"></a><a href="#Footnote_10_10" class="fnanchor">[10]</a> has shown in dilatation of the arch of
the aorta. This auscultatory sign is evidence of some more
or less solid body in the anterior mediastinum which is
lying on the trachea and permits the normal tubular breathing
in the trachea to be audible over the upper part of the
sternum. It is found in cases of dilated aortic arch. Fluoroscopic
examination has confirmed the findings on auscultation.</p>
<p>4. In all high pulse pressure cases, in which the pulse
pressure is over 70 mm. of mercury, there is increase in
the size of all large distributing arteries, carotids, brachials,
femorals, renals, celiac axis, etc., with fibrous changes in
the media, loss of some of the elasticity, and in the palpable
superficial arteries, increase in size of the pulse wave.</p>
<p>Increased pulse pressure means increased volume output,
but does not always mean increased velocity. The proper
distribution of blood to the various organs of the body is
regulated by the vasomotor system acting on the small arteries
which contain considerable unstriated muscle. In
order that there may be enough blood at all times and under
varying conditions of rest and function, there must be a
proper supply coming through the distributing vessels, the
large arteries, those containing much elastic tissue, and
only a very small amount of unstriated muscle tissue or
none whatever. Fibrous sclerosis of these vessels causes
them to become enlarged and tortuous and to lose much<span class="pagenum"><a name="Page_111" id="Page_111">[111]</a></span>
of their elasticity, which is essential for the even distribution
of blood. A greater blood volume is therefore necessary
in order that the organs may receive their quota of
blood. A force which is sufficient to send blood through
elastic normal distributing tubes becomes totally insufficient
to send the same amount of blood through tortuous and
more or less inelastic tubes. As a compensatory process
the pulse pressure increases. For this to increase, the left
ventricular cavity dilates, the arch dilates, and as a greater
force must be exerted to keep the increased mass in motion,
the heart responds by hypertrophy of its left ventricle and
becomes itself the subject of fibrous changes in the myocardium.
The mass movement of blood is therefore greater
in high pulse pressure cases than in cases of normal pulse
pressure.</p>
<p>In cases of chronic interstitial nephritis—contracted
granular kidney—it may well be that the sclerosis of the
arteries is a secondary process caused, as Adami thinks,
by the hypertension itself. In aortic insufficiency the situation
is somewhat different. The high pulse pressure is due
to a very low diastolic pressure, for in my experience with
uncomplicated aortic insufficiency the systolic pressure is,
as a rule, not much increased above the normal for the individual's
age. Here peripheral resistance is so low that
a capillary pulse is common. The volume output per unit
of time is greatly increased, the arch of the aorta is dilated,
and the pulse is large. The fact that a large part of the
blood regurgitates during diastole back into the ventricle,
and the fact that the diastolic pressure is low means that
there is no increased resistance to overcome, and the systolic
pressure is not raised.</p>
<p>Stone<a name="FNanchor_11_11" id="FNanchor_11_11"></a><a href="#Footnote_11_11" class="fnanchor">[11]</a> has divided the cases of hypertension into the cerebral
and cardiac types. He finds that there is a difference
in prognosis and in the mode of death in the two groups.
He has further attempted to judge of the work placed upon<span class="pagenum"><a name="Page_112" id="Page_112">[112]</a></span>
the heart by calculating what he calls the heart load or pressure-ratio.
For example, he takes a normal pressure at
120-80-40. The relation between 80 and 40 is ½ or 50 per
cent. That he considers normal. When the heart load increases
so that the pulse pressure equals or exceeds the
diastolic pressure, the heart load is 100 per cent or more,
he considers the danger of myocardial exhaustion graver
than when the heart load is normal or less than 50 per cent.</p>
<p>It is his opinion, in which I heartily concur, "that an
individual with a systolic pressure of 200 and a diastolic
pressure of 140, is in greater danger of cerebral death than
an individual with a systolic pressure of 200 and a diastolic
pressure of 100." He is "likewise certain that the individual
with a systolic pressure of 200 and a diastolic of
90 to 100 is in greater danger of a cardiac death. It is
apparently the constant high diastolic pressure rather than
the intermittently high systolic pressure which predisposes
to cerebral accident."</p>
<p>I have not been able to confirm all of Stone's conclusions.
His contention holds good for some cases, but not, in my
experience, for the great majority of the hypertension cases.
I feel that in the classification of the chronic high pressure
case we can go one step farther and split his first group
into two usually differentiable groups. Syphilis is not an
etiological factor in any of these groups. It is not considered
that these groups are absolutely distinct and can always
be rigidly separated. There are variations and combinations
which render an exact separation impossible.
But bearing this in mind the following classification is proposed
as a working classification.</p>
<p>Group A. Chronic nephritis.</p>
<p>Group B. Essential hypertension.</p>
<p>Group C. Arteriosclerotic hypertension.</p>
<p>Group A. <i>Chronic Nephritis.</i> These are the cases with
a high-pressure picture, that is to say, high systolic (200+)
and high diastolic (120-140+). The pulse pressure is much<span class="pagenum"><a name="Page_113" id="Page_113">[113]</a></span>
increased. The palpable arteries are hard and fibrous.
There is puffiness of the under eyelids, which is more pronounced
in the morning on arising. Polyuria with low
specific gravity and nycturia are present. There are almost
constant traces of albumin in the urine, with hyaline and
finely granular casts.</p>
<p>Functionally these kidneys are much under normal. The
functional capacity determined by Mosenthal's modification
of the Schlayer-Hedinger method shows a marked inability
to concentrate salts and nitrogen. The phthalein output
is below normal. As the case advances the phthalein output
becomes less and less, until a period is reached when there
are only traces or complete suppression at the end of a two-hour
period. Such patients may live for ten weeks (one of
our cases) or longer, all the time showing mild uremic
symptoms, and suddenly pass into coma and die.</p>
<p>The natural end of patients in this group is either uremia
or cardiac decompensation (so-called cardiorenal disease).
Cerebral accidents may happen to a small number. It is
only to this group, in my opinion, that the term cardiorenal
disease should be applied. Formerly I believed that all high
systolic pressure cases were cases of chronic nephritis of
some definite degree. From the purely pathologic standpoint
that is true, but from the important, functional standpoint
it is far from being the true state of the cases.</p>
<p>In this group there is marked hypertrophy and moderate
dilatation of the left ventricle with dilatation and nodular
sclerosis of the aorta. The kidneys are firm, red, small,
coarsely granular, the cortex much reduced, the capsule
adherent. Cysts are common. It is the familiar primary
contracted kidney. Mallory calls this capsular-glomerulonephritis.
The etiology is obscure. Often no cause can be
found. Again, there is a history of some kidney involvement
following one of the acute infectious diseases, or it
may follow the nephritis of pregnancy. Usually, however,<span class="pagenum"><a name="Page_114" id="Page_114">[114]</a></span>
these cases fall into the group of secondary contracted kidneys,
chronic parenchymatous nephritis.</p>
<blockquote><p>Illustrative Case.—R. Z., a woman, aged thirty-six years, was seen July 26,
1916, in coma. There was a history of typhoid fever at nineteen years, but no
other disease. She had had nine full-term pregnancies, the last one thirteen
months previously. For a week before the onset of the present illness she had
complained of severe headaches and dizziness. There were no heart symptoms.
For the past year she has had nycturia. Physical examination revealed tubular
breathing beneath the manubrium, a few rales in the chest, an enlarged heart
(left side), with a systolic murmur over the aortic area. Blood pressure was
178-125-53, the pulse rate 96, leucocytes 27,250. Venesection of 500 c.c. of
blood and intravenous injections of 500 c.c. of 5 per cent NaHCO<sub>3</sub> in normal
saline were employed. Lumbar puncture withdrew 60 c.c. of clear fluid under
pressure with 6 cells per cubic millimeter. The eye grounds showed distinct
haziness of the disks and dilatation of the veins. Blood pressure after venesection
was 164-122-42, pulse 76, but in a few days rose to 222-142-80, pulse 70.
A second venesection of 400 c.c. and proctoclysis of 1000 c.c. saline solution
was tried. The blood-pressure now was 198-140-58. The pH of the blood was
7.6, the alkaline reserve was 35 volume per cent (van Slyke), and the CO<sub>2</sub>
tension of the alveolar air (Marriott) was 25 mm. The phthalein on the day
following the second venesection was 45 per cent in two hours. The urine
at first showed 500 c.c. in twenty-four hours, specific gravity 1016, albumin
and casts. Later she passed 1300 to 1600 c.c. with specific gravity around
1010. The blood-pressure fluctuated considerably, reaching as low as 138-98-40,
pulse 88. She was discharged improved September 10, 1916. She had
constant headache but managed to keep up. In June, 1917, she suddenly
died in an uremic coma.</p></blockquote>
<p>Group B. This one might designate as the hereditary
type, although there is not always a history in the antecedent.
This group includes the robust, florid, exuberantly
healthy people. They often are heard to boast that they
have never had a doctor in their lives. They are usually
thick-set or very large, fleshy people. The pressure picture
is exceedingly high. The pulse pressure is moderately
increased. The arteries are rather large, fibrous, and often
quite tortuous, although this is not always the case. Some
persons have hard, small, fibrous arteries. There is no
puffiness beneath the eyes, no polyuria, and no nycturia as
a rule. The urine is of normal amount, color, and specific
gravity. Albumin is only rarely found and then in traces,
but careful search of a centrifuged specimen invariably reveals<span class="pagenum"><a name="Page_115" id="Page_115">[115]</a></span>
a few hyaline casts. The phthalein excretion is normal
or only slightly reduced. The kidneys excrete salt and
nitrogen normally. It is in this group that apoplexy is
found most frequently. The rupture of the vessel occurs
when the victim is in perfect health, often without any
warning. Occasionally when such a case recovers sufficiently
to be around, cardiac decompensation sets in later
and he dies then of the cardiac complications.</p>
<p>Pathologically the hearts of such persons are found to
have the most enormous hypertrophy of the wall of the left
ventricle. The cavity is somewhat enlarged, as is always
the case when the pulse-pressure is increased, but the size
of the cavity is not the striking feature. The aorta is
fibrous, thick walled, and the arch is slightly dilated. There
are patches of arteriosclerosis. One such case seen only
at autopsy had a rupture of the aorta just above the sinus
of Valsalva and died of hemopericardium. The kidneys
are of normal size, dark red, firm, the capsule strips readily,
the surface is smooth or finely granular, the cortex is not
decreased. The pyramids are congested and red streaks extend
into the cortex. Microscopically the capsules of the
glomeruli are a trifle thickened; a few show hyaline
changes. There is rather diffuse, mild, round-cell infiltration
between the tubules. The tubular epithelium shows little
or no demonstrable changes. The arterioles are generally
the seat of a moderate thickening of the intima and media,
but it is not usual to find obliterating endarteritis.
There is evidently a diffuse fibrous change which has not
affected either the tubules or glomeruli to any great extent.</p>
<blockquote><p>Illustrative Case.—L. C., a man, aged fifty-six years, stonemason by trade,
is a stocky, thick-necked individual. He had never been ill in his life until
a year ago, when he fell from his chair unconscious. He had a right-sided
hemiplegia which has cleared up so completely that except for a very slight
drag to his foot he walks perfectly well. He came in complaining of shortness
of breath and cough. There was no swelling of the feet. Here evidently
was left-heart decompensation. Examination showed the blood pressure
to be 240-130-110, pulse irregular, 104 to the minute. There were cyanosis
and rales throughout both chests. The urine was normal in color, specific<span class="pagenum"><a name="Page_116" id="Page_116">[116]</a></span>
gravity 1025, small amount of albumin, few casts, hyaline and granular.
The phthalein elimination was 65 per cent in two hours. Under rest, purgatives,
and digitalis he was much improved. He has since had two other
apoplectic strokes, the last of which was fatal.</p></blockquote>
<p>When these patients are seen with acute cardiac decompensation,
there are, of course, much albumin and many
casts in the urine, and the phthalein output is, for the time
being, decreased.</p>
<p>Group C. This might be called the arteriosclerotic high-tension
group (Stone's cardiac group). The cases are usually
over fifty years old. They are men and women who
have lived high and thought hard. Often they have had
periods of great mental strain. Many men in this group
were athletes in their young manhood. Many have been
fairly heavy drinkers, although never drinking to excess.
They are usually well nourished and inclined to stoutness.
The pressure picture is high systolic with normal or only
slightly increased diastolic and large pulse pressure. The
arteries are large, full, fibrous, usually tortuous. The heart
is very large, the apex far down and out. There is no polyuria;
nycturia is uncommon, quite the exception. The urine
is normal in color, amount, and specific gravity. Albumin
is only rarely found and hyaline casts are not invariably
present. The phthalein excretion is quite normal and the
excretions of salt and nitrogen are also normal. The terminal
condition in most of the patients in this group is cardiac
decompensation. They may have several attacks from
which they recover, but after every attack the succeeding
one is produced by less exertion than the preceding one, and
it becomes more and more difficult to control attacks.
Eventually the patients become bed- or chair-ridden, and
finally die of acute dilatation of the heart.</p>
<p>Occasionally patients in this group may have a cerebral
attack, but in my experience this is uncommon. Pathologically
the heart is large, at times true <i>cor bovinum</i>, dilated
and hypertrophied. The cavity of the left ventricle is much
dilated. The aorta is dilated and sclerosed.</p>
<p><span class="pagenum"><a name="Page_117" id="Page_117">[117]</a></span>The kidneys are increased in size, are firm, dark red
in color, with fatty streaks in the cortex. The capsule strips
readily and the cortex is normal in thickness or only
slightly increased. The organ offers some resistance to the
knife. The microscope shows small areas scattered
throughout where the glomeruli are hyalinized, the stroma
full of small round cells, the tubules dilated, and the cells
are almost bare of protoplasm. Naturally the tubules are
full of granular cast material. Also the arterioles show
extensive intimal thickening, fibrous in character, with occasional
obliterating endarteritis. One gets the impression
that the small sclerotic lesions are the result of anemia and
gradual replacement of scattered glomeruli by fibrous tissue.
For the most part the kidney, except for the chronic
passive congestion, appears quite normal. One can readily
understand that in such a kidney function could not have
been much interfered with.</p>
<blockquote><p>Illustrative Case.—C. K., an active, stout, business man, aged fifty-six
years, consulted me on account of shortness of breath and swelling of the feet
in May, 1915. He had just returned from a hospital in another city, where
he had gone with what was apparently cardiac decompensation. In his early
manhood he had been a gymnast and a prize winner. He has worked hard,
often given way to violent paroxysms of temper, has eaten heavily but drunk
very moderately. The heart was greatly enlarged, the arch of the aorta
dilated, a mitral murmur was audible at the apex. The radials and temporals
were large, tortuous, and fibrous. The blood pressure picture ranged around
180-90-90. He was easily made dyspneic and had a tendency to swelling of
the lower legs. The urine was acid, of normal specific gravity, normal in
amount, normal phthalein, normal concentration of salt and nitrogen, contained
albumin only when he was suffering from decompensation of the heart.
Casts were always found. He finally died, after sixteen months, with all
the symptoms of chronic myocardial insufficiency. The heart was enormous,
a true <i>cor bovinum</i>. The kidneys were typical of this condition, possibly
somewhat larger than usual.</p></blockquote>
<h4>Hypotension</h4>
<p>When the pressure is constantly below the normal, it is
called hypotension. This may be transient—as in fainting—it
may be a normal state of the individual, it occurs in<span class="pagenum"><a name="Page_118" id="Page_118">[118]</a></span>
most fevers and in a great variety of diseases, including
anemias.</p>
<p>In arteriosclerosis, especially the diffuse (senile) type,
the blood pressure is invariably low, and may be spoken of
as hypotension. The heart in such a case is small, the
muscle is flabby, there is brown atrophy of the fibers, and
some replacement of the muscle cells by connective tissue.
The same causes which have produced general arteriosclerosis
have also produced sclerosis of the coronary arteries,
and probably the lessened blood supply accounts for much
of the atrophy of the heart muscle.</p>
<p>In typhoid fever the maximum blood pressure during
beginning convalescence may be as low as 65 mm. Hg. I
have frequently seen hypotension of 80 mm. This is common.</p>
<p>Meningitis is the only acute infectious disease in which
the blood pressure is more often high than low. This is
accounted for by the increased intracranial tension.</p>
<p>Following large hemorrhages the blood pressure is reduced.
In venesection the withdrawal of blood may not
affect the blood pressure. The procedure is done to relieve
overdistension of the heart.</p>
<p>In pleurisy with effusion and in pericarditis with effusion
there is hypotension.</p>
<p>Collapse, whether from poisoning by drugs or as the result
of dysentery, cholera, or profuse vomiting from whatever
cause, reduces the blood pressure.</p>
<p>In cachectic states, such as cancer, the blood pressure is
low. General wasting of the whole musculature includes
that of the heart and the heart muscle shows the condition
known as "brown atrophy."</p>
<p>A most interesting and important condition in which
hypotension occurs is pulmonary tuberculosis. Haven
Emerson has recently gone over the whole subject in a careful
piece of work and his summary is as follows:</p>
<p>"Hypotension or subnormal blood pressure is universally<span class="pagenum"><a name="Page_119" id="Page_119">[119]</a></span>
found in advanced pulmonary tuberculosis, in which
condition emaciation may play a part in its causation.
Hypotension is found in almost all cases of moderately advanced
tuberculosis, or in early cases in which the toxemia
is marked except when arteriosclerosis, the so-called arthritic
or gouty diathesis, chronic nephritis, or diabetes
complicate the tuberculosis and bring about a normal pressure
or a hypertension. Occasionally the period just preceding
a hemoptysis or during a hemoptysis may show hypertension
in a patient whose usual condition is that of
hypotension.</p>
<p>"Hypotension has been found by so many observers in
early, doubtful or suspected cases with or before physical
signs of the disease in the lungs, and is considered by competent
clinicians so useful a differential sign between various
conditions and tuberculosis, that it should be sought for
as carefully as it is the custom at present to search for
pulmonary signs.</p>
<p>"Hypotension when found persistently in individuals or
families or classes living under certain unhygienic conditions
should put us on our guard against at least a predisposition
to tuberculosis. Most unhygienic conditions,
overwork, undernourishment and insufficient air, are of
themselves causes of a diminished resistance, and it seems
likely that a failure of normal cardiovascular response to
exercise or change of position may be found to indicate this
stage of susceptibility, especially to tuberculous infection.</p>
<p>"... Hypotension, when it is present in tuberculosis, increases
with an extension of the process. Recovery from
hypotension accompanies arrest or improvement. Return
to normal pressure is commonly found in those who are
cured. Continuation of hypotension seems never to accompany
improvement. Prognosis can as safely be based on
the alteration in the blood pressure as on changes in the
pulse or temperature...."</p>
<p>There are a few drugs which lower the blood pressure,<span class="pagenum"><a name="Page_120" id="Page_120">[120]</a></span>
but, as a rule, their effects are more or less transitory. We
know of no drug, unless it be iodide of potassium, which has
the property of causing changes in the blood (decrease in
viscosity?), which tends to reduce the blood pressure when
it is excessive. This drug fails us many times.</p>
<div class="center">SOME DRUGS WHICH INFLUENCE THE BLOOD PRESSURE</div>
<p>
<b>Pressure Raisers</b><br />
<br />
Adrenalin, when injected directly<br />
into a vein or deep into the muscles.<br />
The action is transitory.<br />
<br />
Caffeine, preferably in the form<br />
of caffeine-sodium-benzoate. A good<br />
drug.<br />
<br />
Strychnine, which does not act directly<br />
but seemingly through the<br />
higher centers.<br />
<br />
Ergot, somewhat uncertain.<br />
<br />
Nicotine, not used therapeutically.<br />
<br />
Camphor, used in sterile olive oil<br />
and injected deeply into the muscles.<br />
<br />
Digitalis, when the cardiac tone is<br />
low and decompensation is present.<br />
Its action is prolonged but slow. Injections<br />
of the infundibular portion<br />
of the pituitary body. Not in use<br />
clinically.<br />
<br />
<br />
<b>Pressure Depressors</b><br />
<br />
Nitroglycerine and amyl nitrite,<br />
action transitory but rapid.<br />
<br />
Sodium nitrite and erythrol tetranitrate.<br />
Action somewhat more prolonged.<br />
<br />
Aconite, veratrum viride, chloral,<br />
etc. These depress the heart.<br />
<br />
Purgatives, drastic and hydragogue.<br />
<br />
Potassium and sodium iodide may<br />
lower blood pressure. When they do,<br />
the action is prolonged.<br />
<br />
Diuretin and theocin-sodium-acetate.<br />
</p>
<h4>Venous Pressure</h4>
<p>Comparatively little work has been done upon the determination
of the pressure in the veins in man. It is conceivable
that this procedure may, at times, be of great
value. A number of attempts have been made to measure
the venous pressure by compressing the arm veins and noting
on a manometer the force necessary to obliterate the
vein. As the pressure is so slight, water is used instead
of mercury, and readings have been given in centimeters
of water.</p>
<div class="figcenter" style="width: 330px;">
<a name="Venous_blood_pressure_instrument" id="Venous_blood_pressure_instrument"></a>
<img src="images/fig_033.png" width="330" height="500" alt="Fig. 33.—Apparatus for estimating the venous blood pressure in man, devised by
Drs. Hooker and Eyster. The small figure is the detail of the box B. See explanation
in text." title="Fig. 33.—Apparatus for estimating the venous blood pressure in man, devised by
Drs. Hooker and Eyster. The small figure is the detail of the box B. See explanation
in text." />
<span class="caption">Fig. 33.—Apparatus for estimating the venous blood pressure in man, devised by
Drs. Hooker and Eyster. The small figure is the detail of the box B. See explanation
in text.</span>
</div>
<p>In the apparatus shown in the figure (Fig. 33), Drs.
Hooker and Eyster succeeded in making estimations of the
venous pressure. The box <i>B</i> is held in position by the tapes
<i>A</i>, so that the vein is visible through the rectangular opening
in the thin rubber covering the bottom. The box is connected
with the water manometer <i>G</i>, by a rubber tube,
from which a T-tube enters the rubber bulb <i>E</i>. When the
bulb <i>E</i> is compressed between the plates <i>D</i>, by the coarse<span class="pagenum"><a name="Page_121" id="Page_121">[121]</a></span>
thumbscrew <i>C</i>, air is forced into the box <i>B</i>, exerting a pressure
on the vein lying exposed beneath. This pressure is
transmitted directly to the manometer <b>G</b>, and may be read
off in centimeters of water on the accompanying scale. The
veins of the back of the hand are used and there must be no
obstruction between them and the heart. The rubber-covered
box is accurately and lightly fitted over a vein and
pressure made until it is obliterated. By measuring the
distance above or below the heart level that the hand was
when the observation was made, and subtracting or adding<span class="pagenum"><a name="Page_122" id="Page_122">[122]</a></span>
these figures to the manometer reading, we obtain the
venous pressure at the heart level.</p>
<p>Eyster has modified this instrument so that it is now
much simpler to operate. He uses a small glass cup with a
flaring edge and a diameter of about 2 cm. This is sealed
to the skin directly over a vein on the back of the hand by
means of collodion. The stem of the cup has a rubber tube
leading to a small hand bulb and to the manometer tube
which contains colored water. Slight compression of the
hand bulb obliterates the vein which can be seen through
the glass cup. The pressure in centimeters of water is then
read off. (Fig. 34.) The principle is the same as in the
earlier instrument, but the application is easier.</p>
<div class="figcenter bord" style="width: 500px;">
<a name="New_venous_pressure_instrument" id="New_venous_pressure_instrument"></a>
<img src="images/fig_034.png" width="500" height="424" alt="Fig. 34.—New venous pressure instrument. (After Eyster.)" title="Fig. 34.—New venous pressure instrument. (After Eyster.)" />
<span class="caption">Fig. 34.—New venous pressure instrument. (After Eyster.)</span>
</div>
<p>Practically Hooker and Eyster found that the normal
variation in healthy subjects was from 3 to 10 cm. of water.
The pressure rose in cases of decompensated hearts with<span class="pagenum"><a name="Page_123" id="Page_123">[123]</a></span>
dyspnea and venous stasis, and returned to normal with
improvement in the condition of the patient. It might be
possible with this instrument to foretell an oncoming decompensation
by the rise in venous pressure.</p>
<p>The venous pressure may also be estimated roughly by
slowly elevating the arm and noting the instant at which
a particular vein collapses. By measuring the height of
the vein above the heart some idea may be obtained of the
pressure within the right auricle.</p>
<h4>The Pulse</h4>
<p>There is nothing characteristic about the pulse of a
person suffering from arteriosclerosis, except it be the difference
in the pulse of high tension and of low tension.
The pulse of high tension has a gradual rise, a more or less
rounded apex, and the dicrotic wave is slightly marked and
occurs about half-way down on the descending limb. In
arteriosclerosis with low tension the radial artery is usually
so rigid that very little pulse wave can be obtained. The
general form of a low tension pulse is a sharp upstroke, a
pointed summit, and a secondary wave on the base line,
which corresponds to the dicrotic wave. Such a pulse can
be easily palpated, and is known as a dicrotic pulse. However,
such a pulse can occur only when the artery still retains
all or a large part of its elasticity; hence in arteriosclerotic
low tension we would never see such a pulse as
the typical dicrotic.</p>
<h4>The Venous Pulse</h4>
<p>It would carry us too far to discuss fully the character
of the venous pulse, but a brief summary of the essential
features of the normal venous pulse is presented. The
venous pulse is a term used to express the tracing obtained
from the internal or external jugular vein at the root of
the neck. Normally a very characteristic curve is produced,
which can be readily analyzed into a series of waves corresponding<span class="pagenum"><a name="Page_124" id="Page_124">[124]</a></span>
to the fluctuations in the cardiac cycle. To understand
these waves and their values, the accompanying
figure is helpful. (Fig. 35.)</p>
<div class="figcenter" style="width: 500px;">
<a name="Events_in_the_cardiac_cycle" id="Events_in_the_cardiac_cycle"></a>
<img src="images/fig_035.png" width="500" height="459" alt="Fig. 35.—Semidiagrammatic representation of the events in the cardiac cycle: Jug.,
pulse in the jugular vein; Aur., contraction of auricle; V. Pr., intraventricular pressure;
Pap. M., contraction of the papillary muscles; Car., carotid pulse. Below are
given the times of occurrence of the heart sounds and of the opening and closing of
the heart valves. (After Hirschfelder.)" title="Fig. 35.—Semidiagrammatic representation of the events in the cardiac cycle.... (After Hirschfelder.)" />
<span class="caption">Fig. 35.—Semidiagrammatic representation of the events in the cardiac cycle: Jug.,
pulse in the jugular vein; Aur., contraction of auricle; V. Pr., intraventricular pressure;
Pap. M., contraction of the papillary muscles; Car., carotid pulse. Below are
given the times of occurrence of the heart sounds and of the opening and closing of
the heart valves. (After Hirschfelder.)</span>
</div>
<p>Bachmann summarizes the normal waves in the venous
pulse tracing as follows:</p>
<p>"The physiological or so-called venous pulse consists of
three positive and three negative waves, bearing a more or
less definite relation to the events of the cardiac cycle, and
having their origin in the various movements of the chambers
and structures of the right heart. The first positive
wave (<i>a</i>) is presystolic in time, and is due to the contraction
of the auricle, causing a slowing of the venous current
and producing a centrifugal wave through a sudden arrest
of the inflowing blood. The second positive wave (<i>S</i>) is
presystolic in time, and originates in the sudden projection<span class="pagenum"><a name="Page_125" id="Page_125">[125]</a></span>
of the tricuspid valve into the cavity of the auricle during
the quick, incipient rise in the intraventricular pressure
occurring in the protosystolic period. The third positive
wave (<i>v</i>) occurs toward the end of ventricular systole. It
consists of two lesser waves separated by a shallow notch.
The factors entering into its formation are the relaxation
of the papillary muscle at a time when the intraventricular
is still higher than the intraauricular pressure, resulting
in an upward movement of the tricuspid leaflets and a return
of the auriculoventricular septum to its position of
rest.</p>
<p><span class="pagenum"><a name="Page_126" id="Page_126">[126]</a></span>"The first negative wave (between positive wave <i>a</i> and
<i>S</i>) is due to the relaxing auricle. The second negative
wave (<i>Af</i>) occurs during the diastole of the auricle. It
is due to the dilatation of its walls, to the displacement of
the auriculoventricular septum toward the apex occurring
at the time of ventricular systole, and to the pull of the
papillary muscles on the tricuspid valve leaflets. The third
negative wave (<i>Vf</i>) appears during ventricular diastole and
in the common pause of the heart chambers. Its cause is
found in the passage of the blood from the auricle into the
ventricle. It is somewhat modified possibly by the continual
ascent of the auriculoventricular septum and by a wave
of stasis due to the accumulation of blood coming from the
periphery." (Fig. 36.)</p>
<div class="figcenter" style="width: 500px;">
<a name="Simultaneous_tracings_of_the_jugular_and_carotid_pulses" id="Simultaneous_tracings_of_the_jugular_and_carotid_pulses"></a>
<img src="images/fig_036.png" width="500" height="295" alt="Fig. 36.—Simultaneous tracings of the jugular and carotid pulses showing normal waves
in the venous pulse and relation to carotid pulse. (After Bachmann.)" title="Fig. 36.—Simultaneous tracings of the jugular and carotid pulses showing normal waves
in the venous pulse and relation to carotid pulse. (After Bachmann.)" />
<span class="caption">Fig. 36.—Simultaneous tracings of the jugular and carotid pulses showing normal waves
in the venous pulse and relation to carotid pulse. (After Bachmann.)</span>
</div>
<p>Hirschfelder has described another wave which he calls
the "h" wave, which is due to the floating up of the tricuspid
valve by the blood in the ventricle before the complete
filling of the ventricle following the auricular systole. (Fig.
37.)</p>
<div class="figcenter" style="width: 500px;">
<a name="Jugular_and_carotid_tracings" id="Jugular_and_carotid_tracings"></a>
<img src="images/fig_037.png" width="500" height="169" alt="Fig. 37.—Jugular and carotid tracing from a normal individual with a well-marked
third heart sound showing a large "h" and a smaller pre-auricular wave "w." ? indicates
a small wave in mid-diastole following the "h" wave, occasionally found though
perhaps an artefact. (After Hirschfelder.)" title="Fig. 37.—Jugular and carotid tracing from a normal individual with a well-marked
third heart sound.... (After Hirschfelder.)" />
<span class="caption">Fig. 37.—Jugular and carotid tracing from a normal individual with a well-marked
third heart sound showing a large "h" and a smaller pre-auricular wave "w." ? indicates
a small wave in mid-diastole following the "h" wave, occasionally found though
perhaps an artefact. (After Hirschfelder.)</span>
</div>
<h4>The Electrocardiogram</h4>
<p>In the past few years an immense amount of work has
been done by numerous observers on the changes in the
electrical potential of the various portions of the heart
during contraction. The very elaborate and delicate electrocardiograph
with the string galvanometer devised by
Einthoven is used. It has been definitely determined that
the impulse to cardiac contraction originates in the sinus
node, a collection of differentiated nerve cells situated at
the junction of the superior vena cava with the right auricle.
From there the impulse travels in certain fibers in the interauricular
wall, passes through another node, the auriculoventricular
or Tawara node, situated in the auricular
wall just above the auriculoventricular ring, thence via
the Y-bundle, or bundle of His to the ventricles. This sequence<span class="pagenum"><a name="Page_127" id="Page_127">[127]</a></span>
is orderly, regular, and normally invariable. (Fig.
38.)</p>
<div class="figcenter" style="width: 473px;">
<a name="Right_side_of_the_heart_showing_distribution_of_the_two_vagus_nerves" id="Right_side_of_the_heart_showing_distribution_of_the_two_vagus_nerves"></a>
<img src="images/fig_038.png" width="473" height="500" alt="Fig. 38.—Right side of the heart showing diagrammatically the distribution of the
two vagus nerves to different parts of the viscus....(Hare's Practice of Medicine.)" title="Fig. 38.—Right side of the heart showing diagrammatically the distribution of the
two vagus nerves to different parts of the viscus.... (Hare's Practice of Medicine.)" />
<span class="caption">Fig. 38.—Right side of the heart showing diagrammatically the distribution of the
two vagus nerves to different parts of the viscus. The impulse to contraction originates
at the sino-auricular node and passes over the wall of the auricle to Tawara's node, and
thence over His' bundle across the auriculoventricular septum to be distributed throughout
the ventricular wall. If the upper, sino-auricular, node is damaged, or if its impulses
fail to get across the wall of the auricle, Tawara's node acts in its place to start
off the ventricle. If a lesion at the base of the mesial segment of the tricuspid valve
damages His' bundle, so that Tawara's node is cut off from the ventricle, then the ventricle
may originate its own impulses to contraction. (Hare's Practice of Medicine.)</span>
</div>
<p>The sino-auricular (s-a) node is the most irritable portion
of the heart, it is endowed with the greatest amount<span class="pagenum"><a name="Page_129" id="Page_129">[129]</a></span><span class="pagenum"><a name="Page_128" id="Page_128"></a></span>
of rhythmicity as well. It is under the control of the vagus
nerve. Its inherent rate of rhythmicity is probably more
rapid than the usual numbers of impulses per minute, but
it is inhibited by the vagus. Paralysis of the vagus endings
increases the rate of impulse formation and therefore the
rate of the heart.</p>
<p>The electrocardiogram is a graphic representation on a
photographic film or sensitive bromide paper of the changes
of electrical potential during muscular activity. The lines
are made by the highly magnified string of the galvanometer
as it moves across the slit in the photographic apparatus
in response to the induction currents set up in the
heart magnified by the special galvanometer.</p>
<p>The record is made in three so-called Leads.</p>
<div class="center">
Lead I<br />
<br />
The electrodes are attached to right arm and left arm.<br />
<br />
Lead II<br />
<br />
The electrodes are attached to right arm and left leg.<br />
<br />
Lead III<br />
<br />
The electrodes are attached to left arm and left leg.<br />
</div>
<p>A series of regular figures is normally obtained in which
are depressions and elevations and regular spacing of these
elevations and depressions. The waves so-called have been
arbitrarily designated <i>P</i>, <i>Q</i>, <i>R</i>, <i>S</i>, <i>T</i>. There is some difference
in the three leads. "The wave <i>P</i> is positive in <i>all
leads</i>. <i>P</i> to <i>R</i> interval varies slightly in the <i>three leads</i>.
All the waves of <i>Lead II</i> are greater than those of <i>Leads I</i>
and <i>III</i>. The wave <i>R</i> is positive in <i>all leads</i>. <i>T</i> is usually
positive in <i>all leads</i>, but is occasionally negative in Lead
III. Even in normal individuals there is a considerable
range of variation in the electrocardiogram which is within
the limits of the normal." (Hart.) (Fig. 39.)</p>
<div class="figcenter" style="width: 312px;">
<a name="Normal_electrocardiogram" id="Normal_electrocardiogram"></a>
<img src="images/fig_039.png" width="312" height="500" alt="Fig. 39.—Normal electrocardiogram. (After Hart.)" title="Fig. 39.—Normal electrocardiogram. (After Hart.)" />
<span class="caption">Fig. 39.—Normal electrocardiogram. (After Hart.)</span>
</div>
<p>The <i>P</i> wave is admitted to be the wave of auricular contraction.
<i>Q</i>, <i>R</i>, <i>S</i>, is the ventricular complex caused, it is<span class="pagenum"><a name="Page_130" id="Page_130">[130]</a></span>
thought, by the current passing over the ventricles. <i>T</i>
wave is not yet definitely settled. It has been thought by
some that it represented actual ventricular contraction and
its height and shape had some meaning in heart force.
This is denied by others. Hart defines it as "The final activity
of the ventricle." The <i>T</i> wave is usually increased
in size during exercise.</p>
<p>The <i>P-R</i> interval is almost the most important feature
of the tracing. It is the actual conduction time in fractions
of a second of the impulse from s-a node to the ventricles.
Normally this is about 0.2 second or slightly less. Much
that was hoped for from the electrocardiograph in the clinic
has not been forthcoming. Its greatest value is in states
of abnormal conductivity, such as various grades of heart
block, extrasystoles, whether originating in auricles or in
either ventricle, abnormalities of rhythm, as flutter and
fibrillation. It has, however, aided materially in the intelligent
interpretation of many phenomena heretofore not
well understood, and has enormously increased our knowledge
of the physiology and pathologic physiology of the
heart.</p>
<p>It is not possible to enter farther into the subject here.
This brief discussion must suffice. The reader is referred
to works on this subject in connection with diseases of the
heart.</p>
<hr style="width: 65%;" />
<p><span class="pagenum"><a name="Page_131" id="Page_131">[131]</a></span></p>
<h2><a name="CHAPTER_IV" id="CHAPTER_IV"></a>CHAPTER IV.</h2>
<h3>IMPORTANT CARDIAC IRREGULARITIES
ASSOCIATED WITH ARTERIOSCLEROSIS</h3>
<p>Arteriosclerosis of the aorta, of the coronary arteries,
or of both, is practically always found in cases dying of
various cardiac irregularities other than those the result
of rheumatic cardiac lesions. It is not that arteriosclerosis
causes the cardiac lesions (although the thickening of the
walls of the coronary arteries does interfere mechanically
with the nutrition of the heart muscle), but the arteriosclerosis
is a part of the tissue reaction in the arteries to
some set of causes affecting the whole body. It is true
when one boils down the question to its last analysis, general
arteriosclerosis may mechanically so interfere with the
blood supply to tissues that the tissue is thrown out of
function either in the reduction or even loss of function.
So it may be that occasionally the arteriosclerosis in the
arteries supplying the heart is really responsible for the
cardiac irregularity. The past few years have been fruitful
ones in increasing our knowledge of the various irregularities
of the heart. We can do no more than sketch
briefly some of them in relation to arteriosclerosis.</p>
<p>The chief irregularities are (1) auricular flutter, (2)
auricular fibrillation, (3) ventricular fibrillation, (4) auricular
extrasystole, (5) ventricular extrasystole, (6) heart
block, partial or complete.</p>
<h4>Auricular Flutter</h4>
<p>Auricular flutter is an abnormal rhythm characterized by
very rapid, but rhythmic auricular contractions usually 250
to 300 per minute. The auricular contractions are so rapid
that the ventricle can not respond, so that an electrocardiagram<span class="pagenum"><a name="Page_132" id="Page_132">[132]</a></span>
of a heart in such a state (Fig. 40) shows the
ventricle beating regularly but at a much slower rate than
the auricle.</p>
<div class="figcenter" style="width: 459px;">
<a name="Auricular_flutter" id="Auricular_flutter"></a>
<img src="images/fig_040.png" width="459" height="500" alt="Fig. 40.—(After Hart.)" title="Fig. 40.—(After Hart.)" />
<span class="caption">Fig. 40.—(After Hart.)</span>
</div>
<p>The majority of cases exhibiting this peculiar rhythm are
over 40 years of age. In many cases sclerosis of the coronary
arteries as a part of general arteriosclerosis has been
found. Auricular flutter can be suspected when the pulse
is regular or not particularly irregular and a fluttering,
rapid pulsation is seen in the jugular vein on the right side.
One can only be sure of the condition by making graphic
records of the heart.</p>
<p><span class="pagenum"><a name="Page_133" id="Page_133">[133]</a></span>Attacks usually come on suddenly and may disappear as
suddenly, suggesting paroxysmal tachycardia. The patient
feels a commotion in his chest, dyspnea, precordial distress,
etc. The attack may last for weeks or months, in which
case the patient may carry on his usual work but be conscious
of palpitation in his chest. One may safely assume
that the flutter is a sign of a failing myocardium and sooner
or later the heart will pass to the graver stage of auricular
fibrillation.</p>
<h4>Auricular Fibrillation</h4>
<p>In this condition the auricle is widely dilated and over its
surface are countless twitchings of individual muscles giving
to the auricle the appearance of a squirming bunch of
worms. Such a condition may be readily produced in a
dog's exposed heart by direct faradization of the auricle.
It should be seen by every physician in order fully to appreciate
the passive, dilated sac part which the auricle
plays when in such a state. There is no auricular wave on
the electrocardiogram (Figs. 41 and 42) only a series of fine
tremulous lines, and the ventricles beat irregularly with
many dropped beats and variations in the size and force of
individual beats. Extrasystoles are also frequent. The heart
is absolutely irregular. Such a condition is readily recognizable
as the state of broken compensation. Graphic records
are not essential as in auricular flutter to establish
the condition. Inspection of the root of the neck for jugular
pulsations and examination of the pulse with the patient's
evident dyspneic, cyanotic, edematous condition settles the
diagnosis.</p>
<div class="figcenter" style="width: 487px;">
<a name="Auricular_fibrillation" id="Auricular_fibrillation"></a>
<img src="images/fig_041.png" width="487" height="500" alt="Fig. 41.—Electrocardiogram showing auricular fibrillation in Leads I (upper) and II
(middle and lower). (Courtesy of Dr. G. C. Robinson.)" title="Fig. 41.—Electrocardiogram showing auricular fibrillation in Leads I (upper) and II
(middle and lower). (Courtesy of Dr. G. C. Robinson.)" />
<span class="caption">Fig. 41.—Electrocardiogram showing auricular fibrillation in Leads I (upper) and II
(middle and lower). (Courtesy of Dr. G. C. Robinson.)</span>
</div>
<div class="figcenter" style="width: 500px;">
<a name="Auricular_fibrillations" id="Auricular_fibrillations"></a>
<img src="images/fig_042.png" width="500" height="218" alt="Fig. 42.—Auricular fibrillation. (After Hart.)" title="Fig. 42.—Auricular fibrillation. (After Hart.)" />
<span class="caption">Fig. 42.—Auricular fibrillation. (After Hart.)</span>
</div>
<p>In no case of auricular fibrillation is the heart muscle
free from extensive fibrous changes. These may be the result
of general arteriosclerotic changes or may result from
toxic changes. It is the general consensus of opinion that
auricular fibrillation may persist for months or even years.
Some hold that the state of perpetual irregular pulse is
associated with auricular fibrillation. If that is true, then<span class="pagenum"><a name="Page_135" id="Page_135">[135]</a></span><span class="pagenum"><a name="Page_134" id="Page_134"></a></span>
auricular fibrillation may last for many years. Patients
may go about their work but always live with the imminent
danger of a sudden dilatation of the ventricle and symptoms
of acute cardiac decompensation.</p>
<p>In these cases the blood pressure is of particular interest.
It is often stated that the blood pressure is lowered as compensation
returns and digitalis has exhibited its full action.
As a matter of fact this statement needs some modification.
If one takes the highest pressure at the strongest beat,
which may be only one in a dozen or more, that may be true,
but that does not represent the action of the much embarrassed
heart. We know that the circulation is much interfered
with, that there is hypostatic congestion, that the
mass action is slow. The pulse pressure is greatly disturbed
and the head of pressure which should force the
blood to the periphery is so little that the circulation almost
ceases.</p>
<p>A count of the cardiac contractions heard with the stethoscope
and a count of the pulse shows a great discrepancy
in number. This has been called the "pulse deficit" (Hart).
In order to arrive at the true average systolic pressure the
following procedure is done. "The apex and radial are<span class="pagenum"><a name="Page_136" id="Page_136">[136]</a></span>
counted for one minute, at the same time by two observers,
(if possible) then a blood pressure cuff is applied to the
arm, and the pressure raised until the radial pulse is completely
obliterated; the pressure is then lowered 10 mm.,
and a second radial count is made; this count is repeated
at intervals of 10 mm. lowered pressure until the cuff-pressure
is insufficient to cut off any of the radial waves (between
each estimation the pressure on the arm should be
lowered to zero). From the figures thus obtained the
average systolic blood pressure is calculated by multiplying
the number of radial beats by the pressures under which
they came through, adding together these products and
dividing their sum by the number of apex-beats per minute,
the resulting figure is what we have called the 'average
systolic blood pressure.'" (Fig. 43.)</p>
<div class="figcenter" style="width: 500px;">
<a name="Pulse_deficit" id="Pulse_deficit"></a>
<img src="images/fig_043.png" width="500" height="243" alt="Fig. 43.—The shaded area represents the pulse deficit; the upper edge is the apex
rate, the lower edge the radial rate. The broken line indicates the "average systolic
blood pressure." (Compare these values with the figures at the bottom of the chart,
which show the systolic blood pressure determined by the usual method.) (After Hart.)" title="Fig. 43.—The shaded area represents the pulse deficit..." />
<span class="caption">Fig. 43.—The shaded area represents the pulse deficit; the upper edge is the apex
rate, the lower edge the radial rate. The broken line indicates the "average systolic
blood pressure." (Compare these values with the figures at the bottom of the chart,
which show the systolic blood pressure determined by the usual method.) (After Hart.)</span>
</div>
<p>For example: "B. S., April 29, 1910, Apex 131; radial, 101; deficit, 30.</p>
<p>
BRACHIAL PRESSURE RADIAL COUNT<br />
<span style="margin-left: 1.5em;">100 mm. Hg. 0</span><br />
<span style="margin-left: 2em;">90 mm. 13 13 x 90 = 1170</span><br />
<span style="margin-left: 2em;">80 mm. 47 - 13 = 34 x 80 = 2720</span><br />
<span style="margin-left: 2em;">70 mm. 75 - 47 = 28 x 70 = 1960</span><br />
<span style="margin-left: 2em;">60 mm. 82 - 75 = 7 x 60 = 420</span><br />
<span style="margin-left: 2em;">50 mm. 101 - 82 = 19 x 50 = 950</span><br />
<span style="margin-left: 21em;">——</span><br />
<span style="margin-left: 16em;">Apex = 131) 7220</span><br />
<span style="margin-left: 21em;">——</span><br />
<span style="margin-left: 6em;">Average systolic blood-pressure 55 plus</span><br />
</p>
<p>B. S., May 11, 1910, Apex 79; radial, 72; deficit 7.</p>
<p>
BRACHIAL PRESSURE RADIAL COUNT<br />
<span style="margin-left: 1.5em;">120 mm. Hg. 0</span><br />
<span style="margin-left: 1.5em;">110 mm. 44 44 x 110 = 4840</span><br />
<span style="margin-left: 1.5em;">100 mm. 64 - 44 = 20 x 100 = 2000</span><br />
<span style="margin-left: 2em;">90 mm. 72 - 64 = 8 x 90 = 720</span><br />
<span style="margin-left: 21.5em;">——</span><br />
<span style="margin-left: 16.5em;">Apex = 79) 7560</span><br />
<span style="margin-left: 21.5em;">——</span><br />
<span style="margin-left: 1.5em;">Average systolic blood-pressure 95 plus"</span><br />
</p>
<p>The diastolic pressure in these cases can not be determined
except approximately. This may be done by using
an instrument with a dial and noting the pressure where
the oscillations of the dial hand show the maximum excursion.
The diastolic pressure is not at all important under
such conditions of acute cardiac breakdown. It would
make no difference in treatment whether the case was one<span class="pagenum"><a name="Page_138" id="Page_138">[138]</a></span><span class="pagenum"><a name="Page_137" id="Page_137"></a></span>
of pure cardiac disease or one of the hypertension groups.
After the heart has rallied and the circulation is reestablished,
then a careful determination of the diastolic pressure
can be made and the prognosis will rest on what is
found at the compensated stage.</p>
<h4>Ventricular Fibrillation</h4>
<p>Ventricular fibrillation as its name implies, is fibrillation
of the ventricle analogous to that of the auricle, but the
condition is rarely observed as it is incompatible with life.
It has been shown that hearts at the time of death at times
enter a state of fibrillation of the ventricles and that cases
of sudden death may be due to this condition. Recently
G. Canby Robinson<a name="FNanchor_12_12" id="FNanchor_12_12"></a><a href="#Footnote_12_12" class="fnanchor">[12]</a> has seen and made electrocardiograms
of a case of ventricular fibrillation. (Fig. 44.) The case
was that of a woman forty-five years old, "who had a series
of attacks of prolonged cardiac syncope, closely resembling
Stokes-Adams syndrome, from which she recovered."
During an attack of unconsciousness in which there
was no apex beat for about four minutes, the electrocardiogram
was taken. Following this the tracings showed an
almost regular heart beating at the rate of 85 to 100 per
minute. The patient had three convulsions and died with
edema of lungs about 30 hours after the attack of ventricular
fibrillation.</p>
<div class="figcenter" style="width: 500px;">
<a name="Ventricular_fibrillation" id="Ventricular_fibrillation"></a>
<img src="images/fig_044.png" width="500" height="169" alt="Fig. 44.—Upper curve. Record obtained during period of cardiac syncopy at 2:48 p.m., Lead II. Lower curve from dog.
Ventricular fibrillation observed in the exposed heart. Lead from right foreleg and left hind leg. (Courtesy of Dr. G. C. Robinson.)" title="Fig. 44.—Upper curve. Record obtained during period of cardiac syncopy at 2:48 p.m., Lead II. Lower curve from dog.
Ventricular fibrillation observed in the exposed heart. Lead from right foreleg and left hind leg. (Courtesy of Dr. G. C. Robinson.)" />
<span class="caption">Fig. 44.—Upper curve. Record obtained during period of cardiac syncopy at 2:48 p.m., Lead II. Lower curve from dog.
Ventricular fibrillation observed in the exposed heart. Lead from right foreleg and left hind leg. (Courtesy of Dr. G. C. Robinson.)</span>
</div>
<p>Autopsy revealed chronic fibrous endocarditis of aortic
and mitral valves, arteriosclerosis, bilateral carcinoma of
the ovaries, and signs of general chronic passive congestion.</p>
<p>It is possible that the syncopal attacks in this case were
the result of sclerosis of the vessels supplying the heart
muscle although careful microscopical examination did not
throw much light on the ultimate cause.</p>
<h4>Extrasystole</h4>
<p>Whenever there is a dropped beat or an intermittent pulse
one may be sure that it is the result of an extrasystole.<span class="pagenum"><a name="Page_139" id="Page_139">[139]</a></span>
Such extrasystoles are produced in the ventricle at some
point other than the regular path of conduction of impulses.
The extrasystole may have its origin in either the auricle
or the ventricle. If there is auricular extrasystole it can
not usually be recognized except by graphic methods. (Fig.
45.) The ventricular extrasystole on the contrary is commonly
seen and readily recognized. Most of those seen in
the clinic have their origin in some part of the ventricular
wall. Their two characteristics are that they occur too
early and that they are followed by a pause longer than the
normal diastolic pause. (Fig. 46.)</p>
<div class="figcenter" style="width: 500px;">
<a name="Auricular_extrasystoles" id="Auricular_extrasystoles"></a>
<img src="images/fig_045.png" width="500" height="259" alt="Fig. 45.—Electrocardiogram showing auricular extrasystoles (P). (Courtesy of Dr. G. C.
Robinson.)" title="Fig. 45.—Electrocardiogram showing auricular extrasystoles (P). (Courtesy of Dr. G. C.
Robinson.)" />
<span class="caption">Fig. 45.—Electrocardiogram showing auricular extrasystoles (P). (Courtesy of Dr. G. C.
Robinson.)</span>
</div>
<div class="figcenter" style="width: 500px;">
<a name="Ventricular_extrasystole" id="Ventricular_extrasystole"></a>
<img src="images/fig_046.png" width="500" height="122" alt="Fig. 46.—Electrocardiogram showing ventricular extrasystole. Heart rate 56-60
beats per minute. Note that diastolic pause in which extrasystole occurs is practically
equal to two normal diastolic pauses. (Courtesy of Dr. G. C. Robinson.)" title="Fig. 46.—Electrocardiogram showing ventricular extrasystole.... (Courtesy of Dr. G. C. Robinson.)" />
<span class="caption">Fig. 46.—Electrocardiogram showing ventricular extrasystole. Heart rate 56-60
beats per minute. Note that diastolic pause in which extrasystole occurs is practically
equal to two normal diastolic pauses. (Courtesy of Dr. G. C. Robinson.)</span>
</div>
<p>When one listens over the chest to a heart when extrasystoles
are occurring, one suddenly hears a weak beat<span class="pagenum"><a name="Page_140" id="Page_140">[140]</a></span>
which has taken place rather too early after the previous
systole to be strong enough to effect the opening of the
aortic valves. Consequently there is no pulse, the blood
does not move, and that beat is lost to the circulation.
Moreover, when the next regular stimulus comes from the
s-a node it finds the ventricle in a refractory condition,
having just ceased a contraction, and it is not until the next
sinus impulse that the ventricle responds normally. (Fig.
46.)</p>
<p>Patients who have occasional extrasystoles will say that
all of a sudden the heart turns upside down in the chest.
Sometimes there is slight sharp twinge of pain. Patients
are at times quite alarmed about their condition. Provided
there is no evidence of gross myocardial lesion, the extrasystole
itself is of no great significance.</p>
<p>While many cases showing pathologic causes for extrasystoles
have more or less marked arteriosclerosis, there
are other states in which no arteriosclerosis is found where
the extrasystole is present.</p>
<h4>Heart Block</h4>
<p>As heart block occurs frequently in cases characterized
by extensive arteriosclerosis, a brief discussion of the essential
features will be given. It is, however, probable that
arteriosclerosis is not the cause of any of the cases of heart
block directly, but it is only a result of the same etiological
conditions which produce the lesion or lesions which result
in heart block. We may define heart block as the condition
in which the auricles and ventricles beat independently
of each other. There may be delayed conduction (Fig. 47),
partial (Fig. 48), or complete heart block (Fig. 49). In
the former there are ventricular silences, during which the
auricles beat two, three, four, five, even up to nine times,
with only one ventricular contraction. It is believed by
most physiologists that the essential factor in the production
of heart block is an interference in the conduction of<span class="pagenum"><a name="Page_141" id="Page_141">[141]</a></span>
impulses from the auricles to the ventricles through the
band of tissue known as the auriculoventricular bundle.</p>
<div class="figcenter" style="width: 500px;">
<a name="Delayed_conduction" id="Delayed_conduction"></a>
<img src="images/fig_047.png" width="500" height="86" alt="Fig. 47.—Electrocardiogram showing delayed conduction (lengthening of P-R interval).
These P-R intervals are quite regular. When irregular there is apt to be extrasystole
of ventricle or occasional blocking of impulse going to ventricle. (Courtesy of
Dr. G. C. Robinson.)" title="Fig. 47.—Electrocardiogram showing delayed conduction (lengthening of P-R interval).... (Courtesy of
Dr. G. C. Robinson.)" />
<span class="caption">Fig. 47.—Electrocardiogram showing delayed conduction (lengthening of P-R interval).
These P-R intervals are quite regular. When irregular there is apt to be extrasystole
of ventricle or occasional blocking of impulse going to ventricle. (Courtesy of
Dr. G. C. Robinson.)</span>
</div>
<div class="figcenter" style="width: 500px;">
<a name="Partial_heart_block" id="Partial_heart_block"></a>
<img src="images/fig_048.png" width="500" height="383" alt="Fig. 48.—Electrocardiogram showing partial heart-block in the three leads. Note
the variability of P-R interval calculated in seconds in Lead II. (Courtesy of Dr.
G. C. Robinson.)" title="Fig. 48.—Electrocardiogram showing partial heart-block in the three leads. Note
the variability of P-R interval calculated in seconds in Lead II. (Courtesy of Dr.
G. C. Robinson.)" />
<span class="caption">Fig. 48.—Electrocardiogram showing partial heart-block in the three leads. Note
the variability of P-R interval calculated in seconds in Lead II. (Courtesy of Dr.
G. C. Robinson.)</span>
</div>
<div class="figcenter" style="width: 500px;">
<a name="Complete_heart_block" id="Complete_heart_block"></a>
<img src="images/fig_049.png" width="500" height="377" alt="Fig. 49.—Complete heart block. (Courtesy of Dr. G. C. Robinson.)" title="Fig. 49.—Complete heart block. (Courtesy of Dr. G. C. Robinson.)" />
<span class="caption">Fig. 49.—Complete heart block. (Courtesy of Dr. G. C. Robinson.)</span>
</div>
<p>The bundle of muscles described by His in 1905, connecting
the auricles and ventricles, has been definitely
shown to be the path through which impulses having their
origin in the orifices of the great veins pass to the ventricles.<span class="pagenum"><a name="Page_142" id="Page_142">[142]</a></span>
The situation and size of this bundle has been thus
described in man by Retzer:</p>
<p>"When viewed from the left side, the bundle lies just
above the muscular septum of the ventricles and below the
membranous septum. In some hearts the muscular septum
is so well developed that it envelops the bundle. It is then
difficult to find, but occasionally it can be seen directly
by means of transmitted light. From the left side the bundle
can be followed no farther posteriorly than the right
fibrous trigone, for here the connective tissue becomes so
dense that it is difficult to dissect it away. The impression
is, therefore, received that this mass of connective tissue
forms the insertion of the bundle. The bundle may be followed
anteriorly until it becomes intimately mixed with the
musculature of the ventricles.</p>
<p><span class="pagenum"><a name="Page_143" id="Page_143">[143]</a></span>"When viewed from the right side of the heart, the
bundle can not be seen, because it is covered by the mesial
leaflet of the tricuspid valve, whose line of attachment
passes obliquely over the membranous septum. Then, if
the endocardium is removed from the posterior part of the
septum of the auricle up to the membranous septum, the
posterior part of the auriculoventricular bundle will be exposed.
If, in addition, the membranous septum be removed,
the bundle may be traced from the point to which it could
be followed when viewed from the left side as it passes
posteriorly over the muscular septum. In the region of the
auriculoventricular junction it loses its compactness, the
fibers divide, and the bundle seems to fork. One branch
passes into the superficial part of the valve musculature
which descends from the auricles, and the other branch
passes directly into the musculature of the auricle.</p>
<p>"Briefly, the auriculoventricular bundle runs posteriorly
in the septum of the ventricles about 10 mm. below the
posterior leaflet of the aortic semilunar valves; with a gentle
curve it passes posteriorly just over the upper edge of
the muscular septum and sends its fibers into the musculature
of the right auricle and of the auricular valves. In
the heart of the adult the bundle is 18 mm. long, 2.5 mm.
wide, and 1.5 mm. thick." (Erlanger.)</p>
<p>All normal impulses have their origin in the sino-auricular
node at the junction of the superior vena cava with
the right auricle (Fig. 50). From there the impulse travels
in the wall of the auricle in the interauricular septum to the
node of Tawara or A-V node (Fig. 51), thence through the
bundle of His to be distributed to the fibers of the right and
left ventricles. This sequence is orderly and perfectly
regular.</p>
<div class="figcenter" style="width: 500px;">
<a name="Alternating_periods_of_sinus_rhythm_and_auriculoventricular_rhythm" id="Alternating_periods_of_sinus_rhythm_and_auriculoventricular_rhythm"></a>
<img src="images/fig_050.png" width="500" height="95" alt="Fig. 50.—Showing alternating periods of sinus rhythm and auriculoventricular rhythm.
(After Eyster and Evans.)" title="Fig. 50.—Showing alternating periods of sinus rhythm and auriculoventricular rhythm.
(After Eyster and Evans.)" />
<span class="caption">Fig. 50.—Showing alternating periods of sinus rhythm and auriculoventricular rhythm.
(After Eyster and Evans.)</span>
</div>
<div class="figcenter" style="width: 500px;">
<a name="Auriculoventricular_or_nodal_rhythm" id="Auriculoventricular_or_nodal_rhythm"></a>
<img src="images/fig_051.png" width="500" height="264" alt="Fig. 51.—Period of auriculoventricular or "nodal" rhythm following exercise in sitting
posture. (After Eyster and Evans.)" title="Fig. 51.—Period of auriculoventricular or "nodal" rhythm following exercise in sitting
posture. (After Eyster and Evans.)" />
<span class="caption">Fig. 51.—Period of auriculoventricular or "nodal" rhythm following exercise in sitting
posture. (After Eyster and Evans.)</span>
</div>
<p>It has also been shown that the independent auricular
and ventricular rates vary somewhat, that of the auricle
being in general faster than that of the ventricle. A strip
of mammalian ventricle placed outside of the body in<span class="pagenum"><a name="Page_144" id="Page_144">[144]</a></span>
proper surroundings will begin to beat automatically at
the rate of about 40 beats a minute. Experimentally various
grades of heart block have been produced in the dog's
heart by more or less compression of the bundle at the A-V
ring. The block may be partial, when two to nine auricular
beats occur to every one of the ventricle, up to absolute<span class="pagenum"><a name="Page_145" id="Page_145">[145]</a></span>
complete block when the auricles and ventricles beat independently
of one another.</p>
<p>In any stage of partial block, pressure on the vagus nerve<span class="pagenum"><a name="Page_146" id="Page_146">[146]</a></span>
in the neck produces certain specific changes. (Fig. 52.)
Robinson and Draper<a name="FNanchor_13_13" id="FNanchor_13_13"></a><a href="#Footnote_13_13" class="fnanchor">[13]</a> have found qualitative differences
in the two vagi. The right vagus sends most of its fibers to
the s-a node (Fig. 53) and has a more evident influence on
the rate and force of the cardiac contractions. The majority
of fibers from the left vagus are distributed to the A-V
node so that its most evident action is upon the conductivity
of the impulse. Pressure then on the right vagus will
have a tendency to slow the whole heart. Pressure on the
left vagus will have a tendency to prolong the P-R interval
until even complete block occurs. Even when the heart
block is complete, stimulation of the accelerator nerve, as a
rule, increases the rate of both auricles and ventricles.</p>
<div class="figcenter" style="width: 500px;">
<a name="Influence_of_mechanical_pressure_on_the_right_vagus_nerve" id="Influence_of_mechanical_pressure_on_the_right_vagus_nerve"></a>
<img src="images/fig_052.png" width="500" height="69" alt="Fig. 52.—Influence of mechanical pressure on the right vagus nerve. (After Eyster
and Evans.)" title="Fig. 52.—Influence of mechanical pressure on the right vagus nerve. (After Eyster
and Evans.)" />
<span class="caption">Fig. 52.—Influence of mechanical pressure on the right vagus nerve. (After Eyster
and Evans.)</span>
</div>
<div class="figcenter" style="width: 356px;">
<a name="Schematic_distribution_of_right_and_left_vagus" id="Schematic_distribution_of_right_and_left_vagus"></a>
<img src="images/fig_053.png" width="356" height="500" alt="Fig. 53.—Schematic distribution of right and left vagus. (After Hart.)" title="Fig. 53.—Schematic distribution of right and left vagus. (After Hart.)" />
<span class="caption">Fig. 53.—Schematic distribution of right and left vagus. (After Hart.)</span>
</div>
<p>If the block is functional, depending upon some temporary
overstimulation of the vagus nerve, atropin, which
paralyzes the endings of the vagus, will naturally lift the
block. If the block is due to some actual lesion of the bundle
of His, such as fibrosis, gumma, or other lesion, then
atropin will have no influence to terminate the block. In
this manner we are able to distinguish between functional
and organic heart block.</p>
<hr style="width: 65%;" />
<p><span class="pagenum"><a name="Page_147" id="Page_147">[147]</a></span></p>
<h2><a name="CHAPTER_V" id="CHAPTER_V"></a>CHAPTER V.</h2>
<h3>BLOOD PRESSURE IN ITS CLINICAL APPLICATIONS</h3>
<p>It is well to bear constantly in mind the point made over
and over in this work, that blood pressure is only one of
many methods of acquiring information. He who worships
his sphygmomanometer as a thing apart and infallible will
sooner or later come to grief. Judgment must be used in
interpreting changes in blood pressure just as judgment is
essential in properly evaluating any instrumental help in
diagnosis. One must not forget the personal equation
which enters into even accurate instrumental recording in
medicine and surgery.</p>
<p>In this chapter there will be no attempt to quote largely
from what others have said or thought. Every one has
his own opinion as to the value of certain methods after he
has worked with them for a long time. The ideas here expressed,
except in cases where no opportunity has offered
to make personal studies, are those gathered from personal
experience.</p>
<h4>Blood Pressure in Surgery</h4>
<p>Careful estimation of the blood pressure in surgical cases
has, at times, great value. In all surgical diseases the most
important fact to know is not the systolic pressure, but the
pulse pressure. If the pulse pressure keeps within the
range of normal, does not drop much below 30 mm. in an
adult, then so far as we can tell the circulation is being
carried on. When the systolic pressure is gradually falling
and the diastolic remains the same, the circulation is
failing and unless the pulse pressure can be established
again the patient will die. Again we see the value of the
pulse pressure.</p>
<p><span class="pagenum"><a name="Page_148" id="Page_148">[148]</a></span>All prolonged febrile diseases tend to produce a lowering
of the blood pressure picture. The diastolic does not fall to
the same extent as the systolic so that there is a pulse pressure
smaller than normal. This is to be expected from what
we know of the general depression of the circulation in
fevers. The blood pressure reading is only a graphic record
of what we have long known, and enables us from day
to day accurately to measure the general circulation.</p>
<h4>Head Injuries</h4>
<p>It was claimed that in fracture of the skull or in concussion
much could be gained by frequent estimations of
the blood pressure. This seemed probable in the light of
experiments on compressing the brains of dogs by the use
of bags inserted through trephine openings (Cushing). In
the clinic, however, it has not been found of any material
value. It has a value in differentiating a simple fracture,
let us say, from a case of uremia which is picked up on the
street with a bump on the head. There the high pressure
usually found would at once direct attention to the kidneys
and the newer methods of blood examination would at once
settle the question. Naturally uremics may also have skull
fracture. There the diagnosis would be complicated. A
decompression done at once would be indicated. If the
skull fracture happened in a uremic, the decompression
would probably do no harm. In fact, there are some who
advise decompression for uremia.</p>
<h4>Shock and Hemorrhage</h4>
<p>In shock the blood pressure picture is low but the pulse
pressure drops to abnormally low figures. It seems to me
that the blood pressure instrument has its greatest value
in surgery in the warning it gives to the operating surgeon
in cases of impending shock.</p>
<p>It is well known that the first effect of ether, the commonly<span class="pagenum"><a name="Page_151" id="Page_151">[151]</a></span><span class="pagenum"><a name="Page_150" id="Page_150"></a></span><span class="pagenum"><a name="Page_149" id="Page_149"></a></span>
used anesthetic, is to raise the blood pressure and
quicken the pulse rate. The whole blood pressure picture
is at first elevated (Fig. 54). Soon the whole pressure falls
slightly but continues at a higher level than normal. The
diastolic pressure drops back nearly to normal and the increased
pulse pressure is due almost entirely to the slight
rise in the systolic pressure. Now the whole duty of the anesthetist
is to administer the ether so that this ratio of systolic
and diastolic is maintained throughout the operation.
Warning comes to him of impending shock before it comes
to any one in the neighborhood (Fig. 55). Any sudden
change in the pressure is a signal for increased watchfulness.
Should the pressure all at once drop he can immediately
notify the surgeon and institute measures to resuscitate
the patient.</p>
<div class="figcenter" style="width: 368px;">
<a name="Blood_pressure_record_from_a_normal_reaction_to_ether" id="Blood_pressure_record_from_a_normal_reaction_to_ether"></a>
<img src="images/fig_054.png" width="368" height="500" alt="Fig. 54.—Blood pressure record from a normal reaction to ether. Note that the
systolic and diastolic rise and fall together. At the end of the anesthetization the pulse
pressure is practically the same as at the beginning. Compare this with the record in
Fig. 55, where the operation had to be discontinued on account of the onset of shock." title="Fig. 54.—Blood pressure record from a normal reaction to ether. " />
<span class="caption">Fig. 54.—Blood pressure record from a normal reaction to ether. Note that the
systolic and diastolic rise and fall together. At the end of the anesthetization the pulse
pressure is practically the same as at the beginning. Compare this with the record in
Fig. 55, where the operation had to be discontinued on account of the onset of shock.</span>
</div>
<div class="figcenter" style="width: 440px;">
<a name="Chart_showing_the_method_of_recording_blood_pressure_during_an" id="Chart_showing_the_method_of_recording_blood_pressure_during_an"></a>
<img src="images/fig_055.png" width="440" height="600" alt="Fig. 55.—Beginning of operative shock. Chart showing the method of recording blood pressure
during operation.
Note that the pulse and respiration show no remarkable changes, but the blood pressure
steadily fell, the systolic more than the diastolic so that the pulse pressure was gradually reaching
the danger point. Further work on this case was stopped following the warning given by the
blood pressure. The patient was returned to the ward and a week later anesthesia was again
given, the operation was completed, and the patient had a satisfactory convalescence." title="Fig. 55.—Beginning of operative shock. Chart showing the method of recording blood pressure
during operation...." />
<span class="caption">Fig. 55.—Beginning of operative shock. Chart showing the method of recording blood pressure
during operation.
Note that the pulse and respiration show no remarkable changes, but the blood pressure
steadily fell, the systolic more than the diastolic so that the pulse pressure was gradually reaching
the danger point. Further work on this case was stopped following the warning given by the
blood pressure. The patient was returned to the ward and a week later anesthesia was again
given, the operation was completed, and the patient had a satisfactory convalescence.</span>
</div>
<p>A method which is widely used is as follows: The anesthetist
wraps the cuff of one of the dial instruments around
the patient's arm, and arranges the dial so that it can easily<span class="pagenum"><a name="Page_152" id="Page_152">[152]</a></span>
be seen by him at all times. This does not in any way interfere
with the work of the surgeon. Over the brachial artery
below the cuff is the bell of a binaural stethoscope held
in place by the strap attachment now on the market. The
tubes of the stethoscope are long enough to reach conveniently
to the ear pieces. A watch is pinned to the sheet of
the table. He has a chart, as illustrated (Fig. 56) on a
board and makes a dot in every space for five minute intervals.
By joining the lines a curve is obtained which tells
at a glance what the circulation is doing. I feel sure that
more attention and care exercised on the part of the anesthetist
would be the means of conserving many lives lost
from shock following operation.</p>
<div class="figcenter bord" style="width: 500px;">
<a name="Method_of_using_blood_pressure_instrument_during_operation" id="Method_of_using_blood_pressure_instrument_during_operation"></a>
<img src="images/fig_056.png" width="500" height="398" alt="Fig. 56.—Showing method of using blood pressure instrument during operation without
interfering with the operator or assistants. Sheet thrown back to show cuff on
arm of patient. Anesthetist has chart on table beside him, dial pinned to pad in full
view, bulb near hand. Extra tubing must be put on the blood pressure instrument." title="Fig. 56.—Showing method of using blood pressure instrument during operation without
interfering with the operator or assistants." />
<span class="caption">Fig. 56.—Showing method of using blood pressure instrument during operation without
interfering with the operator or assistants. Sheet thrown back to show cuff on
arm of patient. Anesthetist has chart on table beside him, dial pinned to pad in full
view, bulb near hand. Extra tubing must be put on the blood pressure instrument.</span>
</div>
<p>A sudden drop in the pressure picture may mean a large
hemorrhage. The gradual return of the pressure picture
means that the vasomotor mechanism has acted to keep up
the pulse pressure. Should the diastolic pressure continually
fall, it may mean that the hemorrhage is still taking
place (Wiggers).</p>
<h4>Blood Pressure in Obstetrics</h4>
<p>One might affirm almost without fear of contradiction
that the constant determination of blood pressure during
pregnancy is more important than the examination of the
urine. Within recent years a number of observers having
access to a large material, have given the results of their
findings. There is a striking unanimity of opinion, although
now and then a difference in minor details.</p>
<p>The blood pressure should be taken frequently during
pregnancy. The usual and highly essential precautions in
taking pressure in general apply most particularly in these
cases. Towards the end of pregnancy the pressure should
if possible be taken daily and oftener if necessary.</p>
<p>Pressure in women is usually below 120 mm. Many patients
have a temporary rise in blood pressure during pregnancy,
due oftenest to constipation, without developing<span class="pagenum"><a name="Page_153" id="Page_153">[153]</a></span>
other symptoms. This is common to all conditions and has
no significance. Some think that an abnormally low pressure,
that is, a systolic below 90 mm., suggests that the
patient is likely to react unduly to the strain of labor. This
is denied by others. Among 1000 cases (Irving) the pressure
was below 90 in only one case. A gradually rising
pressure precedes albuminuria, as a rule. If there is albumin
without change in pressure the albumin may usually
be disregarded. Some think that a pressure over 130 mm.
systolic should be carefully watched. The danger limit
is set by some at 150 mm. If the blood pressure from the
very first is high, it may mean only that that was the patient's
normal pressure. This calls for increased watchfulness.
It is held by some that high blood pressure favors
hemorrhage and probably explains the hemorrhagic lesions
in the placenta and some viscera in eclampsia and albuminuria.</p>
<p>All are agreed that the most significant change is the
gradual but sure rise from a low pressure. When this is
combined with albuminuria the danger of toxemia is imminent.
The high blood pressure in those under thirty
years of age seems to be a more certain sign of approaching
toxemia than the same pressure in those older. The
pressure falls within a few days to its normal after delivery
in the toxic cases.</p>
<p>Although the emesis gravidarum is held to be a sign of
a toxemia of some unknown nature, the blood pressure is
never raised even in the pernicious form.</p>
<h4>Infectious Diseases</h4>
<p>In all infectious diseases the blood pressure tends to be
lower than normal. During chills the systolic may rise to
great height due to the violent muscular contractions.</p>
<p>We found the blood pressure of great value in giving
information concerning the circulation. Again we repeat<span class="pagenum"><a name="Page_154" id="Page_154">[154]</a></span>
that it is not the systolic alone or the diastolic alone but the
pulse pressure which we wish to keep informed about. In
pneumonia we have tried out Gibson's law only to discard
it. This so-called law is that in pneumonia the systolic
pressure in millimeters should remain above the figure for
the pulse rate. When the figure in mm. of pressure is
equalled by or exceeded by the pulse rate the prognosis is
grave.</p>
<p>In typhoid fever we have made many estimations at various
stages of the disease. We can only say that the pressure
picture tends to fall during the course. The systolic
falls more than the diastolic so that it is not uncommon
to see pulse pressures of 20 mm. at the beginning of convalescence
in spite of the high caloric feeding practiced.
At the time of perforation the systolic pressure may be
raised. This is only the reflex from the initial pain. Soon
the pressure falls and if peritonitis sets in, the pressure is
exceedingly low and the pulse pressure gradually falls until
the circulation can no longer be carried on. In large
hemorrhage the pressure suddenly falls. If only one hemorrhage
has occurred a gradual rise takes place, but the
general pressure picture remains at a lower level for days,
gradually returning where it was before the hemorrhage.</p>
<p>In beginning failure of the circulation we found elevation
of the foot of the bed about nine inches to be of such
value that we felt there must be some increase in blood pressure.
Numerous readings were made covering a period of
several months. Although we felt certain that the circulation
was improved, we rarely needed cardiac stimulation,
we never could prove any increase of blood pressure with
the sphygmomanometer.</p>
<p>In all infectious diseases there is no help offered by blood
pressure estimations in diagnosis. The sole and important
use is that of keeping track of the circulation.</p>
<p><span class="pagenum"><a name="Page_155" id="Page_155">[155]</a></span></p>
<h4>Valvular Heart Disease</h4>
<p>No rules can be laid down for blood pressure in valvular
heart disease. Aortic stenosis, the rarest of the valvular
lesions, is practically always accompanied by high pressure
picture. Mitral stenosis on the contrary usually shows a
low pressure picture. Mitral insufficiency may show an
exceedingly low picture or an exceedingly high picture.
Aortic insufficiency also may be accompanied by a high
systolic or by a normal systolic pressure. It depends on the
etiology. Practically all the rheumatic cases have low pressure,
the syphilitic cases have a high pressure. It is characteristic
of all cases of aortic insufficiency that the diastolic
pressure is low, even as low as 30 mm. The pulse
pressure is invariably high. Usually there is no difficulty
in determining the diastolic pressure. The intense third
tone suddenly becomes dull at the point of diastolic pressure
and frequently the dull sound can be distinctly heard
over the artery down to the zero of the scale. If difficulty
is found in reading the diastolic as the pressure is reduced,
the estimation may be reversed and the pressure gradually
increased from zero to the point where the dull tone suddenly
becomes loud and clear. These points always coincide.</p>
<h4>Kidney Diseases</h4>
<p>This has already been discussed somewhat fully in Chapter
III and will receive more consideration later. It might
be remarked in passing that in a case of seeming coma
where albumin is found in the urine but where the blood
pressure is low or normal, I have found at autopsy in several
cases pyonephrosis and not chronic nephritis. The
blood pressure may be useful in differentiating uremic coma
from the coma of pyonephrosis. Also in the cases of coma
with anasarca, either the acute, subacute or chronic form
the blood pressure is not raised as a rule. Other diseases
of the kidney, as tuberculosis, cancer, infection with pyogenic<span class="pagenum"><a name="Page_156" id="Page_156">[156]</a></span>
organisms, are not accompanied with any notable
changes in blood pressure.</p>
<h4>Other Diseases, Liver, Spleen, Abdomen, etc.</h4>
<p>Blood pressure is only of value in the above diseases in
affording information concerning the state of the circulation.
There is nothing characteristic about the pressure
in any of these diseases.</p>
<hr style="width: 65%;" />
<p><span class="pagenum"><a name="Page_157" id="Page_157">[157]</a></span></p>
<h2><a name="CHAPTER_VI" id="CHAPTER_VI"></a>CHAPTER VI.</h2>
<h3>ETIOLOGY</h3>
<p>The causes of arteriosclerosis are many and varied. No
two persons have the same resisting power toward poisons
that circulate in the blood. Some go through life exposed
to all the infectious diseases without ever becoming infected,
while others fall easy victims to every disease that
comes, no matter how careful they may be, and it is quite
the same in regard to the resistance of the arterial tissues.
If the tubing is of first class quality and the individual does
not place too much strain on it, he may live to the biblical
three-score years and ten, and possess arteries which have
undergone such slight changes that they are not palpable.
Such a person is, however, the exception. On the other
hand, if the tissue is of poor quality, even the ordinary
wear and tear of life causes early changes in the vessels,
and a person of forty may have hard arteries.</p>
<p>We have described in a previous chapter the changes
which normally occur in the arteries as age advances. An
artery that is normal for a man of fifty years would be
distinctly abnormal for a boy of fifteen.</p>
<p>Two broad divisions of arteriosclerosis may be made:
(1) congenital, or the result of inherited tendency; (2)
acquired.</p>
<h4>Congenital Form</h4>
<p>When Dr. O. W. Holmes was asked how to live to the age
of seventy, he replied that a man should begin to pick his
ancestors one hundred years before he was born. Our
parents determine the character of the tissues with which
we start in life, and this determines our general resistance.
We might properly speak of congenital arteriosclerosis<span class="pagenum"><a name="Page_158" id="Page_158">[158]</a></span>
where the affected individual had poor arterial tissue with
which to begin life, for that, in a sense, is a congenital defect,
and arterial tissue that is poor in quality is prone to
disease.</p>
<p>The author is more and more impressed with the part that
heredity plays in the determination of arterial degeneration.
Especially does syphilis in the parents or grandparents
leave its stigma in the succeeding generations in
the shape of poor arterial tissue which is prone to early
degeneration. Recently W. W. Graves has called attention
to a malformation of the vertebral border of the scapula
which consists in a concavity instead of the normal
convexity of the bone. To this malformation he has given
the name, scaphoid scapula. He considers this to be but
one manifestation of a general lack of development in the
individual. He speaks of this maldevelopment as a blight
and considers that syphilis in the ancestors is responsible
for the condition in the offspring. He finds that even in
children, the subjects of the scaphoid scapula, the arteries
are very definitely thickened. While confirmation of his
observations is lacking, there is no doubt that we must lay
the blame for much of the arteriosclerosis in our patients
to the poor quality of arterial tissue transmitted by ancestors
who have acquired some constitutional disease. It
may have been syphilis, it may have been the degeneration
produced by alcohol or other drug. We can not ignore the
part which heredity plays. The various factors to be considered
in the production of the acquired form of arteriosclerosis
appear to me to be but contributory factors to
a very great extent, the essential and fundamental factor
being the quality of arterial tissue with which the individual
is endowed.</p>
<p>Arteriosclerosis may occur in infants. Cases have been
reported of calcification of the arteries in infants and children.
The arteriosclerosis may occur without nephritis or
rise of blood pressure. Cerebral hemorrhage in a child<span class="pagenum"><a name="Page_159" id="Page_159">[159]</a></span>
of two years has been seen. Heredity in these cases plays
a most important rôle. In many of the reported cases there
was no question of congenital syphilis. Aneurysms, single
or multiple, have been found in the arteries of children,
and even the pulmonary artery may show sclerotic changes.</p>
<h4>Acquired Form</h4>
<p>As a rule the cases usually seen belong in this group
because it seems as if a connection could be established almost
always between one or more of the etiologic factors
to be described and the disease. While this apparently is
the case, we must never lose sight of the part which the
quality of the tissue plays. When we leave this out of our
calculations we undoubtedly make many false deductions.
When two men of the same age who have been exposed to
the same conditions as far as we can learn, are found to
have quite different arteries, the one normal, the other
thickened, we must postulate congenitally poor tissue on
the part of the latter. Such tissue readily becomes diseased
following conditions which would very likely have
produced no noticeable effect on perfectly normal, healthy
tissue.</p>
<h4>Hypertension</h4>
<p>Hypertension must still be reckoned with in the etiology
of arteriosclerosis although the rôle that it was thought to
play does not seem so important. Changes of blood pressure
alone are not considered by many to be sufficient for
the production of arteriosclerosis. This may play some
part, but there are many other factors mostly unknown
which determine in any case the production of arterial
lesions.</p>
<p>With every systole of the heart, blood is forced out into
the arterial system against a certain amount of resistance
represented by the tonicity of the capillary area, and the
amount of cohesion between the viscous blood and the walls<span class="pagenum"><a name="Page_160" id="Page_160">[160]</a></span>
of arterioles. When a dilatation of the capillaries over
any large area takes place, the blood pressure falls, provided
there is no compensatory contraction in other areas
to make up for the decreased resistance in the dilated vessels.
The viscosity of the blood, as such, probably has
very little effect on the resistance to the flow. With the
systole of the heart there is a sudden dilatation of the arch
of the aorta, and a wave of expansion follows, which is
transmitted to the periphery and is lost only in the capillaries.</p>
<p>The blood pressure is constantly changing. Physiologically
there are relatively wide variations in the pressure
in a perfectly normal individual. There are some
persons who have hypotension, a blood pressure much below
the normal. Such persons have usually small hearts,
small aortas, and they seem to have but little resistance
to disease. Many diseases, especially the prolonged fevers,
diminish markedly the blood pressure. Whether the hypertension
is the cause of the structural changes that are found
in the walls of the vessels, or is the result of the diminished
area of the arterial tree through which the same amount
of blood has to be driven as before the vessel walls became
narrowed, is still disputed. As has been stated, experimental
evidence would tend to place the initial blame upon
the poisons circulating in the blood, which first damage the
vessel walls. The subsequent changes then produce thickening
and inelasticity. Some think (Allbutt) that the
hypertension is primary. There are cases seen clinically
that lend support to this view and there is experimental
evidence also (v. Chap. II). Not infrequently individuals
in middle life begin to show increase of arterial blood pressure
without discoverable cause. In such case it may be
that there is slowly progressing chronic nephritis. The
urine if examined only superficially in single specimens may
not reveal any abnormalities. Careful functional examination
by means of the newer tests may reveal functional<span class="pagenum"><a name="Page_161" id="Page_161">[161]</a></span>
deficiency. It must not be supposed that all cases of increasing
hypertension are cases of chronic nephritis. The
opinion has already been expressed (Chap. III) concerning
this point. Experience has convinced me that the opinion
expressed in former editions is not altogether correct.</p>
<h4>Age</h4>
<p>No age is exempt from the lesions of arteriosclerosis if we
consider the two groups. However, the disease is seen for
the most part in persons past middle life. The relative
frequency with which it is found in the different decades
depends on so many factors that it is of no value to tabulate
them. As has been stated, arteriosclerosis of all types is
an involution process that advances with age. Longevity
is a question of the integrity of the arterial tissue, and no
one can tell what sort of "vital rubber" (Osler) any one
of us has. However, many with poor tubing may make
such use of it that it will outlast good tubing that is badly
treated. Unfortunately we have no way of telling early
enough with just what sort of arterial tissue we are starting
life.</p>
<h4>Sex</h4>
<p>There is no doubt that men are far more prone to arterial
disease than women are; all statistics are in accord on this
point. This is explained by the greater exposure of men
to those conditions of life which tend to produce circulatory
strain, and so to produce arteriosclerosis, or vice versa.
Arteriosclerosis in women is not often seen until after the
fiftieth year. Cases of the most extreme grade of pipe
stem arteries are, however, seen in old women, and calcified
arteries are not hard to find among the inmates of an old
woman's home.</p>
<h4>Race</h4>
<p>Some of the most beautiful examples of arteriosclerosis
in this country are seen in the negro. Not only is this<span class="pagenum"><a name="Page_162" id="Page_162">[162]</a></span>
disease more frequent in the black race, but the age of onset
is much earlier than in the Caucasian. The accidents of
arteriosclerosis, viz., aneurysm, cerebral hemorrhage, etc.,
are more common among the negro males. The etiologic
factors that are most often found in the history are the
prevalence of syphilis and hard physical labor.</p>
<h4>Occupation</h4>
<p>Certain occupations have a distinct causal relationship to
arteriosclerosis; among such are particularly those entailing
prolonged muscular exercise, especially if much lifting
is necessary. Every one is familiar with the phenomena
accompanying the exertion of lifting. The breath is drawn
in, the glottis is closed, and the muscles of the chest wall
are held rigidly while the exertion lasts. This causes a
great increase in blood pressure, and constant repetition
of this will produce permanent high tension. In hospitals,
the stevedores as a class have marked arteriosclerosis, and,
almost without exception, they are comparatively young
men. Occupations that are accompanied with prolonged
mental strain, such as now occur to the heads of large manufacturing
and financial institutions, also predispose to
early arterial changes. Psychic activity, especially when it
is accompanied by worry, is a potent factor in the production
of the increased blood pressure which is the chief factor
in producing arterial disease. It has been suggested that
sexual continence in high-strung men produces changes in
the nervous system which can conceivably lead to the production
of high tension and further to arteriosclerosis. This,
however, I can not think has any foundation in fact except
in so far as such men are prone to live at high speed and
wear themselves out sooner than the normal person. The
sexual continence <i>per se</i> is not harmful. There are, however,
men who seem not to be harmed by the constant wear
and tear of our modern life. These are the exceptions.</p>
<p>Workers in factories where paint is made and the ingredients<span class="pagenum"><a name="Page_163" id="Page_163">[163]</a></span>
hand-mixed, are prone to develop arteriosclerosis
early in life. It has been found that the laborers most apt
to be victims of lead intoxication are those who are careless
in their habits of cleanliness, particularly in regard to the
fingernails. The continuous absorption of lead into the
system, brings about a condition of hypertension that has
its inevitable results.</p>
<p>The fact is that any occupation which entails either the
absorption of toxic substances, or prolonged muscular labor,
will hasten markedly the onset of arterial disease.</p>
<h4>Food Poisons</h4>
<p>The opinion that arteriosclerosis is due in large part to
poisoning by end products or by-products of protein digestion
is now receiving much support. Experiments on
dogs and rabbits have lent some confirmation to chemical
observations. It has been shown that dogs fed for a long
time on putrefied meat developed inflammation and degeneration
of the adventitia and media, with hyperplasia and
calcification of the intima of many arteries. In the pulmonary
and carotid arteries, in the vena cavas and myocardium,
there were extensive necroses and hyaline degeneration.
Moreover, injections of sodium urate and ergot
caused necroses in the muscularis and elastica of the aorta,
pulmonary artery, vena cavas inferior and heart muscle, but
there was no calcification. Guinea pigs which were fed
indol in small doses by the mouth over a long period showed
atheromatous degeneration of the aorta.</p>
<h4>Infectious Diseases</h4>
<p>As more study has been given to the arteries in persons
who have died of the acute infectious diseases, more has
come to light concerning the effects of the toxins of these
diseases on the vessel walls. In the arteries of children
who have died of measles, scarlet fever, diphtheria, cerebrospinal<span class="pagenum"><a name="Page_164" id="Page_164">[164]</a></span>
meningitis, etc., degenerative changes in the arteries
occur, modified only by the length of time that the
toxins have acted.</p>
<p>Thayer has shown that the arteries of those who have
passed through an attack of moderately severe or severe
typhoid fever are as a rule more readily palpable than are
the vessels of persons of corresponding years who have
never had the disease. Clinically the typhoid toxin appears
to cause the early production of arteriosclerosis. The
changes in the arteries occur for the most part, and always
earlier, in the peripheral arteries, and the media is chiefly
affected. Minute yellowish patches are found on the aorta,
carotids, and coronaries. In persons who have passed
through an attack of one of the fevers, and have later died
from some other cause, regenerative changes are sometimes
found to have taken place in the arteries, consisting of an
ingrowth of elastic fibers from the intact adventitia to the
diseased media.</p>
<p>That there are some other factors than the infectious disease
which are concerned in the production of arterial
changes seems evident from a study<a name="FNanchor_14_14" id="FNanchor_14_14"></a><a href="#Footnote_14_14" class="fnanchor">[14]</a> made recently among
a group of almshouse inmates ranging in age from 38 to
90 years. The study included 500 persons of both sexes.
Careful histories were taken to determine the presence of
antecedent infectious disease. The radial artery was palpated
to determine the presence of sclerosis. Among the
cases giving a history of one infectious disease the following
table gives the results:</p>
<div class="center">
<table border="0" cellpadding="4" cellspacing="0" summary="">
<tr><td align="left">DISEASE </td><td align="left">NO. </td><td align="left">+ </td><td align="left">++ </td><td align="left">+++ </td><td align="left">POSITIVE </td><td align="left">NEGATIVE</td></tr>
<tr><td align="left">Measles</td><td align="right">47</td><td align="right">10</td><td align="right">6</td><td align="right">12</td><td align="right">28</td><td align="right">19</td></tr>
<tr><td align="left">Infectious arthritis</td><td align="right">38</td><td align="right">9</td><td align="right">6</td><td align="right">4</td><td align="right">19</td><td align="right">19</td></tr>
<tr><td align="left">Pneumonia</td><td align="right">30</td><td align="right">5</td><td align="right">8</td><td align="right">5</td><td align="right">18</td><td align="right">12</td></tr>
<tr><td align="left">Typhoid</td><td align="right">27</td><td align="right">6</td><td align="right">8</td><td align="right">3</td><td align="right">17</td><td align="right">10</td></tr>
<tr><td align="left">Scarlet fever</td><td align="right">10</td><td align="right">0</td><td align="right">0</td><td align="right">4</td><td align="right">4</td><td align="right">6</td></tr>
<tr><td align="left">Smallpox</td><td align="right">14</td><td align="right">1</td><td align="right">4</td><td align="right">0</td><td align="right">5</td><td align="right">9</td></tr>
<tr><td align="left">Miscellaneous</td><td align="right">12</td><td align="right">2</td><td align="right">5</td><td align="right">2</td><td align="right">9</td><td align="right">3</td></tr>
<tr><td align="left"> </td><td align="right">178</td><td align="right">33</td><td align="right">37</td><td align="right">30</td><td align="right">100</td><td align="right">78</td></tr>
</table></div>
<p><span class="pagenum"><a name="Page_165" id="Page_165">[165]</a></span></p>
<p>A summary of the cases showed: 252 cases without sclerosis;
248 with sclerosis; 147 cases with infections but no
sclerosis; 180 cases with infections and sclerosis.</p>
<p>This study failed to throw any positive light on the question.
Infectious diseases undoubtedly play a certain rôle,
particularly those continuing a long time and certain particular
infectious diseases, as measles.</p>
<h4>Syphilis</h4>
<p>Syphilis is one of the most important of the etiologic
factors in the production of arteriosclerosis. It has been
shown that in 85 per cent of cases of aortic insufficiency in
persons, usually males, over forty-five years, who did not
have chronic infective endocarditis, the Wassermann reaction
was positive. Acute aortitis affecting the ascending
and transverse portions of the arch of the aorta is very
commonly seen, and the irregular, scattered, slightly raised,
yellowish-white patches of sclerosis in the arch which are
found years after the syphilitic lesion, are considered by
some to be very characteristic of syphilis. Mesaortitis is
the primary lesion and acts as a <i>locus minoris resistentiæ</i>
where an aneurysm forms.</p>
<p>Hypertensive cardiovascular cases have been serologically
studied, and a positive Wassermann reaction found
in a large percentage of one series. In fifty cases, 90 per
cent either gave a positive Wassermann reaction or luetin
test, were known to have syphilis, or had children with
hereditary syphilis. This suggests what might be called
"familial cardiovascular syphilis."</p>
<p>Hypertensive disease is possibly one of the common so-called
"late" manifestations of syphilis. That syphilis is
responsible for the arterial disease in the vessels of the
brain, resulting in apoplexy or sudden cardiac death in middle
life, has long been known. In fact, it is claimed (Osler)
that all aneurysms occurring in persons under thirty years<span class="pagenum"><a name="Page_166" id="Page_166">[166]</a></span>
of age are due to syphilitic aortitis. In the late stages of
syphilis the arterial lesions may be of a diffuse character.</p>
<h4>Chronic Drug Intoxications</h4>
<p>Lead, tobacco, and according to some, tea and coffee, are
to be classed as causal factors in the production of arteriosclerosis.
Certain it is that all these substances have a
tendency to raise the arterial pressure, but whether the
drug itself causes first a degeneration, and later a hypertension
results, or vice versa, is not yet positively known.
We have just mentioned that lead particularly has a marked
effect in producing arterial lesions. Other drugs as adrenalin,
barium chloride, physostigmin, etc., while producing
experimental arteriosclerosis, hardly could produce
the disease in man. <b>Alcohol</b> has been blamed for much, and
as an etiologic factor in the production of arteriosclerosis
formerly was accorded a first place. More recently much
doubt has been thrown on this supposition by the work of
Cabot, who showed that the mere drinking of even large
quantities of spirits had no effect in producing arterial
disease.</p>
<p>This observation has been recently substantiated by
Hultgen, who carefully studied clinically 460 cases of
chronic alcoholism. He says, "There are no cardiovascular
symptoms which might be termed characteristic of
chronic alcoholism, unless it be the peculiar fetal qualities
of the heart sounds which we know as embryocardia. I
find this very frequent among drinkers, but I can offer only
a tentative explanation for it, namely the following: Embryocardia
can only occur with low tension blood pressure,
and in the absence of renal insufficiency. Hence it
might be considered as a useful condition of no pathologic
significance at all. That alcohol is a sclerogenic pharmakon
and productive of arteriosclerosis with its usual train of
symptoms may be a fact, but its demonstration would be<span class="pagenum"><a name="Page_167" id="Page_167">[167]</a></span>
difficult and is really not shown by my tabulations. There
were cardiovascular changes, such as myocarditis, aortitis,
valvular heart disease and arteriosclerosis in chronic alcoholics
in 54.3 per cent of 461 cases, but this by no means
constitutes a proof of the causal relationship between these
lesions and the abuse of liquors. I believe it, nevertheless,
to be good reasoning to ascribe the bulk of cardiovascular
symptoms to the sclerogenic action of alcohol, while abstaining
from an interpretation of its pathogenesis." Just
what rôle <b>tobacco</b> plays is difficult to say. My own opinion
is, that of itself when used in moderation, it has no ill
effects. However, as tobacco is a drug that may raise the
blood pressure, excessive use must be held responsible for
the production of arteriosclerosis. It is difficult to separate
its effects from those produced by eating and drinking.</p>
<h4>Overeating</h4>
<p>There can be no doubt but that the constant overloading
of the stomach with rich or difficultly digestible food is
responsible for a large number of cases of arteriosclerosis.
Every one must have noted the increase in force and volume
of the heart beat after the ingestion of a large meal. The
constant repetition of such processes conceivably can lead
to damage to the vessel walls through hypertension.</p>
<p>In the metabolism of food in the intestines there are substances
produced which are poisonous when absorbed directly
into the circulation. Ordinarily these substances
are rendered harmless either before absorption or are detoxicated
in the liver to harmless substances. It is conceivable
that a constant overproduction of such poisons
would eventually damage the defensive mechanism of the
body to such an extent that some of the poisons would
circulate in the blood. An expression of a surplus of one,
at least, of these decomposition products is the appearance
of indican in the urine. It is not believed that indicanuria
has the importance attached to it which some authors would<span class="pagenum"><a name="Page_168" id="Page_168">[168]</a></span>
have us believe. It is found too often and in too many varying
conditions, nevertheless it undoubtedly does reveal the
presence of perverted metabolism.</p>
<p>In how far the toxins absorbed from the intestinal tract
are responsible for the production of arterial disease, it is
not possible to say. Some observers lay great stress on
this factor as a cause of arteriosclerosis. The author believes
that the rôle played by the absorption of products of
perverted intestinal metabolism is an important one. The
primary change is an increased tension in the arterioles
which later leads to thickening of the coats of the vessels
and to the other consequences of arterial disease. A vicious
circle is thus established which has a tendency to become
progressively worse.</p>
<h4>Mental Strain</h4>
<p>More and more does one become impressed with the fact
that patients with arteriosclerosis are very often those who
take life too seriously and either from ambition or from an
exalted sense of duty lead especially strenuous lives. Not
always are these persons addicted to drug or liquor habit.
Many are rather abstemious in their habits. It is not so
often that we see as a victim of arteriosclerosis, the carefree
person who laughs his way through life without worrying
about the morrow. He is not so prone to arteriosclerosis.
Worry is a far more potent cause of breakdown than
actual manual work. It is the rule to find thickened arteries
among neurasthenics. This may be only part of a generalized
degeneration of all tissue in the body. The blood pressure
in such persons is usually low. So many men of our
better class live under a continuous mental strain in the
business world. The increase in arteriosclerosis cases is
real, not apparent. The intense mental strain seems to cause
a marked increase in blood pressure (for short periods of
mental effort this has been proved) over a period of time<span class="pagenum"><a name="Page_169" id="Page_169">[169]</a></span>
sufficient to cause permanent changes in the vessel walls.
The same sequence of events repeats itself; high tension,
arterial strain, compensatory thickening, hypertrophied
heart, etc.</p>
<p>Certainly the character of the arterial tissue has much to
do with the determination of degenerative changes which
may result from the action of one or more of the etiologic
factors.</p>
<h4>Muscular Overwork</h4>
<p>Muscular overwork is to be reckoned with as an etiologic
factor. One sees it especially among the laboring class in
both whites and negroes. Possibly other factors, as alcohol
and coarse heavy food, contribute to the early arterial
degeneration. Hypertrophy of the heart occurs in athletes,
and statistics gathered among the oarsmen especially, show
a relatively high mortality at the different decades traceable
to the high tension produced while in training. This
question deserves more consideration than has been accorded
it.</p>
<h4>Renal Disease</h4>
<p>Chronic disease of the kidneys (contracted red kidney) is
one of the most certain producers of hypertension; in fact,
some maintain that high tension, even without demonstrable
kidney lesions, as revealed by careful urine examinations,
is a valuable sign pointing to chronic nephritis. This
is doubted by others, myself among them. Just what causes
the increase in blood pressure sometimes to over 270 mm.
of Hg, is not definitely known. It seems most probable that
it is some poison elaborated by the diseased kidneys and
absorbed into the general circulation. There it acts primarily
on the musculature of the arterioles causing tonic
contraction and an increase of work on the part of the heart
to force the blood through narrowed channels. One fact is
certain. We see patients in coma due to renal disease with<span class="pagenum"><a name="Page_170" id="Page_170">[170]</a></span>
blood pressure much over 200 mm of Hg. As these cases
clear up, the pressure may fall, and should they seemingly
recover, the recovery is accompanied with a marked decrease
in blood pressure, finally reaching the normal for
the individual. Moreover, in the course of a severe acute or
subacute nephritis, hypertension is associated with headache,
partial or total blindness, and drowsiness. When the
pressure is reduced, all these symptoms disappear.</p>
<p>There is also the chronically shrunken and scarred kidney
known pathologically as the arteriosclerotic kidney.
It is probable that there are two groups of cases which we
may designate: (1) primary; (2) secondary. In the primary
group the kidney disease antedates the sclerosis of
the arteries, and the sclerosis is most probably dependent on
the constant high tension. We know that prolonged hypertension
will produce severe forms of arteriosclerosis. The
arterial disease in this group is caused by the renal disease.</p>
<p>In the second group the kidney changes are apparently
due to the general arteriosclerosis which, affecting the kidney
vessels, causes changes leading to atrophy and subsequent
fibrous tissue ingrowth of scattered areas. These
cases are not necessarily associated with hypertension; on
the contrary there is more apt to be hypotension. Where
the first group occurs for the most part in young and active
middle-aged people, the second group is the result of involutionary
processes which accompany advanced age.</p>
<p>However careful a urinalysis may be, there is no assurance
that one can predict the pathologic state of the kidney.
Often so-called normal urine will be secreted by a badly
diseased kidney, whereas a urine which contains considerable
albumin and many casts may be secreted by a kidney
which is only temporarily the seat of inflammation. What
matters after all is not the state of the kidney which the
pathologist describes, but the actual functional response
of the kidney in the body to the various tests now well
known.</p>
<p><span class="pagenum"><a name="Page_171" id="Page_171">[171]</a></span></p>
<h4>Ductless Glands</h4>
<p>At the present time the tendency among some writers
is to make the ductless glands the responsible agents in
almost all diseases. Arteriosclerosis is no exception to this
tendency. Sajous, for example, divides the morbid process
producing arteriosclerosis into three types; (1) autolytic,
(2) adrenal, (3) denutrition. In the first type he finds
the pancreas to be the most important gland. It supplies
an internal secretion which "takes a direct part in the protein
metabolism of the tissue cells, and also in the defensive
reactions within these cells, as well as in the phagocytes and
in the blood stream." This being the case exaggeration of
this digestive process has tissue destruction as its result,
arteriosclerosis among them.</p>
<p>In the adrenal type Sajous argues that adrenalin produces
lesions experimentally, therefore the adrenal gland
has a profound influence by its internal secretion in connection
with the sympathetic system in producing degenerations
leading to arteriosclerosis.</p>
<p>The denutrition type has as its particular gland the thyroid.
The sclerotic process in the arteries is due to the lack
of thyroid as in cases of myxedema. After a long résumé
of his ideas he concludes "that arteriosclerosis is the result
of excessive or deficient activity of certain ductless glands,
the thyroid and adrenal in particular."</p>
<p>No one can dogmatically deny the part which the ductless
glands may play in the production of arteriosclerosis, but it
hardly seems that there is enough actual experimental evidence
to show that they take such an important part as Sajous
believes. Until further and more convincing evidence
is offered by competent investigators, I prefer to look with
some skepticism upon the ductless gland theory of the causation
of arteriosclerosis. The field lends itself too easily
to speculation and imagery. Some are already allowing
themselves the mental debauch of this nature.</p>
<hr style="width: 65%;" />
<p><span class="pagenum"><a name="Page_172" id="Page_172">[172]</a></span></p>
<h2><a name="CHAPTER_VII" id="CHAPTER_VII"></a>CHAPTER VII.</h2>
<h3>THE PHYSICAL EXAMINATION OF THE HEART
AND ARTERIES</h3>
<h4>Heart Boundaries</h4>
<p>In order to be able to estimate the departures from normal
in the boundaries of the heart, it is essential that there
be a definite appreciation of the boundaries of the normal
heart in relation to the chest wall.</p>
<p>It is frequently stated that the right limit of cardiac dullness
is normally, in the adult, just at the right border of
the sternum. This is not strictly accurate. Careful dissections
at the autopsy table and x-ray plates of the chest
made at a distance of two meters from the tube show that
the border of the right auricle is from one to one and a
half and even two centimeters from the edge of the sternum
at the level of the fourth rib, and on the living subject this
can be also demonstrated. The right border of the heart
usually is from 3 to 4 cm. from the midsternal line at the
level of the fourth rib.</p>
<p>Again there is a term used in defining the apex, known as
the point of maximum impulse. As this does not always
coincide with the apex beat and with the outer lower left
border of the heart, it would be better to use the term apex
beat.</p>
<p>Normally, then, the cardiac dullness, the so-called relative
cardiac dullness, begins above at the upper border of the
third costal cartilage, as a rule, and taking a somewhat
curved line with the concavity inward, descends to the fifth
interspace or beneath the fifth rib from 9 to 10 cm. from a
line drawn through the center of the sternum parallel to its
length, the midsternal line. This seems to me to be a better
method of recording the size of the heart than by the<span class="pagenum"><a name="Page_173" id="Page_173">[173]</a></span>
lines commonly used; viz., the nipple, or midclavicular, or
parasternal line. Below, the cardiac dullness is merged into
the tympany from the stomach and the dullness from the
liver. At the sixth right costosternal articulation there is
a sharp turn upwards forming at that point with the liver
the cardiohepatic angle. At the fourth right cartilage or
the third interspace, the dullness is from one to two centimeters
from the edge of the sternum. We have then a somewhat
pear-shaped area or triangular area with the apex at
the apex of the heart. The so-called absolute cardiac dullness
does not appear to me to be of any great significance.
In reality it is the limit of lung resonance and may be
greater or less, not so much on account of variations in the
size of the heart, as of variations in size of the lungs and
shape of the chest wall.</p>
<p>The really crucial question which should always be asked
is, Is the heart enlarged or decreased in size? The position
of the apex beat alone can not determine this, neither can the
limit to the right of the sternum. The distance between
these two points and the depth of the dullness at a distance
of 5 cm. from the midsternal line on the left side, will give
the size of the heart as nearly as can be obtained in the living
subject. A series of measurements in normal adults
average 13 to 14 cm. and 9 to 10 cm. respectively. For
women they are about 1 cm. less in each direction.</p>
<p>The elaborate mechanism known as the orthodiagraph is
probably the best means of determining the actual limits
of the heart, but few men have such an expensive instrument,
and, moreover, at the bedside such an instrument
could not be used. From comparative measurements I concur
in the belief of those who affirm that careful percussion
will furnish equally as accurate limits.</p>
<p>The first step in making an examination of the heart is to
expose the patient's chest in a good light, and, sitting at his
right side, carefully inspect the chest. The position of the
apex beat, heaving, bulging, retraction of interspaces, etc.,<span class="pagenum"><a name="Page_174" id="Page_174">[174]</a></span>
can easily be seen if visible. After careful inspection has
given all the data which it is possible to obtain, one next
lays the palm of the hand over the heart and attempts to
palpate the apex beat. The thrust of the apex in a hypertrophied
heart can readily be felt, and one can feel whether
the heart is regular, irregular, intermittent, or has other
change in rhythm. The shock of the closing valves, particularly
the aortic, can be felt, and that and the forcible apical
impulse are very suggestive signs of hypertrophy and
hypertension. Thrills may also be felt and can be timed
in relation to the heart cycle.</p>
<h4>Percussion</h4>
<p>It is to percussion that we next proceed, and for the data
in regard to the size of the heart, it is, for our purpose, the
most valuable of all the physical methods of heart examination.</p>
<p>First and foremost we wish by percussion to learn the
actual size of the heart, in other words what is ordinarily
called the relative cardiac dullness. With the absolute dullness
we are not concerned. That irregular area represents,
as has been said, actually the <b>limits of lung resonance</b>. The
heart may or may not be covered with lung; there may or
may not be the incisura cardiaca. What I wish to insist
upon is that the size of the area of absolute dullness can
give us no data in regard to the size of the heart. What we
must endeavor to learn is the actual size of the heart as
nearly as our crude means will permit.</p>
<p>Light, very light, almost inaudible percussion, what Goldscheider
called "Schwellungsperkussion," must be practiced.
Use the middle finger of the right (left) hand as the
hammer and the last joint of the middle finger of the left
(right) hand pressed firmly against the chest, as pleximeter.
I believe it is better to place the pleximeter finger parallel
to the boundary to be limited although some place the finger
perpendicularly, that is, pointing toward the boundary.<span class="pagenum"><a name="Page_175" id="Page_175">[175]</a></span>
Now and then it helps to bend the pleximeter finger at the
second joint, hold it perpendicularly to the chest wall, and
strike the joint directly in line of the finger. This in my
hands has been of great assistance in percussing the limits
of the heart dullness. Pottenger's "light touch palpation"
is a modification of the light palpation and, to my mind, has
no very special advantages. Auscultatory percussion is of
great value at times. The bell of the stethoscope is placed
over the portion of heart uncovered by lung (should such
be the case), and with this point as a center the chest is
lightly and quickly tapped along radii converging toward
the stethoscope. One soon learns to recognize the change
of pitch as the tapping reaches the border of the heart. It
is well to use all methods, especially in difficult cases, and
to compare the results. Personally I have found that by
light percussion I can limit with much accuracy the upper,
right, and left borders of the heart.</p>
<p>There is much to be gained by using light percussion.
Strong blows set in vibration not only the underlying structures,
but also more or less of the chest wall. We wish to
avoid this source of error, we do not wish to differentiate by
pitch alone. Finally one's pleximeter finger becomes, after
long practice, so sensitive to changes in the resonance of
structures lying below it, that there is actual feeling of impairment
to the slightest degree. This delicate touch is
what we should endeavor to cultivate.</p>
<p>It is at times of advantage to use immediate percussion.
This is done by bending the fingers of the striking hand,
bringing the tips in a line and striking the chest lightly with
the four fingers as one finger. Some find it easier to percuss
the dullness due to the heart in this way than by mediate
percussion.</p>
<p>The little hammer and hard rubber, celluloid, bone, or
ivory pleximeter does not seem to me to be nearly as good
as the fingers. Moreover, one always has his hands, but
may forget his hammer and pleximeter.</p>
<p><span class="pagenum"><a name="Page_176" id="Page_176">[176]</a></span></p>
<h4>Auscultation</h4>
<p>In auscultating the heart I prefer the binaural stethoscope
of the Ford pattern. The recent substitution of an
aluminum bell for the hard rubber bell is an improvement.
Personally I do not favor the phonendoscope or any of the
new patent non-roaring instruments now for sale by urgent
instrument makers. The phonendoscope has its uses, for
example in auscultating the back when a patient is lying
in bed or in listening to the heart sounds when a patient is
under an anesthetic; but for differentiating the murmurs
and for heart diagnosis, I much prefer the regular bell
stethoscope.</p>
<p>In arteriosclerosis the two places over which it is important
to listen are the apex and the second right cartilage,
the aortic area. Over the former, one gains data in regard
to the strength of the heart as indicated by the first sound,
over the latter point, one learns of the tension in the aorta
by the character of the sound produced when the aortic
valves close.</p>
<p>The hypertrophy of the heart in arteriosclerosis is invariably
due to the enlargement and thickening of the left
ventricle. From the nature of the position which the heart
assumes in the thorax, this enlargement is downward and
to the left. The apex beat will therefore be found in the
fifth or sixth interspace, and definitely at an increased distance
from the midsternal line. As stated above, it is
most important that this distance be accurately measured
and put down in the notes of the case for future reference.
No satisfactory prognosis can be given unless this is done,
for the gradual increase or the decrease under treatment in
the size of the heart can thus be definitely known, and,
knowing the other factors, a prognosis may be given which
will be of some value to the patient.</p>
<p><span class="pagenum"><a name="Page_177" id="Page_177">[177]</a></span></p>
<h4>The Examination of the Arteries</h4>
<p>It is exceedingly difficult at times to affirm definitely that
an artery, the radial for example, is actually sclerosed.
Much depends on the sensitiveness of the fingers of him
who palpates, and much upon the relation of the palpated
artery to the surrounding, chiefly underlying, structures.
In the examination of arteries it is well to inspect the body
for the pulsations caused by them. Frequently an exceedingly
tortuous artery, such as the brachial, may be seen
throughout its whole extent and yet the radial appear little,
if any, thickened by palpation. Again the artery of a
pulse of high tension which is small in size but full between
the beats, may not be as sclerosed as one which collapses
and feels much softer. It is difficult to obtain accurate data
in regard to the tension in an artery by feeling it with the
fingers of one hand. One should use both hands. With the
middle finger of the right (left) hand the artery is compressed
peripherally, that is, nearest the wrist. The blood
is then pressed out of the artery with the middle finger of
the left (right) hand, so as to obliterate completely the
pulse wave and the two or three inches between the middle
fingers are felt with the index fingers. By holding the finger
firmly on the artery near the wrist so as to block any
wave that may come through the palmar arch by anastomosis
with the ulnar artery and by releasing pressure on the
proximal middle finger, some idea may be had of the degree
of pulse tension. However, no amount of practice can more
than approximate the tension and when one is surest that
he can tell how many millimeters of pressure there are, he
is apt to be farthest wrong when he checks his guess with
the sphygmomanometer.</p>
<p>Much may be learned from carefully palpating the peripheral
arteries, and, as a rule, the sclerosis of these arteries
means general arteriosclerosis, although there are many
exceptions to this.</p>
<p><span class="pagenum"><a name="Page_178" id="Page_178">[178]</a></span>A more recent method, and one which in the author's
hands has been found to be valuable, is that proposed by
Wertheim-Salomonson who palpates the artery not with
the ball of the finger but with the fingernail. The finger is
held so that the nail is perpendicular to the surface of the
skin and the artery is felt with the end of the nail. The sensation
is perceived at the root and makes use of all the sensitive
nerve endings there. In this way it is possible to feel<span class="pagenum"><a name="Page_179" id="Page_179">[179]</a></span>
the arterial wall distinctly, and a little practice will enable
one to determine whether or not the vessel wall is thickened.
It is also possible to determine with a considerable degree of
accuracy the diameter of the artery and the size of the wall
when the current is cut off by pressure on the proximal side
of the artery. It is best to have a firm background when
this "fingernail" palpation is used. This may be obtained
by palpating the radial artery against the lower end of the
radius.</p>
<p>Probably the best method of palpating the arteries, especially
the radial, to determine the degree of sclerosis and
thickening, is to use the tip of the finger and roll it carefully
over the artery. The tip of the finger is exceedingly
sensitive and, moreover, it is a firmer palpating surface
than the ball, thus enabling one to appreciate degrees of
sclerosis which could not be differentiated by palpation
with the soft yielding ball. This finger tip palpation is well
illustrated in the figures here shown. (Figs. 57 and 58.)</p>
<div class="figcenter bord" style="width: 500px;">
<a name="Finger-tip_palpation_of_the_radial_artery" id="Finger-tip_palpation_of_the_radial_artery"></a>
<img src="images/fig_057.png" width="500" height="321" alt="Fig. 57.—A method of finger-tip palpation of the radial artery. (Graves.)" title="Fig. 57.—A method of finger-tip palpation of the radial artery. (Graves.)" />
<span class="caption">Fig. 57.—A method of finger-tip palpation of the radial artery. (Graves.)</span>
</div>
<div class="figcenter bord" style="width: 500px;">
<a name="Finger-tip_palpations_of_the_radial_artery" id="Finger-tip_palpations_of_the_radial_artery"></a>
<img src="images/fig_058.png" width="500" height="316" alt="Fig. 58.—Another method of finger-tip palpation of the radial artery. (Graves.)" title="Fig. 58.—Another method of finger-tip palpation of the radial artery. (Graves.)" />
<span class="caption">Fig. 58.—Another method of finger-tip palpation of the radial artery. (Graves.)</span>
</div>
<h4>Estimation of Blood Pressure</h4>
<p>It must be borne in mind at the outset that arteriosclerosis
and high blood pressure are not always associated. As
a matter of fact in the severest grades of senile arteriosclerosis
the blood pressure is usually below the normal
for the individual's years. However, as high tension is a
frequent factor in the production of arterial thickening,
blood pressure readings are of importance.</p>
<p>The instrument which one uses is of minor importance
provided it is properly standardized. The most important
feature of the instrument is the cuff. This must be 12 cm.
wide and be long enough to wrap around the arm several
times so that the pressure is evenly distributed over the
whole arm and not over a small portion. One mercury instrument
we had in the hospital was reported to be at great
variance with a dial instrument. This mercury instrument
was provided with a cuff which was short and was tied<span class="pagenum"><a name="Page_180" id="Page_180">[180]</a></span>
around the arm by means of a piece of tape. This caused
a tight constriction over a small area and rendered the estimation
too high. A new, long tailed cuff easily remedied
the apparent defect in the instrument.</p>
<p>In taking blood pressures the difference from day to day
of 10 or even 15 mm. of systolic pressure has no great significance.
Fluctuations of the systolic pressure alone, it is
insisted upon, have very little meaning. One must take the
whole pressure picture into consideration and determine
how the picture changes in order to draw any conclusion in
regard to the state of the blood pressure. Failure to pay
attention to this evident point has caused much futile work
to be written and published.</p>
<p>It is well to emphasize again the point that the blood
pressure picture consists of the systolic, the diastolic, the
pulse pressure and the pulse rate.</p>
<h4>Palpation</h4>
<p>Hoover has called attention to the direct palpation of the
femoral artery just below Poupart's ligament as a more accurate
index of the pressure in the aorta than the palpation
of the radial artery. Possibly one can obtain a more accurate
estimate of the blood pressure in this way. This,
however, is open to dispute. To estimate the blood pressure
by palpating the radial artery is most deceptive. In
about 75 per cent of cases one can tell fairly well whether
the pressure is abnormally high or abnormally low. Small
variations are impossible to determine. Unquestionably it
is most advantageous to get into the habit of palpating the
femoral artery and checking the result with the sphygmomanometer
so that the fingers may be trained to appreciate
as accurately as possible changes of pressure.</p>
<p>It may be that one day when the instrument is needed it
is not at hand. A well-trained touch then becomes a great
asset.</p>
<p><span class="pagenum"><a name="Page_181" id="Page_181">[181]</a></span></p>
<h4>Precautions When Estimating Blood Pressure</h4>
<p>There are certain precautions which must be strictly observed
when deductions are drawn from the manometer
readings. The psychic factor must be reckoned with. Any
emotion may cause marked variations in the pressure. Excitement
and anger are especial sources of error. Even the
slight excitement arising from taking the first blood pressure
on a nervous patient especially is apt to give false
values. Usually the readings must be taken many times at
the first sitting and the first few may have to be set aside.
Worry is a potent factor in raising the pressure. A walk
to the physician's office, especially if rapid, has its effect.</p>
<p>The position of the patient when the blood pressure is
taken is important. Usually in the office the pressure is
taken when the patient sits in a chair. He should assume a
relaxed, comfortable attitude. The readings should be
made at the same time of day and at the same interval between
meals. The pressure in both arms should be
measured and comparisons should be made only between
readings on the same arm. These precautions may seem
useless and even somewhat trivial, and the conditions difficult
to control. But unless they are carefully observed the
readings will be false, no comparisons can be drawn between
the readings on different days, and the instrument
will most probably be blamed. I have known this to happen
so often that I can not emphasize too strongly the importance
of controlling all the essential conditions which
go to make accurate work.</p>
<h4>The Value of Blood Pressure</h4>
<p>In the past few years there has been a veritable avalanche
of blood pressure instrument salesmen who have
covered the country, sold instruments, and have made many
startling claims for the instrument. They have emphasized
its value out of proportion to what the instrument can do<span class="pagenum"><a name="Page_182" id="Page_182">[182]</a></span>
even in the hands of one familiar will all the defects. Consequently
it is not necessary to emphasize the value of blood
pressure. It seems best to utter a few words of caution in
regard to its interpretation.</p>
<p>The value lies not in the occasional estimation compared
with some other one reading, but in the frequent estimation
and in the visualization of the blood pressure picture. For
the great majority of diseases the blood pressure has no
particular value except to show that the circulation is not
materially disturbed. The limits of normal are rather wide,
so that consideration of the patient's age, sex, build, etc.,
will give us some idea of a base line, so to speak, for any one
person. Wide departures from relatively normal figures
are important, but are not diagnostic or, rather, pathognomonic.
I can not help but feel that the diastolic pressure is
<i>the</i> most important part of the blood pressure picture. Persistent
high diastolic pressure means increased work for the
heart, which, if acting for a long time against the high
peripheral resistance, must eventually hypertrophy. The
arteries become thickened, lose their wonderful elasticity,
fibrous tissue is deposited in their walls, and the vicious
circle is established which leads to pathologic hypertension.</p>
<p>Blood pressure readings must be intimately mixed with
brains in order to be of any great value in diagnosis or
prognosis.</p>
<hr style="width: 65%;" />
<p><span class="pagenum"><a name="Page_183" id="Page_183">[183]</a></span></p>
<h2><a name="CHAPTER_VIII" id="CHAPTER_VIII"></a>CHAPTER VIII.</h2>
<h3>SYMPTOMS AND PHYSICAL SIGNS</h3>
<h4>General</h4>
<p>Well developed arteriosclerosis shows four pathognomonic
signs: (1) hypertrophy of the heart; (2) accentuation
of the aortic second sound; (3) palpable thickening of
the arteries; and (4) heightened blood pressure. However,
it must not be inferred that these signs must be present in
order to diagnose arteriosclerosis. It has already been said
that a very marked degree of thickening, with even calcification
of the palpable arteries, may occur with absolutely
no increase of blood pressure, and at autopsy a small flabby
heart may be found.</p>
<p>While arteriosclerosis is usually a disease which is of
slow maturation, nevertheless cases are occasionally seen
which develop rather rapidly. The peripheral arteries have
been noticed to become stiff and hard in as relatively brief
a time as two years from the recognized onset of the disease.</p>
<p>Since involution processes are physiologic, as has been
described (vide infra), arteriosclerosis may assume an
advanced grade and run its course devoid of symptoms
referable to diseased arteries. It is doubtful whether the
sclerosis itself could produce symptoms, except in cases
later to be described, were it not that the organs supplied
by the diseased arteries suffer from an insufficient blood
supply and the symptoms then become a part of the symptom-complex
of any or all the affected organs.</p>
<p>There are cases, however, in comparatively young persons
where a combination of certain ill-defined symptoms
gives a clue to the underlying pathologic processes. These
symptoms of early arteriosclerosis are the result of slight<span class="pagenum"><a name="Page_184" id="Page_184">[184]</a></span>
and variable disturbances in the circulation of the various
organs. Normally there are frequent changes in the blood
pressure in the organs, but the vasomotor control of normal
elastic vessels is so perfect that no symptoms are noted by
the individual. When the arteries are sclerosed, they are
less elastic and the blood supply is, therefore, less easily
regulated. At times symptoms occur only after effort. The
patient may tire more readily than he should for a given
amount of mental or bodily exercise; he is weary and depressed,
and occasionally there is noted an unusual intolerance
of alcohol or tobacco. Vertigo is common, especially
on rising in the morning or in suddenly changing from a
sitting to a standing position. Some complain of constant
roaring or ringing in the ears. There may be dull headache
that the accurate fitting of glasses does not alleviate.
Unusual irritability or somnolency with a disinclination
to commence a new task may be present. Sometimes the
effort of concentrating the attention is sufficient to increase
the headache. This has been called "the sign of the painful
thought." Numbness and tingling in the hands, feet,
arms, or legs are also complained of, and neuralgias, not
following the course of the nerves but of the arteries, also
occur. It is important to remember that the train of symptoms
resembling neurasthenia in a person over forty-five
years old may be due to incipient arteriosclerosis. This
tardy neurasthenia frequently accompanies cancer, tuberculosis,
diabetes, and incipient general paralysis, as well as
incipient arteriosclerosis.</p>
<p>Bleeding from the nose, epistaxis, taking place frequently
in a middle-aged person, sometimes is an early symptom.
The bleeding may be profuse, but is rarely so large as to be
positively harmful. In fact, it may do much good in relieving
tension. Slight edema of the ankles and legs is seen.
Dyspnea on slight exertion is not uncommon. Dyspeptic
symptoms are not infrequent, pyrosis (heartburn), a feeling
of fullness after meals with belching or a feeling of<span class="pagenum"><a name="Page_185" id="Page_185">[185]</a></span>
weight in the epigastrium. The dyspeptic symptoms may
be so marked that one might almost speak of a variety of
arteriosclerosis, the dyspeptic type. For quite a while before
any symptoms that would definitely fix the case as one
of undoubted arteriosclerosis, the patient complains that
foods which previously were digested with no difficulty now
give him gastric distress. The examination of the stomach
contents of a patient presenting gastric symptoms reveals
usually a subacidity. The total acidity measured after the
Ewald test meal may be only 20 and the free HCl may be
absent. Attention has been called to an unnatural pallor
of the face in early arteriosclerosis. Progressive emaciation
is sometimes seen in cases of arteriosclerosis and may
be the only symptom of which the patient complains.</p>
<h4>Hypertension</h4>
<p>Not all cases of arteriosclerosis are accompanied by increased
arterial tension. As has been stated in a previous
chapter, the blood pressure in the arterial system depends
chiefly on two factors; viz., the degree of peripheral (capillary)
resistance, and the force of the ventricular contraction.
The highest arterial pressures recorded with the
sphygmomanometer occur not in pure arteriosclerosis but
in cases where there is concomitant chronic interstitial disease
of the kidneys. When this is found there is always
arteriosclerosis more or less marked. In cases where the
arteries are so sclerosed that they feel like pipe stems there
may be an actual decrease in the blood pressure. Hence
the clinical measuring of the pressure in the brachial artery
alone is not sufficient for a diagnosis of arteriosclerosis. A
persistent high blood pressure even with normal urinary
findings is not a sign of arteriosclerosis. The high tension
later may lead to the production of sclerosis of the arteries,
but in these cases the kidney may be primarily at fault.</p>
<p>The impression must not be gained that hypertension in<span class="pagenum"><a name="Page_186" id="Page_186">[186]</a></span>
itself always constitutes a disease or even a symptom of disease.
Hypertension itself is practically always a compensatory
process. That is to say, it is the attempt on the part
of the body to equalize the distribution of blood in the body
when there is some poison causing constriction of the small
arteries. In this sense hypertension is not only essential,
but actually life-saving. A heart which is so diseased that
it can not respond to the call for increased action by hypertrophy
of its fibers, would shortly wear out. The very fact
that the heart becomes enlarged and the tension in the
arteries becomes high, indicates that in such a heart there
was great reserve power. But while hypertension is largely
an effort at adjustment among the various parts of the circulation,
it nevertheless tends to increase, provided the
cause or causes which produced it act continuously. Moreover,
as has been said (Chap. II), the arterioles do not respond
to increased work on the part of the heart by expanding,
but by contracting. A vicious circle is thus maintained
which eventually must lead to serious consequences.</p>
<p>Hypertension is then, if anything, only a symptom which
may or may not demand treatment. That hypertension
leads to the production of sclerosis of the arteries has been
repeatedly affirmed here. In certain cases it is good and
should not be experimented with. In other cases it is bad
and some treatment to reduce the tension must be tried.
The main point is to regard hypertension as one regards a
compensated heart lesion.</p>
<p>Prof. T. Clifford Allbutt divides the causes of arteriosclerosis
clinically into three classes: (1) The toxic class—the
results of poisons of the most part of extrinsic origin,
chiefly those of certain infections. In some of these
diseases, the blood pressures, as for example, in syphilis,
are ordinarily unaffected; in others, as in lead poisoning,
they are raised. (2) The class he calls hyperpietic,<a name="FNanchor_15_15" id="FNanchor_15_15"></a><a href="#Footnote_15_15" class="fnanchor">[15]</a> in<span class="pagenum"><a name="Page_187" id="Page_187">[187]</a></span>
which an arteriosclerosis is the consequence of tensile
strength, of excessive arterial blood pressure persisting for
some years. A considerable example of this class is the
arteriosclerosis of granular kidney, but in many cases kidney
disease is, clinically speaking, absent. (3) The involutionary
class, in which the change depends upon a senile, or
quasisenile degradation. This may be no more than wear
and tear, a disposition of all or of certain tissues to premature
failure—partly atrophic, partly mechanical—under
ordinary stresses; or it also may be toxic, a slow poisoning
by the "faltering rheums of age." In ordinary cases
of this class the blood pressures for the age of the patient
are not excessive. Although the toxins of the specific
fevers, notably typhoid, as stated above, and influenza, have
been shown to produce arteriosclerosis, this, under favorable
circumstances he believes tends to disappear. This
has been shown by Wiesel.</p>
<p>As the blood pressure is dependent on the resistance
offered by the capillaries and arterioles, there are only two
ways in which increased pressure can be brought about;
either by rendering the blood more viscous, or by the generation
of some poison from the food taken into the body
which, acting on the vasomotor center or directly on the
finer vessels, arteriolar or capillary, sets up a constriction
over any large area, and mainly in the splanchnic area. In
regard to the liability to arteriosclerosis, this area stands
second only to the aortic and coronary areas. He believes
that arteriosclerosis itself has little effect in raising arterial
pressure. Many cases are seen in which with extreme arteriosclerosis
there was no rise in blood pressure, and some
in which pressures have been rising even long before the
appearance of arterial disease. Prof. Allbutt also believes
that in the hyperpietic cases the arteries undergo a transient
thickening, which can be removed if the causes can be
reached and overcome.</p>
<p>Clinically speaking, then, hyperpietic arteriosclerosis is<span class="pagenum"><a name="Page_188" id="Page_188">[188]</a></span>
not a disease, but a mechanical result of disease. If the narrowing
of the arterioles is brought about by thickening due
to arteriosclerosis, then it would seem <i>a priori</i> that such
obliteration should cause a rise in pressure. Were the
vascular system a mere mechanical set of tubes and a pump,
this would happen, but other factors of great importance
must be taken into consideration besides the mechanical
factors; viz., chemical and biological factors. Thus, whole
parts may be closed and with compensatory dilatation in
other parts there would be little or no change in pressure,
unless there were hyperpiesis. In established hyperpiesis,
we note two conditions in the radial artery: first, a comparatively
straight vessel with a small diameter; secondly, a
larger, more tortuous vessel, "the large leathery artery."
In the cases of the first group, hyperpiesis is often more
marked, although not appearing so to the examining finger,
than in the second class. In view of the difficulty of estimating
by touch alone the amount of hyperpiesis in a contracted
hard artery, it is often overlooked until a ruptured
vessel in the brain startles us to a realization of our mistake.
The "narrow" artery is more dangerous than the
tortuous one, for with every change in pressure the passive
vessels of the brain must receive blood that under normal
conditions would go to other parts of the circulation.</p>
<p>In involutionary sclerosis there is a gradual thickening
and tortuosity of the vessel, which although it may be
greater than in the hyperpietic cases, yet is never so dangerous
to life. The heart in hyperpiesis hypertrophies and
dilates, but such a heart is the result, not an integral part,
of the arterial disease.</p>
<h4>The Heart</h4>
<p>When the arterial tree becomes narrowed and the resistance
offered to the flow of blood thereby is increased, more
muscular work is required of the left ventricle and according<span class="pagenum"><a name="Page_189" id="Page_189">[189]</a></span>
to the general laws which govern muscles the ventricle
hypertrophies. There is an actual increase in number of
fibers as well as an increase in the size of the individual
fibers. Some of the best examples of simple hypertrophy
of the left ventricle are found under such circumstances.
The chambers as a rule do not dilate until the resistance becomes
greater than the contraction can overcome, when
symptoms of broken compensation of the heart take place.
The hypertrophy of the left ventricle brings more of this
portion of the heart toward the anterior chest wall. The
enlargement is toward the left, also, consequently the apex-beat
is found below and to the left of its usual site, even an
inch or more beyond the nipple line. The impulse is heaving,
pushing the palpating hand forcibly up from the chest
wall. The visible area of pulsation may occupy three interspaces
and the precordium is seen to heave with every systole.
On auscultation the second sound at the aortic cartilage
is ringing, clear, and accentuated. Not infrequently,
too, the first sound is loud and booming, but has a curious
muffled sound that may even be of a murmurish quality.
The leaflets of the mitral valve may be the seat of sclerosis,
the edges are slightly thickened and do not quite approximate,
thus causing a definite murmur with every systole.
This murmur may be transmitted out into the axilla and be
heard at the inferior angle of the left scapula.</p>
<h4>Palpable Arteries</h4>
<p>Not every artery that can be felt is the subject of arteriosclerosis,
and, as has been stated, palpable arteries being
more or less a condition of advancing years, judgment as
to whether the artery is pathologically or physiologically
thickened may be a matter of individual opinion. A radial
artery that lies close to the lower end of the radius and can
actually be seen to pulsate when the hand is held slightly
extended on the back of the wrist, is easily felt, but must<span class="pagenum"><a name="Page_190" id="Page_190">[190]</a></span>
not, therefore, be considered a sclerosed artery. The radial
may be so deeply situated in the wrist of a fat subject that
it is difficultly palpable. Yet the two cases just described
may have arteries of identical structure, there being no
more retrogressive changes in the one than in the other.
"Experience is fallacious and judgment difficult."</p>
<p>The small, contracted, wiry artery of a chronic nephritic
may feel like a pipe stem, but if properly felt the mistake
will not be made of considering such an artery an unusually
sclerosed one. When the wave is pressed out of such a
high tension artery, it is found that what seemed to be a
firm sclerosed vessel, was in reality an artery tightly
stretched over the column of blood.</p>
<h4>Ocular Signs and Symptoms</h4>
<p>It would not exaggerate too much to say that the examination
of the eye grounds with the ophthalmoscope is the
most important aid in the early diagnosis of arteriosclerosis.
Long before there are any subjective symptoms,
changes can be seen in the blood vessels of the retina which,
while not always diagnostic, at least call attention to a beginning
chronic disease. As I become more proficient in the
use of the ophthalmoscope, I am impressed with the importance
of the ocular signs of arterial disease. I would urge
practitioners to familiarize themselves with this instrument.
The electrically lighted instruments on the market now have
so simplified the technic that any physician should be able
to see the grosser changes which take place in the arteries
and veins of the retina and in the disc. Frequently the
ophthalmologist is the first to recognize early arteriosclerosis.
In the fundus are seen increased tortuosity of the retinal
vessels and their terminal twigs with more or less bending
of the vessels at their crossings. The arteries are terminal
ones, and small patches of retinitis are therefore found.
The changes have been divided into (1) suggestive, (2)
pathognomonic.</p>
<p><span class="pagenum"><a name="Page_191" id="Page_191">[191]</a></span></p>
<p>Under (1) are:</p>
<p>(a) Uneven caliber of the vessels,</p>
<p>(b) Undue tortuosity,</p>
<p>(c) Increased distinctness of the central light streak,</p>
<p>(d) An unusually light color of the breadth of the
artery.</p>
<p>Under (2) are:</p>
<p>(a) Changes in size and breadth of the retinal arteries
so that they look beaded,</p>
<p>(b) Distinct loss of translucency,</p>
<p>(c) Alternate contractions and dilatations in the veins,</p>
<p>(d) Most important of all, the indentation of the veins
by the stiffened arteries.</p>
<p>There is yet another sign which appears to be pathognomonic.
The arteries are pale, appear rigid and through the
center, parallel to the course, is a rather bright, fine threadlike
line. The appearance is known as the "silverwire"
artery. It is particularly constant in hypertension where
the most beautiful examples are seen.</p>
<p>Moreover, there is the arcus senilis, the fine translucent
to opaque circle surrounding the outer portion of the iris.
Practically every one with a well-marked arcus senilis has
arteriosclerosis, but vice versa not every one with even
marked arteriosclerosis has an arcus senilis.</p>
<p>In general, the symptoms are gradual loss of acute vision,
and attacks of transient loss of vision. The explanation
which has been offered for these phenomena is the contraction
in a diseased central artery.</p>
<h4>Nervous Symptoms</h4>
<p>The onset of arteriosclerosis is, in the majority of cases,
so insidious that certain nervous manifestations, due in all
probability to disturbances in blood pressure, are present
long before the actual sclerosis of the arteries can be felt.<span class="pagenum"><a name="Page_192" id="Page_192">[192]</a></span>
These nervous symptoms are at times the sign posts to show
us the way to accurate diagnosis. There may be gradual
increase in irritability of temper, inability to sleep,
vertigo even extending to transient attacks of unconsciousness.
Loss of memory for details frequently is an early
symptom of sclerosis of the cerebral arteries. Nervous indigestion
may be present. Various paresthesias as numbness,
tingling, a sense of coldness or of heat or burning, a
sense of stiffness or even actual stiffness or weakness may
occur in the arms and legs, more frequently in the legs.
The pain complained of may be due to occlusion of an artery,
although evidence for this is lacking. It has been
thought by some that the pain in angina pectoris might be
due to this cause.</p>
<p>Several curious and interesting diseases which have
been thought by some to have arteriosclerosis as a basis are
accompanied by pain. Such are erythromelalgia, Raynaud's
disease, "dead fingers," and intermittent claudication.</p>
<p>Erb has reported a large series of intermittent limp
(claudication) from his private practice. He finds that the
large majority of the cases occur in men. The abuse of
tobacco was evidently the main etiologic factor in about
half of the cases. Repeated exposure to cold and the abuse
of alcohol were responsible for most of the other cases.
Curiously enough he finds that a history of syphilis was
present in only a small proportion of his cases. It is his
firm conviction that intermittent limping—which he thinks
should be called angiosclerotic dysbasia—is frequently incorrectly
diagnosed. It is mistaken for other troubles and
treated wrongly. As gangrene may develop this is particularly
dangerous. The affection generally develops gradually,
although he has seen cases where the onset was rather
acute. The partial or complete lack of the pulse in the foot
is the one striking sign, together with the varying behavior
of the pulse, its disappearance when the feet are cold and<span class="pagenum"><a name="Page_193" id="Page_193">[193]</a></span>
its return after a warm foot bath or under other treatment.
Signs of general arteriosclerosis were present in nearly
every case. When there is a tendency to the development
of intermittent limp he finds that a valuable sign is the manner
in which the leg blanches when it is lifted repeatedly
while the patient is recumbent and becomes hyperemic later
when placed horizontally. In health this change occurs
more rapidly.</p>
<hr style="width: 65%;" />
<p><span class="pagenum"><a name="Page_194" id="Page_194">[194]</a></span></p>
<h2><a name="CHAPTER_IX" id="CHAPTER_IX"></a>CHAPTER IX.</h2>
<h3>SYMPTOMS AND PHYSICAL SIGNS</h3>
<h4>Special</h4>
<p>Our conception of arteriosclerosis as a degenerative process
affecting the vascular tree rather than a disease, removes
the possibility of discussing special symptoms. As
a matter of fact, we know of very few organs where even
profound pathologic changes in the vascular system produced
during life any symptoms which could be laid to
these arterial changes. Kind nature has given to us such
an excess of organs of every kind that the destruction of
large portions of any organ seems to affect the function
but little. So only particular groups of organs, which show
symptomatic changes as the result of arteriosclerotic processes,
will be discussed. It is realized that this may not
give Teutonic completeness to the discussion, but it certainly
saves paper and has a distinct practical value to the
long suffering reader.</p>
<p>Although arteriosclerosis is a disease which affects the
whole arterial system, it nevertheless never reaches the
same grade all over the body. The difference in the structure
and functions of the various organs determines to great
extent the eventual symptomatology. Endarteritis obliterans
of a small sized artery in the liver or leg would lead to
no marked symptoms, as the circulation is so rich that the
anastomoses of the blood vessels would soon establish a
collateral circulation that would be perfectly competent to
sustain the function of the part. Quite different would it
be should one of the small arteries of the brain, the lenticulo-striate,
for example, which supplies the corpus striatum,
become the seat of a thrombosis or embolism caused by
arteriosclerosis. The arteries of the brain are terminal<span class="pagenum"><a name="Page_195" id="Page_195">[195]</a></span>
arteries and the blood supply would be cut off entirely with
a resulting anemic necrosis of the part supplied by the
artery and a loss of function of the part. What would be
of no moment in the leg or arm might prove even fatal in
the brain.</p>
<p>The further symptomatology, therefore, of arteriosclerosis
depends entirely on the organ or organs most affected
by the interference with the blood supply. The following
groups may be recognized:</p>
<p>
1. Cardiac.<br />
<br />
2. Renal.<br />
<br />
3. Abdominal.<br />
<br />
4. Cerebral.<br />
<br />
5. Spinal.<br />
<br />
6. Local vasomotor effects.<br />
<br />
7. Pulmonary.<br />
</p>
<h4>Cardiac</h4>
<p>Most cases of arteriosclerosis sooner or later present
symptoms referable to the heart. When the organ is hypertrophied
and is already working against an enormous
peripheral resistance, a slight excess of work put upon it
may cause a dilatation of the chambers with the resulting
broken compensation. There is dyspnea on slight exertion,
possibly some precordial distress, slight edema of the ankles
and lower legs and possibly scanty urine. With proper
care, a patient with such symptoms may recover, but the
danger of another break in compensation is enhanced. The
next attack is more severe. The edema is greater, there
may be signs of edema of the lungs, effusions into the serous
cavities may occur. The heart shows marked dilatation.
There is gallop or canter rhythm and there are loud murmurs
at the apex. When a patient is first seen in this stage,
it may be quite impossible to state whether or not there is
true valvular disease of the heart. The muscle is usually
diseased in that there is fibroid degeneration of more or<span class="pagenum"><a name="Page_196" id="Page_196">[196]</a></span>
less extensive character. This factor causes the heart to
lose much of its elasticity and increases the tendency to
permanent dilatation. Such cases must be watched before
one can say that true valvular insufficiency is not present.
The fatal termination of such a case is quite like that of
true valvular disease. There is increasing dyspnea, increasing
anasarca, and the patient usually succumbs to
edema of the lungs, drowned in his own secretions.</p>
<div class="figcenter" style="width: 422px;">
<a name="Aneurysm_of_the_heart_wall" id="Aneurysm_of_the_heart_wall"></a>
<img src="images/fig_059.png" width="422" height="500" alt="Fig. 59.—Aneurysm of the heart wall. (Milwaukee County Hospital.)" title="Fig. 59.—Aneurysm of the heart wall. (Milwaukee County Hospital.)" />
<span class="caption">Fig. 59.—Aneurysm of the heart wall. (Milwaukee County Hospital.)</span>
</div>
<p>A very rare complication of the fibroid degeneration of
the heart muscle is aneurysm of the heart wall. (Fig. 59.)<span class="pagenum"><a name="Page_197" id="Page_197">[197]</a></span>
The apex of the left ventricle is most commonly the site of
the aneurysm and rupture occasionally occurs. Such an accident
is rapidly fatal. In the arteriosclerotic process which
occurs at the root of the aorta, the coronary arteries become
involved both at the openings and along the courses of the
vessels. A branch or branches or even one artery may
become blocked as a result of obliterating endarteritis.
The arteries of the heart are not terminal vessels but as a
rule blocking of a large branch leads to anemic infarct.
These areas become replaced by fibrous tissue which in the
gross specimen appears as streaks of whitish or yellowish
color in the musculature. Anemic infarcts may not occur.
In such cases the anastomosis between branches of the coronary
arteries is unusually free. Through arteriosclerosis
of the coronary vessels extensive fibrous changes may occur
that lead to a myocardial insufficiency with its attending
symptoms—dyspnea, irregular and intermittent heart,
gallop rhythm, edema, etc. One of the most distressing
and dangerous results of sclerosis of the coronary arteries
and of the root of the aorta is angina pectoris. While in
almost every case of angina pectoris there is disease of the
coronary arteries, the contrary does not hold true, for most
extensive disease, even embolism, of the arteries is frequently
found in persons who never suffered any attacks of
pain. This symptom group is more common in males than
in females and as a rule occurs only in adult life. "In men
under thirty-five syphilitic aortitis is an important factor."
(Osler.)</p>
<p>Since the valuable experiments of Erlanger on heart
block, considerable attention has been paid to lesions of the
Y-shaped bundle of fibers, a bundle arising at the auriculoventricular
node and extending to the two ventricles,
known also as the auriculoventricular bundle of His.
Interference with the transmission of impulses through this
bundle gives rise to the symptom group known as the
Stokes-Adams syndrome, which is characterized by: (a)<span class="pagenum"><a name="Page_198" id="Page_198">[198]</a></span>
slow pulse, (b) cerebral attacks—vertigo, syncope, transient
apoplectiform and epileptiform seizures, (c) visible
auricular impulses in the veins of the neck. Many of the
cases which occur are in elderly people the subjects of
arteriosclerosis.</p>
<div class="figcenter bord" style="width: 314px;">
<a name="Large_aneurysm_of_the_aorta_eroding_the_sternum" id="Large_aneurysm_of_the_aorta_eroding_the_sternum"></a>
<img src="images/fig_060.png" width="314" height="500" alt="Fig. 60.—Large aneurysm of the aorta eroding the sternum. Death from rupture through
the skin preceded by frequent small hemorrhages. (Milwaukee County Hospital.)" title="Fig. 60.—Large aneurysm of the aorta eroding the sternum. Death from rupture through
the skin preceded by frequent small hemorrhages. (Milwaukee County Hospital.)" />
<span class="caption">Fig. 60.—Large aneurysm of the aorta eroding the sternum. Death from rupture through
the skin preceded by frequent small hemorrhages. (Milwaukee County Hospital.)</span>
</div>
<p>So far as we now know all cases of the Stokes-Adams
syndrome are caused by heart block which is only another
name for disease in the auriculoventricular bundle. Of
interest here is the fact that besides gummata, ulcers, and
other lesions of the bundle, definite arteriosclerotic changes
have been found.</p>
<p>"The investigation of a typical case of Stokes-Adams disease
has shown that the symptoms of this case are caused
by some lesion in the heart which gives rise to the condition<span class="pagenum"><a name="Page_199" id="Page_199">[199]</a></span>
now generally termed heart block. Practically all degrees
of heart block have been observed, namely, complete
heart block and partial block with 4:1, 3:1, and 2:1 rhythm,
and occasionally ventricular silences. These stages occurred
during recovery.</p>
<p>"Experiments testing the reaction of the heart to various
extrinsic influences demonstrate that when the block is complete
the ventricles do not respond to influences presumably
of vagus origin, although the auricles still respond normally
to such influences, that effects exerted upon the heart
presumably through the accelerators still influence the rate
of the ventricles as well as that of the auricles.</p>
<p>"When the block is partial the rate of the ventricular contraction
varies proportionally with the rate of the auricular
contractions but only within certain limits. When these
limits are exceeded the block becomes more complete, i. e.,
a 2:1 rhythm may be changed into a 3:1 rhythm, this into
a 4:1 rhythm, and this into complete block, and vice versa.</p>
<p>"The syncopal attacks are, in all probability, directly dependent
upon a marked reduction of the ventricular rate.
Such reductions of the ventricular rate are always associated
with an increase of the auricular rate, and it is
believed that the latter is the cause of the former." (Erlanger.)</p>
<p>The epileptiform seizures of the syndrome may be caused
by the anemia of the brain resulting from failure of the
heart to supply a sufficient quantity of blood.</p>
<p>The apoplectiform attacks are most probably caused by
venous congestion when the slowing of the ventricular contractions
is not sufficient to cause convulsions, but will just
cause complete unconsciousness.</p>
<h4>Renal</h4>
<p>Chronic nephritis, hypertension, arteriosclerosis form a
most important trinity. Some stoutly affirm that in all
cases of high tension there is chronic renal disease. Certainly<span class="pagenum"><a name="Page_200" id="Page_200">[200]</a></span>
the very highest blood pressures which we see occur
in the chronic interstitial forms of kidney disease. The
cause is most probably to be sought in some poison which
is elaborated in the kidney, is absorbed into the circulation
and acts powerfully either on the vasoconstrictor center
as a stimulus, or directly on the musculature of the
small arteries all over the body. Usually hypertension is
progressive but it may be temporary.</p>
<p>A man, 43 years old, entered the Milwaukee County Hospital
in uremic coma. The systolic blood pressure was
280-290 mm. Hg, the diastolic pressure 220 mm. (Janeway
instrument). Under treatment his blood pressure gradually
became lower, at the same period the albumin and
casts gradually disappeared from the urine. In two weeks
from admission he seemed perfectly well, there were no
albumin or casts found in the urine, and the systolic blood
pressure was 136 mm., not a high figure for a muscular man
of the laboring class. It must be admitted, however, that
such cases are the exception, not the rule.</p>
<p>Patients suffering from the association of chronic nephritis
with hypertension die slowly, usually. There is gradual
development of anasarca. Headache is frequent and
severe. Pains all over the body may occur. The sight
may suddenly become dim or may even be lost. Dizziness
may be complained of and dyspnea is usually marked.
Cyanosis comes on, the pulse becomes weak, irregular or
intermittent, heart failure sets in, and the patient dies with
edema of the lungs.</p>
<p>Another class of renal arteriosclerosis is characterized
by a small granular kidney in which fibrous changes of a
patchy character have taken place. These scattered areas
are the result of obliterating endarteritis of renal arteries
here and there with consequent anemia, death of cells, and
replacement by fibrous tissue. It occurs as part of a generalized
arteriosclerosis in which the whole arterial system
is the seat of diffuse (senile) sclerosis. The palpable arteries<span class="pagenum"><a name="Page_201" id="Page_201">[201]</a></span>
are usually beaded or even encircled with calcareous
deposits and the aorta is the seat of an extensive nodular
and ulcerating sclerosis. The heart is usually small, shows
extensive fibrous and fatty changes and possibly the condition
known as "brown atrophy;" the blood pressure is low.
Such cases do not show any special symptoms. They are
anemic, short of breath on exertion, have the appearance
and show the signs of senility.</p>
<p>In the first group it is, at times, difficult to say whether
the kidney disease or the arterial disease is the most important.
From a clinical standpoint the decision is not
essential as the end results are much the same in both.
However, when actual uremic symptoms dominate the
picture, it becomes evident that the disease of the kidney is
the chief feature in the causation of the symptoms.</p>
<h4>Abdominal or Visceral</h4>
<p>There is an important group of cases to which but little
attention has been paid until quite recently. This is the
abdominal or visceral type of arteriosclerosis. It has been
stated that arteriosclerosis of the splanchnic vessels almost
invariably causes high tension. Among others, Janeway
has shown that general arteriosclerosis without marked
disease of the splanchnic vessels does not cause as a rule
increase of blood pressure.</p>
<p>There are cases in which the brunt of the lesion falls upon
the abdominal vessels. Such cases have been called
"angina abdominalis." It has been suggested (Harlow
Brooks) that this type of arteriosclerosis may be determined
by constant overloading of the stomach with food,
especially rich and spiced food. This causes overwork of
the special arteries connected with digestion and so leads
to sclerosis of the vessels of the stomach, pancreas, and intestines.
Personal habits probably influence to great extent
the production of this more or less <b>localized</b> condition.</p>
<p>The organs supplied by the diseased arteries suffer from<span class="pagenum"><a name="Page_202" id="Page_202">[202]</a></span>
changes analogous to those occurring in general or local
malnutrition, such as starvation, old age, or local anemias.
These changes are atrophy with hemachromatosis (brown
atrophy) or fatty infiltration and degeneration. Following
the degenerative changes there result connective tissue
growth and further limitation of the functionating power of
the affected organs.</p>
<p>Pain is a more or less constant symptom of visceral
sclerosis. In the early stages there may be only a sense
of oppression, of weight, or of actual pressure in the abdomen
or pit of the stomach. There may be only recurring
attacks of violent abdominal pain accompanied by vomiting.
In some cases symptoms of tenderness in the epigastrium,
pains in the stomach after eating, vomiting and backache
may suggest gastric ulcer. There may be dyspnea and a
sense of anguish accompanied with a rapid and feeble pulse.
Hematemesis may make the symptom group even more like
ulcer of the stomach, and only the course of the disease
with the failure of rigid ulcer treatment and the substitution
of treatment directed toward relief of the arterial
spasm with resulting betterment, enables one to make a
diagnosis. The condition may be present for years and the
symptoms only epigastric tenderness with dizziness and
sweating on lying down after dinner, as in one of Perutz's
patients. The attacks are probably due to spasmodic contraction
of the sclerosed intestinal vessels with a resulting
local rise in blood pressure. The pains are most probably
due to the spasm of the intestinal muscles, and some think
they are located in the sympathetic and mesenteric plexuses.</p>
<p>This result of arteriosclerosis is not so uncommon, and
by keeping this cause of obscure abdominal pain in mind
we are now and then enabled to save a patient from operation.</p>
<p>An autopsy on a case which for many years had attacks
of abdominal pain and cramp-like attacks, with high blood
pressure and heart hypertrophy, showed extensive sclerosis<span class="pagenum"><a name="Page_203" id="Page_203">[203]</a></span>
of the abdominal aorta, superior mesenteric and iliacs.
These vessels were calcified. Hypertrophy of the left
ventricle was found. The kidneys were microscopically
normal. There were no changes in the ascending aorta but
in the descending portion there were scattered nodules and
small calcified plaques.</p>
<p>The attacks of pain from which this patient suffered for
many years, the hypertrophy of the left ventricle and the
increased blood pressure were thought to be directly due
to the sclerosis of the abdominal vessels.</p>
<h4>Cerebral</h4>
<p>It has been stated that arteriosclerosis is a general disease,
yet certain systems of vessels may be affected far
more than others, and indeed there may be marked sclerosis
at one part of the body and none demonstrable at another
part.</p>
<p>In advanced sclerosis there may be one or more of a series
of accidents due to embolism, thrombosis, or rupture of the
vessels. Such conditions as transient hemiplegia, monoplegia
or aphasia may occur. The attacks may come on
suddenly and be over in a few minutes; what Allbutt calls
"Larval apoplexies." They may last from a few hours
up to a day, and are very characteristic. A patient aged
64 years with pipe stem radials and tortuous hard temporals
would be lying quietly in bed when suddenly he would
stiffen, the eyes would become fixed and the breathing
cease. In a few seconds consciousness returned, the patient
would shake himself, pass his hand over his brow and ask,
"Where am I? Oh, yes, that's all right." He had as many
as thirty of these attacks in twenty-four hours, none of
them lasting over one minute. To just what such attacks
are due, it is hard to say. Some have attributed them to
spasm of the smaller blood vessels of the brain, but there
have never been demonstrated in the vessels any constrictor
fibers.</p>
<p><span class="pagenum"><a name="Page_204" id="Page_204">[204]</a></span>There is a well recognized form of dementia caused by
arteriosclerosis. In general paralysis of the insane and
in senile dementia the blood vessels are always diseased.
Milder grades of psychic disturbances are accompanied by
such symptoms as mental fatigue, persistent headaches,
vertigo, memory weakness and fainting. Aphasia, periods
of excitement and mental confusion occur in some. Later
stages are at times accompanied by inclination to fabulate,
loss of judgment, disorientation, narrowing of the external
interests, episodes of confusion and hallucinatory delirium.</p>
<p>The hemiplegias, monoplegias and paraplegias may occur
again and again and last for one or two days. Unless
there has been rupture of the vessels, there is complete recovery
as a rule.</p>
<p>In persons who have arteriosclerosis with high tension
attacks of melancholia are seen. There are at the same
time fits of depression, insomnia, irritability, fretfulness,
and a generally marked change in disposition. When the
tension is reduced by appropriate treatment these symptoms
disappear, to recur when the tension again becomes
high. On the contrary, attacks of mania are accompanied
by low blood pressure. The dizziness and vertigo in cerebral
arteriosclerosis are probably due to the stiffness of the
vessels which prevents them from following closely the variations
of pressure produced by position, and thus, at
times, the brain is deprived of blood and a transient anemia
occurs.</p>
<p>Arteriosclerosis of the cerebral vessels is always a serious
condition. The greatest danger is from rupture of a
blood vessel. Another of the dangers is gradual occlusion
of the arteries bringing about necrosis with softening of the
brain substance. The latter is more apt to be associated
with psychic changes, dementia, etc.; the former, with
hemiplegia. It is curious that a small branch of the Sylvian
artery, the lenticulo-striate, which supplies the corpus striatum,
should be the one which most frequently ruptures.<span class="pagenum"><a name="Page_205" id="Page_205">[205]</a></span>
Where the motor fibers from the whole cortex are gathered
together in one compact bundle, a very small hemorrhage
may and does cause very serious effects. A comparatively
large hemorrhage in the silent area of the brain may cause
few or no symptoms.</p>
<h4>Spinal</h4>
<p>It is conceivable that arteriosclerosis of the vessels of
the spinal cord might cause symptoms which would be referred
to the areas of the cord where the process was most
advanced. The lesions would be scattered and consequently
the symptoms might be protean in character.</p>
<p>True epileptic convulsions dependent on arteriosclerotic
changes are also seen and are not so uncommon.</p>
<p>This is on the whole a rare condition, much less common
than arteriosclerosis of the cerebral vessels. Collins and
Zabriskie report the following typical case:</p>
<blockquote><p>"H., a fireman, fifty-one years old, was in ordinary good health until toward
the end of 1902. At that time he noticed that his legs were growing
weak and that they tired easily. Later he complained of a jerking sensation
in different parts of the lower extremities and at times of sharp pain, which
might last from several minutes to two or three hours. The legs were the
seat of a heavy, unwieldy sensation, but there was no numbness or other
paresthesia. About the same time he began to have difficulty in holding the
urine, a symptom which steadily increased in severity. These symptoms continued
until March, 1903, i. e., for three months, then he awakened one morning
to find that he was unable to stand or walk, and the sphincters of the
bowels and bladder relaxed. There was no complaint of pain in the back or
legs, no difficulty in moving the arms, in swallowing or in speaking. He says
he was able to tell when his lower extremities were touched and he could
feel the bed and clothes. He was admitted to the City Hospital three weeks
later and the following record was made on April 21, 1903.</p>
<p>"The patient was a frail, emaciated man of medium height, who had the
appearance of being 55-60 years of age. He was unable to stand or walk.
When he was lying, he could flex the thigh and the legs slowly and feebly.
There was slight atrophy of the anterior and inner muscles, more of the left
than of the right side. The knee jerks and ankle jerks were absent. Irritation
of the soles caused quite a typical Babinski phenomenon. The patient
had fair strength in the upper extremities, but the arms tired very soon, he
said. The grip was moderate and alike in each hand. The motility of the
face, head, and neck was not noticeably impaired. There was no difficulty<span class="pagenum"><a name="Page_206" id="Page_206">[206]</a></span>
in swallowing, and articulation was not defective. Tactile sensibility was
slightly disordered in the lower extremities, although he could feel contact of
the finger, the point of a pin, and the like. Sensibility was not so acute as
normal; there was a quantitative diminution. Sensory perception was not
delayed. There was a distinct zone of slight hyperesthesia about as wide as
the hand above the femoral trochanters. Above that, sensibility was normal.
There was no discernible impairment of thermal sensibility. No part of the
body was particularly tender on pressure. A bedsore existed over the sacrum,
and there was excoriation of the genitals from constant dribbling of urine.</p>
<p>"Examination of the chest showed shallow respiratory movements. The
heart was regular, weak, there were no murmurs, the second sound was accentuated.
Examination of the abdomen showed that the liver and spleen
were palpable, but were not enlarged. The abdominal reflexes, both upper and
lower, were sluggish. The patient was slow of speech, likewise apparently of
thought. He did not seem to show an adequate interest in his condition, still
he was fully oriented and seemed to have a fair memory. His mental reflex
was slow. There were indications in the peripheral blood vessels and heart of
a moderate degree of general arteriosclerosis. The peripheral vessels
such as the radial, were palpable, the walls thickened, the blood pressure
increased.</p>
<p>"The patient did not complain of pain while he was in the hospital, a
period of four weeks, nor was there any particular change in the patient's
symptoms, subjective and objective, during this time. His mental state remained
clear until forty-eight hours before death, when he became sleepy,
stuporous, and comatose, dying apparently of cardiac weakness, which had set
in simultaneously with the clouding of consciousness."</p>
<p>At autopsy, except for a few small hemorrhages in the posterior horns of
the lower dorsal segments on the right side and a similar condition of the left
anterior horns, there was nothing noticed. On microscopic examination, there
was found widespread sclerosis of the vessels of the cord to a marked degree
with only slight thickening of the vessels of the brain. There were secondary
degenerations of ascending and descending type particularly marked at the
ninth dorsal segment. They included portions of all the tracts, the pyramidal
tract as well. The symptoms in brief were: (1) weakness and easily induced
fatigue of the legs; (2) peculiar sensations in the lower extremities, described
as jerky, numbness, heaviness, and occasionally sharp pain; (3)
progressive incontinence of urine; (4) progressive paraplegia.</p></blockquote>
<p>Since one of the chief manifestations of syphilis is sclerosis
of the arteries, neurologic cases characterized by irregular
symptoms and signs which can not be placed in any of
the definite system disease groups, are possibly due to
irregularly scattered areas of sclerosis throughout the
spinal cord caused by obliterating arteritis. Such cases
are not so very uncommon. Several have come under my<span class="pagenum"><a name="Page_207" id="Page_207">[207]</a></span>
observation. Further studies of the spinal cords of these
cases at autopsy are necessary before a final opinion can
be given as to their dependence on arteriosclerosis of the
spinal vessels.</p>
<h4>Local or Peripheral</h4>
<p>When the arteriosclerosis in the peripheral arteries
reaches a stage where endarteritis obliterans supervenes,
there is usually no chance for a compensatory or collateral
circulation to be established. The area supplied by the vessel
undergoes dry gangrene. A portion of a toe or finger or
a whole foot or hand may shrivel up. It is more common to
see the spontaneous amputation take place in the lower extremities.
The same effect may be produced by the plugging
of a vessel with a thrombus. There may be much pain
connected with the sudden blocking, whereas the gradual
obliteration of the blood supply of a toe or foot is not as a
rule at all painful. The condition is at times revealed more
or less accidentally when a patient injures his toe or foot
and discovers that there is no sensation in the part and that
the wound instead of healing is inclined to grow larger.</p>
<p>Other interesting vasomotor phenomena are frequently
connected with arteriosclerosis. Such a one is the curious
condition known as Raynaud's disease, a vascular disorder
which is divided into three grades of intensity: (1) local
syncope, (2) local asphyxia, (3) local or symmetrical gangrene.
This is not the place to describe this condition except
to say that the condition called "dead fingers" is the
most characteristic feature of the first stage. Chilblains
represent the mildest grade of the second stage. The parts
are intensely congested and there may be excruciating pain.
Any one who has ever had chilblains knows how painful
they can be. The general health is not impaired as a rule,
although the attacks are apt to come on when the person is
run down. The third stage may vary from a very mild<span class="pagenum"><a name="Page_208" id="Page_208">[208]</a></span>
grade, with only small necrotic areas at the tips of the
fingers, to extensive multiple gangrene.</p>
<p>Another and very rare condition in which chronic endarteritis
was the only constant finding is the disease described
by S. Weir Mitchell and called by him erythromelalgia (red
neuralgia). This is "A chronic disease in which a part or
parts—usually one or more extremities—suffer with pain,
flushing, and local fever, made far worse if the parts hang
down." (Weir Mitchell.)</p>
<p>Probably the most frequently seen result of arteriosclerosis
in the leg arteries is the remarkable condition, first described
by Charcot, known as intermittent claudication.
Persons the subject of this disease are able to walk if they
go slowly. If, however, any attempt be made to hurry the
step, there results total disability accompanied at times by
considerable cramp-like pain. The condition is much more
prone to occur in men than in women, and Hebrews seem
more frequently affected. The cause is most probably to
be sought in the anemia which results from the narrowing
of the channels through which the blood reaches the part.
The stiff, much narrowed arteries allow sufficient blood to
pass along for the nutrition of the part at rest or in quiet
motion. Just as soon as more violent exercise is taken,
calling for more blood, an ischemia of the part supervenes,
for the stiff vessels can not accommodate themselves to
changes in the necessary vascularity of the part. A rest
brings about a gradual return of blood and the function of
the part is restored. Pulsation may be totally absent in the
dorsal arteries of the feet and when the legs are allowed to
hang down there is apt to be deep congestion.</p>
<p>In this connection a curious case reported by Parkes
Weber will not be out of place. The patient, a male, aged
42 years, complained of cramp-like pains in the sole of the
left foot and calf of the leg occurring after walking for a
few minutes and obliging him to rest frequently. When
the legs were allowed to hang over the side of the bed, the<span class="pagenum"><a name="Page_209" id="Page_209">[209]</a></span>
distal portion of the left foot became red and congested
looking. No pulsation could be felt in the dorsal artery of
the left foot or in the posterior tibial artery. There was no
evidence of cardiovascular or other disease. An ulcer on
the little toe had slowly healed, but cramp-like muscular
pains still occurred on walking. The disease had lasted
about five years without the appearance of gangrene.</p>
<p>Weber calls this case one of arteritis obliterans with intermittent
claudication.</p>
<h4>Pulmonary Artery</h4>
<p>In the symptomatology of sclerosis of the pulmonary
artery the clinical signs and symptoms are mostly referable
to the obliterating endarteritis of the smaller vessels, while
the physical signs are more apt to reveal the involvement of
the main trunk. A history of severe infection in the past
is frequent, especially smallpox, and accompanying aortic
sclerosis with insufficiency of the mitral valve or stenosis of
this valve is the rule. Striking cyanosis is an early symptom,
while there is little if any dyspnea and edema. Intermittent
dyspragia is common. There seems to be no
tendency to clubbed fingers. Repeated hemorrhages from
the lungs without the formation of infarcts may occur.
There is usually an area of dullness at the upper left margin
of the sternum and nearby parts, sensitive to pressure
and to percussion, and the heart dullness extends unusually
far towards the right. The diagnosis of the right ventricular
hypertrophy may be substantiated by a fluoroscopic examination.</p>
<hr style="width: 65%;" />
<p><span class="pagenum"><a name="Page_210" id="Page_210">[210]</a></span></p>
<h2><a name="CHAPTER_X" id="CHAPTER_X"></a>CHAPTER X.</h2>
<h3>DIAGNOSIS</h3>
<h4>Early Diagnosis</h4>
<p>Arteriosclerosis is essentially a disease of middle life
and old age. It is not unusual, however, to find evidences
of the disease in persons in the third decade and
even in the second decade. Hereditary influences play
a most important rôle, syphilis and the abuse of alcohol
in the family history are particularly momentous. The
recognition of the early changes in the arteries among
young persons depends largely upon how carefully these
changes are looked for. The difference in the point of view
of one man who finds many cases in the comparatively
young, and another man who rarely finds such changes early
in life, at times, depends upon the acuity of perception and
observation and not upon the fact that one man has had a
series of unusually young arteriosclerotic subjects. The
diagnosis of arteriosclerosis may be so easily made that the
tyro could not fail to make it. It is, however, the purpose
of this volume to lay stress on the earliest possible diagnosis
and, if possible, to point out how the diagnosis may be arrived
at. It is obviously much to the advantage of the patient
to know that certain changes are beginning in his
arteries, which, if allowed to go on, will inevitably lead to
one or more of the symptom groups described in the preceding
chapters.</p>
<p>The combination of (1) hypertrophied heart, (2) increased
blood pressure, (3) palpable arteries, and (4)
ringing, accentuated second sound at the aortic cartilage is,
in reality, the picture of advanced arteriosclerosis. If the
individual is in good condition much may be done by judicious<span class="pagenum"><a name="Page_211" id="Page_211">[211]</a></span>
advice and treatment to ward off complications and
prolong life with a considerable degree of comfort. But we
should not wait until such signs are found before making a
diagnosis and instituting treatment. As in all forms of
chronic disease the early diagnosis is all important.</p>
<p>The history of the case is the first essential. Often a careful
inquiry into the personal habits of a patient, with the
record of all the preceding infectious diseases will give us
valuable information and may be the means of directing the
attention at once to the possible true condition. Particularly
must we inquire into the family history of gout and
rheumatism. An individual who comes of gouty stock is
certainly more prone to arterial degeneration than one who
can show a healthy heredity. Alcoholism in the family also
is of importance because of the fact that the children of
alcoholics start in life with a poor quality of tissue, and
conditions that would not affect a man from healthy stock
might cause early degeneration of arterial tissue in one of
bad ancestry.</p>
<p>What infectious diseases has the patient had? Even the
exanthemata may cause degenerations in the arteries, but,
as has been shown, such lesions probably heal completely
with no resulting damage to the vessel. Should the patient
have passed through a long siege of typhoid fever the problem
is quite different. Here (vide supra) (Thayer), the
palpable arteries do appear to be sclerosed permanently.
Probably the length of time that the toxin has had a chance
to act determines the permanent damage to the vessel wall.
More potent than all other diseases to cause early arteriosclerosis
is syphilis, and hence very careful inquiry should
be made in regard to the possibility of infection with this
virus. Not only the fact of actual infection but the duration
and thoroughness of treatment are important matters
for the physician to know.</p>
<p>What is the patient's occupation? Has he been an
athlete, particularly an oarsman? Has he been under any<span class="pagenum"><a name="Page_212" id="Page_212">[212]</a></span>
severe, prolonged, mental strain? Is he a laborer? If so,
in what form of manual labor is he engaged? Such questions
as these should never be overlooked, as they form the
foundation stones of an accurate diagnosis, and early, accurate
diagnosis, we repeat, is essential to successful
therapy.</p>
<p>We have called attention to the factor of sustained high
pressure in the production of arteriosclerosis. Constant
overstretching of the vessels leads to efforts of the body to
increase the strength of the part or parts. The material
which is used to strengthen the weakened walls has a higher
elastic resistance than muscle and elastic tissue, but a lower
limit of elasticity, and is none other than the familiar connective
tissue. In athletes, laborers, brain workers who are
under constant mental strain, and in those whose calling
brings them into contact with such poisons as lead, there is
every factor necessary for the production of high tension
and consequently of arteriosclerosis.</p>
<p>Another question in regard to personal habits is how
much tobacco does the patient use and in what form does he
use it? Our experience is that the cigar smoker is more
prone to present the symptoms of arteriosclerosis than the
cigarette smoker, the pipe smoker, or the one who chews the
tobacco. A very irritable heart results not infrequently
from cigarette smoking but such is almost always found in
young men in whom the lesions of arteriosclerosis are exceedingly
rare. The probabilities are that the arteriosclerosis
in cigar smoking results from the slowly acting poison
which causes a rapid heart rate with an increase of pressure.</p>
<p>Last but not least, and perhaps the most important question
is, has the patient been a heavy eater? This I believe
to be a potent cause of splanchnic arteriosclerosis with the
resulting indigestion, cramp-like attacks, high blood pressure,
etc. In a joking manner we are accustomed to remark,
"Overeating is the curse of the American people."
There is, however, much truth in that sentence. Osler, than<span class="pagenum"><a name="Page_213" id="Page_213">[213]</a></span>
whom there is no keener observer, states that he is more
and more impressed with the fact that overloading the
stomach with rich or heavy or spiced foods is today one of
the first causes of arterial degeneration. It stands to reason
that this is true. We know that organs exposed constantly
to hard work undergo hypertrophy, and that the
blood tension in those organs is high. Blood tension is,
after all, dependent on capillary resistance, and if the capillaries
are distended with blood, the resistance is great.
The digestive organs can be no exception to this rule. Increased
work means an increase of blood. This inevitably
causes distension of the capillaries with stretching of the
arteries and consequent damage to the walls. Once arteriosclerosis
is present a vicious circle is established.</p>
<p>A man about forty-five consults us and says that he has
noticed recently that he gets out of breath easily; in tying
his shoes he experiences some dizziness. He finds that he
has palpitation of the heart and possibly pain over the
precordial region now and then. He notices also that he is
irritable, that is, his family tell him he is, and he notices
that things that formerly did not annoy him, now are almost
hateful to him. On examination, one finds a palpable radial,
a somewhat hypertrophied heart and slightly accentuated
second aortic sound. The blood pressure may be
high. The urine may or may not reveal any abnormalities.
Not infrequently, although no albumin may be found, there
are hyaline casts. Such a case of arteriosclerosis is evidently
not to be regarded as early. Then the question
arises, How are we to recognize early arteriosclerosis? I
do not believe that the solution of this problem lies entirely
in the hands of the physician. Some men are fortunate
enough to come up for an examination for life insurance
before an observant doctor who recognizes the palpable
artery, makes out the beginning heart hypertrophy and the
slightly accentuated second aortic sound. The patient will
tell you that he never felt better in his life. He gets up at<span class="pagenum"><a name="Page_214" id="Page_214">[214]</a></span>
seven, works all day, plays golf, drinks his three to six
whiskies, and is proud of his physical development. But
the great mass of people are not fortunate from this standpoint.
They do not seek the advice of the physician until
they are stretched out in bed. They boast of the fact that
for twenty years they have never had a doctor. One may
well say that it is a problem how to reach such persons. It
seems to me that there can be but one way to do this. The
people must be taught that the duty of a physician is just
as much to keep them in health as it is to bring them back
to health when they are ill. To that end people should be
taught that at least twice a year they should be carefully
examined. I do not mean that the patient should present
himself to the doctor and, after a few questions the doctor
say cheerfully, "You are all right." The patient should
be systematically examined. That means a removal of the
clothing and examination on the bare skin. Such cooperation
on the part of patient and doctor would save the patient
years of active life and make of the doctor, what his
position entitles him to be, the benefactor to the community.
Too often careless work on the physician's part lulls the
patient into a false sense of security and he wakes up too
late to find that he has wasted months or years of life.
Early diagnosis of arteriosclerosis is only possible in exceptional
cases unless people present themselves to the physician
with the thought in mind that he is the guardian of
health as well as the healer.</p>
<p>There are patients who go to the ophthalmologist for
failing vision. Physically they feel quite well. They have
been heavy eaters, hard workers, men and women who have
been under great mental strain. On examination of the
fundus of the eye there is found slight tortuosity of the vessels
with possibly areas of degeneration in the retina. A
careful physical examination will usually reveal the signs
of arteriosclerosis elsewhere. We have mentioned frequently
high tension as an early sign. This must be taken<span class="pagenum"><a name="Page_215" id="Page_215">[215]</a></span>
with somewhat of a reservation, for this reason: not infrequently
a persistent high tension is the earliest sign of
chronic nephritis. The arteries may be pipe stem in character
and the heart small and flabby. However, if one
watches for the palpably thickened superficial arteries (always
bearing in mind the normal palpability as age advances)
and the high tension, he can not go far wrong in his
treatment whether the case is one of chronic nephritis or of
arteriosclerosis.</p>
<p>There is also this to bear in mind. Arteriosclerosis may
be marked in some vessels and so slight in the peripheral
vessels that it can not with certainty be made out. But
when the radials are sclerosed, it is usually the case that
similar changes exist in other parts. Then too, there may
be marked changes at the root of the aorta leading to
sclerosis of the coronary vessels alone, and the first intimation
that the patient or any one else has that there is disease,
may be an attack of angina pectoris. Except for
symptoms on the part of the heart there is no way to make
the diagnosis of sclerosis of the coronary arteries.</p>
<h4>Differential Diagnosis</h4>
<p>In arriving at a diagnosis, when the question is whether
or not arteriosclerosis is the main etiologic factor, the
most important fact to know is the age of the patient.
Other points that have been dwelt on fully must of necessity
also be borne in mind.</p>
<p>Possibly the chief conditions that may be confused with
some of the results of arteriosclerosis are pseudo angina
pectoris which may be mistaken for true angina pectoris,
and ulcer of the stomach, appendicitis (?) or other inflammatory
abdominal condition which may be mistaken for
angina abdominalis.</p>
<p>Differential tables are sometimes of value in fixing the
chief points of difference graphically.</p>
<p><span class="pagenum"><a name="Page_216" id="Page_216">[216]</a></span></p>
<p> </p>
<table border="0" cellpadding="4" cellspacing="0" summary="Angina Pectoris">
<tr>
<td><b>Pseudo angina pectoris</b>.</td><td><b>True angina pectoris</b>.</td>
</tr>
<tr>
<td> </td>
</tr>
<tr>
<td>Etiology rather certain; hysteria,
neurasthenia, toxic agents, and reflex
irritations.</td><td>Etiology not certain but almost always
associated with arteriosclerosis
of the coronary arteries and also
aortic regurgitation.</td></tr>
<tr>
<td> </td>
</tr>
<tr>
<td>No age is exempt. Usually in
young people, chiefly females.</td>
<td>Age is important factor. Rare before
forty, and males usually affected.</td>
</tr>
<tr>
<td> </td><td> </td>
</tr>
<tr>
<td>Paroxysms of pain occur spontaneously,
are periodic and often nocturnal.</td>
<td>Paroxysms brought on by overexertions
or excessive mental emotion.
Rarely periodic.
</td></tr>
<tr>
<td> </td><td> </td>
</tr>
<tr>
<td>Pain, while severe, is diffuse and
sensation is of distension of heart.
No sense of real anguish.</td>
<td>Intense pain, radiating down arm;
heart felt as in a vise. Sense of anguish
and impending dissolution.</td></tr>
<tr>
<td> </td><td> </td>
</tr>
<tr>
<td>Duration may be an hour or more.</td>
<td>Duration from few seconds to several
minutes.</td></tr>
<tr>
<td> </td><td> </td>
</tr>
<tr>
<td>Restlessness and emotional symptoms
of causative conditions are
prominent.</td>
<td>Silent and fixed attitude, rigidity
rather than restlessness.</td>
</tr>
<tr>
<td> </td><td> </td>
</tr>
<tr>
<td>Usually no increase in arterial tension.</td>
<td>Arterial tension is as a rule increased.</td>
</tr>
<tr>
<td> </td><td> </td>
</tr>
<tr>
<td>Prognosis favorable.</td>
<td>Prognosis most unfavorable.</td>
</tr>
</table>
<p> </p>
<p>In differentiating between ulcer of the stomach and
angina abdominalis the following points may be of service:</p>
<p> </p>
<table border="0" cellpadding="4" cellspacing="0" summary="Ulcer">
<tr>
<td><b>Ulcer</b>.</td>
<td><b>Angina abdominalis</b>.</td>
</tr>
<tr>
<td> </td><td> </td>
</tr>
<tr>
<td>Occurs as a rule in young persons,
more often females.</td>
<td>Only occurs in adults over forty
who have been heavy eaters and
drinkers, mostly males.</td></tr>
<tr>
<td> </td><td> </td>
</tr>
<tr><td>Pain of boring character increased
by food and by certain positions with
food in stomach. Felt through to
left of spine.</td>
<td>Pain cramp-like, diffuse, although
more localized in epigastrium. Not
necessarily any connection with food.</td>
</tr>
<tr>
<td> </td><td> </td>
</tr>
<tr>
<td>Occult blood found in stools.</td>
<td>
No occult blood in stools.</td>
</tr>
<tr>
<td> </td><td> </td>
</tr>
<tr><td>Considerable anemia apt to be
present.</td>
<td>Anemia more often absent.</td>
</tr>
<tr>
<td> </td><td> </td>
</tr>
<tr>
<td>Arterial tension usually low.</td>
<td>Arterial tension high. (Splanchnic
sclerosis.)</td>
</tr>
</table>
<h4>Diseases in Which Arteriosclerosis Is Commonly Found</h4>
<p>There are certain more or less chronic diseases in which
arteriosclerosis is found either as a separate disease or as
a result of the chronic disease itself, or the sclerosis may be
the cause of the disease. As examples of the first class
are diabetes mellitus and cirrhosis of the liver. As examples<span class="pagenum"><a name="Page_217" id="Page_217">[217]</a></span>
of the second class are chronic nephritis, gout, syphilis,
and lead poisoning. Examples of the third class have already
been fully described. Then certain rare diseases
that have been briefly described in this chapter, viz.: Raynaud's
disease and erythromelalgia are frequently associated
with demonstrable arteriosclerosis.</p>
<hr style="width: 65%;" />
<p><span class="pagenum"><a name="Page_218" id="Page_218">[218]</a></span></p>
<h2><a name="CHAPTER_XI" id="CHAPTER_XI"></a>CHAPTER XI.</h2>
<h3>PROGNOSIS</h3>
<p>In a disease that presents as many vagaries as arteriosclerosis,
it is not possible to give a certain prognosis.
Unfortunately we do not as a rule see the arteriosclerotic
until the disease is well advanced, or even after some of the
more serious complications have taken place. By that time
the condition is progressive, and while the prognosis is
grave the individual may live a number of years.</p>
<p>It is fortunate for the arteriosclerotic that mild grades
of the disease are compatible with a fairly active life. The
disease in this stage may become arrested and the patient
may live many years. Not only in the mild grades is this
possible. Even patients with advanced sclerosis may enjoy
good health provided the organs have not been so damaged
as to render them unfit to perform their functions. The
frequency with which we see advanced arteriosclerosis at
the postmortem table as an accidental discovery, attests
the truth of the foregoing statement. Yet how often does
it happen that individuals, apparently in the best of health,
suddenly succumb to an asthmatic or uremic attack, an
apoplexy, cessation of the heart beat, or a rupture of the
heart due to arteriosclerosis!</p>
<p>In order to arrive at an intelligent opinion in regard to
prognosis certain factors must be taken into consideration,
chief of which are: the seat of the sclerosis; the probable
stage; the existing complications; and, last and most important,
the patient himself. The whole man must be studied
and even then our prognosis must be most guarded.</p>
<p>It is much more dangerous for the patient when the
process is in the ascending portion of the arch of the aorta
than when it has attacked the peripheral arteries. Here,
at the root of the aorta, are the openings of the coronary<span class="pagenum"><a name="Page_219" id="Page_219">[219]</a></span>
arteries and the arteries supplying the brain are close by.
The coronary arteries here control the situation. When
loud murmurs are heard at the aortic orifice and the heart
is evidently diseased, it is useful to divide the endocarditis
into two types, the arteriosclerotic and the endocarditic.
The etiology of the former is sclerosis and the prognosis is
grave because of the liability, nay the probability, that the
orifices of the coronary arteries will become narrowed.
The etiology of the second type is in most cases rheumatic
fever or some other infectious disease, and the prognosis
is far better than in the first type. True, the two may be
combined. In such a case, the prognosis is entirely dependent
upon the course of the arteriosclerosis.</p>
<p>The involvement of the arteries in the kidneys is of considerable
importance, for it is usually bilateral and widespread.
As a rule, the disease makes but slow progress
provided that the general condition of the patient is good,
but at any time from a slight indiscretion or for no assignable
cause, symptoms of renal insufficiency may appear and
may rapidly prove fatal.</p>
<p>It must not be thought that because the localization of
the arteriosclerosis in the peripheral arteries is usually the
most favorable condition that it is therefore devoid of ill
effects. On the contrary, very serious, even fatal, results
may be brought about by interference with the circulation
with resultant extensive gangrene of the part supplied by
the diseased arteries. The amputation of a portion of a
leg, for instance, may relieve, to some extent, an overburdened
heart and prove life-saving to the patient, but the
neuritic pains are not necessarily relieved. The torture
from these pains may be excruciating.</p>
<p>No stage of the disease is exempt from its particular
danger. In the early stages of the disease before the
artery or arteries have had time to become strengthened by
proliferation of the connective tissue, there is the danger of
aneurysm. Later, the very same protective mechanism
leads to stiffening and narrowing of the arteries and hence<span class="pagenum"><a name="Page_220" id="Page_220">[220]</a></span>
to increased work on the part of the heart with all of its
consequences. Thrombosis is favored, and where atheromatous
ulcers are formed, embolism is to be feared.</p>
<p>As the complications and results of arteriosclerosis come
to the front every one must be considered by itself and as
if it were the true disease. There may be a slight apoplectic
attack from which the patient fully recovers, but the
prognosis is now of a grave character, as the chances are
that another attack may supervene and carry off the subject.
Yet, after an apoplectic attack, patients have lived for many
years. Probably the most noted illustration of this is the
life of Pasteur. He had at forty-six hemiplegia with gradual
onset. He recovered with a resulting slight limp, did
some of his best work after the stroke, and lived to be
seventy-three years old. Yet the exception but proves the
rule and the prognosis after one apoplectic stroke should
always be guarded.</p>
<p>The first attack of cardiac asthma is to be looked upon
as the beginning of the end. The end may be postponed
for some time, but it comes nearer with every subsequent
attack. One may recover from what appears to be a fatal
attack of cardiac asthma accompanied by edema of the lungs
and irregular, intermittent, laboring heart, but the recovery
is slow and the chances that the next attack will be the
fatal one are increased.</p>
<p>The significance of albuminuria is difficult to determine.
The kidneys secrete albumin under so many conditions that
the mere presence of albumin in the urine may have but
little prognostic value. Many cases are seen where there is
no demonstrable albumin, and yet the patient may suddenly
have a cerebral hemorrhage. As a general rule the urine
should be carefully examined, but not too much stress should
be laid on the discovery of albumin and casts. It is not
always possible to determine the extent of the kidney lesion
by the urinary examination, yet at any time a uremic attack
may appear and prove fatal.</p>
<p><span class="pagenum"><a name="Page_221" id="Page_221">[221]</a></span>After all the most important fact for the patient is not
what the pathologist finds in his kidneys after he is dead,
but what the living functional capacity of the kidneys is.
This can now be determined in a variety of ways as the
result of extensive work carried out in quite recent years.
The simplest method of determining the functional capacity
of the kidneys is by the injection into the muscles of the
back of a solution containing 6 mg. of the drug phenolsulphonephthalein
in one c.c. of fluid. This comes already
prepared in ampules, with full directions for its employment.<a name="FNanchor_16_16" id="FNanchor_16_16"></a><a href="#Footnote_16_16" class="fnanchor">[16]</a>
Some clinicians use indigo-carmine in place of
phthalein. The general consensus of opinion is in favor
of phthalein.</p>
<p>The nephritic test meal carefully worked out by Mosenthal<a name="FNanchor_17_17" id="FNanchor_17_17"></a><a href="#Footnote_17_17" class="fnanchor">[17]</a>
gives much valuable information. The determination
of the nonprotein nitrogen or the creatinin in the blood also
reveals the functional capacity of the kidneys.<a name="FNanchor_18_18" id="FNanchor_18_18"></a><a href="#Footnote_18_18" class="fnanchor">[18]</a></p>
<p>One might say that the appearance of albumin in the
urine of an arteriosclerotic where it had not been before,
is a bad sign, and in making a prognosis this must be taken
into consideration.</p>
<p>Bleeding from the nose is not infrequently seen in those
who have arteriosclerosis. It can hardly be called a dangerous
symptom as it can always be controlled by tampons.
There are times when epistaxis is decidedly beneficial as it
relieves headache, dizziness, and may avert the danger of
a hemorrhage into the brain substance. It is rare to have
nose bleed except in cases of high tension in plethoric
individuals. My experience has been that it has saved me
the trouble of bleeding the patient. It is always of serious
import in that it indicates a high degree of tension, but
there is scarcely ever any immediate danger from the nose
bleed itself.</p>
<p>Intestinal hemorrhage is always a grave sign. As has<span class="pagenum"><a name="Page_222" id="Page_222">[222]</a></span>
been shown, arteriosclerosis of the splanchnic vessels not
infrequently occurs, and an embolus or thrombus may completely
occlude the superior mesenteric artery. The
chances of the establishment of a collateral circulation are
small, as the arteries of the intestines are end arteries.
Necrosis of the part follows, blood is found in the stools,
and perforation or gangrene, or both, are apt to follow.
There may be blocking of small branches only, leading to
ulceration of the intestine. Under all conditions the prognosis
is serious.</p>
<p>The general condition of the patient, his build, physical
strength, powers of recuperation, etc., must be taken into
account in giving a prognosis. The more powerful the individual,
the more favorable, as a rule, is the prognosis, with
this reservation always in mind, that the greater the body
development, the greater is the heart hypertrophy, and the
accidents from high tension must not be overlooked. Many
puny individuals with stiff, calcified arteries go about with
more ease than a robust man with thickened arteries only.
The differentiation as pointed out by Allbutt (page 186),
is well to keep in mind in giving a prognosis. It can not be
too strongly emphasized that it is the whole patient that we
must consider and not any one system that at the time happens
to be the seat of greatest trouble, and by its group of
symptoms dominates the picture.</p>
<p>It is evident from what has been said that an accurate
prognosis in arteriosclerosis is no easy matter. Were
arteriosclerosis a simple disease of an acute character there
might be grounds for giving a more or less definite prognosis.
The most that can be said is that arteriosclerosis
is always a serious disease from the time that symptoms
begin to make themselves known. The gravity depends altogether
on the seat of the greatest arterial changes, and
is necessarily greater when the seat is in the brain than
when it is in the legs or arms.</p>
<p>The attitude of the patient himself also determines to a<span class="pagenum"><a name="Page_223" id="Page_223">[223]</a></span>
great extent the prognosis. Some men, especially those
who have always enjoyed good health, turn a deaf ear to
warnings and instead of ordering their lives according to
the advice of the physician, persist in going their own way
in the hope that the luck that has always been with them will
continue to stand at their elbows. Neither firmness nor
pleadings avail with some men. The only salve for the conscience
of the physician is that he has done his best to steer
the patient away from the shoals and breakers. In others
who realize their condition and take advantage of the advice
given as to the regulation of their lives, the prognosis is
generally favorable.</p>
<p>To sum up the chapter in a few words, I should say:
Always remember that the patient is a human being; study
his habits and character and mode of life; look at him as a
whole; take everything into consideration, and give always
a guarded prognosis.</p>
<hr style="width: 65%;" />
<p><span class="pagenum"><a name="Page_224" id="Page_224">[224]</a></span></p>
<h2><a name="CHAPTER_XII" id="CHAPTER_XII"></a>CHAPTER XII.</h2>
<h3>PROPHYLAXIS</h3>
<p>Arteriosclerosis comes to almost every one who lives out
his allotted time of life. As has been noted within, many
diseases and many habits of life are conducive to the early
appearance of arterial degeneration. Decay and degeneration
of the tissues are necessary concomitants of advancing
years and none of us can escape growing old. From
the period of adolescence certain of the tissues are commencing
a retrograde metamorphosis, and hand in hand
with this goes the deposit of fibrous tissue which later may
become calcified. The arterial tissue is no exception to this
rule, and we have already shown that certain changes normally
take place as the individual grows older, changes
which are arteriosclerotic in type and are quite like those
caused in younger people by many of the etiologic factors
of the disease.</p>
<p>We are absolutely dependent upon the integrity of our
hearts and blood vessels for the maintenance of activity and
span of life. Respiration may cease and be carried on artificially
for many hours while the heart continues to beat.
Even the heart has been massaged and the individual has
been brought back to life after its pulsations have ceased,
but such cases are few in number. We can not live without
the heart beat and the prophylaxis of arteriosclerosis consists
in the adjustment of our lives to our environment, so
that we may get the maximum amount of work accomplished
with the minimum amount of wear and tear on the blood
vessels.</p>
<p>The struggle for existence is keen. Competition in every
profession or trade is exceedingly acute, so much so that to
rise to the head in any branch of human activity requires<span class="pagenum"><a name="Page_225" id="Page_225">[225]</a></span>
exceptional powers of mind. Among those who are entered
in this keen competition, the fittest only can survive for any
period of time. The weaklings are bound to succumb. A
scion of healthy stock will stand the wear and tear far better
than will the progeny of diseased parentage.</p>
<p>It is only necessary to call attention to the part that
alcohol, syphilis and insanity play in heredity. These have
been discussed fully in the earlier part of this book.</p>
<p>We live rapidly, burning the candle at both ends. It is
not strange that so many comparatively young men and
women grow old prematurely. While heredity is a factor
as far as the prophylaxis of arteriosclerosis is concerned,
of far more importance is the mode of life of the individual.
Scarcely any of us lead strictly temperate lives. If
we do not abuse our bodies by excessive eating and drinking
and so wear out our splanchnic vessels and cause general
sclerosis by the high tension thereby induced, we abuse
our bodies by excessive brain work and worry with all their
multitudinous evils. The prophylaxis of arteriosclerosis
might well be labeled, "The plea for a more rational mode
of life." Moderation in all things is the keynote to health,
and to grow old gracefully is an art that admits of cultivation.
Excesses of any kind, be they mental, moral, or
physical, tend to wear out the organism.</p>
<p>People habitually eat too much; many drink too much.
They throw into the vascular system excessive fluid combined
frequently with toxic products that cause eventually
a condition of high arterial tension. It has been shown how
poisonous substances absorbed from the intestines have
some influence on the blood pressure. Anything that causes
constant increase of pressure should be studiously avoided.</p>
<p>Mild exercise is an essential feature of prophylaxis. One
may, by judicious exercise and diet, make of himself a
powerful muscular man without, at the same time, raising
his average blood pressure. The man who goes to excess
and continually overburdens his heart, will suffer the consequences,<span class="pagenum"><a name="Page_226" id="Page_226">[226]</a></span>
for the bill with compound interest will be
charged against him. It is a great mistake for any one to
work incessantly with no physical relaxation of any kind,
and yet, after all, it is not so much physical relaxation that
is necessary, as the pursuit of something entirely different,
so that the mind may be carried into channels other than
the accustomed routes. Diversification of interests is as a
rule restful. That is what every man who reaches adult
life should aim at. Hobbies are sometimes the salvation of
men. They may be ridden hard, but even then they are
helpful in bearing one completely away from daily cares
and worries. The man who can keep the balance between
his mental and physical work is the man who will, other
things being equal, live the longest and enjoy the best
health.</p>
<p>Nowadays the trend of medicine is toward prophylaxis.
We give the state authority to control epidemics so far as
it is possible by modern measures to control them.</p>
<p>We urge over and over again the value of early diagnosis
in all chronic diseases, for we know that many of them, and
this applies particularly to arteriosclerosis, could be prevented
from advancing by the recognition of the condition
and the institution of proper hygienic and medicinal treatment.</p>
<p><i>It is the patent duty of every physician to instruct the
members of his clientele in the fundamental rules of health.</i>
Recently the President of the American Medical Association,
in his address before the 1908 meeting, urged the
dissemination of accurate knowledge concerning diseases
among the laity. While this may be done by city and state
boards of health, it seems far better for the modern trained
physician to work among his own people. With concise
information concerning the modes of infection and the dangers
of waiting until a disease has a firm hold before consulting
the health mender, people should be able to protect
themselves from infections and be able to nip chronic processes<span class="pagenum"><a name="Page_227" id="Page_227">[227]</a></span>
in the bud. But it is difficult to turn the average
individual away from the habit of having a drug-clerk prescribe
a dose of medicine for the ailment that troubles him.
It is really unfortunate that most of the pains and aches and
morbid sensations that one has speedily pass away with
little or no treatment. Herein lies the strength of charlatanism
and quackery. Unfortunate, yes, for a man can not
tell whether the trivial complaint from which he suffers is
any different from the one that was so easily conquered six
months ago. But instead of recovering, he grows worse.
Hope that springs eternal in the human breast, leads him
to dilly-dally until he at last seeks medical advice, only to
find that the disease has made such progress that little can
be done.</p>
<p><i>Instruct the public to consult the doctors twice a year.</i>
The dentists have their patients return to them at stated
intervals only to see if all is well. <i>How much more rational
it would be if men and women past the age of forty had
a physical examination made twice a year to find out if all
is well.</i></p>
<p>The prophylaxis of arteriosclerosis is moderation in all
the duties and pleasures of life. This in no sense means
that a man has to nurse himself into neurasthenia for fear
that something will happen to him. As one grows in years
exercise should not be as violent as it was when younger,
and food should be taken in smaller quantities. Many forms
of exercise suggest themselves, particularly walking and
golf. Walking is a much neglected form of exercise which,
in these modern days with our thousand and one means of
locomotion, is becoming almost extinct. There is no better
form of exercise than graded walking. To strengthen the
heart selected hill climbing is one of the best therapeutic
methods that we have. The patient is made to exercise his
heart just as he is made to exercise his legs, and as with
exercise of voluntary muscles comes increase in strength,
so by fitting exercise may the heart muscle be increased in<span class="pagenum"><a name="Page_228" id="Page_228">[228]</a></span>
power. A warning should be sounded, however, against
over exercise. This leads naturally to hypertrophy with
all its disastrous possibilities. Men who have been athletes
when young should guard against overeating and lack of
exercise as they grow older. Many of the factors which
favor the development of arteriosclerosis are already there,
and a sedentary, ordinary life, such as office all day, club
in afternoon, a few drinks and much rich food, will inevitably
lead to well-advanced arterial disease.</p>
<p>Karl Marx in his famous Socialistic platform said: "No
rights without duties; no duties without rights." So we
may paraphrase this and say: "No brain work without
moderate physical exercise in the open air; no physical exercise
without moderate brain work."</p>
<p>There is yet one other point that is important, the combination
of concentrated brain work and constant whiskey
drinking. This is most often seen in men of forty-five to
fifty-five, heads of large business concerns who habitually
take from six to twelve drinks of whiskey daily, and with
possibly a bottle of wine for dinner. Such men appear
ruddy and in prime health but, almost invariably, careful
examination will reveal unmistakable signs of arterial disease.
There is usually the enlarged heart and pulse of high
tension with or without the trace of albumin in the urine.
The lurking danger of this group of manifestations has so
impressed the medical directors of several of the large insurance
companies that a blood pressure reading must be
made on all applicants over forty years of age. Should high
blood pressure be found, the premium is increased, as the
expectation of life is proportionately shorter in such men
than in normal persons.</p>
<p>Therefore, let every physician act his part as guardian
of health. Only in this way is the prophylaxis of arteriosclerosis
possible.</p>
<hr style="width: 65%;" />
<p><span class="pagenum"><a name="Page_229" id="Page_229">[229]</a></span></p>
<h2><a name="CHAPTER_XIII" id="CHAPTER_XIII"></a>CHAPTER XIII.</h2>
<h3>TREATMENT</h3>
<p>Although it has been rather dogmatically stated (vide
supra) that every one who reaches old age has arteriosclerosis,
it must not be inferred that absolutely no exceptions to
this rule are found. Cases are known where persons of
ninety years even had soft arteries, and we have seen persons
of eighty whose arteries could not be palpated. When
infants and children are seen with considerable sclerosis,
it proves that, after all, it is the quality of the tissue even
more than the wear and tear, that is the determining factor
in the production of arteriosclerosis. It would be well if
those who can not bring healthy progeny into the world
were to leave this duty to those who can.</p>
<p>In general the treatment of arteriosclerosis is prophylactic
and symptomatic. In the preceding chapter I had something
to say about prophylaxis in general; I must again
refer to it in detail.</p>
<p>Arteriosclerosis is essentially a chronic progressive disease,
and the secret of success in the management of it is
not to treat the disease or the stage of the disease, but to
treat the patient who has the disease. To infer the stage
of the disease from the feeling of the sclerosed artery, may
lead to serious mistakes. Persons with calcified arteries
may be perfectly comfortable, while those with only moderate
thickening may have many severe symptoms. The
keynote is individualization. It is manifestly absurd to
treat the laboring man with his arteriosclerosis as one
would treat the successful financier. The habits, mode of
life, every detail, should be studied in every patient if we
expect to gain the greatest measure of success in the treatment.
One may treat fifty patients who have typhoid fever<span class="pagenum"><a name="Page_230" id="Page_230">[230]</a></span>
by a routine method and all may recover. Individualizing,
while of great value in the treatment of acute diseases, yet
is not absolutely essential in order that good results may
be obtained. Far different is it when treating a disease
like arteriosclerosis. One who relies on textbook knowledge
will find himself at a loss to know what to do. Textbooks
can only outline, in the briefest manner, the average
case, and no one ever sees the average book case. At the
bedside with the patients is the place to learn therapeutics
as well as diagnosis. All that can be hoped for in outlining
the treatment of arteriosclerosis is to lay down a few principles.
The tact, the intuition, the subtle something that
makes the successful therapeutist, can not be learned from
books. So the man who treats cases by rule of thumb is a
failure from the beginning. There are certain general
principles that will be our sheet anchors at all times and
for all cases. The art of varying the application of these
fundamentals to suit the individual case, is not to be culled
from printed words.</p>
<h4>Hygienic Treatment</h4>
<p>Every man is more or less the arbiter of his own fate.
Granted that he has good tissue to begin life, his own habits
and actions determine his span of comfortable existence.
No one cares to live after his brain begins to fail, and the
failing brain is often due to disease of the cranial arteries.
The hygienic treatment resolves itself into advice in regard
to prophylaxis.</p>
<p>First and foremost is exercise. It has seemed to us that
the revival of out-of-door sports is one of the best signs of
promise of the preservation of a virile, hardy race. That
women, as well as men, indulge in the lighter forms of out-of-door
exercise should bring it about that the coming
generation will start in life under the most advantageous
conditions of bodily resistance.</p>
<p>Among all the forms of exercise, golf probably is the best.<span class="pagenum"><a name="Page_231" id="Page_231">[231]</a></span>
It is not too violent for the middle-aged man, yet it gives
the young athlete quite enough exercise to tire him. It is
played in the open. One is compelled to walk up and down
in pleasant company, for golf is essentially a companionable
game, while he reaps the full benefit of the invigorating exercise.
The blood courses through the muscles and lungs
more rapidly; the contraction of the skeletal muscles serves
to compress the veins and so to aid the return of blood to
the heart: the lungs are rendered hyperemic, deeper and
fuller breaths must be taken; oxidation is necessarily more
rapid, and effete products, which if not completely oxidized
would possibly act as vasoconstrictors, are oxidized to
harmless products and eliminated without irritating the
excretory organs.</p>
<p>Other forms of out-door exercise that can be recommended
are tennis, canoeing, rowing, fishing, horseback riding,
swimming, etc. Tennis is the most violent of all the
sports mentioned and might readily be overdone. Rowing
as practiced by the eights at college is undoubtedly too violent
a form of exercise, and may be productive in later life
of very grave results. Canoeing is a delightful and invigorating
exercise. The muscles of the arms, shoulders,
and trunk are especially used, the leg muscles scarcely at
all. Nevertheless, the deep breathing that necessarily
comes with all chest exercises aerates every portion of the
lungs, and is of great benefit to the whole body.</p>
<p>Swimming as an exercise has much to recommend it. In
this sport all the muscles take part and at the same time the
chest is broadened and deepened.</p>
<p>All these methods of using the muscles to keep oneself in
trim, so to speak, are part and parcel of the general hygienic
mode of life that is conducive to a healthy old age. Exercise
can be overdone, as eating can be overdone. Both are
essential and yet both can be the means of hastening an individual
to a premature grave.</p>
<p>When the arteriosclerosis has advanced so far that it is<span class="pagenum"><a name="Page_232" id="Page_232">[232]</a></span>
easily recognizable, certain forms of exercise should be absolutely
prohibited. Such are tennis, rowing and swimming.
Horseback riding to be allowed must be strictly supervised.
At times this may be an exceedingly violent exercise. As
an out-of-door sport, there is nothing that equals golf.
The physician, knowing the character of the course, and
the length of it, can say to his patient that he may play six,
nine, twelve, or eighteen holes, depending on the patient's
condition.</p>
<p>For those who are not able to get out, exercise in the
room with the windows open must take the place of out-of-door
sports. Here the use of chest weights is a most
excellent means of keeping up the tone of the muscles. By
adjusting the weights, the exercise may be made light,
medium, or heavy. Every physician should be familiar
with the chest weight exercises. They are not as good as
open air exercise but they undoubtedly have been the means
of saving years of life to many patients with arterial
disease.</p>
<p>There comes a time when all forms of exercise must be
prohibited on account of the dyspnea, edema, dizziness, etc.
It seems unwise to keep such a patient in bed, even though
the edema be considerable. Once on his back in bed he
becomes weak, and the danger of edema of the lungs or
hypostatic congestion of the bases, with subsequent bronchopneumonia,
is very great.</p>
<p>Such patients may be allowed to sit up in a comfortable
chair with the legs supported straight out on a stool or
other chair. The half reclining position is not easy to assume
in bed. Considerable ingenuity must often be exercised
by the physician in making the patient comfortable
without increasing the symptoms from which the patient
suffers following the least amount of exercise. Although
such persons can not exercise actively, they should have
passive exercise in the form of massage, carefully given, so
that no injury is done to the rigid vessels. It is possible to<span class="pagenum"><a name="Page_233" id="Page_233">[233]</a></span>
rupture a vessel, the walls of which are encrusted with lime
salts, and full of small aneurysmal dilatations. Every patient
must be watched carefully and measures instituted for
the individual.</p>
<h4>Balneotherapy</h4>
<p>As a tonic and invigorator, the cold or cool bath (shower
or tub), in the morning on arising can be highly recommended.
It promotes skin activity, is a stimulant to the
bowels and kidneys and to the general circulation, besides
being cleansing. We find today that the morning bath has
become such a necessity to the average American that all
new hotels are fitted with private baths, and old hotels, in
order to get patronage, are arranging as many baths connected
with sleeping rooms as is possible. Our generation
assuredly is a ruddy, clean-bodied one. What the actual
results of this out-door life and frequent bathing will be
for the race remains to be seen, but one can not but feel
that it must build up a stronger, more resistant race of
people, who not only enjoy better health than did their forefathers,
but enjoy it longer.</p>
<p>Not every one can stand a cold bath. It is folly to urge
it on one to whom it is distasteful, or on one who does not
feel the comfortable glow that should naturally result. For
the well, or those with a tendency to arteriosclerosis, or
those in whose families there have been several members
who had early arteriosclerosis, such proceedings as recommended
could not be improved upon. However, for the
person who has well recognized sclerosis, only warm baths
should be advised, and these not daily. The water should
be at a temperature of 90-95° F. Care should be taken
that persons sent to spas be cautioned against hot baths.
It is not inconceivable that the increased force of the heart
beat that accompanies a hot bath might be sufficient to rupture
a small cranial vessel. Hence, Turkish and Russian
baths should be most unqualifiedly condemned. As a matter<span class="pagenum"><a name="Page_234" id="Page_234">[234]</a></span>
of fact, persons vary so in their habits with regard to
bathing that what might suit one person would do another
much harm.</p>
<h4>Personal Habits</h4>
<p>The personal habits of the individual, more than any
other factor, determine whether or not arteriosclerosis sets
in early in his life. The man or woman who is moderate in
eating and drinking, sees that the kidneys are kept in good
condition, and attends strictly to regularity of the bowels,
lays a good basis for the measure of health which is so
essential for happiness. It has been shown that sclerosis
of the splanchnic vessels may be due to constant irritation
of toxic products elaborated in digesting constantly enormous
meals. In obstinate constipation, many poisons, the
nature of which we do not know, are absorbed and circulate
in the blood. We have not sufficient data to prove that
constipation favors the production of arteriosclerosis, but
our impression has been that it does favor it. Constipation
can often be relieved by a glass of water before breakfast,
a regular time to go to stool, and abdominal massage
or exercises. Some maintain that it is a bad habit only,
and can be readily overcome. Whatever is done, avoid
leading the patient into the drug habit, for the last state
of the patient will be worse than the first. Habits of sleep
are not of such great importance. Most persons get enough
sleep except when under severe mental strain. Most adults
need from seven to eight hours' sleep, although some can
do all their work and keep in prime health on five or six
hours' sleep.</p>
<p>Tobacco has been accused of causing many ills and has
been thereby much maligned. We can not see that the use
of tobacco in any form in moderation is harmful to most
men. Undoubtedly the blood pressure is raised when mild
tobacco poisoning occurs, and individual peculiarities of reaction
to the weed are multitudinous. But to condemn offhand<span class="pagenum"><a name="Page_235" id="Page_235">[235]</a></span>
its use is the height of folly. There is no reason why
the arteriosclerotic who has always used tobacco in moderation,
should not continue to use it, whether he smoke cigarettes,
cigars, or pipe. His supply should be decreased, but
there is no sense in depriving a man of one of the solaces of
life, unless, as is sometimes the case, abstinence is easier
for the patient than moderation.</p>
<p>As for alcohol, opinions differ widely.<a name="FNanchor_19_19" id="FNanchor_19_19"></a><a href="#Footnote_19_19" class="fnanchor">[19]</a> Some see in alcohol
one of the most frequent causes of arteriosclerosis;
others do not believe that the part played by alcohol is a
serious one, only in conjunction with other poisonous substances
is it dangerous. Probably unreasoning fanaticism
has had much to do with the wholesale condemnation of
alcoholic beverages. The general effect of alcohol is to
lower the blood pressure by causing marked dilatation of
all the vessels of the skin. True, the alcohol circulates in
the blood, and is broken up in the liver, and this organ
would seem to bear the brunt of the harm done. Alcoholic
drinks in moderation, I do not believe have any deleterious
effect on health. On the contrary, I believe that they may
in some cases assist digestion and assimilation. Indiscriminate
indulgence is to be condemned, as is overindulgence
in exercise or eating. What may be moderate for A, might
be excessive for B. Every man is then the arbiter of his
own fortune and within his own limits can indulge moderately
(a relative term after all) without fear of doing himself
harm. In advanced arteriosclerosis it is necessary to
decrease the supply of alcohol just as it is necessary to cut
down the food supply. This must rest entirely on the
judgment of the physician, who must not act arbitrarily,
but must have his reasons for every one of his orders.</p>
<h4>Dietetic Treatment</h4>
<p>Most persons eat too much. We not only satisfy our
hunger, but we satisfy our palates, and, instead of putting<span class="pagenum"><a name="Page_236" id="Page_236">[236]</a></span>
substantial foodstuffs into our stomachs, we frequently take
unto ourselves concoctions that defy description.</p>
<p>Foodstuffs are composed of one or all of three classes:
(1) proteins, (2) fats, (3) carbohydrates. As examples
of the first are beef and white of egg; of the second, the
oils, butter, lard; of the third, sugar, potato, beet, corn, etc.</p>
<p>The physiologists and chemists have shown us that both
endogenous and exogenous uric acid in excess will cause a
rise of blood pressure, but the bodies most concerned in
the production of elevated blood pressure are the purin
bodies, those organic compounds which are formed from
proteins and represent chemically a step in the oxidation
of part of the protein molecule to uric acid. Red meat
contains more of the substances producing purin bodies
than any other one common foodstuff, and for this reason
the excessive meat eater is, <i>ceteris paribus</i>, more apt to
develop arteriosclerosis comparatively early in life.</p>
<p>The fats and carbohydrates contain practically no substances
that react on the body of the ordinary individual
in a deleterious manner during their digestion. The extra
work that is put on the heart by the formation of many
new blood vessels in adipose tissue is the only harmful effect
of overindulgence in these foodstuffs.</p>
<p>It has been found that nitrogen equilibrium can be maintained
at a wide range of levels. Formerly 135-150 gms.
of protein daily were considered necessary for a man doing
light work. Now it is known that half that amount is sufficient
to keep one in nitrogenous equilibrium, and to enable
one to keep his weight. A person at rest requires even less
than that. One who is engaged in hard physical labor burns
up more fuel in the muscles, and so must have a larger
fuel supply.</p>
<p>Although we habitually eat too much we drink too little
water. For those who have any form of arterial disease
an excess of fluid is harmful, as the vessels become filled
up and a condition of plethora results, which necessarily<span class="pagenum"><a name="Page_237" id="Page_237">[237]</a></span>
reacts injuriously on the heart and circulation. The drinking
of a glass of water during meals is, in the author's
opinion, good practice. The water must be taken mouthful
at a time, and not gulped down. If this is done, there
results sufficient dilution of the solid food to enable the
gastric juices successfully and rapidly to reach all parts
of the meal.</p>
<p>Some are in favor of a rigid milk diet for those who
have arteriosclerosis. Some men have lived on nothing
but milk for several years and have not only kept in good
health, but have actually gained weight and led at the
same time active lives. It has been held by others that rigid
milk diet is positively harmful on account of the relatively
large quantity of calcium salts that are ingested. This was
thought to favor the deposition of calcareous material in
the walls of the already diseased arteries. While possibly
there may be some danger of increased calcification, the
majority of clinicians are in favor of a milk cure given at
intervals. Thus the patient is made to take three to
four quarts daily for a period of a month. There is then a
gradual return to a general diet, exclusive of meat, for
several weeks, then another rigid milk diet period.</p>
<p>If we are bold enough to follow Metschnikoff in his theories
of longevity, we might advise resection of the large
intestine, on the ground that it is an enormous culture tube
that produces prodigious amounts of poisonous substances
which are thrown into the general circulation. To combat
such a grave (?) condition as the carrying of several feet
of large intestine, we are recommended to take buttermilk
or milk soured by means of the <i>b. acidus lacticus</i>. Clinical
experience has taught that in arteriosclerosis buttermilk
is of great value, whether it be the natural product, or made
directly from sweet milk by the addition of the bacilli. The
latter is a smoother product and has, to my mind, a delightful
flavor. It may be diluted with Vichy or plain soda
water. Cases that can not take milk or any other food will<span class="pagenum"><a name="Page_238" id="Page_238">[238]</a></span>
often take buttermilk, and do well on this restricted diet.
From two to four quarts daily should be taken. It should
be drunk slowly as should milk.</p>
<h4>Medicinal</h4>
<p>It has long been thought that the iodides have some specific
effect on the advancing arteriosclerosis, checking its
spread, if not really aiding nature to a limited restoration
of the diseased arteries. It is possible that the eulogies
upon the iodides owe their origin to the successful treatment
of syphilitic arteriosclerosis, in which condition these
drugs have a specific action. However that may be, there
is no doubt that the administration of sodium or potassium
iodide is good therapeutics in cases of arteriosclerosis.</p>
<p>Unfortunately many persons have such irritable stomachs
that they can not take the iodides, even though they be
diluted many times. They may be made less irritating by
giving them with essence of pepsin. Unless the case is
syphilitic, it is doubtful whether it is of value to increase the
dose gradually until a dram or even more is taken three
times daily after meals. Usually a maximum dose of ten
grains seems to be quite sufficient. This may be taken three
times a day, well diluted, for three months. There follows
a month's rest, then the treatment is resumed for another
period of three months, and so on. Either sodium or potassium
iodide in saturated solution may be given. The sodium
salt is possibly less irritating, and contains more free
iodine than the potassium salt, although the latter is more
generally used. The strontium iodide may also be used.</p>
<p>One sees a patient now and then who can not take the
iodides, however they may be combined. For such patients
one may obtain good results with iodopin, sajodin, or other
of the preparations put up by reputable firms. Personally I
have never yet seen a patient who could not take the ordinary
iodides in some form or other, and I am opposed to
ready made drugging.</p>
<p><span class="pagenum"><a name="Page_239" id="Page_239">[239]</a></span>The action of the iodides is to lower the blood pressure,
and they are of greatest value when the blood pressure
is high, and when headache and precordial pain are present.</p>
<p>When the case is moderately advanced, very mild doses,
gr. ½, morning and evening, of the thyroid extract may be
given. It is generally believed that the internal secretion
of the thyroid and the adrenal are antagonistic. That the
thyroid secretion lowers blood pressure in certain forms of
hypertension is certain, possibly on account of its iodine
content. Some combinations of iodine and thyroid such as
the iodothyroidin have been used and have had some measure
of success attributed to them.</p>
<p>Hypertension does not always demand active measures
for its reduction. Viewed from the physiologic standpoint,
hypertension is but the expression of a compensating
mechanism which is designed to keep the blood moving
through narrowed channels. Heart hypertrophy then is
absolutely essential to the maintenance of life. It has been
said that the highest blood pressures occur in chronic disease
of the kidneys. The poisonous substances produced
in the kidneys must exert their action through absorption
into the general blood stream. This toxin may be completely
eliminated, if we accept as our criterion the reduction
of tension to normal together with the complete return
of the affected individual to health. A concrete example
is as follows: A man aged 44 years was brought to the
Milwaukee County Hospital in coma. His systolic blood
pressure was over 280 mm. Hg, diastolic 170 mm., his urine
contained considerable albumin and many casts. He had
general anasarca. Venesection was done at once and 300
c.c. blood obtained. Immediately following this operation
the pressure was 210-150, but within twelve hours it was
again above 280-170. He was given no medication to reduce
pressure except that he was freely purged. He was
given a steam sweat bath daily. Frequent blood pressure
readings were taken. Within seven days the pressure was<span class="pagenum"><a name="Page_240" id="Page_240">[240]</a></span>
130-86. He had, in the meantime, completely recovered
from his symptoms. He was kept in the hospital for two
weeks longer assisting in the work on the ward, and he was
discharged with a pressure (systolic) between 130 and 136
diastolic 80-84. The treatment was rest in bed, free purging,
venesection, and sweat baths, simple but exceedingly
effective.</p>
<p>Should there be actual indications for reducing the blood
pressure, I must admit that it can not always be done. The
majority of cases will do well on the sodium nitrite or
erythrol tetranitrate. However, these do not always lower
blood pressure and keep it within normal limits. When a
man has very high tension we do not wish to reduce it to
what it should normally be for the age of the patient, as
symptoms of collapse might set in at any time under such
conditions.</p>
<p>Observations made with the sphygmomanometer<a name="FNanchor_20_20" id="FNanchor_20_20"></a><a href="#Footnote_20_20" class="fnanchor">[20]</a> show
that the effect of nitroglycerin is transient or of no effect
except in doses which are relatively enormous (one drop of
the one per cent solution given every hour). Sodium nitrite
may lower the blood pressure but the effects will have
worn off in two hours. It is the same with erythrol tetranitrate.
Sodium sulphocyanate in doses of from one to three
grains three times a day is highly recommended by some.
My own experience with it does not lead me to believe that it
is of any great value in hypertension. It, however, may be
tried. Benzyl benzoate has been used recently to reduce
the high blood pressure of hypertension. Macht has reported
some success. In the author's hands it has been
efficacious in a few cases. As long as the patient takes the
drug the pressure may be slightly reduced, but upon the
withdrawal of the drug the pressure returns to its former
level. It is well worth a trial and further experimentation<span class="pagenum"><a name="Page_241" id="Page_241">[241]</a></span>
may reveal better methods of administration. The dose is
from 2 to 6 c.c. mixed with water at intervals.</p>
<p>In the hypertension of the menopause some have had
success with large doses of corpus luteum extract. As
a matter of fact the drug treatment of hypertension,
when it becomes necessary to treat this condition with
drugs, has suffered a notable set-back since more careful
control has been made with the blood pressure instruments.
In giving any of the depressor drugs their action should
be controlled by blood pressure measurements, for only
in this way can we be sure that the drug is exerting its
physiological effect and we may expect results. The individual
reaction to these drugs varies greatly and no rule
for dosage can be dogmatically laid down. The only successful
therapy is rigid individualization. This is the keystone
to treatment in cases of arteriosclerosis and high
tension.</p>
<p>It must not be inferred from what has been said that the
nitrites are of no value. They are of decided value but
they have their limitations. The most evanescent of these
drugs is amyl nitrite. This is put up in the form of capsules,
or pearls, containing from one to three minims. When
it is desired to dilate the peripheral vessels suddenly, one
or two of these capsules are broken in a cloth held to the
nose. The effect is almost instantaneous. There is flushing
of the face and other peripheral vessels, particularly
near the head, denoting a relaxation and widening of the
bed of the blood stream, and a consequent decrease in pressure
in the arteries. These effects are over in a short
while. It is only used in attacks of cardiac spasm, as in
angina pectoris. Nitroglycerin, the Spiritus Glonoini of
the U. S. P., acts in about the same manner as amyl nitrite
but the effects last usually a trifle longer. One drop
of the one per cent solution may be given every hour until
physiologic effects are produced. It may be given hypodermically.
This may be a means of reducing pronounced<span class="pagenum"><a name="Page_242" id="Page_242">[242]</a></span>
high tension. This drug has been found of benefit especially
in cases where arteriosclerosis combined with chronic
nephritis causes cardiac asthma. The other drug which
may be of service in these conditions, one whose sphere
of action is somewhat broader, because its effects are more
lasting, is sodium nitrite. This is given in water in doses
of one to three or five grains every four hours. Some
have objected to the use of this drug, but my experience
has made me place considerable confidence in its harmlessness,
provided that the patient is carefully watched. This,
however, applies to all of the nitrite compounds. My experience
with erythrol tetranitrate is not large. It may
be used in place of sodium nitrite.</p>
<p>For a mild case, one often finds that sweet spirits of
niter is sufficient to control the pressure and relieve the
distressing symptoms, and it is undoubtedly the least harmful
of all the nitrites. Drugs that are of great value, but
of which little is noted in textbooks, are aconite and veratrum
viride. Both of these drugs are well known to be
marked circulatory depressors. Veratrum viride in my experience
should be very cautiously used, and never used
unless a trained attendant is constantly at hand. With regard
to aconite I have no such feeling, and a mixture of
tincture of aconite and spiritus etheris nitrosi may be
given for several weeks with no fear of doing any harm.
Personally, of all the drugs mentioned, I prefer the nitrite
of sodium or the combination just given. They may be advantageously
alternated.</p>
<p>My own feeling is that the most successful means of treatment
of acute high tension is without the use of drugs.
The most important measure is absolute rest in bed. This
often suffices to lower the blood pressure and to arrest the
symptoms produced by high tension. Venesection I believe
is also of value. True the arterioles appear to contract
almost immediately upon the lessened quantity of blood,
or there is immediate interchange of serum from the tissues<span class="pagenum"><a name="Page_243" id="Page_243">[243]</a></span>
which brings the blood volume back to the original amount.
Whatever happens the pressure is not greatly reduced, at
times not reduced at all, but often the symptoms are relieved.
Hot packs or sweat baths assuredly do reduce the
pressure in many cases. This seems to me to be an exceedingly
valuable measure. Finally the diet should be
nourishing, but very light, not too much fluid should be
ingested, and the bowels should be freely opened.</p>
<p>With the fibrolysin of Merck, I have had no experience.
Some men assert that they have had good results from
its use, but on the whole the evidence is not highly favorable.</p>
<p>Morphine is invaluable. No drug is of such value in the
nocturnal dyspneic attacks that occur in the late stages of
arteriosclerosis when the heart or the kidneys are failing.
Morphine not only relaxes spasm and quiets the cerebral
centers, but is an actual heart stimulant under such conditions,
and should never be withheld, as the danger of the
patient's becoming addicted to its use is more fanciful than
real. However, morphine, at times, suppresses the secretion
of urine. So that if after trial the urine becomes
scanty and the edema increases, recourse must be had to
other drugs. The various hypnotics may be used with
caution. One which seems to be very useful is adalin.</p>
<p>As heart stimulants, one may use strychnine, spartein,
caffein, or camphor. In desperate cases, where a rapidly
diffusible stimulant is needed, a hypodermic syringeful of
ether may be given, and repeated in a short while.</p>
<p>Several years ago a so-called serum was brought out by
Trunecek which was said to have a favorable effect on the
metabolism of the vessel walls. It was given at first hypodermatically
or intravenously but the former method was
painful. It was later stated that given by mouth it acted
just as well. The results with the Trunecek serum have not
come up to the expectations that the early favorable reports
promised. The original serum was composed as follows:<span class="pagenum"><a name="Page_244" id="Page_244">[244]</a></span>
NaCl, 4.92 gm.; Na<sub>2</sub>SO<sub>4</sub>, 0.44 gm.; Na<sub>2</sub>CO<sub>3</sub>, 0.21 gm.;
K<sub>2</sub>SO<sub>4</sub>, 0.40 gm.; aqua destil. q. s. ad. 100.0 c.c. Later
this was modified for internal use to the following prescription:</p>
<p>
℞<span style="margin-left: 2em;"> Natrii chlor. 10. gm.</span><br />
<span style="margin-left: 3em;">Natrii sulphat. 1. gm.</span><br />
<span style="margin-left: 3em;">Natrii carbonat. 0.40 gm.</span><br />
<span style="margin-left: 3em;">Natrii phosphat. 0.30 gm.</span><br />
<span style="margin-left: 3em;">Calcii phosphat.</span><br />
<span style="margin-left: 3em;">Magnesii phosphat. aa. 0.75 gm.</span><br />
M. Ft. cachets No. XIII.
</p>
<p>The contents of every cachet corresponds to 15 c.c. of the
fluid serum or to 150 c.c. of blood serum. The preparation
called antisclerosin consists of the salts contained in the
serum. As to its efficacy, I can not judge, as I have never
felt that it was worth while to use it. Reports of cases in
which it has been tried do not speak very highly of it.</p>
<p>In the general treatment of arteriosclerosis, there is no
one factor of more importance than the regular daily bowel
movement. Attention to this may save the patient much
discomfort and even acute attacks of cardiac embarrassment.
The choice of the purgative is immaterial, with this
reservation only, that the mild ones, such as cascara, rhubarb,
licorice powder and the mineral waters, should be
thoroughly tried before we resort to the more drastic purgatives.
Plenolphthalein in 3 to 5 grain doses acts remarkably
well in some people as a pleasant laxative. Agar-agar
with or without cascara may be useful.</p>
<p>Liquid paraffin under a variety of names is a most useful
and efficacious laxative. As its action is purely mechanical
it may be taken indefinitely without doing harm to the intestinal
musculature.</p>
<p>The old Lady Webster dinner pill is an excellent tonic
aperient. When the heart is embarrassed and edema of the
legs and effusion into the serous cavities have taken place,
then it becomes necessary to use the drastic purgatives
that cause a number of watery movements. Epsom salts<span class="pagenum"><a name="Page_245" id="Page_245">[245]</a></span>
given in concentrated form, elaterin gr. 1-12, the compound
cathartic pill, blue mass and scammony, or even croton
oil may be used. Since the observation of a greatly congested
intestine from a patient who had been given croton
oil, I have ceased to use this purgative, and I doubt much
whether its use is ever justifiable in these cases.</p>
<p>The management of the ordinary case of arteriosclerosis
resolves itself into a careful hygienic and dietetic regime
with the addition of the iodides, aconite, or the nitrites.
A diet consisting of very little meat, alcohol in moderation
or even absolutely prohibited, and not too much fluid should
be prescribed. Condiments and spices should also be used
sparingly. Cold baths, shower baths, cold and hot sheets
alternating, are of great benefit in assisting the heart to do
its best work by making the large capillary area of the skin
more permeable. It is not true that such baths raise the
blood pressure so markedly. Certain acts, as sneezing, violent
coughing, etc., increase the blood pressure much more
than judicious bathing.</p>
<h4>Symptomatic Treatment</h4>
<p>The fact that arteriosclerosis really loses much of its own
identity and, in later stages, becomes merged with the symptomatology
of the diseases of various organs, as the kidney,
brain, heart, compels us, for completeness' sake, to say a
few words about the treatment of these complications.</p>
<p>One of the results of arteriosclerosis of the coronary
arteries, angina pectoris, demands prompt treatment. In
the acute attack, the chief object is to relieve the spasm and
pain. Pearls of amyl nitrite should be inhaled, and morphine
sulphate with atropine sulphate given hypodermatically
at the very earliest moment. It is senseless to withhold
morphine. The only possible reason for withholding
it would be uncertainty as to the diagnosis. It is probably
better to err on the safe side, and should the case prove to<span class="pagenum"><a name="Page_246" id="Page_246">[246]</a></span>
be one of pseudo angina, in the next attack sterile water
can be given instead of the morphine and atropine.</p>
<p>When a patient is seen in the condition of broken compensation
with the much dilated heart, anasarca, dyspnea
and suppression of urine, there is no better practice than
venesection. Especially is this valuable when the tension is
still fairly high and the individual is robust. Following the
abstraction of six to eight ounces of blood (300-500 c.c.)<a name="FNanchor_21_21" id="FNanchor_21_21"></a><a href="#Footnote_21_21" class="fnanchor">[21]</a>
the whole picture changes, so that a man who a short while
before was apparently at death's door, notices his surroundings
and takes an interest again in life. This should be followed
up with thorough purgation, and cardiac stimulants
should be ordered. In such cases digitalis is useful, but its
action is never so striking as in cases of this general character
due to uncompensated valvular disease. It must be remembered
that in arteriosclerosis the changes in the myocardium
must be of a considerable grade for the heart to
give away. Therefore, digitalis can not be expected to act
on a diseased muscle as it acts on a comparatively healthy
muscle. It is only in such cases of broken compensation
that digitalis should ever be used.</p>
<p>Digitalis is not a general vasoconstrictor as used to be
taught. Its action on the kidney is actually a vasodilator
one. And in its action on the heart the digitonin dilates
the coronary arteries, according to Macht, while the digitoxin
acts on the heart muscle. Overdosing with digitalis
has produced partial heart block in many cases. It is absolutely
contraindicated in Stokes-Adams syndrome.</p>
<p>There are, however, some cases, especially those with
transudations, when digitalis may be carefully tried even
though high tension be present. It is sometimes of advantage
to combine digitalis with the nitrites although they are
said to be physiologically incompatible.</p>
<p>Still another drug, that is of great value in conditions such
as have been described, is diuretin. This may be given in
capsule or tablets, grs. x. three times daily. There is only<span class="pagenum"><a name="Page_247" id="Page_247">[247]</a></span>
one caution to express in the use of this drug. It should not
be given when the kidneys are the seat of chronic inflammatory
changes; in fact, actual harm may be done by administering
the drug under such conditions.</p>
<p>The same is true even to a greater extent with theocin.
This is a powerful diuretic. If given by mouth it should be
well diluted as it is most irritating to the stomach. It is
best given intravenously in doses of two and a half to
three grains dissolved in five to six cubic centimeters of
distilled water. One must be reasonably sure that the kidneys
are not the subject of chronic disease and are functionally,
therefore, below par. The intravenous dose should
not be given oftener than once in four days.</p>
<p>For the pain in aneurysm, nothing (except, of course,
morphine) is so valuable as iodide of potassium. Patients
who are suffering agony, when put to bed and given KI
grs. x. three times a day, soon lose all the distressing symptoms.
This applies particularly to aneurysms of the arch
of the aorta.</p>
<p>When the sclerosis has affected the cerebral arteries to
such an extent that symptoms result, the case is, as a rule,
exceedingly grave. Not much can be done except to relieve
the headaches and keep down the blood pressure, if this is
high, by means of rest in bed, the iodides, aconite, or the
nitrites. The cases of transient monoplegias or hemiplegias
can be much relieved by careful hygienic measures and judicious
administration of drugs. Much ingenuity is sometimes
required to overcome the idiosyncrasies of patients,
but care and patience will succeed in surmounting all such
difficulties.</p>
<p>The treatment of intermittent claudication is the treatment
of arteriosclerosis in general. Sometimes the circulation
in the affected leg or legs is much helped by daily warm
foot baths. Light massage might be tried and the galvanic
current may be used once or twice daily.</p>
<p><span class="pagenum"><a name="Page_248" id="Page_248">[248]</a></span>There are a few distressing symptoms that occur usually
late in the disease, when complications have already occurred,
which frequently baffle the therapeutic skill of the
physician. The chief of these—insomnia, dyspnea, and
headache—may not be late manifestations, but insomnia and
headache are frequently associated with the moderately
advanced stages of arteriosclerosis. At times all the symptoms
seem to be due to the high tension, the relief of which
causes them to disappear. There are, unfortunately, times
when high tension is not responsible for the headache and
insomnia. Under these circumstances such drugs as trional,
veronal, amylene hydrate, ammonol, etc., may be tried until
one is found which produces sleep. For the headaches,
phenacetin, alone or in combination with caffein and bromide
of sodium, may be tried. Acetanilid, cautiously used,
is at times of value. There have been cases of arteriosclerosis
with low blood pressure, accompanied by severe headaches,
that have been relieved by ergot. Codeine should be
used with care, and morphine only as a very last resource.</p>
<p>Great care must always be exercised in giving drugs that
depress the circulation, for it is easily conceivable that more
harm than good can come from injudicious drugging.</p>
<hr style="width: 65%;" />
<p><span class="pagenum"><a name="Page_249" id="Page_249">[249]</a></span></p>
<h2><a name="CHAPTER_XIV" id="CHAPTER_XIV"></a>CHAPTER XIV.</h2>
<h3>ARTERIOSCLEROSIS IN ITS RELATION TO LIFE
INSURANCE</h3>
<p>The value of the early recognition of cases of arteriosclerosis
and hypertension has been spoken of within, but it
needs to be further emphasized. There is perhaps no class
among physicians to whom is afforded a better opportunity
of seeing early cases than the medical examiners of life
insurance companies.</p>
<p>The relationship between a patient and the physician
whom he consults, and the applicant for life insurance and
the examiner are diametrically opposite. In the former
the patient desires to conceal nothing and the physician is
called upon to diagnose and treat disease. In the latter the
applicant, a presumably healthy person, may have much to
conceal and the examiner is there to pass upon the state of
health. The question is this—"Is the applicant now in
good health?" It becomes then of vital importance for the
examiner to be able to detect among other abnormal conditions
the incipient signs of arteriosclerosis and of hypertension.
Parenthetically it may be stated that arteriosclerosis
and hypertension are not one and the same disease as has
been so frequently insisted upon within; the former may
occur without the latter but the latter can not from its very
nature be present for long without arterial thickening supervening.
It is necessary in discussing the question here
to group the two conditions together in order to prevent
needless repetition.</p>
<p>Such a case as the following is common. A successful
business man of forty-four years was brought to me by an
agent in 1905 for examination. The man was six feet tall,
weighed 218 pounds, had a ruddy color and looked to be the<span class="pagenum"><a name="Page_250" id="Page_250">[250]</a></span>
picture of health. He was not strictly intemperate, he
never became intoxicated, but every day he drank three or
four whiskies and often he had a bottle of wine for dinner
in the evening. When he was examined his pulse was of
good quality and owing to the fleshiness of the wrist it was
difficult to say positively whether the radial artery was
sclerosed or not. In the heart no murmurs were heard, and
it was difficult to be sure that the left ventricle was enlarged.
There was, however, a slight but definite accentuation of the
second sound at the aortic cartilage which might readily
have been overlooked had the patient not been stripped and
a careful examination made with the stethoscope. Upon
taking the blood pressure it was found to be from 170-175
mm. of Hg. The urine specimen examined at the visit was
normal, no casts were found. The applicant was seen at
his home and the blood pressure measured. It was again
the same. He was seen a third time and practically the
same systolic blood pressure was found. Under protests
from all the agency staff the man was declined. Two years
later he died of apoplexy. The man was angry at being
refused. Instead of looking the matter squarely in the face
he thrust aside the idea that there was anything the matter
with him. He had never had one ill day in his life, his forebears
had lived to ripe old age, and he was sure that he knew
more about himself than the examiner.</p>
<p>Had this applicant showed a sense of reasonableness he
should have been grateful to the doctor for calling his attention
to a condition which surely would sooner or later prove
either fatal itself or lead to some fatal lesion. It was
learned that this man had gone directly to his family physician
who laughed at such nonsense as had been told the
(now) patient by the examiner.</p>
<p>Another illustration of a slightly different type of case is
afforded in the following history.</p>
<p>A man of fifty years of age, five feet ten in height and 164
lbs. in weight, was brought for examination. In his youth<span class="pagenum"><a name="Page_251" id="Page_251">[251]</a></span>
there was a history of a mild attack of scarlet fever. He
was almost a total abstainer, rarely taking liquor in any
form. Physically he appeared to be an excellent risk.
However, on examining the heart it was found that there
was slight hypertrophy with an accentuated second aortic
sound at the base, and the blood pressure was 180 mm. of
Hg. Some sclerosis of the radial arteries was found. One
company had refused him on account of albumin in the
urine. There was none in the first specimen which was
passed while in the office. The specific gravity was 1014.
A morning specimen was obtained and contained a trace of
albumin. Several specimens were then examined. Some
contained albumin, some had no albumin content. The man
was declined; no protests from the agent as albumin had
been found. There was something tangible in that. Had
the applicant been refused on account of his high tension,
sclerosis of the radials, and slightly enlarged heart there
would undoubtedly have been protests. And yet an applicant
revealing such a state of the cardiovascular system
without albumin in the urine should unhesitatingly be declined.
Attention has been called to hypertension as an
early, and some think an invariable, sign of chronic nephritis.
My own experience has confirmed me in the belief
that in hypertension the kidneys are often the seat of
chronic interstitial changes. Careful palpation of the radial
and brachial arteries will in every case reveal more
or less thickening.</p>
<p>There is yet another group of cases which the examiner
sees as healthy subjects, namely those cases of sclerosis of
the peripheral arteries without sclerosis of the aorta and
without high tension. In such cases the radials, brachials,
temporals and other superficial arteries are readily palpable,
sometimes even revealing irregularities along the
course of a vessel. Such cases are not subjects for insurance.
The recognition of such a condition is of great importance
to the one who has it and he should be urged to go to<span class="pagenum"><a name="Page_252" id="Page_252">[252]</a></span>
his regular physician for thorough examination. Should the
physician ridicule the idea, as has happened to me more
than once when I was actively engaged in insurance work,
the examiner has done his full duty to the company, the
applicant, and himself.</p>
<p>A life insurance examiner has a difficult position to fill.
He has four people to satisfy; the applicant, the agent, the
medical director and himself. The straight and narrow
path of strict honesty is his only salvation. By being honest
with himself he necessarily gives a square deal to the
other three parties.</p>
<p>No applicant who has palpable arteries or hypertension
can be considered a first class risk. It can not be denied
that men with arteriosclerosis live to an advanced age and
may even outlive those who have apparently normal arteries,
but the average life expectancy at any age for an
arteriosclerotic is less than that for a normal person. The
apparently healthy applicant who learns for the first time
when examined for life insurance that he has the early or
moderately advanced signs of arterial disease, should thank
the agent and examiner for showing him the danger signals
ahead. The sensible man then orders his life so that he
puts as little strain on his heart, arteries, and kidneys as
possible and may add many years to his life.</p>
<p>It is on account of this very insidiousness of onset that I
have elsewhere urged as a prophylactic measure the examination
every six months of all persons over forty years of
age. I am more and more convinced that it is of vital importance
to the health of the public.</p>
<p>As I have remarked, the average man consults his dentist
at least once a year so that no tooth may be so far diseased
that it can not be saved. It is purely a means of preserving
the teeth. Why not do the same with the whole body? Of
what use is it to save the teeth and lose the body? It seems
to me that the great army of life insurance examiners are
in an enviable position in their ability to add years of life<span class="pagenum"><a name="Page_253" id="Page_253">[253]</a></span>
to many men and women. I doubt whether they realize
their importance in the campaign for health. I should urge
life insurance companies not to employ recent graduates
unless they have had at least a year's hospital experience.
For the company as well as for the individuals I believe
that there is a prognostic sense which the examiner should
have and this can only be acquired by experience.</p>
<p>I believe that arteriosclerosis and hypertension are increasing
for the reasons which have been given in another
chapter. There can be no doubt that when these conditions
are recognized long before symptoms would naturally supervene,
men and women would not only live longer but
also die more comfortably and many very likely would be
carried off by some disease having no relationship whatever
to arteriosclerosis. Slight enlargement of the heart downward
and to the left, accentuation of the second aortic
sound at the base, a full pulse, arteries which are palpably
thickened, increased blood pressure are signs to which attention
must be paid.</p>
<p>When the peripheral arteries are palpable they are not
always sclerosed. The radial artery, the one usually palpated,
may lie very close to the bone in a thin person. Under
these conditions the artery can be easily felt. It is
better then to palpate for the brachial as it lies beneath the
inner edge of the biceps muscle. Should this artery be felt
then very probably sclerosis is present. Opinion as to
whether or not sclerosis is present, when it is slight, may
differ. It is difficult at times to say definitely. Should
such be the case the applicant should be most carefully
questioned as to his family and past history, the heart
should be carefully outlined by percussion and the blood
pressure should be taken, both the systolic and diastolic
pressures. The urine should be examined with particular
care. I am aware that the average examination for life insurance
is not made with the care which is bestowed upon a
patient. Yet I see no reason why the same attention to detail<span class="pagenum"><a name="Page_254" id="Page_254">[254]</a></span>
should not be given in one as in the other. The examination
of the great majority of applicants can he made in a
short time, as there is no question of latent chronic disease.
When the exception turns up he should be given a searching
examination and a full report should be sent to the Medical
Director. Only in this way will it be possible to weed out
the undesirable risks.</p>
<p>On the surface it does not seem to require any great diagnostic
acumen to be a life insurance examiner. In the old
days of many of the companies there were no examiners.
The applicant was brought before the president or other
appointed official and he was passed or rejected on his
general appearance. This has changed, and now the medical
department with its scores of examiners in the field is
a well organized department.</p>
<p>It seems to me that the examiner should be an exceedingly
able diagnostician and prognosticator. There is no telling
when he may be called upon to pass judgment on a borderline
case. From personal experience I know how difficult
it is to make a decision in some cases. These suspicious
cases after a careful examination had better be passed by
the examiner and a supplementary report sent to the
medical director containing unbiased details. But no applicant
with readily palpable arteries, even though the
blood pressure be normal, should be considered a first class
insurance risk.</p>
<p>The question of the value of the diastolic pressure reading
in examinations for life insurance is not yet settled to
the satisfaction of all medical directors. Certain medical
directors with clinical experience behind them, lay great
stress on the increased diastolic pressure and consider a
persistent diastolic of 100 mm. really more significant as
an indication of hypertension than a systolic pressure of
160 mm. Other directors pay little or no attention to the
diastolic reading. Should an applicant show a systolic
above the average normal on several successive readings,<span class="pagenum"><a name="Page_255" id="Page_255">[255]</a></span>
he is declined. When one takes into consideration the
psychic effect of knowing that he is being examined for
high blood pressure, it seems unfair to refuse insurance on
such grounds as is constantly done.</p>
<p>Up to the present there are no extensive series of life-expectancy
tables in which hundreds of thousands of cases
are analyzed from the diastolic pressure values. There are
many such tables for the systolic pressures alone. In the
tabulation of such statistics one must not lose sight of the
important fact that the figures are taken by thousands of
men of varying capacity and different degrees of intelligence.
Such studies to be of any real value must be taken
from records made at the home offices by capable men. We
shall await these tables with interest. In the meantime we
must be permitted to have the impression that the diastolic
pressure has been much neglected. This has no doubt been
due to the difficulty of measuring it with any degree of accuracy.
Now with the auscultatory method and the correct
place to read the diastolic pressure the results of blood
pressure estimations should begin to have some value for
statistical data.</p>
<p>Clinically the diastolic is probably more important than
the systolic. Until proof is brought to the contrary we shall
believe that in life insurance examinations it has the same
importance.</p>
<hr style="width: 65%;" />
<p><span class="pagenum"><a name="Page_256" id="Page_256">[256]</a></span></p>
<h2><a name="CHAPTER_XV" id="CHAPTER_XV"></a>CHAPTER XV.</h2>
<h3>PRACTICAL SUGGESTIONS</h3>
<p>The time spent in obtaining a careful history of a case
is time well spent. Often the diagnosis can be made from
the history alone, the physical examination merely adding
confirmation to the data already obtained.</p>
<p>The younger the patient who has arteriosclerosis, the
more probable is it that syphilis is the etiologic factor.
A denial of infection should have little weight if the history
of possible exposure is present. Miscarriages in a woman
should arouse the suspicion of lues in her husband. The
complement-fixation reaction will often clear up an apparently
obscure diagnosis.</p>
<p>There are various ways of examining a patient but there
is only one right way; the examination should be made on
the bare skin. However skillful one may be in the art of
physical diagnosis, he can gather few accurate data by examining
over the clothes even if he use a phonendoscope.</p>
<p>The immoderate eater is laying up for himself a wealth
of trouble at the time when he can least afford to bear it.
The ounce of advice in time is worth more to him than the
pounds of medicine later.</p>
<p>It is a wise maxim never to drive a horse too far. Apply
that to the human being and the rule holds equally well.</p>
<p>There may be no symptoms in a case of advanced arteriosclerosis.
Do not on that account neglect to advise a patient
in whom the disease is accidentally discovered.</p>
<p>Many a man owes a debt of gratitude to the life insurance
examiner. He rarely feels grateful.</p>
<p>When a competent ophthalmologist refers a case to a general
practitioner with the statement that he believes from
the appearance of the fundus of the eye that arteriosclerotic<span class="pagenum"><a name="Page_257" id="Page_257">[257]</a></span>
changes are present over the body, the case should be most
carefully examined. The earliest diagnoses are not infrequently
made by the ophthalmologist.</p>
<p>It is the part of wisdom never to have such a firmly preconceived
idea of the diagnosis that facts observed are
perverted in order to fit into the diagnosis. Let the facts
speak for themselves.</p>
<p>Beware of the snap diagnosis. Even in a case of well-marked
arteriosclerosis when the diagnosis seems to be
written in large letters all over the patient, go through the
routine. Nine times out of ten this may seem needless.
The tenth time it saves your conscience and reputation.
Always consider that you are examining a tenth case.</p>
<p>Gradual loss of weight in a person over fifty years old
should arouse the suspicion of arteriosclerosis.</p>
<p>Do not call the nervous symptoms displayed by a middle-aged
man or woman neurasthenia until you have ruled out
all organic causes, particularly arteriosclerosis.</p>
<p>When palpating the radial artery, always use both hands
according to the method already described. Pay attention
to the superficial or deep situation of the artery.</p>
<p>The examination of one specimen of urine does not give
much information, especially if it should be found to contain
no abnormal elements. Fairly accurate data may be
gathered from the mixed night and morning urine; most
accurate data from the twenty-four hour specimen. To be
of any real value there should be frequent examinations of
the day's excretion.</p>
<p>In measuring the day's output a good rule is as follows:
begin to collect urine after the first morning's micturition
and collect all including the first quantity passed the next
morning. It is best to examine the centrifugated urine for
casts even though no albumin be present. It is useless to
look for casts in an alkaline urine.</p>
<p>Casts are not infrequently found in chemically normal
urine from a middle-aged patient. Other things being normal,<span class="pagenum"><a name="Page_258" id="Page_258">[258]</a></span>
the finding has no significance. The kidneys must be
carefully tested functionally.</p>
<p>Blood pressure readings should always be taken with the
patient in the same posture at every estimation. At the
first examination it is advisable to take readings from both
brachial arteries. Let the patient sit comfortably and relax
all muscles.</p>
<p>Differentiate as soon as possible between the uncompensated
heart caused by valvular disease and that caused
by arteriosclerosis. There is a difference in prognosis.
Both give the same symptoms, and are treated similarly until
compensation returns; thereafter the management of the
two forms is different.</p>
<p>Aortic incompetence that comes on late in life is generally
the result of curling of the free margins of the valves
caused by syphilitic arteriosclerosis. Prognosis is grave
because of the fact that the heart muscle also is the seat of
degenerative changes and compensatory hypertrophy is established
with difficulty.</p>
<p>When laying down a regime for a patient, consider his
disposition, and individualize the treatment. Remember
that exercise is an essential feature of the hygiene of the
patient's life but do not forget to be explicit about the
amount and character of the permissible exercise.</p>
<p>In the prophylaxis of arteriosclerosis, a rational mode of
living is the all-important factor. As a rule, the less meat
one eats, the less is the liability of arterial degeneration as
age advances. The exceptions to this rule are many, and
probably depend upon the character of the "vital rubber"
with which the individual begins life.</p>
<p>The diet in well-marked cases of arteriosclerosis should
be carefully selected with regard to its nutritive and non-irritating
character. Animal proteins should be sparingly
used. Milk should have an important place in the dietary.</p>
<p>No drug relieves the pain of uncomplicated aneurysm as
surely as iodide of potassium.</p>
<p><span class="pagenum"><a name="Page_259" id="Page_259">[259]</a></span>Iodides frequently upset the stomach. Be cautious in the
use of them. The irritable stomach may turn the scales
against your patient.</p>
<p>Use cardiac stimulants with care and judgment. If all
the valuable ammunition is used up at first, the fight will be
lost.</p>
<p>Use digitalis with especial care. Its chief usefulness is
in steadying the decompensated heart, improving the conduction
of impulses, and increasing the tone of the cardiac
muscle. <i>It should never be given to patients with very slow
pulses, the subjects of Stokes-Adams syndrome.</i> Digitalis
has been found to produce partial to complete heart block
when therapeutically administered.</p>
<p>Remember that in the uncompensated heart morphine not
only eases the oppressive dyspnea, but also steadies and
stimulates the heart.</p>
<p>See to it that the patient has a daily movement of the
bowels. In the early stage try the effect of liquid paraffin
or of the mineral waters such as Pluto, or Hunyadi Janos,
or artificial Carlsbad salts (Sprudel salts). These last can
be made as follows: Sodium chloride, ℥I; sodium bicarbonate,
℥II; sodium sulphate, ℥IV. Take two tablespoonsful of
this in a glass of hot water before breakfast. Should these
not succeed, assist the action of the drugs by the use of
enemata. The pill of aloin, strychnine sulphate, and extract
of cascara, with the addition of a small quantity of hyoscyamus,
is a mild tonic purgative. In cases of constipation
with high tension, there is no drug as valuable as calomel or
one of the other mercurials given occasionally.</p>
<p>Never give Epsom salts unless copious watery stools are
desired to deplete effusion into the serous cavities or into
the subcutaneous tissue.</p>
<p>Chronic constipation increases the gravity of the prognosis.</p>
<p>In case of suppression of urine and anasarca, hot air
packs may be of value. The patient may be wrapped in a<span class="pagenum"><a name="Page_260" id="Page_260">[260]</a></span>
hot wet sheet and covered with blankets. I do not believe in
administering pilocarpine to assist the sweating.</p>
<p>Remember to treat the patient and not the disease. The
careful hygienic and dietetic treatment, combined with the
least amount of drugging, is the best and most rational
method of treatment.</p>
<hr style="width: 65%;" />
<p><span class="pagenum"><a name="Page_261" id="Page_261">[261]</a></span></p>
<h2>INDEX</h2>
<div>
A<br />
<br />
Abdominal symptoms, <a href="#Page_201">201</a><br />
<br />
Aconite in treatment, <a href="#Page_242">242</a><br />
<br />
Acquired arteriosclerosis, <a href="#Page_159">159</a><br />
<br />
Adami, effect of syphilis in aorta, <a href="#Page_45">45</a><br />
<br />
Adventitia, <a href="#Page_28">28</a><br />
<br />
Age in arteriosclerosis, <a href="#Page_161">161</a><br />
<br />
Albuminuria, <a href="#Page_221">221</a><br />
<br />
Albutt's classification of arteriosclerosis, <a href="#Page_186">186</a><br />
<br />
Alcohol, <a href="#Page_166">166</a>, <a href="#Page_228">228</a>, <a href="#Page_235">235</a><br />
<br />
Anatomy, <a href="#Page_25">25</a><br />
<br />
Angina abdominalis, <a href="#Page_201">201</a>, <a href="#Page_216">216</a><br />
<span style="margin-left: 1em;">pectoris, <a href="#Page_197">197</a>, <a href="#Page_216">216</a></span><br />
<span style="margin-left: 2em;">pseudo, <a href="#Page_216">216</a></span><br />
<br />
Angiosclerosis, <a href="#Page_26">26</a>, <a href="#Page_64">64</a><br />
<br />
Aorta, <a href="#Page_27">27</a><br />
<span style="margin-left: 1em;">anatomical lesions in, <a href="#Page_33">33</a></span><br />
<span style="margin-left: 1em;">Aschoff on, <a href="#Page_35">35</a></span><br />
<span style="margin-left: 1em;">normal, <a href="#Page_41">41</a></span><br />
<span style="margin-left: 1em;">syphilis in, <a href="#Page_44">44</a></span><br />
<span style="margin-left: 1em;">thoracic, <a href="#Page_29">29</a></span><br />
<span style="margin-left: 1em;">thoracic and abdominal, arteriosclerosis of, <a href="#Page_39">39</a></span><br />
<span style="margin-left: 1em;">velocity of blood in, <a href="#Page_66">66</a></span><br />
<br />
Aortic incompetence, <a href="#Page_61">61</a>, <a href="#Page_258">258</a><br />
<span style="margin-left: 1em;">stenosis, <a href="#Page_60">60</a></span><br />
<br />
Aortitis, acute, <a href="#Page_165">165</a><br />
<br />
Arcus senilis, <a href="#Page_191">191</a><br />
<br />
Arrhythmia, tonal, <a href="#Page_92">92</a>, <a href="#Page_102">102</a><br />
<br />
Arterial pressure, <a href="#Page_85">85</a><br />
<span style="margin-left: 1em;">symptoms, <a href="#Page_189">189</a></span><br />
<br />
Arteries, <a href="#Page_29">29</a><br />
<span style="margin-left: 1em;">examination of, <a href="#Page_172">172</a>, <a href="#Page_177">177</a></span><br />
<span style="margin-left: 1em;">general structure of, <a href="#Page_27">27</a></span><br />
<span style="margin-left: 1em;">large, <a href="#Page_30">30</a></span><br />
<span style="margin-left: 2em;">adventitia of, <a href="#Page_30">30</a></span><br />
<span style="margin-left: 1em;">palpable, <a href="#Page_189">189</a></span><br />
<span style="margin-left: 1em;">pulmonary, arteriosclerosis of, <a href="#Page_63">63</a></span><br />
<br />
Arteriocapillary fibrosis, <a href="#Page_26">26</a><br />
<br />
Arteriosclerotic endocarditis, <a href="#Page_60">60</a>, <a href="#Page_219">219</a><br />
<br />
Artery, coronary, cross-section of, <a href="#Page_36">36</a><br />
<span style="margin-left: 1em;">pulmonary, <a href="#Page_209">209</a></span><br />
<span style="margin-left: 1em;">radial, <a href="#Page_29">29</a></span><br />
<br />
Aschoff on aorta, <a href="#Page_35">35</a><br />
<br />
Atheroma, simple, <a href="#Page_32">32</a><br />
<br />
Atheromatous abscess, <a href="#Page_38">38</a><br />
<br />
Auricular fibrillation, <a href="#Page_133">133</a><br />
<span style="margin-left: 1em;">flutter, <a href="#Page_131">131</a></span><br />
<br />
Auscultation, <a href="#Page_176">176</a><br />
<br />
Auscultatory blood pressure phenomenon, <a href="#Page_90">90</a><br />
<span style="margin-left: 1em;">method of taking blood pressure, <a href="#Page_83">83</a></span><br />
<span style="margin-left: 1em;">percussion, <a href="#Page_175">175</a></span><br />
<br />
<br />
B<br />
<br />
Balneotherapy, <a href="#Page_233">233</a><br />
<br />
Basch's blood pressure instrument, <a href="#Page_70">70</a><br />
<br />
Blood, circulation of, <a href="#Page_65">65</a><br />
<span style="margin-left: 1em;">velocity of, <a href="#Page_65">65</a></span><br />
<span style="margin-left: 2em;">in animals, <a href="#Page_66">66</a></span><br />
<span style="margin-left: 2em;">in aorta, <a href="#Page_66">66</a></span><br />
<span style="margin-left: 2em;">in capillaries, <a href="#Page_66">66</a></span><br />
<span style="margin-left: 1em;">viscosity of, <a href="#Page_68">68</a></span><br />
<br />
Blood pressure, <a href="#Page_68">68</a><br />
<span style="margin-left: 1em;">auscultatory method of taking, <a href="#Page_83">83</a></span><br />
<span style="margin-left: 1em;">clinical applications of, <a href="#Page_147">147</a></span><br />
<span style="margin-left: 1em;">diurnal variations of, <a href="#Page_102">102</a></span><br />
<span style="margin-left: 1em;">drugs influencing, <a href="#Page_120">120</a></span><br />
<span style="margin-left: 1em;">estimation of, <a href="#Page_179">179</a></span><br />
<span style="margin-left: 1em;">in cancer, <a href="#Page_118">118</a></span><br />
<span style="margin-left: 1em;">in collapse, <a href="#Page_118">118</a></span><br />
<span style="margin-left: 1em;">in exercise, <a href="#Page_105">105</a></span><br />
<span style="margin-left: 1em;">in head injuries, <a href="#Page_148">148</a></span><br />
<span style="margin-left: 1em;">in hemorrhages, <a href="#Page_105">105</a>, <a href="#Page_118">118</a>, <a href="#Page_148">148</a></span><br />
<span style="margin-left: 1em;">in infectious diseases, <a href="#Page_153">153</a></span><br />
<span style="margin-left: 1em;">in kidney diseases, <a href="#Page_155">155</a></span><br />
<span style="margin-left: 1em;">in meningitis, <a href="#Page_118">118</a></span><br />
<span style="margin-left: 1em;">in obstetrics, <a href="#Page_152">152</a></span><br />
<span style="margin-left: 1em;">in pulmonary tuberculosis, <a href="#Page_119">119</a></span><br />
<span style="margin-left: 1em;">in shock, <a href="#Page_105">105</a>, <a href="#Page_148">148</a></span><br />
<span style="margin-left: 1em;">in surgery, <a href="#Page_147">147</a></span><br />
<span style="margin-left: 1em;">in typhoid fever, <a href="#Page_118">118</a>, <a href="#Page_154">154</a></span><br />
<span style="margin-left: 1em;">in valvular heart disease, <a href="#Page_155">155</a></span><br />
<span style="margin-left: 1em;">increase of, <a href="#Page_55">55</a></span><br />
<span style="margin-left: 1em;">instruments, <a href="#Page_70">70</a></span><br />
<span style="margin-left: 2em;">Brown's, <a href="#Page_74">74</a></span><br />
<span style="margin-left: 2em;">Cook's, <a href="#Page_71">71</a></span><br />
<span style="margin-left: 2em;">Erlanger's, <a href="#Page_72">72</a></span><br />
<span style="margin-left: 2em;">Faught's, <a href="#Page_75">75</a>, <a href="#Page_80">80</a></span><br />
<span style="margin-left: 2em;">Hill and Barnard's, <a href="#Page_70">70</a></span><br />
<span style="margin-left: 2em;">Hirschfelder's, <a href="#Page_73">73</a></span><br />
<span style="margin-left: 2em;">K. Vierordt's, <a href="#Page_70">70</a></span><br />
<span style="margin-left: 2em;">Marcy's, <a href="#Page_70">70</a></span><br />
<span style="margin-left: 2em;">Potain's, <a href="#Page_70">70</a></span><br />
<span style="margin-left: 2em;">Riva Rocci's, <a href="#Page_70">70</a></span><br />
<span style="margin-left: 2em;">Roger's, <a href="#Page_77">77</a></span><br />
<span class="pagenum"><a name="Page_262" id="Page_262">[262]</a></span><span style="margin-left: 2em;">Sanborn's, <a href="#Page_80">80</a></span><br />
<span style="margin-left: 2em;">Stanton's, <a href="#Page_72">72</a></span><br />
<span style="margin-left: 2em;">technique of, <a href="#Page_80">80</a></span><br />
<span style="margin-left: 2em;">"Tycos," <a href="#Page_77">77</a></span><br />
<span style="margin-left: 2em;">v. Basch's, <a href="#Page_70">70</a></span><br />
<span style="margin-left: 2em;">v. Recklinghausen's, <a href="#Page_76">76</a></span><br />
<span style="margin-left: 1em;">mechanism of, <a href="#Page_55">55</a></span><br />
<span style="margin-left: 1em;">normal variations of, <a href="#Page_88">88</a></span><br />
<span style="margin-left: 1em;">phenomenon, auscultatory, <a href="#Page_90">90</a></span><br />
<span style="margin-left: 1em;">precautions when estimating, <a href="#Page_181">181</a></span><br />
<span style="margin-left: 1em;">value of, <a href="#Page_181">181</a></span><br />
<br />
Bowman's capsules, sclerosis of, <a href="#Page_62">62</a><br />
<br />
Brain, changes in, <a href="#Page_62">62</a><br />
<br />
Brown atrophy, <a href="#Page_60">60</a>, <a href="#Page_118">118</a>, <a href="#Page_201">201</a><br />
<br />
<br />
C<br />
<br />
Calcification of media, <a href="#Page_43">43</a>, <a href="#Page_59">59</a><br />
<br />
Cancer, blood pressure in, <a href="#Page_118">118</a><br />
<br />
Capillaries, anatomy of, <a href="#Page_27">27</a>, <a href="#Page_31">31</a><br />
<br />
Capillary pulse, <a href="#Page_67">67</a><br />
<br />
Cardiac dullness, <a href="#Page_172">172</a><br />
<span style="margin-left: 1em;">irregularities in arteriosclerosis, <a href="#Page_131">131</a></span><br />
<span style="margin-left: 1em;">symptoms, <a href="#Page_195">195</a></span><br />
<br />
Cerebral symptoms, <a href="#Page_203">203</a><br />
<br />
Circulation of blood, <a href="#Page_65">65</a><br />
<span style="margin-left: 1em;">physiology of, <a href="#Page_65">65</a></span><br />
<br />
Cirrhosis of liver, <a href="#Page_64">64</a>, <a href="#Page_216">216</a><br />
<br />
Classification of arteriosclerosis, <a href="#Page_32">32</a>, <a href="#Page_37">37</a><br />
<span style="margin-left: 1em;">Allbutt's, <a href="#Page_186">186</a></span><br />
<br />
Collapse, blood pressure in, <a href="#Page_118">118</a><br />
<br />
Congenital arteriosclerosis, <a href="#Page_157">157</a><br />
<br />
Cook's blood pressure instrument, <a href="#Page_71">71</a><br />
<br />
Cor bovinum, <a href="#Page_116">116</a><br />
<br />
Coronary artery, cross section of, <a href="#Page_36">36</a><br />
<br />
Corpus luteum, <a href="#Page_241">241</a><br />
<br />
<br />
D<br />
<br />
Definition of arteriosclerosis, <a href="#Page_26">26</a><br />
<br />
Diabetes mellitus, <a href="#Page_216">216</a><br />
<br />
Diagnosis, <a href="#Page_210">210</a><br />
<span style="margin-left: 1em;">differential, <a href="#Page_215">215</a></span><br />
<span style="margin-left: 1em;">early, <a href="#Page_210">210</a></span><br />
<span style="margin-left: 1em;">ophthalmic examination in, <a href="#Page_214">214</a></span><br />
<br />
Diastolic pressure, <a href="#Page_69">69</a>, <a href="#Page_83">83</a>, <a href="#Page_85">85</a>, <a href="#Page_94">94</a><br />
<span style="margin-left: 1em;">importance of, <a href="#Page_97">97</a></span><br />
<br />
Dicrotic pulse, <a href="#Page_123">123</a><br />
<br />
Dietetic treatment, <a href="#Page_235">235</a><br />
<br />
Differential diagnosis, <a href="#Page_166">166</a>, <a href="#Page_215">215</a><br />
<br />
Diffuse arteriosclerosis, <a href="#Page_32">32</a>, <a href="#Page_37">37</a>, <a href="#Page_38">38</a>, <a href="#Page_57">57</a><br />
<br />
Digitalis in treatment, <a href="#Page_246">246</a>, <a href="#Page_259">259</a><br />
<br />
Diuretin in treatment, <a href="#Page_246">246</a><br />
<br />
Drug intoxications, <a href="#Page_166">166</a><br />
<br />
Drugs influencing blood pressure, <a href="#Page_105">105</a>, <a href="#Page_120">120</a><br />
<br />
Ductless glands, <a href="#Page_171">171</a><br />
<br />
Dullness, cardiac, <a href="#Page_172">172</a><br />
<br />
Dyspeptic symptoms, <a href="#Page_184">184</a><br />
<br />
Dyspnea, <a href="#Page_184">184</a><br />
<span style="margin-left: 1em;">treatment of, <a href="#Page_248">248</a></span><br />
<br />
<br />
E<br />
<br />
Electrocardiogram, <a href="#Page_126">126</a><br />
<br />
Embolism, <a href="#Page_59">59</a><br />
<br />
Endarteritis deformans, <a href="#Page_47">47</a><br />
<span style="margin-left: 1em;">obliterans, <a href="#Page_46">46</a></span><br />
<br />
Endocarditis, arteriosclerotic, <a href="#Page_60">60</a>, <a href="#Page_219">219</a><br />
<br />
Endothelial lining, <a href="#Page_27">27</a><br />
<span style="margin-left: 1em;">tubes, <a href="#Page_31">31</a></span><br />
<br />
Epistaxis, <a href="#Page_184">184</a>, <a href="#Page_221">221</a><br />
<br />
Erlanger's blood pressure instrument, <a href="#Page_72">72</a><br />
<br />
Erythromelalgia, <a href="#Page_192">192</a>, <a href="#Page_208">208</a><br />
<br />
Estimation of blood pressure, <a href="#Page_179">179</a><br />
<br />
Etiology, <a href="#Page_157">157</a><br />
<br />
Examination of arteries, <a href="#Page_172">172</a>, <a href="#Page_177">177</a><br />
<span style="margin-left: 1em;">of heart, <a href="#Page_172">172</a></span><br />
<span style="margin-left: 1em;">of urine, <a href="#Page_257">257</a></span><br />
<br />
Exercise, blood pressure in, <a href="#Page_105">105</a><br />
<span style="margin-left: 1em;">in prophylaxis, <a href="#Page_225">225</a></span><br />
<span style="margin-left: 1em;">in treatment, <a href="#Page_230">230</a></span><br />
<br />
Experimental arteriosclerosis, <a href="#Page_50">50</a><br />
<br />
Extrasystole, <a href="#Page_138">138</a><br />
<br />
<br />
F<br />
<br />
Faught's blood pressure instrument, <a href="#Page_75">75</a>, <a href="#Page_80">80</a><br />
<br />
Fibrillation, auricular, <a href="#Page_133">133</a><br />
<span style="margin-left: 1em;">ventricular, <a href="#Page_138">138</a></span><br />
<br />
Fibrolysin in treatment, <a href="#Page_243">243</a><br />
<br />
Fingernail palpation, <a href="#Page_178">178</a><br />
<br />
Finger tip palpation, <a href="#Page_179">179</a><br />
<br />
Flutter, auricular, <a href="#Page_131">131</a><br />
<br />
Food poisons in arteriosclerosis, <a href="#Page_163">163</a><br />
<br />
<br />
G<br />
<br />
Gibson's law, <a href="#Page_154">154</a><br />
<br />
<br />
H<br />
<br />
"H" wave, <a href="#Page_126">126</a><br />
<br />
Habits, personal, <a href="#Page_234">234</a><br />
<br />
Head injuries, blood pressure in, <a href="#Page_148">148</a><br />
<br />
Headache, <a href="#Page_184">184</a><br />
<span style="margin-left: 1em;">treatment of, <a href="#Page_248">248</a></span><br />
<br />
Heart block, <a href="#Page_140">140</a><br />
<span style="margin-left: 1em;">boundaries, <a href="#Page_172">172</a></span><br />
<span style="margin-left: 1em;">examination of, <a href="#Page_172">172</a></span><br />
<span style="margin-left: 1em;">hypertrophy of, <a href="#Page_60">60</a></span><br />
<span style="margin-left: 1em;">physical examination of, <a href="#Page_172">172</a></span><br />
<span style="margin-left: 1em;">stimulants, <a href="#Page_243">243</a>, <a href="#Page_246">246</a>, <a href="#Page_259">259</a></span><br />
<span style="margin-left: 1em;">symptoms, <a href="#Page_188">188</a></span><br />
<span class="pagenum"><a name="Page_263" id="Page_263">[263]</a></span><br />
Hemorrhages, blood pressure in, <a href="#Page_118">118</a><br />
<br />
Henle, membrane of, <a href="#Page_29">29</a><br />
<br />
Hill and Barnard's blood pressure instrument, <a href="#Page_70">70</a><br />
<br />
Hirschfelder's blood pressure instrument, <a href="#Page_73">73</a><br />
<br />
His, bundle of, <a href="#Page_141">141</a>, <a href="#Page_197">197</a><br />
<br />
Hygienic treatment, <a href="#Page_230">230</a><br />
<br />
Hyperpietic arteriosclerosis, <a href="#Page_186">186</a><br />
<br />
Hypertension, <a href="#Page_60">60</a>, <a href="#Page_106">106</a>, <a href="#Page_169">169</a>, <a href="#Page_185">185</a>, <a href="#Page_249">249</a><br />
<span style="margin-left: 1em;">cause of arteriosclerosis, <a href="#Page_159">159</a></span><br />
<span style="margin-left: 1em;">classification of cases, <a href="#Page_112">112</a></span><br />
<br />
Hypertrophy of left ventricle, <a href="#Page_58">58</a><br />
<br />
Hypotension, <a href="#Page_117">117</a><br />
<br />
<br />
I<br />
<br />
Incompetence, aortic, <a href="#Page_61">61</a>, <a href="#Page_258">258</a><br />
<br />
Indicanuria, <a href="#Page_167">167</a><br />
<br />
Infants, arteriosclerosis in, <a href="#Page_158">158</a><br />
<br />
Infectious diseases in arteriosclerosis, <a href="#Page_163">163</a><br />
<span style="margin-left: 1em;">blood pressure in, <a href="#Page_153">153</a></span><br />
<br />
Insomnia, treatment of, <a href="#Page_248">248</a><br />
<br />
Intermittent claudication, <a href="#Page_192">192</a>, <a href="#Page_208">208</a><br />
<span style="margin-left: 1em;">treatment of, <a href="#Page_247">247</a></span><br />
<br />
Intoxications, chronic drug, <a href="#Page_166">166</a><br />
<br />
Intracranial tension, <a href="#Page_105">105</a><br />
<br />
Involutionary arteriosclerosis, <a href="#Page_187">187</a><br />
<br />
Iodides in treatment, <a href="#Page_238">238</a>, <a href="#Page_247">247</a>, <a href="#Page_259">259</a><br />
<br />
<br />
K<br />
<br />
Kidney diseases, blood pressure in, <a href="#Page_155">155</a><br />
<br />
Kidneys, sclerosis of, <a href="#Page_61">61</a>, <a href="#Page_170">170</a><br />
<br />
<br />
L<br />
<br />
Life insurance, relation to, <a href="#Page_249">249</a><br />
<br />
Light percussion, <a href="#Page_174">174</a><br />
<span style="margin-left: 1em;">touch palpation, <a href="#Page_175">175</a></span><br />
<br />
Liver, cirrhosis, <a href="#Page_64">64</a>, <a href="#Page_216">216</a><br />
<br />
Local symptoms, <a href="#Page_207">207</a><br />
<br />
<br />
M<br />
<br />
Marey's blood pressure instrument, <a href="#Page_70">70</a><br />
<br />
Maximum pressure, <a href="#Page_85">85</a>, <a href="#Page_94">94</a><br />
<br />
Mean pressure, <a href="#Page_85">85</a><br />
<br />
Media, calcification of, <a href="#Page_43">43</a>, <a href="#Page_59">59</a><br />
<br />
Medicinal treatment, <a href="#Page_238">238</a><br />
<br />
Meningitis, blood pressure in, <a href="#Page_118">118</a><br />
<br />
Mental strain, <a href="#Page_168">168</a><br />
<br />
Mesaortitis, <a href="#Page_45">45</a>, <a href="#Page_47">47</a>, <a href="#Page_49">49</a>, <a href="#Page_165">165</a><br />
<br />
Mesentery, cross-section of small artery in, <a href="#Page_56">56</a><br />
<br />
Milk diet, <a href="#Page_237">237</a><br />
<br />
Minimum pressure, <a href="#Page_86">86</a>, <a href="#Page_94">94</a><br />
<br />
Moenckeberg type of arteriosclerosis, <a href="#Page_43">43</a><br />
<br />
Morphine in treatment, <a href="#Page_243">243</a><br />
<br />
Mosenthal test meal, <a href="#Page_221">221</a><br />
<br />
Muscular overwork, <a href="#Page_169">169</a><br />
<br />
<br />
N<br />
<br />
Nervous symptoms, <a href="#Page_191">191</a><br />
<br />
Nitrites in treatment, <a href="#Page_240">240</a><br />
<br />
Nitroglycerin in treatment, <a href="#Page_241">241</a><br />
<br />
Nodular arteriosclerosis, <a href="#Page_32">32</a>, <a href="#Page_37">37</a><br />
<br />
Normal blood pressure variation, <a href="#Page_88">88</a><br />
<br />
<br />
O<br />
<br />
Obstetrics, blood pressure in, <a href="#Page_152">152</a><br />
<br />
Occupation in arteriosclerosis, <a href="#Page_162">162</a><br />
<br />
Ocular symptoms, <a href="#Page_190">190</a><br />
<br />
Ophthalmic examination, importance in early diagnosis, <a href="#Page_214">214</a>, <a href="#Page_256">256</a><br />
<br />
Orthodiagraph, <a href="#Page_173">173</a><br />
<br />
Overeating, <a href="#Page_167">167</a>, <a href="#Page_212">212</a>, <a href="#Page_225">225</a>, <a href="#Page_235">235</a><br />
<br />
Overwork, muscular, <a href="#Page_169">169</a><br />
<br />
<br />
P<br />
<br />
"P" wave, <a href="#Page_129">129</a><br />
<br />
"P-R" interval, <a href="#Page_130">130</a><br />
<br />
Palpable arteries, <a href="#Page_189">189</a><br />
<br />
Palpation, <a href="#Page_174">174</a>, <a href="#Page_180">180</a><br />
<span style="margin-left: 1em;">fingernail, <a href="#Page_178">178</a></span><br />
<span style="margin-left: 1em;">finger tip, <a href="#Page_179">179</a></span><br />
<span style="margin-left: 1em;">light touch, <a href="#Page_175">175</a></span><br />
<br />
Pathology, <a href="#Page_32">32</a><br />
<br />
Percussion, <a href="#Page_174">174</a><br />
<span style="margin-left: 1em;">auscultatory, <a href="#Page_175">175</a></span><br />
<span style="margin-left: 1em;">light, <a href="#Page_174">174</a></span><br />
<br />
Peripheral symptoms, <a href="#Page_207">207</a><br />
<br />
Personal habits, <a href="#Page_234">234</a><br />
<br />
Phlebosclerosis, <a href="#Page_64">64</a><br />
<br />
Phthalein test, <a href="#Page_221">221</a><br />
<br />
Physical signs, <a href="#Page_183">183</a><br />
<br />
Physiology of the circulation, <a href="#Page_65">65</a><br />
<br />
Potain's blood pressure instrument, <a href="#Page_70">70</a><br />
<br />
Practical suggestions, <a href="#Page_256">256</a><br />
<br />
Pressure, arterial, <a href="#Page_85">85</a><br />
<span style="margin-left: 1em;">ausculatory method of determining, <a href="#Page_83">83</a></span><br />
<span style="margin-left: 1em;">diastolic, <a href="#Page_83">83</a>, <a href="#Page_94">94</a></span><br />
<span style="margin-left: 1em;">estimation of, <a href="#Page_179">179</a></span><br />
<span style="margin-left: 1em;">in surgery, <a href="#Page_147">147</a></span><br />
<span style="margin-left: 1em;">maximum, <a href="#Page_85">85</a>, <a href="#Page_94">94</a></span><br />
<span style="margin-left: 1em;">normal variations, <a href="#Page_88">88</a></span><br />
<span style="margin-left: 1em;">pulse, <a href="#Page_83">83</a>, <a href="#Page_85">85</a>, <a href="#Page_87">87</a>, <a href="#Page_100">100</a></span><br />
<span style="margin-left: 1em;">systolic, <a href="#Page_82">82</a>, <a href="#Page_85">85</a></span><br />
<span style="margin-left: 1em;">technique, <a href="#Page_80">80</a></span><br />
<span style="margin-left: 1em;">venous, <a href="#Page_120">120</a></span><br />
<span class="pagenum"><a name="Page_264" id="Page_264">[264]</a></span><br />
Prognosis, <a href="#Page_218">218</a><br />
<br />
Prophylaxis, <a href="#Page_224">224</a><br />
<span style="margin-left: 1em;">exercise in, <a href="#Page_225">225</a></span><br />
<br />
Pseudo angina pectoris, <a href="#Page_216">216</a><br />
<br />
Pulmonary artery, <a href="#Page_209">209</a><br />
<span style="margin-left: 1em;">arteriosclerosis of, <a href="#Page_63">63</a></span><br />
<span style="margin-left: 1em;">tuberculosis, blood pressure in, <a href="#Page_119">119</a></span><br />
<br />
Pulse, <a href="#Page_123">123</a><br />
<span style="margin-left: 1em;">capillary, <a href="#Page_67">67</a></span><br />
<span style="margin-left: 1em;">deficit, <a href="#Page_135">135</a></span><br />
<span style="margin-left: 1em;">dicrotic, <a href="#Page_123">123</a></span><br />
<span style="margin-left: 1em;">in arteriosclerosis, <a href="#Page_123">123</a></span><br />
<span style="margin-left: 1em;">pressure, <a href="#Page_69">69</a>, <a href="#Page_83">83</a>, <a href="#Page_85">85</a>, <a href="#Page_87">87</a>, <a href="#Page_100">100</a></span><br />
<span style="margin-left: 1em;">rate, <a href="#Page_69">69</a></span><br />
<span style="margin-left: 1em;">venous, <a href="#Page_123">123</a></span><br />
<br />
Purgatives in treatment, <a href="#Page_244">244</a>, <a href="#Page_259">259</a><br />
<br />
Pyrosis, <a href="#Page_184">184</a><br />
<br />
<br />
Q<br />
<br />
"Q R S" complex, <a href="#Page_129">129</a><br />
<br />
<br />
R<br />
<br />
Rabbits, lesions produced experimentally in, <a href="#Page_50">50</a><br />
<br />
Race in arteriosclerosis, <a href="#Page_161">161</a><br />
<br />
Radial artery, <a href="#Page_29">29</a><br />
<br />
Radials, sclerosis of, <a href="#Page_43">43</a><br />
<br />
Raynaud's disease, <a href="#Page_192">192</a>, <a href="#Page_207">207</a><br />
<br />
Recklinghausen's blood pressure instrument, <a href="#Page_76">76</a><br />
<br />
Renal disease, <a href="#Page_169">169</a><br />
<span style="margin-left: 1em;">symptoms, <a href="#Page_199">199</a></span><br />
<br />
Rest in treatment, <a href="#Page_242">242</a><br />
<br />
Riva-Rocci's blood pressure instrument, <a href="#Page_70">70</a><br />
<br />
Rogers' blood pressure instrument, <a href="#Page_77">77</a><br />
<br />
<br />
S<br />
<br />
Sanborn's blood pressure instrument, <a href="#Page_80">80</a><br />
<br />
Scaphoid scapula, <a href="#Page_158">158</a><br />
<br />
Schwellungsperkussion, <a href="#Page_174">174</a><br />
<br />
Sclerosis of veins, <a href="#Page_64">64</a><br />
<br />
Senile arteriosclerosis, <a href="#Page_32">32</a>, <a href="#Page_37">37</a>, <a href="#Page_43">43</a>, <a href="#Page_59">59</a><br />
<br />
Sex in arteriosclerosis, <a href="#Page_161">161</a><br />
<br />
Shock, blood pressure in, <a href="#Page_105">105</a>, <a href="#Page_148">148</a><br />
<br />
Spinal symptoms, <a href="#Page_205">205</a><br />
<br />
Spirochaeta pallida, <a href="#Page_45">45</a><br />
<br />
Stanton's blood pressure instrument, <a href="#Page_72">72</a><br />
<br />
Stenosis, aortic, <a href="#Page_60">60</a><br />
<br />
Stokes-Adams syndrome, <a href="#Page_197">197</a><br />
<br />
Stomach, ulcer of, <a href="#Page_216">216</a><br />
<br />
Strain hypertrophy, <a href="#Page_47">47</a>, <a href="#Page_54">54</a>, <a href="#Page_55">55</a><br />
<br />
Surgery, blood pressure in, <a href="#Page_147">147</a><br />
<br />
Symptomatic treatment, <a href="#Page_245">245</a><br />
<br />
Symptoms, <a href="#Page_183">183</a><br />
<span style="margin-left: 1em;">abdominal, <a href="#Page_201">201</a></span><br />
<span style="margin-left: 1em;">arterial, <a href="#Page_189">189</a></span><br />
<span style="margin-left: 1em;">cardiac, <a href="#Page_195">195</a></span><br />
<span style="margin-left: 1em;">cerebral, <a href="#Page_203">203</a></span><br />
<span style="margin-left: 1em;">dyspeptic, <a href="#Page_184">184</a></span><br />
<span style="margin-left: 1em;">dyspnea, <a href="#Page_184">184</a></span><br />
<span style="margin-left: 1em;">general, <a href="#Page_183">183</a></span><br />
<span style="margin-left: 1em;">headache, <a href="#Page_184">184</a></span><br />
<span style="margin-left: 1em;">heart, <a href="#Page_188">188</a></span><br />
<span style="margin-left: 1em;">local, <a href="#Page_207">207</a></span><br />
<span style="margin-left: 1em;">nervous, <a href="#Page_191">191</a></span><br />
<span style="margin-left: 1em;">ocular, <a href="#Page_190">190</a></span><br />
<span style="margin-left: 1em;">peripheral, <a href="#Page_207">207</a></span><br />
<span style="margin-left: 1em;">pyrosis, <a href="#Page_184">184</a></span><br />
<span style="margin-left: 1em;">renal, <a href="#Page_199">199</a></span><br />
<span style="margin-left: 1em;">special, <a href="#Page_194">194</a></span><br />
<span style="margin-left: 1em;">spinal, <a href="#Page_205">205</a></span><br />
<span style="margin-left: 1em;">vertigo, <a href="#Page_184">184</a></span><br />
<span style="margin-left: 1em;">visceral, <a href="#Page_201">201</a></span><br />
<br />
Syphilis, <a href="#Page_165">165</a><br />
<span style="margin-left: 1em;">in aorta, <a href="#Page_44">44</a></span><br />
<br />
Syphilitic arteriosclerosis, <a href="#Page_37">37</a><br />
<br />
Systolic pressure, <a href="#Page_69">69</a>, <a href="#Page_82">82</a>, <a href="#Page_85">85</a>, <a href="#Page_94">94</a><br />
<span style="margin-left: 1em;">importance of, <a href="#Page_97">97</a></span><br />
<br />
<br />
T<br />
<br />
"T" wave, <a href="#Page_130">130</a><br />
<br />
Technique of blood pressure instruments, <a href="#Page_80">80</a><br />
<br />
Thayer and Fabyan, <a href="#Page_34">34</a><br />
<br />
Theocin, <a href="#Page_247">247</a><br />
<br />
Thoma on arteriosclerosis, <a href="#Page_33">33</a><br />
<br />
Thoracic aorta, <a href="#Page_29">29</a><br />
<br />
Thyroid extract in treatment, <a href="#Page_239">239</a><br />
<br />
Tobacco, <a href="#Page_167">167</a>, <a href="#Page_212">212</a>, <a href="#Page_234">234</a><br />
<br />
Tonal arrhythmia, <a href="#Page_92">92</a>, <a href="#Page_102">102</a><br />
<br />
Toxic arteriosclerosis, <a href="#Page_186">186</a><br />
<br />
Treatment, <a href="#Page_229">229</a><br />
<span style="margin-left: 1em;">aconite in, <a href="#Page_242">242</a></span><br />
<span style="margin-left: 1em;">balneotherapy in, <a href="#Page_233">233</a></span><br />
<span style="margin-left: 1em;">corpus luteum, <a href="#Page_241">241</a></span><br />
<span style="margin-left: 1em;">dietetic, <a href="#Page_235">235</a></span><br />
<span style="margin-left: 1em;">digitalis in, <a href="#Page_246">246</a>, <a href="#Page_259">259</a></span><br />
<span style="margin-left: 1em;">diuretin in, <a href="#Page_246">246</a></span><br />
<span style="margin-left: 1em;">exercise in, <a href="#Page_230">230</a></span><br />
<span style="margin-left: 1em;">fibrolysin in, <a href="#Page_243">243</a></span><br />
<span style="margin-left: 1em;">heart stimulants in, <a href="#Page_243">243</a></span><br />
<span style="margin-left: 1em;">hygienic, <a href="#Page_230">230</a></span><br />
<span style="margin-left: 1em;">iodides in, <a href="#Page_238">238</a>, <a href="#Page_247">247</a>, <a href="#Page_259">259</a></span><br />
<span style="margin-left: 1em;">medicinal, <a href="#Page_238">238</a></span><br />
<span style="margin-left: 1em;">morphine in, <a href="#Page_243">243</a></span><br />
<span style="margin-left: 1em;">nitrites in, <a href="#Page_240">240</a></span><br />
<span style="margin-left: 1em;">nitroglycerin in, <a href="#Page_241">241</a></span><br />
<span style="margin-left: 1em;">of dyspnea, <a href="#Page_248">248</a></span><br />
<span class="pagenum"><a name="Page_265" id="Page_265">[265]</a></span><span style="margin-left: 1em;">of headache, <a href="#Page_248">248</a></span><br />
<span style="margin-left: 1em;">of insomnia, <a href="#Page_248">248</a></span><br />
<span style="margin-left: 1em;">of intermittent claudication, <a href="#Page_247">247</a></span><br />
<span style="margin-left: 1em;">personal habits in, <a href="#Page_234">234</a></span><br />
<span style="margin-left: 1em;">purgatives in, <a href="#Page_244">244</a>, <a href="#Page_259">259</a></span><br />
<span style="margin-left: 1em;">rest in, <a href="#Page_242">242</a></span><br />
<span style="margin-left: 1em;">symptomatic, <a href="#Page_245">245</a></span><br />
<span style="margin-left: 1em;">theocin in, <a href="#Page_247">247</a></span><br />
<span style="margin-left: 1em;">thyroid extract in, <a href="#Page_239">239</a></span><br />
<span style="margin-left: 1em;">Trunecek's serum in, <a href="#Page_243">243</a></span><br />
<span style="margin-left: 1em;">venesection in, <a href="#Page_242">242</a></span><br />
<span style="margin-left: 1em;">veratrum viride in, <a href="#Page_242">242</a></span><br />
<br />
Trunecek's serum in treatment, <a href="#Page_243">243</a><br />
<br />
Tuberculosis, blood pressure in, <a href="#Page_119">119</a><br />
<br />
Tunica intima, <a href="#Page_28">28</a><br />
<span style="margin-left: 1em;">media, <a href="#Page_28">28</a></span><br />
<br />
"Tycos" blood pressure instrument, <a href="#Page_77">77</a><br />
<br />
Typhoid fever as cause of arteriosclerosis, <a href="#Page_164">164</a><br />
<span style="margin-left: 1em;">blood pressure in, <a href="#Page_118">118</a></span><br />
<br />
<br />
U<br />
<br />
Ulcer of stomach, <a href="#Page_216">216</a><br />
<br />
Urine, examination of, <a href="#Page_257">257</a><br />
<span style="margin-left: 1em;">suppression of, <a href="#Page_259">259</a></span><br />
<br />
<br />
V<br />
<br />
Valvular heart disease, blood pressure in, <a href="#Page_155">155</a><br />
<br />
Vasa vasorum, <a href="#Page_29">29</a><br />
<br />
Veins, anatomy of, <a href="#Page_30">30</a><br />
<span style="margin-left: 1em;">sclerosis of, <a href="#Page_64">64</a></span><br />
<br />
Velocity of blood in animals, <a href="#Page_66">66</a><br />
<span style="margin-left: 1em;">of blood in aorta, <a href="#Page_66">66</a></span><br />
<br />
Venesection in treatment, <a href="#Page_242">242</a><br />
<br />
Venous pressure, <a href="#Page_120">120</a><br />
<span style="margin-left: 1em;">pulse, <a href="#Page_123">123</a></span><br />
<br />
Ventricle, left, hypertrophy of, <a href="#Page_58">58</a><br />
<br />
Ventricular fibrillation, <a href="#Page_138">138</a><br />
<br />
Veratrum viride in treatment, <a href="#Page_242">242</a><br />
<br />
Vertigo, <a href="#Page_184">184</a><br />
</div>
<h3>FOOTNOTES:</h3>
<div class="footnote"><p><a name="Footnote_1_1" id="Footnote_1_1"></a><a href="#FNanchor_1_1"><span class="label">[1]</span></a> Longcope and McClintock, however, conclude that permanent constriction of the
superior mesenteric artery and celiac axis, as well as gradual occlusion of one or both
of these vessels, may be present in dogs for at least five months without giving rise to
definite and constant elevation of blood pressure or to hypertrophy of the heart. Further,
they have been unable to find at autopsy on man a definite association between sclerosis
of the abdominal aorta and great splanchnic vessels and cardiac hypertrophy.</p></div>
<div class="footnote"><p><a name="Footnote_2_2" id="Footnote_2_2"></a><a href="#FNanchor_2_2"><span class="label">[2]</span></a> Warthin, A. S.: Am. Jour. Syph., 1918, i, 693.</p></div>
<div class="footnote"><p><a name="Footnote_3_3" id="Footnote_3_3"></a><a href="#FNanchor_3_3"><span class="label">[3]</span></a> A firm makes a stethoscope so that the bell is clamped on the arm leaving both the
operator's hands free.</p></div>
<div class="footnote"><p><a name="Footnote_4_4" id="Footnote_4_4"></a><a href="#FNanchor_4_4"><span class="label">[4]</span></a> Weyse, A. W., and Lutz, B. R.: Diurnal Variations in Arterial Blood Pressure,
Am. Jour. Physiol., 1915, xxxvii, 330.</p></div>
<div class="footnote"><p><a name="Footnote_5_5" id="Footnote_5_5"></a><a href="#FNanchor_5_5"><span class="label">[5]</span></a> Erlanger and Hooker: An Experimental Study of Blood Pressure and of Pulse
Pressure in Man, Johns Hopkins Hosp. Rep., 1904, xii, 145.</p></div>
<div class="footnote"><p><a name="Footnote_6_6" id="Footnote_6_6"></a><a href="#FNanchor_6_6"><span class="label">[6]</span></a> Dawson and Gorham: The Pulse Pressure as an Index of Systolic Output, Jour.
Exper. Med., 1908, x, 484.</p></div>
<div class="footnote"><p><a name="Footnote_7_7" id="Footnote_7_7"></a><a href="#FNanchor_7_7"><span class="label">[7]</span></a> Isolation of a New Vasoconstrictor Substance from the Blood and the Adrenal Cortex,
Jour. Am. Med. Assn., 1913, lxi, 2136.</p></div>
<div class="footnote"><p><a name="Footnote_8_8" id="Footnote_8_8"></a><a href="#FNanchor_8_8"><span class="label">[8]</span></a> Stone, W. J.: The Differentiation of Cerebral and Cardiac Types of Hyperarterial
Tension in Vascular Diseases, Arch. Int. Med., November, 1915, p. 775.</p></div>
<div class="footnote"><p><a name="Footnote_9_9" id="Footnote_9_9"></a><a href="#FNanchor_9_9"><span class="label">[9]</span></a> Smith, W. H., and Kilgore, A. R.: Dilatation of the Arch of the Aorta in Chronic
Nephritis with Hypertension, Am. Jour. Med. Sc., 1915, cxlix, 503.</p></div>
<div class="footnote"><p><a name="Footnote_10_10" id="Footnote_10_10"></a><a href="#FNanchor_10_10"><span class="label">[10]</span></a> McCrae, Thomas: Dilatation of the Arch of the Aorta, Am. Jour. Med. Sc., 1910,
cxl, 469.</p></div>
<div class="footnote"><p><a name="Footnote_11_11" id="Footnote_11_11"></a><a href="#FNanchor_11_11"><span class="label">[11]</span></a> Stone, W. J.: Arch. Int. Med., 1915, xvl, 775.</p></div>
<div class="footnote"><p><a name="Footnote_12_12" id="Footnote_12_12"></a><a href="#FNanchor_12_12"><span class="label">[12]</span></a> Robinson, G. C., and Bredeck, J. F.: Arch. Int. Med., 1917, xx, 725.</p></div>
<div class="footnote"><p><a name="Footnote_13_13" id="Footnote_13_13"></a><a href="#FNanchor_13_13"><span class="label">[13]</span></a> Jour. Exper. Med., 1911, xiv, 217.</p></div>
<div class="footnote"><p><a name="Footnote_14_14" id="Footnote_14_14"></a><a href="#FNanchor_14_14"><span class="label">[14]</span></a> Warfield, L. M.: Jour. Lab. and Clin. Med., November, 1917.</p></div>
<div class="footnote"><p><a name="Footnote_15_15" id="Footnote_15_15"></a><a href="#FNanchor_15_15"><span class="label">[15]</span></a> From πιεσω to squeeze, oppress or distress. Hyperpiesis, therefore, signifies excessive
pressure.</p></div>
<div class="footnote"><p><a name="Footnote_16_16" id="Footnote_16_16"></a><a href="#FNanchor_16_16"><span class="label">[16]</span></a> I have found the small colorimeter made by Hynson, Westcott and Dunning,
Baltimore, Mo., costing $5.00, a very practical instrument.</p></div>
<div class="footnote"><p><a name="Footnote_17_17" id="Footnote_17_17"></a><a href="#FNanchor_17_17"><span class="label">[17]</span></a> Mosenthal, H. O.: Arch. Int. Med., 1915, xvi, 733.</p></div>
<div class="footnote"><p><a name="Footnote_18_18" id="Footnote_18_18"></a><a href="#FNanchor_18_18"><span class="label">[18]</span></a> Myers and Lough: Arch. Int. Med., 1915, xvi, 536.</p></div>
<div class="footnote"><p><a name="Footnote_19_19" id="Footnote_19_19"></a><a href="#FNanchor_19_19"><span class="label">[19]</span></a> Discussion of alcohol at present has value only as it relates to the past. The present
is dry. The future is in the lap of the gods.</p></div>
<div class="footnote"><p><a name="Footnote_20_20" id="Footnote_20_20"></a><a href="#FNanchor_20_20"><span class="label">[20]</span></a> Miller, Jos. L.: Hypertension and the Value of the Various Methods for Its Reduction.
Jour. Am. Med. Assn., 1910, liv, p. 1666.</p></div>
<div class="footnote"><p><a name="Footnote_21_21" id="Footnote_21_21"></a><a href="#FNanchor_21_21"><span class="label">[21]</span></a> I have taken as much as 1700 c.c. from a large man. He recovered and went back
to work.</p></div>
<hr style="width: 65%;" />
<div class='tn'><h3>Transcriber's Notes:</h3>
<p>Irregular hyphenation has been preserved, as in
blood pressure and blood-pressure. Both "Hg" and "Hg." appear.</p>
<p>Minor typographical errors and inconsistencies have been silently
normalized.</p>
<p>The original printed list of illustrations shows the original locations; they have been moved
closer to their discussion area in the text to not interrupt the flow of reading.
</p>
</div>
<pre>
End of the Project Gutenberg EBook of Arteriosclerosis and Hypertension:, by
Louis Marshall Warfield
*** END OF THIS PROJECT GUTENBERG EBOOK ARTERIOSCLEROSIS AND HYPERTENSION: ***
***** This file should be named 37675-h.htm or 37675-h.zip *****
This and all associated files of various formats will be found in:
http://www.gutenberg.org/3/7/6/7/37675/
Produced by Bryan Ness, Julia Neufeld and the Online
Distributed Proofreading Team at http://www.pgdp.net (This
file was produced from images generously made available
by The Internet Archive/American Libraries.)
Updated editions will replace the previous one--the old editions
will be renamed.
Creating the works from public domain print editions means that no
one owns a United States copyright in these works, so the Foundation
(and you!) can copy and distribute it in the United States without
permission and without paying copyright royalties. Special rules,
set forth in the General Terms of Use part of this license, apply to
copying and distributing Project Gutenberg-tm electronic works to
protect the PROJECT GUTENBERG-tm concept and trademark. Project
Gutenberg is a registered trademark, and may not be used if you
charge for the eBooks, unless you receive specific permission. If you
do not charge anything for copies of this eBook, complying with the
rules is very easy. You may use this eBook for nearly any purpose
such as creation of derivative works, reports, performances and
research. They may be modified and printed and given away--you may do
practically ANYTHING with public domain eBooks. Redistribution is
subject to the trademark license, especially commercial
redistribution.
*** START: FULL LICENSE ***
THE FULL PROJECT GUTENBERG LICENSE
PLEASE READ THIS BEFORE YOU DISTRIBUTE OR USE THIS WORK
To protect the Project Gutenberg-tm mission of promoting the free
distribution of electronic works, by using or distributing this work
(or any other work associated in any way with the phrase "Project
Gutenberg"), you agree to comply with all the terms of the Full Project
Gutenberg-tm License (available with this file or online at
http://gutenberg.org/license).
Section 1. General Terms of Use and Redistributing Project Gutenberg-tm
electronic works
1.A. By reading or using any part of this Project Gutenberg-tm
electronic work, you indicate that you have read, understand, agree to
and accept all the terms of this license and intellectual property
(trademark/copyright) agreement. If you do not agree to abide by all
the terms of this agreement, you must cease using and return or destroy
all copies of Project Gutenberg-tm electronic works in your possession.
If you paid a fee for obtaining a copy of or access to a Project
Gutenberg-tm electronic work and you do not agree to be bound by the
terms of this agreement, you may obtain a refund from the person or
entity to whom you paid the fee as set forth in paragraph 1.E.8.
1.B. "Project Gutenberg" is a registered trademark. It may only be
used on or associated in any way with an electronic work by people who
agree to be bound by the terms of this agreement. There are a few
things that you can do with most Project Gutenberg-tm electronic works
even without complying with the full terms of this agreement. See
paragraph 1.C below. There are a lot of things you can do with Project
Gutenberg-tm electronic works if you follow the terms of this agreement
and help preserve free future access to Project Gutenberg-tm electronic
works. See paragraph 1.E below.
1.C. The Project Gutenberg Literary Archive Foundation ("the Foundation"
or PGLAF), owns a compilation copyright in the collection of Project
Gutenberg-tm electronic works. Nearly all the individual works in the
collection are in the public domain in the United States. If an
individual work is in the public domain in the United States and you are
located in the United States, we do not claim a right to prevent you from
copying, distributing, performing, displaying or creating derivative
works based on the work as long as all references to Project Gutenberg
are removed. Of course, we hope that you will support the Project
Gutenberg-tm mission of promoting free access to electronic works by
freely sharing Project Gutenberg-tm works in compliance with the terms of
this agreement for keeping the Project Gutenberg-tm name associated with
the work. You can easily comply with the terms of this agreement by
keeping this work in the same format with its attached full Project
Gutenberg-tm License when you share it without charge with others.
1.D. The copyright laws of the place where you are located also govern
what you can do with this work. Copyright laws in most countries are in
a constant state of change. If you are outside the United States, check
the laws of your country in addition to the terms of this agreement
before downloading, copying, displaying, performing, distributing or
creating derivative works based on this work or any other Project
Gutenberg-tm work. The Foundation makes no representations concerning
the copyright status of any work in any country outside the United
States.
1.E. Unless you have removed all references to Project Gutenberg:
1.E.1. The following sentence, with active links to, or other immediate
access to, the full Project Gutenberg-tm License must appear prominently
whenever any copy of a Project Gutenberg-tm work (any work on which the
phrase "Project Gutenberg" appears, or with which the phrase "Project
Gutenberg" is associated) is accessed, displayed, performed, viewed,
copied or distributed:
This eBook is for the use of anyone anywhere at no cost and with
almost no restrictions whatsoever. You may copy it, give it away or
re-use it under the terms of the Project Gutenberg License included
with this eBook or online at www.gutenberg.org
1.E.2. If an individual Project Gutenberg-tm electronic work is derived
from the public domain (does not contain a notice indicating that it is
posted with permission of the copyright holder), the work can be copied
and distributed to anyone in the United States without paying any fees
or charges. If you are redistributing or providing access to a work
with the phrase "Project Gutenberg" associated with or appearing on the
work, you must comply either with the requirements of paragraphs 1.E.1
through 1.E.7 or obtain permission for the use of the work and the
Project Gutenberg-tm trademark as set forth in paragraphs 1.E.8 or
1.E.9.
1.E.3. If an individual Project Gutenberg-tm electronic work is posted
with the permission of the copyright holder, your use and distribution
must comply with both paragraphs 1.E.1 through 1.E.7 and any additional
terms imposed by the copyright holder. Additional terms will be linked
to the Project Gutenberg-tm License for all works posted with the
permission of the copyright holder found at the beginning of this work.
1.E.4. Do not unlink or detach or remove the full Project Gutenberg-tm
License terms from this work, or any files containing a part of this
work or any other work associated with Project Gutenberg-tm.
1.E.5. Do not copy, display, perform, distribute or redistribute this
electronic work, or any part of this electronic work, without
prominently displaying the sentence set forth in paragraph 1.E.1 with
active links or immediate access to the full terms of the Project
Gutenberg-tm License.
1.E.6. You may convert to and distribute this work in any binary,
compressed, marked up, nonproprietary or proprietary form, including any
word processing or hypertext form. However, if you provide access to or
distribute copies of a Project Gutenberg-tm work in a format other than
"Plain Vanilla ASCII" or other format used in the official version
posted on the official Project Gutenberg-tm web site (www.gutenberg.org),
you must, at no additional cost, fee or expense to the user, provide a
copy, a means of exporting a copy, or a means of obtaining a copy upon
request, of the work in its original "Plain Vanilla ASCII" or other
form. Any alternate format must include the full Project Gutenberg-tm
License as specified in paragraph 1.E.1.
1.E.7. Do not charge a fee for access to, viewing, displaying,
performing, copying or distributing any Project Gutenberg-tm works
unless you comply with paragraph 1.E.8 or 1.E.9.
1.E.8. You may charge a reasonable fee for copies of or providing
access to or distributing Project Gutenberg-tm electronic works provided
that
- You pay a royalty fee of 20% of the gross profits you derive from
the use of Project Gutenberg-tm works calculated using the method
you already use to calculate your applicable taxes. The fee is
owed to the owner of the Project Gutenberg-tm trademark, but he
has agreed to donate royalties under this paragraph to the
Project Gutenberg Literary Archive Foundation. Royalty payments
must be paid within 60 days following each date on which you
prepare (or are legally required to prepare) your periodic tax
returns. Royalty payments should be clearly marked as such and
sent to the Project Gutenberg Literary Archive Foundation at the
address specified in Section 4, "Information about donations to
the Project Gutenberg Literary Archive Foundation."
- You provide a full refund of any money paid by a user who notifies
you in writing (or by e-mail) within 30 days of receipt that s/he
does not agree to the terms of the full Project Gutenberg-tm
License. You must require such a user to return or
destroy all copies of the works possessed in a physical medium
and discontinue all use of and all access to other copies of
Project Gutenberg-tm works.
- You provide, in accordance with paragraph 1.F.3, a full refund of any
money paid for a work or a replacement copy, if a defect in the
electronic work is discovered and reported to you within 90 days
of receipt of the work.
- You comply with all other terms of this agreement for free
distribution of Project Gutenberg-tm works.
1.E.9. If you wish to charge a fee or distribute a Project Gutenberg-tm
electronic work or group of works on different terms than are set
forth in this agreement, you must obtain permission in writing from
both the Project Gutenberg Literary Archive Foundation and Michael
Hart, the owner of the Project Gutenberg-tm trademark. Contact the
Foundation as set forth in Section 3 below.
1.F.
1.F.1. Project Gutenberg volunteers and employees expend considerable
effort to identify, do copyright research on, transcribe and proofread
public domain works in creating the Project Gutenberg-tm
collection. Despite these efforts, Project Gutenberg-tm electronic
works, and the medium on which they may be stored, may contain
"Defects," such as, but not limited to, incomplete, inaccurate or
corrupt data, transcription errors, a copyright or other intellectual
property infringement, a defective or damaged disk or other medium, a
computer virus, or computer codes that damage or cannot be read by
your equipment.
1.F.2. LIMITED WARRANTY, DISCLAIMER OF DAMAGES - Except for the "Right
of Replacement or Refund" described in paragraph 1.F.3, the Project
Gutenberg Literary Archive Foundation, the owner of the Project
Gutenberg-tm trademark, and any other party distributing a Project
Gutenberg-tm electronic work under this agreement, disclaim all
liability to you for damages, costs and expenses, including legal
fees. YOU AGREE THAT YOU HAVE NO REMEDIES FOR NEGLIGENCE, STRICT
LIABILITY, BREACH OF WARRANTY OR BREACH OF CONTRACT EXCEPT THOSE
PROVIDED IN PARAGRAPH 1.F.3. YOU AGREE THAT THE FOUNDATION, THE
TRADEMARK OWNER, AND ANY DISTRIBUTOR UNDER THIS AGREEMENT WILL NOT BE
LIABLE TO YOU FOR ACTUAL, DIRECT, INDIRECT, CONSEQUENTIAL, PUNITIVE OR
INCIDENTAL DAMAGES EVEN IF YOU GIVE NOTICE OF THE POSSIBILITY OF SUCH
DAMAGE.
1.F.3. LIMITED RIGHT OF REPLACEMENT OR REFUND - If you discover a
defect in this electronic work within 90 days of receiving it, you can
receive a refund of the money (if any) you paid for it by sending a
written explanation to the person you received the work from. If you
received the work on a physical medium, you must return the medium with
your written explanation. The person or entity that provided you with
the defective work may elect to provide a replacement copy in lieu of a
refund. If you received the work electronically, the person or entity
providing it to you may choose to give you a second opportunity to
receive the work electronically in lieu of a refund. If the second copy
is also defective, you may demand a refund in writing without further
opportunities to fix the problem.
1.F.4. Except for the limited right of replacement or refund set forth
in paragraph 1.F.3, this work is provided to you 'AS-IS' WITH NO OTHER
WARRANTIES OF ANY KIND, EXPRESS OR IMPLIED, INCLUDING BUT NOT LIMITED TO
WARRANTIES OF MERCHANTIBILITY OR FITNESS FOR ANY PURPOSE.
1.F.5. Some states do not allow disclaimers of certain implied
warranties or the exclusion or limitation of certain types of damages.
If any disclaimer or limitation set forth in this agreement violates the
law of the state applicable to this agreement, the agreement shall be
interpreted to make the maximum disclaimer or limitation permitted by
the applicable state law. The invalidity or unenforceability of any
provision of this agreement shall not void the remaining provisions.
1.F.6. INDEMNITY - You agree to indemnify and hold the Foundation, the
trademark owner, any agent or employee of the Foundation, anyone
providing copies of Project Gutenberg-tm electronic works in accordance
with this agreement, and any volunteers associated with the production,
promotion and distribution of Project Gutenberg-tm electronic works,
harmless from all liability, costs and expenses, including legal fees,
that arise directly or indirectly from any of the following which you do
or cause to occur: (a) distribution of this or any Project Gutenberg-tm
work, (b) alteration, modification, or additions or deletions to any
Project Gutenberg-tm work, and (c) any Defect you cause.
Section 2. Information about the Mission of Project Gutenberg-tm
Project Gutenberg-tm is synonymous with the free distribution of
electronic works in formats readable by the widest variety of computers
including obsolete, old, middle-aged and new computers. It exists
because of the efforts of hundreds of volunteers and donations from
people in all walks of life.
Volunteers and financial support to provide volunteers with the
assistance they need, are critical to reaching Project Gutenberg-tm's
goals and ensuring that the Project Gutenberg-tm collection will
remain freely available for generations to come. In 2001, the Project
Gutenberg Literary Archive Foundation was created to provide a secure
and permanent future for Project Gutenberg-tm and future generations.
To learn more about the Project Gutenberg Literary Archive Foundation
and how your efforts and donations can help, see Sections 3 and 4
and the Foundation web page at http://www.pglaf.org.
Section 3. Information about the Project Gutenberg Literary Archive
Foundation
The Project Gutenberg Literary Archive Foundation is a non profit
501(c)(3) educational corporation organized under the laws of the
state of Mississippi and granted tax exempt status by the Internal
Revenue Service. The Foundation's EIN or federal tax identification
number is 64-6221541. Its 501(c)(3) letter is posted at
http://pglaf.org/fundraising. Contributions to the Project Gutenberg
Literary Archive Foundation are tax deductible to the full extent
permitted by U.S. federal laws and your state's laws.
The Foundation's principal office is located at 4557 Melan Dr. S.
Fairbanks, AK, 99712., but its volunteers and employees are scattered
throughout numerous locations. Its business office is located at
809 North 1500 West, Salt Lake City, UT 84116, (801) 596-1887, email
business@pglaf.org. Email contact links and up to date contact
information can be found at the Foundation's web site and official
page at http://pglaf.org
For additional contact information:
Dr. Gregory B. Newby
Chief Executive and Director
gbnewby@pglaf.org
Section 4. Information about Donations to the Project Gutenberg
Literary Archive Foundation
Project Gutenberg-tm depends upon and cannot survive without wide
spread public support and donations to carry out its mission of
increasing the number of public domain and licensed works that can be
freely distributed in machine readable form accessible by the widest
array of equipment including outdated equipment. Many small donations
($1 to $5,000) are particularly important to maintaining tax exempt
status with the IRS.
The Foundation is committed to complying with the laws regulating
charities and charitable donations in all 50 states of the United
States. Compliance requirements are not uniform and it takes a
considerable effort, much paperwork and many fees to meet and keep up
with these requirements. We do not solicit donations in locations
where we have not received written confirmation of compliance. To
SEND DONATIONS or determine the status of compliance for any
particular state visit http://pglaf.org
While we cannot and do not solicit contributions from states where we
have not met the solicitation requirements, we know of no prohibition
against accepting unsolicited donations from donors in such states who
approach us with offers to donate.
International donations are gratefully accepted, but we cannot make
any statements concerning tax treatment of donations received from
outside the United States. U.S. laws alone swamp our small staff.
Please check the Project Gutenberg Web pages for current donation
methods and addresses. Donations are accepted in a number of other
ways including checks, online payments and credit card donations.
To donate, please visit: http://pglaf.org/donate
Section 5. General Information About Project Gutenberg-tm electronic
works.
Professor Michael S. Hart is the originator of the Project Gutenberg-tm
concept of a library of electronic works that could be freely shared
with anyone. For thirty years, he produced and distributed Project
Gutenberg-tm eBooks with only a loose network of volunteer support.
Project Gutenberg-tm eBooks are often created from several printed
editions, all of which are confirmed as Public Domain in the U.S.
unless a copyright notice is included. Thus, we do not necessarily
keep eBooks in compliance with any particular paper edition.
Most people start at our Web site which has the main PG search facility:
http://www.gutenberg.org
This Web site includes information about Project Gutenberg-tm,
including how to make donations to the Project Gutenberg Literary
Archive Foundation, how to help produce our new eBooks, and how to
subscribe to our email newsletter to hear about new eBooks.
</pre>
</body>
</html>
|
