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Ventricular Function After Hypothermic Cardiac Arrest
V. L. WILLMAN, M.D.;
H. S. HOWARD, M.D.;
T. COOPER, M.D.;
C. R. HANLON, M.D.
AMA Arch Surg. 1961;82(1):120-127.
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The deleterious effects of cardiac arrest induced by potassium salts, acetylcholine, or anoxia have been demonstrated by several investigators.2,7,8,12-14,20,21 The mechanism of damage to the myocardium remains uncertain, but it may well be associated with a disparity between the amount of available oxygen and the metabolic needs of the heart for oxygen under normothermic conditions. Although the oxygen consumption of the normothermic, nonbeating heart is reduced below that of the beating, nonworking heart,22 a definite oxygen need persists. This oxygen need of the myocardium may be still further reduced by hypothermia,4 which reduces the oxygen needs of most body tissues.1,19
Since profound hypothermia of itself will cause cardiac arrest, it is natural that a variety of hypothermic techniques have been employed to secure a quiet, bloodless heart for experimental or clinical open cardiac surgery. There has been no definitive study of the relative advantages of these
. . . [Full Text PDF of this Article]
Author Affiliations
ST. LOUIS
From the Department of Surgery, St. Louis University School of Medicine.
Footnotes
Submitted for publication June 16, 1960.
Aided by grants H-3826 (Cl) U.S. Public Health Service, National Heart Institute, and from the Missouri Heart Association.
Read before the Eighth Scientific Meeting of the International Cardiovascular Society, North American Chapter, Miami Beach, June 11, 1960.
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