CARDIAC ADAPTATIONS IN ACUTE PROGRESSIVE ANOXIA

Abstract

The circulatory reactions characteristic for man, breathing gas mixtures with decreasing O2 volumes (20 > 6%), can be duplicated in lightly anesthetized dogs. Such expts. have the advantage that the mechanisms by which cardiac Actaptations operate to increase blood flow can be analyzed more thoroughly than in man. During hypoxia, corresponding to progressive decrease in respired O2 vols. to about 12%, to blood O2 saturations above 75% or altitudes of 15,000 feet, blood flow is increased regionally, by reciprocal constriction and dilatation of vessels causing redistribution of blood flow, and generally by acceleration of the heart. The latter is due to decreased vagal tone, increased accelerator nerve activity and perhaps some direct effect on the S-A node. Stroke vol. is not affected otherwise than during any cardiac acceleration. The vigor of ventricular contractions increases and the period of systolic expulsion shortens. Vasomotor changes probably occur, but there is no dynamic evidence that they are reflected in the changing systolic and diastolic pressures. Effective venous pressures fall slightly, not through reduced venous return but owing to greater minute output by the faster heart. During true anoxia, which begins when O of the inspired air is progressively decreased below 12%, the heart responds with greater stroke vols. and with further increase in velocity of ejection. The economy of effort is enhanced. Expts. on dogs with "controlled circulation," i.e., in animals whose heart rate, arterial diastolic and venous pressure, as well as alveolar CO2, are kept constant, show that the increased systolic discharge is accompanied by increase in diastolic size, independently of changes in venous pressure. Such compensatory reactions could probably not occur without the unquestioned dilatation of coronary vessels. Further decline of O2 in the inspired air to 7 or 6%, corresponding to arterial O2 saturations between 50-35% and to altitudes up to 30,000 ft., leads to a circulatory crisis. Arterial pressures decline abruptly, pulse pressure is reduced, systolic discharge decreases, venous pressure rises tremendously, and various types of conduction and rhythm disturbances may occur. No evidence exists that peripheral vasomotor failure is concerned. The circulatory crisis is essentially an acute congestive heart failure due to depressant effect of anoxia on the myocardium. It probably supervenes when the increasing coronary flow can no longer keep pace with the rapidly diminishing tension of O2 in the blood.