Cardiovascular Dynamics of Aortic Insufficiency

Abstract

Dependent upon its severity, AI is variously manifested by complex and protean hemodynamics in the heart and circulation. Significant AI results in decreases in the effective stroke and minute outputs of the heart, and in the mean and diastolic blood pressures, whereas AI increases the total stroke and minute outputs, and the arterial pulse pressure. The circulatory phenomena in the peripheral vessels are caused by the very hemodynamic alterations by AI per se, by their hydraulic modifications induced in the large and medium arterial walls with spccific physical properties, and finally by the neurohumoral regulatory mechanisms of the cardiovascular system secondary to AI. Although AI enhances the absolute coronary blood flow by increasing the cardiac work load, angina pectoris (myocardial anoxia) is not infrequently associated with this condition. This is simply explaened by the fact that AI results in the greater increment of myocardial oxygen demand than that of the coronary blood flow or oxygen supply. The multiple homeostatic mechanisms for the handicapped hemodynamics are observed to be operating in this condition. The physiological significance of those mechanisms responsible for cardiovascular regulation is described and discussed in detail.