Myocardial oxygen requirements are met by coronary blood flow and oxygen extraction from the arterial blood. The myocardial oxygen extraction coefficient (1) expresses the fraction of available oxygen in arterial blood removed by the myocardium: coronary A-Vo2/Ao2 X 100 = myocardial extraction percentage. Myocardial oxygen extraction during rest is approximately 70 to 75 per cent, exceeding that of all other organs (1, 2). This degree of extraction is equalled only by exercising skeletal muscle, in which increased oxygen requirements are met both by additional blood flow and by increased oxygen extraction. Earlier workers have noted a relative constancy of myocardial oxygen extraction under the widely varying conditions of rest, anemia, hypoxia, and increased left ventricular work, suggesting that coronary blood flow is altered commensurate with myocardial oxygen requirements (1, 3, 4). Case, Berglund and Sarnoff demonstrated that when coronary blood flow reserve was limited by experimental coronary constriction, myocardial extraction increased due to the combined stress of anemia and increased left ventricular work (3).The effect of exercise on coronary hemodynamics has received little attention. Lombardo and co-workers reported observations in 13 human subjects with various forms of heart disease (5). As part of another study, Regan and associates reported on the effects of exercise on the coronary circulation in nine normal subjects (6). This report will present myocardial oxygen extraction data from 108 patients at rest, and from 79 subjects during mild exercise. The physiological significance of myocardial oxygen extrac-* This work was supported by grants from the U. S. (7), and routine cardiac catheterization findings. The exercise electrocardiograms were interpreted according to the criteria of Mattingly, Fancher, Bauer and Robb (8).Four clinical states were selected for correlation with myocardial oxygen extraction patterns. The patients were grouped clinically according to the following criteria.Control. Patients having no symptoms or electrocardiographic, radiologic or physical findings suggesting coronary artery disease or congestive heart failure served as controls. Pulmonary capillary pressures were normal in all subjects except those with mild mitral stenosis. The range of diagnoses included functional systolic murmurs, patent ductus arteriosus, ventricular and atrial septal defects, mild aortic insufficiency, noncritical mitral stenosis (valve area greater than 1.5 cm'), tetralogy of Fallot, and mild coarctation of the aorta. Two had atypical chest pain without evidence to suggest coronary insufficiency.Coronary insufficiency. Patients judged to have coronary insufficiency on the basis of classical angina pectoris, documented myocardial infarction, and positive Master's test were placed in this group. In several cases the coronary vessels were assessed at operation, by coronary arteriography (9), or at necropsy. Several patients had coexisting congestive heart failure.Congestive heart failure. Th...

SUMMARYThirteen patients with ischemic coronary heart disease purposely hyperventilated for seven minutes in order to induce hypocapnic alkalosis. One patient experienced chest pain, and one exhibited chemical signs of myocardial hypoxia. Heart rate, blood pressure and myocardial 02 consumption did not change significantly. Coronary blood flow decreased and coronary (a-v)O2 difference widened. Since the alkalosis increased the blood 02 affinity, the fall in Po2 in coronary venous blood was proportionately even greater than the fall in 02 concentration. Thus, hypocapnic alkalosis due to hyperventilation interferes with myocardial 02 supply by 1) coronary vasoconstriction and 2) increased 02 affinity of blood.HYPERVENTILATION increases arterial blood PO2 and, by the Bohr effect, increases the affinity of blood for 02 in proportion to the degree of hypocapnic alkalosis. The hemoglobin is more fully saturated with 02 at any given Po2, i.e., the 02 dissociation curve is shifted to the left. Unless arterial hypoxemia was present initially, these changes only slightly augment oxygenation of arterial blood in the pulmonary capillaries, due to the configuration of the 02 dissociation curve. At the same time, with the higher pH in the systemic capillaries, the hemoglobin will give up the expected amount of its 02 only if the Po2 falls below normal; and a decrease in capillary blood Po2 might significantly impair 02 diffusion into the tissue.' In the coronary circulation where vasomotor regulation is influenced prominently by the needs of the myocardium for 02, decreased capillary blood Po2 might be expected to result in compensatory vasodilation and increased coronary blood flow, as in anemia. Hypocapnic alkalosis, however, increases vascular resistance and decreases blood flow in some tissues, including the forearm2 and brain.3 Although the results of experiments with the coronary circulation in anesthetized animals are inconclusive,`f voluntary hyperventilation has been reported to increase resistance, decrease blood flow and lower venous 02 concentration in the normal coronary circulation of human subjects.6 Thus, in those subjects, the impaired blood 02 release appeared not to be compensated by augmented blood flow but instead to be compounded by coronary vasoconstriction. If increased blood 02 affinity and coronary vasoconstriction also occur in patients with ischemic coronary heart disease, voluntary hyperventilation might result in myocardial hypoxia. The present report is an investigation of voluntary hyperventilation in the resting state in patients with symptomatic chronic ischemic coronary heart disease. We determined the effect of hyperventilation on systemic hemodynamics, coronary blood flow, myocardial 02 supply, and in viVo 02 affinity of coronary venous blood. MethodsWe studied 13 men with stable exertional angina pectoris who were being evaluated for possible coronary bypass graft surgery. Their ages ranged from 45 to 58 years (mean 50 years). Coronary arteriography was performed in 12 of the men and demo...

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A B S T R A C T Eight patients with coronary heart disease and exertional angina pectoris successfully completed an 11-15 wk program of endurance exercise conditioning. Angina threshold was determined by upright bicycle ergometer exercise and by atrial pacing. The product of heart rate and arterial systolic blood pressure at the exercise angina threshold was higher after conditioning, suggesting that conditioning increased the maximum myocardial 02 supply during exercise. However, when angina was induced by atrial pacing, heart rate, arterial blood pressure, coronary blood flow, and myocardial 02 consumption at the angina threshold were the same before and after conditioning. Myocardial lactate extraction during atrial pacing was abnormal in the same five patients before and after conditioning. Conditioning caused no detectable changes in coronary collaterals as judged by coronary arteriograms.The increase in exercise angina threshold appeared to be due to a functional adaptation in either myocardial 02 supply or the relationship between hemodynamic work and myocardial 02 consumption. The adaptation was limited to exercise, and did not occur during a different stress to myocardial 02 supply, atrial pacing.