Impairment of myocardial O2 supply due to hyperventilation.

Abstract

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...

Heart-focused anxiety, illness beliefs, and behavioral impairment: Comparing healthy heart-anxious patients with cardiac and surgical inpatients

“…Assessment of cardiac inpatients was conducted at the patients' bedside. We decided not to conduct a hyperventilation provocation test with cardiac inpatients, because prolonged hyperventilation may impair myocardial oxygen supply and cause other potentially harmful effects in patients with serious heart disease such as coronary vasoconstriction and microspasms (Neill and Hattenhauer, 1975). Postoperative inpatients in the surgical wards who had agreed to participate completed questionnaires in their hospital room.…”

Position Paper on Urine Alkalinization

“…It could therefore pose a risk to patients with ischemic heart disease. Several studies have shown that voluntary hyperventilation in patients with ischemic heart disease can produce mean arterial pH values of as high as 7.58 (H + concentration 26 nmol/L) and ischemic changes in the electrocardiogram (50,51). However, coronary artery constriction does not occur (51) and the ECG changes may be due to potassium fluxes and autonomic nervous system activity rather than alkalemia (52).…”

Myocardial oxygen supply during hypocapnia and hypercapnia in the dog

“…Am increased myocardial ateriovenous oxygen difference without or with only a minor reduction in myocardial blood flow (MBF) has been demonstrated during hypocapnia (Case et al 1975;Ekrrhart and Smith 1988;Neill and Hattenhauer 1975;Wexels et al 1985). It has been proposed that the absence of a significant reduction in MBF during hypocapnia has been a result of an opposing coronary vasodilating force caused by impaired myocardial oxygen supply (Case et al 1975;Neill and Hattenhauer 1975;Wexels et al 1985).…”

“…It has been proposed that the absence of a significant reduction in MBF during hypocapnia has been a result of an opposing coronary vasodilating force caused by impaired myocardial oxygen supply (Case et al 1975;Neill and Hattenhauer 1975;Wexels et al 1985). The first part of the present study was carried out to examine whether a maximal decline in coronary sinus (CS) oxygen content was reached during h y p a p n i a , inhibiting further coronary vasoconstriction.…”