Right to left shunt in patients with acute myocardial infarction: A proposed mechanism

Abstract

Bedside catheterization of femoral and pulmonary arteries allowed serial measurement of pulmonary arterial pressure, cardiac output and percent right to left shunt in 25 patients with (1) acute myocardial infarction with minimal or no evidence of heart failure, (2) severe heart failure, (3) shock, or (4) shock and heart failure. There was positive correlation between mean cardiac output and percent right to left shunt ( r = +0.64, P < 0.01) but no significant correlation between mean shunt flow and pulmonary arterial pressure (when cardiac output was held constant). Deep breathing or intermittent positive pressure breathing resulted in significant decreases in right to left shunt flow. These observations are explained on the basis of atelectasis of dependent lung units and maximal dilatation of vessels to superior lung zones. Increases in blood flow are accommodated by recruitment of more dilatable vessels in the lower pulmonary lobe, hence explaining the relation between right to left shunt and pulmonary flow. Increases in left atrial pressure would be expected to result in less perfusion to dependent zones (decreasing right to left shunt flow) and increased formation of intraalveolar edema (increasing right to left shunt flow), thus explaining the lack of correlation between pulmonary arterial pressure and right to left shunt flow. Prolonged static position, overzealous use of analgesic agents and rapid shallow ventilation patterns are important causes of atelectasis, right to left shunt and arterial hypoxemia in patients with acute myocardial infarction.