The coronary blood flow as a critical determinant of cardiac performance and cardiac size

Abstract

The manner and extent to which the coronary circulation affects myocardial contractility and cardiac size were explored. It was found that heart failure induced by pulmonary artery constriction is essentially metabolic, a consequence of decreased coronary blood flow. Whereas release of pulmonary artery constriction did not restore cardiac working capacity once failure was established, marked functional improvement could be consistently obtained by increasing coronary blood flow by means of a simple veno-arterial shunting procedure, in the face of persistent pulmonary artery constriction. This was to some extent independent of the oxygen tension of the coronary arterial blood. After a period of veno-arterial shunting, some of the animals acquired the capacity to maintain good cardiac function even when the shunt was discontinued, despite continuance of the previously disabling pulmonary artery constriction. Such an adjustment depended upon a sustaining elevation of CBF after the shunt was discontinued. This accommodation phenomenon demonstrates the remarkable capacity of the heart to recover when given temporary assistance that improves the metabolic milieu. The coronary blood flow has been shown to influence the heart size, the strength of contraction, and adaptive mechanisms to increased work loads. A simple “Starling relationship” therefore cannot explain the control of the in vivo cardiac performance observed in these experiments. The clinical ramifications of these observations on the interpretation and management of shock and some forms of heart failure are discussed. Clinical application of the principles is described in a patient with myocardial infarction and prolonged shock.