Volatile Anesthetics and Coronary Collateral Circulation

Abstract

In this chapter, a study demonstrates that isoflurane and a new volatile anesthetic, sevoflurane, do not abnormally redistribute collateral blood flow away from an area distal to a total coronary artery occlusion. Vasodilation in the region supplied by the stenotic artey causes a decrease in coronary artery pressure distal to the stenosis. Agents that produce coronary vasodilation can act at one or more regions in the coronary vasculature. Arterioles are the primary vessels controlling resistance in the coronary circulation, and, thus, arteriolar dilators such as adenosine, dipyridamole, and chromonar are capable of producing maximal increases in flow and a redistribution of flow away from collateraldependent zones. Volatile anesthetics, including isoflurane, enflurane, and halothane, have been shown to cause coronary vasodilation, primarily of small resistance vessels. This property makes these agents potential candidates for the production of coronary steal. Volatile anesthetics also depress sinoatrial (SA) node and cardiac conduction tissue function in vitro . Volatile anesthetic-induced reductions in myocardial contractility, left ventricular afterload, and heart rate contribute to a reduction in myocardial oxygen consumption and lead to a concomitant increase in coronary vascular resistance via metabolic autoregulation. Thus, the sum of indirect and direct effects in vivo determines the observed alterations in coronary blood flow and vascular resistance. In the present investigation, sevoflurane has been shown to increase coronary collateral blood flow during maintenance of heart rate and arterial pressure at levels observed in the conscious state. In contrast, coronary collateral blood flow remains constant with correction of heart rate and blood pressure during isoflurane or desflurane anesthesia.