In most organs, oxygen consumption is maintained at relatively constant levels as oxygen delivery decreases, until a critical level is reached. This biphasic action is not observed in the heart. Myocardial oxygen consumption is supply dependent at all levels of myocardial oxygen delivery, because changes in myocardial oxygen delivery modify ventricular loading conditions and hence myocardial oxygen consumption. Since the oxygen content of coronary sinus blood is very low, only limited increases in oxygen extraction are possible. Therefore, coronary dilation is the primary mechanism for increasing myocardial oxygen delivery. Four- to sixfold increases in coronary blood flow can occur in several animal species and in human beings. Apart from metabolic control mechanisms, the regulation of myocardial oxygen delivery is multifaceted; major factors include extravascular compressive forces, autoregulation, neural controls, and humoral factors. In situations of decreased myocardial oxygen delivery, coronary vessels dilate to increase flow, and as coronary flow reserve falls to zero, flow becomes exquisitely dependent on perfusion pressure. With onset of supply dependency, contractility falls in an effort to maintain cardiac output at a given myocardial oxygen consumption.