Identification of myocardial viability is of increasing clinical importance in managing patients with coronary artery disease and advanced left ventricular dysfunction. Although viable chronically dysfunctional myocardium is always the result of repetitive episodes of reversible ischemia, there may be multiple mechanisms responsible for the contractile dysfunction. Many patients have contractile dysfunction with normal resting perfusion, as determined by imaging, that is related to chronic myocardial stunning. Viability studies are generally unnecessary because normal resting perfusion would preclude significant fibrosis. The clinical problem arises in evaluating patients with depressed resting flow that can be due to hibernating myocardium or nontransmural infarction. In this circumstance viability studies are required to assess the likelihood of functional recovery after revascularization. Although hibernating myocardium was originally posited to develop in response to prolonged episodes of myocardial ischemia (experimentally termed "short-term hibernation"), subsequent studies have shown that this tenuous balance can only be maintained for a period of several hours before resulting in some degree of subendocardial infarction. More recent experimental studies have demonstrated that there is a progression from chronic stunning with normal flow to hibernating myocardium with reduced resting flow. This presumably arises from repetitive episodes of spontaneous ischemia that increase in frequency as the physiologic significance of a coronary stenosis progresses. Thus in this new paradigm reduced flow is a result, rather than the cause, of the contractile dysfunction. This review summarizes basic and clinical pathophysiologic studies supporting the claim that chronic stunning and hibernation are distinct entities that may represent opposite ends of a continuum of mechanisms in viable chronically dysfunctional myocardium.