The underlying mechanisms of<unk>  have remained the subject of debate for several decades. Two leading hypotheses implicate reperfusion-induced oxygen free-radical damage and altered calcium flux resulting in intracellular hypercalcemia and desensitization of myofilaments. After total ischemia occurs, the myocardium switches immediately from aerobic glycolysis to anaerobic glycolysis resulting in the reduced ability to produce high energy phosphates such as ATP and Creatinine Phosphate. At this point, the lack of the energy and lactate accumulation results in cessation of contraction within 60 seconds of ischemia (i.e. Vessel Occlusion). Subsequent to this is a period of<unk> ," in which reversible ischemic damage is taking place. At approximately 30 minutes after the onset of total ischemia the damage becomes irreversible, thereby ending the phase of<unk> . The generation of oxygen-derived free radicals during the initial period of reperfusion after ischemia is believed to contribute to the pathogenesis of<unk> . Some evidence suggests that brief, repetitive episodes of<unk>  ischemia may result in chronic<unk>  and ventricular contractile impairment.
Myocardial stunning
Pulmonary embolism
Coronary steal
Myocarditis
Coronary vasospasm
Hibernating myocardium
Myocardial scarring
Myocardial infarction