The heart normally receives 4% of cardiac output, or ~ 250 mL/min of blood. Fatty acids and lactate are the predominant sources of energy, although glucose can be utilized (depending on glucose and insulin concentrations, as well as PaO2).
Normal mVO2 is 8-10 mL/100g/min. mVO2 is related to the area inside the pressure-volume loop [Chung N et al. Am J Physiol 258: H1208, 1990]. Work by Suga and Sagawa suggest that pressure volume area (PVA), which takes into account differences in internal work required to function at different physiologic states, may be a more accurate measure of mVO2 [Khalafbeigui F et al. Am J Physiol 237: H566, 1979; Suga H et al. Am J Physiol 240: H39, 1981; Suga H et al. Fed Proc 43: 2411, 1984; Suga H et al. Basic Res Cardiol 81 Suppl 1: 39, 1986; Burkhoff D et al. Heart Vessels 3: 66, 1987]
Coronary venous pO2 is 18-20 mm Mg (30% saturation), and normal myocardial ER is 60-70%. Importantly, the myocardium cannot compensate for underperfusion by increasing oxygen extraction significantly (maximal ER is 90%), and thus the only compensatory mechanisms available are to increase blood flow by either changing regional vascular resistance (see Autoregulation below) or perfusion pressure.
Autoregulation is intact across a range of perfusion pressures (50 – 120 mm Hg according to some sources, MAP range 60 – 140 mm Hg according to Kaplan), is tightly coupled to demand and this relationship is difficult to disrupt – even norepinephrine, which exhibits significant alpha effects, leads to increased coronary blood flow due to increases in myocardial contractility [Barash, PG. Clinical Anesthesia, 5th ed. (Philadelphia), p. 869, 2006]. Note that in animal models, autoregulation is location-dependent – the epicardium tolerates lower MAP than the endocardium [Guyton RA et al. Am J Cardiol 40: 373, 1977]
There are two settings in which myocardial supply and demand can be mismatched – profoundly low perfusion pressures, and irreversible stenosis. In the latter setting, vasodilation of non-critically stenoses vessels can shunt blood away from fixed-diameter vessels, leading to a decrease in coronary blood flow to a susceptible region, a phenomena know as “coronary steal.”
Note that tachycardia and increased LVEDV/P are physiologic alterations most likely to cause myocardial ischemia.