Stable angina results from a supply-demand mismatch in myocardial oxygen delivery caused by fixed atherosclerotic coronary stenosis. The myocardium has the highest oxygen extraction ratio of any organ (60-70% at rest vs 25% for skeletal muscle), leaving minimal reserve for increased extraction during stress. Therefore, increased oxygen delivery must come primarily from increased coronary blood flow. Coronary flow is regulated by metabolic autoregulation: adenosine, nitric oxide, and prostacyclin released by ischemic myocytes and endothelial cells cause arteriolar vasodilation. In healthy arteries, flow-mediated dilation of epicardial arteries augments this response. In atherosclerotic arteries, endothelial dysfunction impairs nitric oxide-mediated vasodilation and may produce paradoxical vasoconstriction to acetylcholine. Coronary flow reserve (the ratio of maximal hyperemic flow to resting flow) decreases as stenosis severity increases: a 50% diameter stenosis begins to limit maximal flow, 70% stenosis produces exertional ischemia, and 90% stenosis may cause resting ischemia. The subendocardium is most vulnerable because it experiences highest wall stress during systole and receives blood flow only during diastole (diastolic perfusion time). Tachycardia reduces diastolic filling time and increases subendocardial vulnerability. The nurse interprets stress test...