The coronary circulation supplies oxygen-rich blood to the myocardium. Coronary flow is restricted during systolic compression of vessels and primarily occurs in diastole when ventricular pressure drops. Metabolic autoregulation ensures coronary flow matches the heart's metabolic demand for oxygen, which increases with contractility, heart rate, and wall stress.
The heart faces a paradox that no other organ encounters: during systole, when ventricular muscle contracts most forcefully and needs oxygen most urgently, the pressure it generates simultaneously squeezes its own blood supply nearly shut. From your study of the cardiac cycle, you know that the left ventricle develops 120 mmHg or more during systole — enough to compress the subendocardial coronary vessels against the ventricular wall. This means the left coronary artery does most of its work during diastole, when ventricular pressure drops and the vessels can open. The right ventricle, which develops much lower pressures, has less of this problem and receives flow throughout the cycle.
This diastolic dependence has an important clinical consequence: heart rate directly steals diastolic time. When heart rate rises from 70 to 140 beats per minute, the cardiac cycle halves — but systole shortens only a little, so most of the time lost comes from diastole. Less diastole means less filling time and, critically, less coronary perfusion time. This is why tachycardia is particularly dangerous in patients with coronary artery disease: the heart demands more oxygen (higher rate) at the same moment it receives less delivery (shorter diastole).
The coronary vasculature responds to this changing demand through metabolic autoregulation. When myocardial oxygen extraction rises — which happens whenever contractility increases, wall stress rises, or heart rate climbs — local metabolic byproducts (adenosine, CO₂, H⁺, K⁺) accumulate and trigger coronary vasodilation. The vessels dilate in proportion to metabolic need, increasing flow up to four or five times resting levels during peak exercise. This is called coronary flow reserve, and its erosion is an early sign of disease: a vessel with 70% stenosis may deliver adequate flow at rest but cannot vasodilate sufficiently during exercise, producing ischemia under stress.
Perfusion pressure is the final piece. Coronary perfusion pressure is roughly aortic diastolic pressure minus left ventricular end-diastolic pressure (LVEDP). From your vascular physiology prerequisite, recall that flow depends on the pressure gradient across a vessel. If aortic diastolic pressure falls (hypotension, aortic regurgitation) or LVEDP rises (heart failure, volume overload), the gradient narrows and coronary flow falls. This is why hypotension is immediately dangerous in coronary artery disease, and why elevated filling pressures in heart failure compound myocardial ischemia — the heart is both volume-overloaded and underperfused simultaneously.