5.7 Coronary Blood Flow

Why Coronary Flow Is Different

Quick Answer: The heart is the only organ whose blood flow is largely diastolic — systole compresses intramyocardial vessels. Coronary flow is matched to myocardial O₂ demand through metabolic autoregulation, mainly by adenosine and hypoxia. The PA-CAT Bulletin of Information, rev. 20240815, includes coronary flow under "The Heart" and Circulation.

Coronary Anatomy

The aortic root gives rise to the left and right coronary ostia, just above the aortic valve cusps.

• Left main coronary artery — divides into the left anterior descending (LAD) artery (supplies the anterior wall, septum, and bundle branches; the "widow-maker" when occluded proximally) and the left circumflex (LCx) artery (supplies the lateral and posterior left ventricle).
• Right coronary artery (RCA) — supplies the right ventricle, the SA node (~60% of people), and the AV node (~80% of people); dominant circulation in most people supplies the posterior descending artery (PDA).
• Posterior descending artery (PDA) — from RCA in right-dominant (~85%) circulation, from LCx in left-dominant (~8%) circulation, or both (codominant).

The coronary sinus collects venous drainage into the right atrium. The thebesian vessels drain a small fraction directly into the cardiac chambers.

Flow Occurs in Diastole

During systole, the contracting myocardium compresses intramyocardial vessels — especially those penetrating the thick left ventricle. Left coronary flow therefore falls during systole and peaks during diastole when the myocardium relaxes and the aortic pressure is still high enough to drive perfusion. Right coronary flow is less affected because the right ventricle is thinner and generates lower pressure.

This creates a critical vulnerability: tachycardia shortens diastole disproportionately. At very high heart rates, diastolic filling time falls, reducing coronary perfusion — a problem in ischemic heart disease. The diastolic pressure-time index (DPTI) divided by the systolic pressure-time index (SPTI) gives the endoocardial viability ratio (EVR); EVR < 0.7 indicates subendocardial ischemia risk.

Determinants of Coronary Flow

Coronary flow is governed by:

1. Perfusion pressure — aortic diastolic pressure minus the intramyocardial (or back) pressure. Low diastolic pressure (e.g., shock, severe aortic regurgitation) reduces coronary flow.
2. Vessel radius — atherosclerotic plaques narrow the lumen; vasospasm (Prinzmetal angina) constricts smooth muscle.
3. Extravascular compression — systolic compression and elevated LV end-diastolic pressure both impede flow.
4. Metabolic vasodilation — the dominant physiologic regulator.

Autoregulation

Coronary flow is autoregulated between roughly 60 and 140 mmHg of perfusion pressure. Within that range, flow stays nearly constant despite pressure changes, via:

• Metabolic vasodilation — increased myocardial O₂ consumption releases adenosine (from ATP breakdown), CO₂, H⁺, and K⁺, which dilate arterioles. Adenosine is a particularly powerful coronary vasodilator acting via A₂ receptors → cAMP → smooth muscle relaxation.
• Myogenic response — vessels constrict to stretch, dilate to reduced pressure.
• Endothelial NO — flow-mediated dilation augments metabolic control.

Beyond the autoregulatory range, flow becomes pressure-passive. A stenotic artery that exhausts autoregulatory reserve at rest is a critical lesion; downstream vasodilation is already maximal, leaving no reserve for increased demand.

Myocardial Oxygen Demand and Supply

The myocardium extracts ~70% of arterial O₂ at rest (compared with ~25% in many organs), so it operates near maximal extraction. Increased O₂ demand must be met almost entirely by increased coronary flow, not by increased extraction. This is why coronary stenosis is so consequential — there is little extraction reserve.

Determinants of O₂ demand:

• Heart rate (the biggest factor; tachycardia raises demand and shortens diastole, a double insult).
• Contractility (inotropic state).
• Wall stress = (P × r) / (2 h) — raised by pressure overload (hypertension, aortic stenosis), dilation (heart failure), and reduced by hypertrophy (compensation).
• Basal metabolic needs of myocardium.

Determinants of O₂ supply:

• Coronary blood flow (dominant).
• Arterial O₂ content (Hb × 1.34 × SaO₂ + dissolved O₂) — anemia or hypoxemia reduces supply.
• Duration of diastole.

Ischemia and Infarction

Ischemia arises when demand exceeds supply. Mechanisms:

• Atherosclerotic plaque rupture with thrombus formation — the cause of most acute coronary syndromes.
• Fixed stenosis with exertion — stable angina, relieved by rest or nitroglycerin.
• Vasospasm — Prinzmetal (variant) angina.
• Microvascular dysfunction — angina with normal epicardial arteries (INOCA).
• Demand ischemia — tachyarrhythmia, severe hypertension, aortic stenosis.

Myocardial infarction is necrosis from prolonged ischemia. A PA-CAT Bulletin sample item notes that myocardial infarction damaging the ventricular septum changes electrical conduction — the septum hosts the bundle of His and bundle branches; damage can produce left or right bundle branch block, AV block, or ventricular arrhythmias. The LAD supplies the septum, so an LAD occlusion can damage these conduction tissues.

Drugs That Alter Coronary Flow

• Nitroglycerin — venodilator (reduces preload) and coronary vasodilator; reduces demand and improves supply.
• β-blockers — lower HR, contractility, and BP (lower demand, longer diastole).
• Calcium channel blockers — vasodilate coronary arteries; useful in vasospastic angina.
• Aspirin and P2Y₁₂ inhibitors — prevent thrombus propagation.
• Statins — stabilize plaques and improve endothelial function.

Clinical Pearls

• Aortic stenosis with angina: hypertrophied LV raises demand and diastolic chamber pressure compresses subendocardial vessels, even with normal coronaries — explains syncope, angina, heart failure triad.
• Subendocardial ischemia appears as ST depressions on ECG — the subendocardium is most vulnerable because it is the last to be perfused and the first compressed.
• Collateral circulation develops over time in chronic ischemia, protecting myocardium distal to a slow-progressing stenosis.

Understanding coronary flow integrates cardiac anatomy, the cardiac cycle, and oxygen demand — a synthesis the PA-CAT tests by asking how changes in HR, BP, or vessel radius shift the supply-demand balance.