Coronary Physiology of the Heart

1. Coronary Anatomy Overview

• Left main coronary artery (LMCA): Courses posterolateral to the pulmonary trunk ~1 cm before dividing into:
  • Left anterior descending (LAD): Runs along the interventricular septum, supplying the LV free wall and septum
  • Left circumflex (LCx): Travels in the atrioventricular groove, giving off obtuse marginal branches
• Right coronary artery (RCA): Runs in the anterior AV sulcus, supplying the RV free wall; typically bifurcates into the posterior descending artery (PDA) and right posterolateral artery. In ~85% of people, the PDA arises from the RCA (right-dominant circulation).
• AV nodal artery: Usually a branch of the RCA - its compromise causes arrhythmias or heart block.

2. Determinants of Coronary Blood Flow - Poiseuille's Law

Flow ∝ Pressure gradient / Resistance, where Resistance ∝ 1/r⁴

• Small changes in vessel caliber cause disproportionately large changes in resistance (4th-power relationship with radius)
• Resting coronary blood flow: ~250 mL/min (1 mL/min/g), representing ~5% of cardiac output
• Vessel length remains essentially constant in the intact heart
• Blood viscosity (governed mainly by hemoglobin concentration) plays a minor role unless marked polycythemia or profound hemodilution is present

3. Phasic Nature of Coronary Blood Flow

Figure: Left coronary flow occurs almost entirely during diastole; right coronary flow occurs in late systole and early diastole. (Barash Clinical Anesthesia, 9e)

• LV coronary flow: Occurs almost entirely during diastole because extravascular compressive forces impede subendocardial intramural vessels during systole
• Despite systolic limitation, uniform transmural LV perfusion is preserved (subepicardial:subendocardial ratio = 1:1) via metabolically mediated arteriolar dilation during diastole
• RV, LA, RA: Pressures remain below aortic pressure throughout the cycle, so compressive forces do not impede flow - right coronary flow occurs in both systole and diastole

4. Myocardial Oxygen Supply-Demand Balance

The Heart is Aerobic and Has Limited O₂ Reserve

• The heart depends almost entirely on aerobic metabolism - myocardial O₂ requirements are disproportionately high (7% of total body O₂) relative to its mass (0.5% of body weight)
• ~75% of O₂ carried by hemoglobin is extracted at baseline (coronary sinus O₂ tension = only 20 mmHg)
• Unlike skeletal muscle, the LV has minimal O₂ extraction reserve - it must increase flow to meet increased demand
• Contraction ceases within 10-15 seconds of acute coronary occlusion without collateral flow
• Primary substrates: fatty acids, glucose, and lactate (via mitochondrial oxidative phosphorylation)

Determinants of Myocardial O₂ Supply

Determinants of Myocardial O₂ Demand

5. Metabolic Regulation of Coronary Blood Flow

Nitric Oxide (NO) - Primary Vasodilator

• Synthesized by endothelial NO synthase (eNOS)
• Stimulated by ↑ intracellular Ca²⁺ (via bradykinin, acetylcholine) or wall shear stress
• Diffuses into arteriolar smooth muscle → stimulates cGMP → vasodilation
• Short half-life; rapidly scavenged by hemoglobin
• Inhibited by atherosclerosis, diabetes, and hypercholesterolemia - leading to dysregulated coronary flow

KATP Channels

• Open when ATP decreases → smooth muscle hyperpolarization → inhibit Ca²⁺ entry → vasodilation
• Mediate basal coronary tone and response to reduced perfusion pressure, increased O₂ demand, and reactive hyperemia

Adenosine

• ATP metabolite; relevant mainly during tissue hypoxia (when it is released)
• Previously thought to be the primary mediator - now recognized as a hypoxia-specific dilator

Prostacyclin (PGI₂)

• Arachidonic acid metabolite; opens KATP channels
• Inhibits platelet aggregation + causes arteriolar vasodilation
• Plays a minor role in routine metabolic regulation

Endothelin-1 (ET-1)

• Potent endogenous vasoconstrictor produced by endothelium
• Acts on ET-A and ET-B receptors on smooth muscle
• Counterbalanced by tonic NO under normal conditions
• Pathologic vasoconstriction occurs when NO release is impaired (hypertension, diabetes, heart failure)

6. Coronary Flow Reserve

• Normal CFR: 500-600% in LV and RV
• Measured by reactive hyperemia (brief occlusion) or pharmacologic vasodilation

• Coronary artery stenosis
• Pressure-overload hypertrophy
• Microvascular dysfunction

• 50% luminal diameter reduction: CFR first becomes detectable
• ~90% diameter reduction: Peak reactive hyperemia is abolished; associated with angina at minimal exertion (threshold for unstable angina)

7. Pressure-Flow Autoregulation

Figure: Coronary autoregulation maintains relatively constant flow across 60-140 mmHg of perfusion pressure. Reduced cardiac effort (lower O₂ demand) shifts the entire curve downward. (Barash Clinical Anesthesia, 9e)

• Below 60 mmHg: Maximal vasodilation; vasodilator reserve is exhausted; flow falls passively
• Above 140 mmHg: Coronary vessels are distended beyond the capacity of smooth muscle to constrict; flow rises passively
• Autoregulation is independent of the autonomic nervous system - it is an intrinsic myogenic phenomenon
• The autoregulatory plateau shifts downward with decreased myocardial O₂ demand (and upward with increased demand)

8. Neural Control of Coronary Circulation

9. Subendocardial Vulnerability

1. Myocardial contraction itself impedes blood flow to this innermost layer
2. It has the highest O₂ demand (greatest wall stress per Laplace's law)
3. The transmural perfusion gradient that normally favors the subendocardium during diastole is lost when diastole is shortened (tachycardia) or CPP falls

10. Coronary Microvascular Dysfunction (CMV)

• Barash, Cullen, and Stoelting's Clinical Anesthesia, 9e - "Coronary Physiology," pp. 857-864
• Sabiston Textbook of Surgery, The Biological Basis of Modern Surgical Practice - "Coronary Artery Anatomy and Physiology," pp. 2483-2484