Myocardial Oxygen Supply-Demand Balance

Part 1: Determinants of Myocardial Oxygen Demand (MVO₂)

1. Heart Rate

• The most important determinant. Increased heart rate increases oxygen consumption per unit time AND shortens diastole (the phase during which 70-80% of coronary blood flow occurs), simultaneously increasing demand and reducing supply.
• The relationship between heart rate and diastolic duration is nonlinear - small increases in rate disproportionately shorten diastole.
• This dual effect makes tachycardia the most dangerous hemodynamic perturbation for myocardial oxygen balance.

2. Myocardial Contractility (Inotropy)

• Greater contractile force requires more ATP and therefore more oxygen.
• Increased catecholamine stimulation (pain, anxiety, light anesthesia, laryngoscopy) raises contractility and MVO₂.

3. Myocardial Wall Tension (Wall Stress / Afterload & Preload)

• Hypertension dramatically increases afterload and MVO₂.
• Ventricular dilatation (e.g., heart failure) increases radius and thus wall tension even at normal pressures.
• Myocardial hypertrophy reduces wall thickness → further increase in wall tension per unit.

Minor Determinants

• Basal metabolic rate - constant, obligatory oxygen consumption for cell integrity (~20-25% of total MVO₂)
• Activation energy - electrical depolarization accounts for a small fraction
• External work - primarily stroke volume × pressure (pressure-volume area)

Part 2: Determinants of Myocardial Oxygen Supply

A. Coronary Blood Flow

1. Coronary Perfusion Pressure (CPP)

• Left ventricle (LV): CPP = Aortic diastolic pressure - Left ventricular end-diastolic pressure (LVEDP)
  • Elevated LVEDP (e.g., heart failure, volume overload) critically impairs subendocardial perfusion
  • Hypotension directly reduces CPP
• Right ventricle (RV): Perfused during both systole and diastole (lower intramural pressures)

2. Duration of Diastole

• 70-80% of LV coronary flow occurs in diastole
• During systole, intramyocardial pressure from contraction compresses vessels, especially the subendocardium
• Tachycardia reduces diastolic time per minute → impairs perfusion
• The subendocardium is most vulnerable (highest wall tension, compressed first)

3. Coronary Vascular Resistance

• R1 - Large epicardial arteries (trivial in normal vessels; major site of atherosclerosis)
• R2 - Pre-arteriolar vessels (autoregulatory)
• R3 - Arteriolar and intramyocardial capillaries (metabolic regulation)

4. Coronary Autoregulation

• Vessels dilate with increased demand (metabolic: adenosine, CO₂, O₂) and with decreased perfusion pressure
• In significant CAD, vessels are already maximally dilated distal to stenoses; manipulating perfusion pressure is then the only effective intervention

B. Arterial Oxygen Content

1. Hemoglobin concentration - anemia directly reduces oxygen-carrying capacity
2. Hemoglobin saturation (SaO₂) - hypoxemia reduces supply
3. Dissolved oxygen (PaO₂) - minor contribution at normal PaO₂

Part 3: Factors Affecting Myocardial O₂ Supply-Demand Balance During Anesthesia

Factors That Increase Demand (and thus Risk of Ischemia)

Factors That Reduce Supply (and thus Risk of Ischemia)

Volatile Anesthetic-Specific Effects

• At controlled concentrations, volatile agents (sevoflurane, desflurane, isoflurane) provide ischemic preconditioning (cardioprotective) and reduce MVO₂ by reducing contractility and heart rate
• At excessive concentrations: myocardial depression + systemic vasodilation → hypotension → ↓ CPP
• Isoflurane raised early concern for "coronary steal" (vasodilation of non-stenotic vessels diverting flow away from stenotic territories), though clinical significance remains debated
• Desflurane can cause reflex tachycardia during rapid increase in concentration - directly harmful in CAD

Neuraxial Anesthesia Effects

• High thoracic epidural/spinal: sympathectomy → bradycardia + hypotension → ↓ CPP
• However, in CAD patients, the anti-sympathetic effect can be beneficial by reducing MVO₂ (lower heart rate, lower afterload)
• Risk: abrupt hypotension with single-shot spinal is poorly tolerated; gradual epidural titration is safer

Positive-Pressure Ventilation

• Increases intrathoracic pressure → reduces venous return → ↓ preload → may ↓ cardiac output
• Can reduce LVEDP (beneficial for subendocardial perfusion) or cause hypotension (harmful to CPP)
• PEEP elevates right heart pressures, may reduce coronary perfusion pressure

Summary Diagram

Key Perioperative Targets to Prevent Ischemia

• Miller's Anesthesia 10e, "Determinants of Myocardial Oxygen Supply and Demand," pp. 7585-7586
• Harrison's Principles of Internal Medicine 22e, "Pathophysiology of Ischemic Heart Disease," p. 2134
• Goodman & Gilman's Pharmacological Basis of Therapeutics, "Pathophysiology of Myocardial Ischemia," Fig. 31-1
• Morgan & Mikhail's Clinical Anesthesiology 7e, "Anesthetic Management in Valvular Disease," p. 770