Myocardial oxygen (O₂) demand is influenced by several factors that increase the heart’s workload and energy consumption.
Factors That Increase Myocardial O₂ Demand:
✅ Increased Contractility – Higher force generation requires more ATP, raising oxygen consumption.
✅ Increased Afterload – Since afterload is proportional to arterial pressure (MAP), a higher MAP forces the heart to work harder.
✅ Increased Heart Rate – Faster beats shorten diastolic filling time, reducing coronary perfusion and increasing O₂ demand.
✅ Increased Ventricular Diameter – A larger ventricular radius increases wall tension according to Laplace’s Law, further raising O₂ requirements.
Laplace’s Law and Wall Stress:
Wall Tension=Pressure×Radius\text{Wall Tension} = \text{Pressure} \times \text{Radius}Wall Tension=Pressure×Radius Wall Stress=Pressure×Radius2×Wall Thickness\text{Wall Stress} = \frac{\text{Pressure} \times \text{Radius}}{2 \times \text{Wall Thickness}}Wall Stress=2×Wall ThicknessPressure×Radius
As the ventricle dilates, the heart compensates by increasing wall thickness (hypertrophy) to reduce stress and O₂ demand.
Coronary Oxygen Extraction:
- The coronary sinus carries the most deoxygenated blood in the body since the myocardium extracts ~75-80% of O₂ from coronary blood.
- Unlike other tissues, the heart increases O₂ supply mainly through coronary vasodilation, not higher extraction.
Clinical Relevance:
- Myocardial Ischemia (Angina, MI) occurs when O₂ demand exceeds supply.
- Beta-blockers reduce HR and contractility, lowering O₂ demand.
- Nitrates (e.g., nitroglycerin) decrease preload and wall tension, improving oxygen balance.
Optimizing cardiac O₂ demand is crucial in managing hypertension, heart failure, and ischemic heart disease.