Myocardial oxygen demand is determined primarily by heart rate and the workload of contraction (afterload/blood pressure), since increased cardiac work requires more ATP generated via oxidative phosphorylation in the electron transport chain, which depends on oxygen availability. When myocardial oxygen demand exceeds supply, the therapeutic principle is to reduce demand by lowering heart rate (e.g., via beta blockade) and reducing blood pressure, complementing supply-side interventions such as vasodilation to improve coronary perfusion. This is a core concept in cardiovascular pathophysiology and pharmacology, specifically within the supply-demand model of myocardial ischemia.
Myocardial oxygen demand is determined primarily by heart rate and the workload of contraction (afterload/blood pressure), since increased cardiac work requires more ATP generated via oxidative phosp…