Angina occurs as a result of:

Angina pectoris is chest pain or discomfort that results from myocardial ischemia — a mismatch between myocardial oxygen supply and demand. When coronary artery disease narrows the arterial lumen, blood flow to the myocardium is insufficient to meet metabolic needs, particularly during exertion or stress. The resulting decreased oxygenation to the myocardium triggers anaerobic metabolism and accumulation of metabolic byproducts such as lactic acid, stimulating pain receptors in the cardiac tissue. This ischemic pain is the defining feature of angina. An increased heart rate due to stress does occur and can worsen the supply-demand mismatch, but it is a contributing trigger rather than the direct cause of anginal pain. An irregular heart rhythm describes dysrhythmias such as atrial fibrillation, which are separate conditions and not the mechanism behind angina. Increased workload from increased fluid describes conditions such as volume overload in heart failure, which can precipitate angina in susceptible patients but is not the primary and direct cause. The essential pathophysiological explanation for angina is inadequate oxygen delivery to the cardiac muscle, making decreased oxygenation to the myocardium the correct answer.