What physiological process is mainly responsible for the pain during a myocardial infarction?

The primary physiological process responsible for the pain experienced during a myocardial infarction is the decreased oxygen supply to the heart muscle. When there is a blockage in the coronary arteries, typically due to atherosclerosis or a blood clot, the heart muscle does not receive adequate oxygen. This lack of oxygen, known as ischemia, causes the heart cells to become distressed and release chemicals that stimulate pain receptors, leading to the characteristic chest pain.

This pain is often described as pressure, squeezing, or a feeling of heaviness, and it may also radiate to other areas such as the arms, neck, or jaw. The direct link between oxygen deprivation and pain stems from the heart muscle’s high metabolic demand and sensitivity to changes in oxygen levels. Consequently, when myocardial cells are ischemic, they trigger pain signals that are perceived by the brain, which are interpreted as discomfort or pain in the chest region.

Other options entail processes that can contribute to discomfort or pain in various contexts but are not the main physiological drivers during a myocardial infarction. For instance, localized nerve irritation might occur but is not the primary cause of ischemic pain. Inflammation of the pericardium is generally associated with a different type of chest pain, known as pericarditis