PATHOPHYSIOLOGY OF ANGINA PECTORIS of the patient RISK FACTORS Family History of CHD Hypertension Smoking Stress Age and

e and gender (Male)

Infiltration of atherosclerotic plaque

Maturity of plaque into the arterial walls

Collects platelets, fibrim, and cellular debris

Platelet aggregation

Arterial occlusion caused By form of thrombus

Release of Prostaglandis Vessel spasm

Alteration in myocardial oxygen supply and demand Myocardial ischemia Reduce heart-pumping function Reduction of pumping deprives the ischemic cells of much needed oxygen and glucose Production and accumulation Initiate sensory receptors

CHEST PAIN

SUMMARY OF THE PATHOPHYSIOLOGY OF ANGINA PECTORIS Angina can be caused by any number of factors that prevents the heart muscle from getting enough blood and oxygen. One is during physician exertion related to the occupation of the patient, which can precipitate an attack, by increase myocardial oxygen demand. Likewise, stress or any provoking situation are also one factor in a way that during this time, the body release adrenaline which tends to increase the blood pressure by accelerating the heart rate and increases myocardial workload. Cigarette smoking contributes to the development of and severity of CAD in three ways: The inhalation of smoke increases the blood carbon monoxide level carrying hemoglobin, the oxygen carrying component of blood to combine more readily which carbon monoxide than oxygen, a decreased amount of available oxygen may decrease the heart ability to pump. The nicotinic acid in tobacco triggers the release of catecholamines, which raise both heart rate and blood pressure. Nicotinic acid can also cause the coronary artery to constrict. Cigarette smoking causes a detrimental vascular response and increase platelet adhesion, leading to a higher probability of thrombus formation.

Moreover, the anatomic structure of the coronary arteries make them particularly susceptible to the mechanism of atherosclerosis, that twist and turn as they supply blood to the heart thereby, create site susceptible to atheroma development. Although heart disease is most often due to antherosclerosis of the coronary arteries, other phenomena also reduce blood flow to the heart. Normally, the coronary arteries supply the myocardium with blood to meet the metabolic needs during varying workloads. The coronary vessels are usually quite efficient and perfuse the myocardium during diastole. When the heart needs more blood, the vessels lose their ability to dilate in order to supply the heart with extra blood. They cannot supply the myocardium with blood for normal workloads. A growing mass of plaque in the vessel collects platelet, fibrin and cellular debris. Platelet aggregation is known to release prostaglandins capable of causing vessel spasm. Myocardium ischemic occurs when either supply and demand is altered. Myocardium cells become ischemic within 10 seconds of coronary artery occlusion. After several minutes of ischemia, the heart pumping function is reduced. The reduction of pumping deprives the ischemic cells of much needed oxygen and glucose. The cells convert to an anaerobic metabolism, which leaves lactic acid as a waste product. As lactic acids accumulate, it may initiate sensory receptors and cause pain.