cardiovascular disorders
Angina Pectoris
Pathophysiology of Angina Pectoris
Angina may be Stable Unstable Instable angina,the relationship between workload or demand and ischemia is usually relatively predictable. Unstable Angina is clinically worsening angina (eg, angina at rest or with increasing frequency and/or intensity of episodes). Atherosclerotic arterial narrowing is not entirely fixed; it varies with the normal fluctuations in arterial tone that occur in all people. Thus, more people have angina in the morning, when arterial tone is relatively high. Also, abnormal endothelial function may contribute to variations in arterial tone; eg, in endothelium damaged by atheromas, stress of a catecholamine surge causes vasoconstriction rather than dilation (normal response). As the myocardium becomes ischemic, coronary sinus blood pH falls, cellular potassium is lost, lactate accumulates, ECG abnormalities appear, and ventricular function (both systolic and diastolic) deteriorates. Left ventricular (LV) diastolic pressure usually increases during angina, sometimes inducing pulmonary congestion and dyspnea. The exact mechanism by which ischemia causes discomfort is unclear but may involve nerve stimulation by hypoxic metabolites. 