The classic indication of impaired circulation to the myocardium is a distinctive type of chest pain called angina pectoris. The pain signifies insufficient oxygenation (ischcmia) of the myocardium; it occurs when the oxygen demands of the myocardium exceed the capacity of the coronary circulation to supply oxygen. In other words, angina represents a signal from the heart, indicating that the myocardium is not receiving sufficient oxygen to meet its needs at the moment. Because angina pectoris is usually the key to the diagnosis of CHD, it is essential to understand its clinical features.
Site of Pain. The pain of myocardial ischemia is located most often directly under the center of the breastbone. It may radiate from this substernal location to both sides of the chest, the left or right arm, the neck, the jaws, or the shoulders and upper back. In some instances the pain occurs only at these latter sites without a substernal component; this pattern, however, is much less common than central chest pain.
Quality of Pain. The discomfort is usually described as pressure, tightness, or constriction within the chest. Some patients place a clenched fist against the sternum in attempting to characterize the tight, constricting nature of the sensation. Although angina generally lasts for only a few minutes (as described below), the pain is steady and is not influenced by breathing, breath-holding, or change in body position. This constancy of the pain is a characteristic aspect of angina and is often more significant than other descriptive qualities (e. g., burning, pressure, or ” indigestion”).
Occurrence of Pain. Any situation that increases the myocardial demand for oxygen is capable of producing angina. In general, oxygen demand is determined by the amount of work the heart performs. As would be anticipated on this basis, the pain is usually brought on by physical effort which increases the heart rate and work and, in turn, myocardial oxygen requirements. Certain activities are especially prone to precipitate angina: walking uphill or against the wind, hurrying after meals, unaccustomed exercise. Conversely, angina is relieved by rest. As soon as physical activity stops the oxygen demand falls promptly and as a consequence the pain subsides. This relationship (activity — pain, rest — disappearance of pain) is typical of transient myocardial ischemia and distinguishes angina of effort from other nonischemic causes of chest pain in which this pattern does not occur. In addition to physical exertion, sudden emotional stress (e.g., anger, fear, or even the excitement of watching a football game) may induce an anginal episode. The mechanism is the same as with angina of effort: the workload of the heart is transiently increased beyond the ability of coronary circulation to satisfy the additional demands. In all, any physical or emotional stress that produces a sudden increase in the heart rate or elevation in blood pressure may induce angina.
Duration of Pain. Angina is characteristically of brief duration, lasting usually from 1-5 minutes before abating with rest. Occasionally the pain may last for more than 5 minutes, particularly if the stimulus for the attack persists. The cessation of pain indicates that the myocardial demand for oxygen has been met and that the oxygen deficit was only transient and not destructive to the myocardium. If the pain does not subside within minutes after rest, myocardial damage may be suspected.
Relief of Pain. Another distinctive feature of angina is the prompt relief of pain that follows the use of nitroglycerin. Failure of nitroglycerin, administered sublingually, to terminate ischemic pain is unusual and is cause for suspicion that the attack is not due to angina of effort. Nitroglycerin (and other nitrates) acts by dilating the coronary vessels, thus increasing the blood flow and oxygen supply to the myocardium. At the same time, nitrates lower the blood pressure and thereby reduce the workload of the heart by diminishing pumping resistance.
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