Martha had just finished dinner with her husband, and they had just sat down to watch television. She is 72 years old and has had a history of angina. Shortly after they sat down, Martha said she had indigestion and went to take some antacid tablets. An hour later, she began to feel warm, restless, and anxious. Her husband noticed she was looking pale and said he would take her to a nearby walk-in clinic. By the time they arrived, Martha said her left arm and shoulder were sore. Suspecting Martha was having a heart attack, her husband turned the car around and rushed her to the hospital. Three hours after the onset of her symptoms, Martha was receiving oxygen, fibrinolytic therapy, and nitroglycerin in the emergency ward. Afterward, she was moved to the cardiac unit for STEMI. An ECG of Martha's heart demonstrated an elevated ST segment. What are the physiological effects of myocardial ischemia that produce this finding? What variables affect the ECG tracing of a patient with ACS? W

Martha had just finished dinner with her husband, and they had just sat down to watch television. She is 72 years old and has had a history of angina. Shortly after they sat down, Martha said she had indigestion and went to take some antacid tablets. An hour later, she began to feel warm, restless, and anxious. Her husband noticed she was looking pale and said he would take her to a nearby walk-in clinic. By the time they arrived, Martha said her left arm and shoulder were sore. Suspecting Martha was having a heart attack, her husband turned the car around and rushed her to the hospital. Three hours after the onset of her symptoms, Martha was receiving oxygen, fibrinolytic therapy, and nitroglycerin in the emergency ward. Afterward, she was moved to the cardiac unit for STEMI. An ECG of Martha's heart demonstrated an elevated ST segment. What are the physiological effects of myocardial ischemia that produce this finding? What variables affect the ECG tracing of a patient with ACS? W

•  Venetta 

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•  #1
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•  Answer

An elevated ST segment is indicative of acute, transmural ischemia. The result is a decreased resting membrane potential and shortened action potential in damaged myocardial fibers. The "current of injury" is what appears on the electrocardiogram. Variables affecting the ECG produced include the duration of the ischemic event, the extent of myocardial damage, and the location of the injury in the cardiac tissue.

Myocardial ischemia triggers anaerobic metabolism and subsequent inability for the heart to produce enough energy to function adequately. Fibrinolytic therapy dissolves clot formations so that reperfusion can occur and prevent, or limit, necrosis and microvascular damage. Nitroglycerin mimics endogenous nitric oxide from endothelial tissue and acts as a vasodilator to increase blood flow to cardiac tissue. Vasodilation reduces preload and afterload, therefore reducing demands on the heart. Because nitroglycerin relieves the pain associated with MI, it may assist in the reduction of the sympathetic response. This also contributes to decrease metabolic demand on the heart. The administration of oxygen increases hemoglobin saturation levels to ensure well-oxygenated blood is present in the coronary circulation.

Myocardial damage typically involves a necrotic zone, an area of injury, and an ischemic region. The inner necrotic zone is incapable of recovery or repair. The inflammatory response involves the migration of macrophages to this area to remove the necrotic tissue and cellular debris. Following this process is the lay down of granulation tissue and subsequent deposition of fibrin. Scar tissue finally replaces the area of ischemic insult and has the effect of decreasing extensibility and contractility of the cardiac wall. The initiation and conduction of action potentials are also compromised in the noncontractile area.