Key result
Oxygen therapy is used in myocardial infarction to increase arterial oxygen content, supplying ischemic muscle to prevent necrosis and ventricular fibrillation, and to relieve pain and dyspnea.
This text discusses the physiological rationale for using oxygen therapy to relieve pain and dyspnea and to protect ischemic myocardium in patients with myocardial infarction.
Traditional rationale for oxygen in MI persists; leaves open net benefit in normoxemic patients without contemporary RCTs.
Oxygen therapy has been widely employed in the management of patients with coronary thrombosis and myocardial infarction because it has been reputed to relieve pain.1Thrombosis of a coronary artery leads to necrosis of the myocardium in the area supplied by this vessel. Adjacent to the necrotic muscle is viable but ischemic muscle, which gives rise to pain and represents a threat to the patient in that it, too, may undergo necrosis or give rise to ventricular fibrillation. One of the logical aims of therapy of myocardial infarction is to provide a more adequate supply of oxygen to the ischemic muscle until collateral circulation can develop. The inhalation of oxygen may accomplish this aim by increasing the oxygen content of the arterial blood so that each unit of blood carries more oxygen to the anoxic tissue. Oxygen therapy is also used to relieve dyspnea in myocardial infarction and to
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Craig W. Borden (1952) conducted a review in Myocardial infarction. Oxygen therapy was evaluated. Oxygen therapy is used in myocardial infarction to increase arterial oxygen content, supplying ischemic muscle to prevent necrosis and ventricular fibrillation, and to relieve pain and dyspnea.
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