Myocardial Infarction
MI, an acute coronary syndrome, results from reduced blood flow through one of the coronary arteries, which causes myocardial ischemia and necrosis. The infarction site depends on the vessels involved. For instance, occlusion of the circumflex coronary artery causes a lateral wall infarction; occlusion of the left anterior coronary artery causes an anterior wall infarction. True posterior and inferior wall infarctions result from occlusion of the right coronary artery or one of its branches. Right ventricular infarctions can also result from right coronary artery occlusion, can accompany inferior infarctions, and may cause right ventricular failure. In transmural (Q wave) MI, tissue damage extends through all myocardial layers; in subendocardial (non-Q wave) MI, usually only the innermost layer is damaged.
Males are more susceptible to MI than premenopausal females, although incidence is rising among females who smoke and take oral contraceptives. The incidence in postmenopausal females is similar to that in males. (See Coronary artery disease in females, page 212.)
Causes
MI results from occlusion of one of the coronary arteries. Such occlusion can stem from atherosclerosis, thrombosis, platelet aggregation, or coronary artery stenosis or spasm. Predisposing factors include:
aging
diabetes mellitus
elevated serum triglyceride, low-density lipoprotein, and cholesterol levels and decreased serum high-density lipoprotein levels
excessive intake of saturated fats, carbohydrates, or salt
hypertension
obesity
family history of coronary artery disease (CAD)
sedentary lifestyle
smoking
stress or a type A personality (aggressive, competitive attitude, addiction to work, chronic impatience).
In addition, use of drugs, such as amphetamines or cocaine, can cause an MI.
Complications
Cardiac complications of an acute MI include arrhythmias, cardiogenic shock, heart failure causing pulmonary edema, and pericarditis. Other complications include ventricular aneurysms, extensions of the original infarction, or rupture of the atrial or ventricular septum, ventricular wall, or valves. Mural thrombi, causing cerebral or pulmonary emboli, may also occur. Dressler’s syndrome (post-MI pericarditis) can occur days to weeks after an MI and cause residual pain, malaise, and fever. (See Assessing and managing complications of MI, pages 600 and 601.)
Typically, elderly patients are more prone to complications and death. Psychological problems can also occur, either from the patient’s fear of another MI or from an organic brain disorder caused by tissue hypoxia. Occasionally, a patient may experience a personality change.
Assessment
Typically, the patient reports the cardinal symptom of MI—persistent, crushing substernal pain that may radiate to the left arm, jaw, neck, and shoulder blades. He commonly describes the pain as heavy, squeezing, or crushing, and it may persist for 12 or more hours. However, in some patients—particularly elderly patients or those with diabetes—pain may not occur; in others, it may be mild and may be confused with indigestion.
Patients with CAD may report increasing anginal frequency, severity, or duration (especially when not precipitated by exertion, a heavy meal, or cold and wind). The patient may also report a feeling of impending doom, fatigue, nausea, vomiting, and shortness of breath. Sudden death, however, may be the first and only indication of an MI.
Inspection may reveal an extremely anxious and restless patient with dyspnea and diaphoresis. If right-sided heart failure is present, you may note jugular vein distention. Within the first hour after an anterior wall MI, about 25% of patients exhibit sympathetic nervous system hyperactivity, such as tachycardia and hypertension. Up to 50% of patients with an inferior wall MI exhibit parasympathetic nervous system hyperactivity, such as bradycardia and hypotension.
In patients who develop ventricular dysfunction, auscultation may disclose an S4, an S3, paradoxical splitting of S2, and decreased heart sounds. A systolic murmur of mitral insufficiency may be heard with papillary muscle dysfunction secondary to infarction. A pericardial friction rub may also be heard, especially in patients who have a transmural MI or have developed pericarditis.
Fever is unusual at the onset of an MI. However, a low-grade fever may develop during the next few days.
Diagnostic tests
For critical diagnostic test results, see Key abnormal diagnostic findings in MI, page 602. Other characteristic diagnostic results include the following:
Two-dimensional echocardiography shows ventricular wall dyskinesia with a transmural MI and helps evaluate the ejection fraction.
Scans, using I.V. technetium Tc99m, can identify acutely damaged muscle by picking up accumulations of radioactive nucleotide, which appears as a “hot spot” on the film. Myocardial perfusion imaging with thallium-201 reveals a “cold spot” in most patients during the first few hours after a transmural MI.
Assessing and managing complications of MI
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