A myocardial infarction (MI) is an acute coronary syndrome resulting from prolonged ischemia of the heart muscle and occurs when blood flow to an area of the myocardium is insufficient to meet the myocardial oxygen requirements. Sustained ischemia causes tissue necrosis and irreversible cellular damage, which results in disturbances in mechanical, biochemical, and electrical function in the necrotic or infarcted area. The degree of altered function depends on the area of the heart involved and the size of the infarct.
MIs may be classified in a number of ways. A transmural MI involves the full thickness of the myocardium. A significant Q wave develops with a transmural infarction, so this may be referred to as a Q-wave MI. A subendocardial infarction only involves a partial thickness of the myocardium and is often classified as a non-Q-wave MI because a pathologic Q wave does not develop. MIs may also be classified as an ST-elevation MI or a non-ST-elevation MI (NSTEMI). In addition to these classification systems, many practitioners also describe an MI by the area of the heart that has been damaged (e.g., anterior MI, lateral MI, inferior MI).
The majority of MIs are caused by rupture of atherosclerotic plaque in a coronary artery, which leads to the release of substances that activate platelet aggregation and clotting factors and cause local vasoconstriction. Other less common causes include severe, persistent spasm of a coronary artery; severe or prolonged hypotension; a rapid ventricular rate; and cocaine use.
The classic symptom of an MI is intense retrosternal chest pain/discomfort. It is often described as a tight, heavy, squeezing, or crushing sensation or “heartburn”; may radiate to the left arm, neck, jaw, or back; lasts longer than 20 minutes; and is unrelieved by nitroglycerin and rest. However, 15% to 25% of infarctions go unrecognized because clients have only mild or no chest discomfort. Other signs and symptoms may include shortness of breath, diaphoresis, dizziness, weakness, pallor, nausea, and vomiting.
The extent of myocardial damage can be limited by early (within 4-6 hours of the onset of symptoms) restoration of coronary blood flow. This can be accomplished by injection of a thrombolytic agent to dissolve the clot obstructing the coronary artery or by a coronary angioplasty. In addition to early restoration of coronary blood flow, treatment with an antiplatelet agent, a beta blocker, an angiotensin-converting enzyme (ACE) inhibitor, and an HMG-CoA reductase inhibitor has been found to significantly reduce mortality following an MI. The prognosis for a client who has had an MI is largely influenced by size and location of the infarct, concurrent cardiovascular status, and promptness and effectiveness of treatment.
Risk for decreased cardiac output
Acute pain: chest pain/discomfort that may radiate to arm, neck, jaw, or back
Risk for activity intolerance
rupture of a portion of the heart (e.g., ventricular free wall, interventricular septum, papillary muscle)
infarct extension or recurrence
Deficient knowledge, Ineffective therapeutic regimen management, or Ineffective health maintenance
Disturbed sleep pattern