Medical and Nursing Management of Myocardial Infarction

I. Definition

• Myocardial infarction is destruction of myocardial tissue in regions of the heart abruptly deprived of adequate blood supply because of reduced coronary blood flow.

II. Risk Factors

• Coronary artery narrowing due to atherosclerosis, coronary artery spasm, or complete arterial occlusion by embolism or thrombus
• Decreased coronary blood flow due to hemorrhage or shock, causing a profound imbalance between myocardial oxygen supply and demand.

III. Pathophysiology

• In an MI, inadequate coronary blood flow rapidly results in myocardial ischemia in the affected area. The location and extent of the infarct determine the effects on cardiac function. Ischemia depresses cardiac function and triggers autonomic nervous system responses that exacerbate the imbalance between myocardial oxygen supply and demand. Persistent ischemia results in tissue necrosis and scar tissue formation, with permanent loss of myocardial contractility in the affected area. Cardiogenic shock may develop because of inadequate CO from decreased myocardial contractility and pumping capacity.

IV. Assessment/Clinical Manifestations/Signs and Symptoms

• Chest pain (typically, chest pain is persistent and crushing; located substernally with radiation to the arm, neck, jaw, or back; and unrelieved by rest or nitrates. A silent MI may produce no pain.)
• Diaphoresis and cool, clammy, pale skin
• Nausea and vomiting
• Dyspnea with or without crackles
• Palpitations or syncope
• Restlessness and anxiety or feeling of impending doom
• Tachycardia or bradycardia
• Decreased blood pressure
• Altered S3 heart sound (indicates left ventricular failure)
• Electrocardiogram: Myocardial ischemia causes the T wave to be larger and inverted; in epicardial myocardial ischemia, the ST segment is elevated; in endocardial myocardial ischemia, the ST segment is depressed.
• Serum enzyme studies reveal elevated levels of creatine phosphokinase; lactate dehydrogenase and troponin.
• The white blood cell count is elevated.

V. Medical Management

The goals of medical management are to minimize myocardial damage, preserve myocardial function, and prevent complications such as lethal dysrhythmias and cardiogenic shock.

• Obtain 12-lead ECG to be read within 10 minutes
• Obtain laboratory blood specimens of cardiac biomarkers, including troponin.
• Obtain other diagnostics to clarify the diagnosis
• Begin routine medical interventions. Emergency management of chest pain:
o M orphine IV (IV access and morphine if pain not relieved with nitroglycerin
o O xygen administration is initiated at the onset of chest pain
o N itroglycerin
o A spirin (if not already given in the outpatient setting)
• Evaluate for indications for reperfusion therapy: Percutaneous coronary intervention, thrombolytic therapy
• Full set of vital signs including oxygen saturation, labs including serum markers, pain assessment with focused history taking and physical examination.
• Continue therapy as indicated: intravenous heparin or low-molecular-weight heparin, Clopidogrel (Plavix) or ticlopidine (Ticlid), Glycoprotein IIb/IIIa inhibitor
• Complete bed rest for a minimum of 12 to 24 hours


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