Cardiovascular disorders- MI

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RATIONALE:

​Troponin I levels rise rapidly and are detectable within 1 hour of myocardial injury. Troponin I levels aren't detectable in people without cardiac injury. Lactate dehydrogenase is present in almost all body tissues and not specific to heart muscle. LDH isoenzymes are useful in diagnosing cardiac injury. CBC is obtained to review blood counts, and a complete chemistry is obtained to review electrolytes. Because CK levles may rise with skeletal muscle injury, CK isoenzymes are required to detect cardiac injury.

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Both glucose and fatty acids are metabolites whose levels increase after a myocardial infarction. Mechanical changes are those that affect the pumping action of the heart, and electro physiologic changes affect conduction. Hematologic changes would affect the blood​

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RATIONALE:

• Beta-adrenergic blockers work by blocking beta receptors in the myocardium, reducing the response to catecholamines and sympathetic nerve stimulation. They protect the myocardium, helping to reduce the risk of another infarction by decreasing the workload of the heart and decreasing myocardial oxygen demand.

• Calcium channel blockers reduce the workload of the heart by decreasing the heart rate.

• Narcotics reduce myocardial oxygen demand, promote vasodilation, and decreased anxiety.

• Nitrates reduce myocardial oxygen consumption by decreasing left ventricular end-diastolic pressure (preload) and systemic vascular resistance (afterload).

• Arrhythmias, caused by oxygen deprivation to the myocardium, are the most common complication of an MI.

• cardiogenic shock, another complication of MI, is defined as the end stage of left ventricular dysfunction. The condition occurs in approximately 15% of clients with MI.

• Because the pumping function of the heart is compromised by an MI, heart failure is the second most common complication.

• Pericarditis most commonly results from a bacterial of viral infection but may occur after MI.

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