What are the possible complications post-MI might the NP be aware of when caring for John?

Discussion #2

1. What diagnosis is consistent with John’s history and physical exam?

John’s history and physical exam indicates that he has acute coronary syndromes acute coronary syndrome results when there is sudden coronary obstruction caused by thrombus formation over a ruptured atherosclerotic plaque. John’s stable angina progressed to unstable angina. Unstable angina is angina that occurs randomly without any physical exertion. It is usually a sign of an impending myocardial infarction. According to John’s physical exam and symptoms he had a myocardial infarction. He was awakened from sleep with more aggressive symptoms such as chest pain and shortness of breath. This time the pain radiated to the jaw and left arm. His diaphoresis and paleness are the result of lack of oxygen caused by ischemia. MI is suggestive of a STEMI or NSTEMI and his ECG shows an ST elevation (McCance & Huether, 2014).

2. Please differentiate between a STEMI and Non-STEMI

A STEMI is the result of sudden clot formation completely blocking an artery in the heart. The damage covers a large area of the heart and extends deep into the heart muscle. A NSTEMI heart attack does not extend through the full depth of the heart muscle (“Heart Attack,” n.d.). An NSTEMI presents with ST depression and T wave inversion. A STEMI shows elevated ST segments and this infarction extends from the endocardium to epicardium and myocardium (McCance & Huether, 2014).

3. What are the pathophysiological findings specifying an MI?

The pathophysiological findings associated with an MI includes symptoms of ischemia such as chest pain, diaphoresis, and palor. ECG changes should indicate new ischemia such as ST elevation. New pathological Q waves develop and this indicates an MI. A pathological q wave is a q wave that is more than 0.04 seconds in duration and more than 25 percent of the size of the following R waves in that lead. Elevation of the cardiac markers in the blood and cardiac imaging changes are also indicative of an MI (“ECG’s in Acute,” n.d.).

4.What are the differences between angina, silent ischemia, and myocardial ischemia?

Angina- chest pain caused by myocardial ischemia.

Myocardial ischemia- occurs when myocardial oxygen demands exceed oxygen supply.

Silent ischemia- myocardial ischemia in the absence of chest discomfort or angina (Mahler, n.d.).

5.Provide a description of the three factors associated with Sudden Cardiac Death.

Myocardial stunning- When the heart loses its contractile function. It can persist for hours to days after perfusion has been restored. Stunning is the result of a change in electrolyte pumps, calcium homeostasis, and the release of toxic oxygen radicals. Stunning can lead to heart failure, shock, and dysrhythmias.

Hibernating myocardium- Ischemic tissue that undergoes metabolic adaptation to prolong cardiac cells survival until perfusion can be restored.

Myocardial remodeling- Myocyte hypertrophy, scarring, and loss of contractile ability in the areas of the heart distant to the site of infarction.

6.What are the possible complications post-MI might the NP be aware of when caring for John?

The possible complications post MI the NP might be aware of are arrhythmias and pericarditis. Dysrhythmias are alterations in cardiac rhythm which can be caused by ischemia, hypoxia, and lactic acidosis. Pericarditis is inflammation of the pericardium. Pericardial friction rub happens two to three days after an MI and it is associated with anterior chest pain that happens with respiratory effort. Corticosteroids can relieve symptoms, but treatments are usually not required (McCance & Huether, 2014).