diagnosis consistent with John’s history and physical exam is a type of acute coronary syndrome known as myocardial infarction (MI), specifically a ST-elevation myocardial infarction (STEMI)

Discussion #1

The diagnosis consistent with John’s history and physical exam is a type of acute coronary syndrome known as myocardial infarction (MI), specifically a ST-elevation myocardial infarction (STEMI). A MI results from an interruption or complete obstruction in bloodflow through the coronary arteries for a prolonged period of time by a thrombus, which leads to the death of heart muscle cells (myocyte necrosis) (McCance &Huether, 2014). Atherosclerotic CAD, coronary spasms, and/or coronary artery embolisms are all possible causes of a MI.

A MI can be subdivided into two categories: STEMI and non-STEMI. This depends on where the infarction occurs. If the thrombus breaks apart before complete death of the tissue distant from the site results, it will only affect the subendocardium, and be termed a Non-STEMI. On a ECG, a non-STEMI (subendocardial MI) will present itself with inverted T waves and ST depression. Although the less severe of the two type of MI, non-STEMI patients are at risk of recurrent clot formation on the disrupted plaque and require intervention. Transmural infractions (STEMIs) occur when a clot is permanently lodged in the vessel and affects the endocardium all the way through to the epicardium (McCance &Huether, 2014). Marked ST elevation will be visible on the ECG of a STEMI patient and immediate intervention is required to restore coronary bloodflow.

When atherosclerotic plaque builds up in the coronary arteries, it can be disrupted by means of ulceration or rupture. This occurs “because of shear forces, inflammation with release of multiple inflammatory mediators, secretion of macrophage-derived degradative enzymes, and apoptosis of cells at the edges of the lesions” (McCance &Huether, 2014, p. 1156). When the plaque is disrupted, the clotting cascade is activated due to the exposed vessel wall and platelets aggregate to the site forming a thrombus and causing obstruction of the vessel. Vessel obstruction is further exacerbated when thromboxane A2 and endothelin, vasoconstrictors, are realeased during the process (McCance &Huether, 2014). This ischemic injury can lead to infarction of the heart muscle.

Angina pectoris is the term used to describe chest pain that is often caused by myocardial ischemia (a lack of blood supply to the heart). The pain is the result of lactic acid accumulation irritating nerve fibers in the myocardium (McCance &Huether, 2014). Silent ischemia is a lack of bloodflow, and therefore oxygen, to the heart that does not produce pain, and is commonly experienced in individuals with mental stress, women, and diabetics. “Myocardial ischemia also can result from other causes of decreased blood and oxygen delivery to the myocardium, such as coronary spasm, hypotension, dysrhythmias, and decreased oxygen-carrying capacity of the blood (anemia, hypoxemia)” (McCance &Huether, 2014, p. 1153).

Over 400,000 annual deaths in the U.S. are related to sudden cardiac death (Sara, Eleid, Gulati, & Holmes, 2014). Three factors associated with sudden cardiac death (SCD) include: coronary artery disease (CAD), myocardial ischemia and infarction, and dysrhythmias. Coronary artery disease occurs when the coronary arteries become hardened and/or narrowed due to the buildup of plaque (atherosclerosis).“Myocardial ischemia is the most common underlying causal disorder for SCD” (Wang, Wang, Wu, Su, Kong & Yu, 2017, para. 1). As previously stated, myocardial ischemia is a lack of blood supply to the myocardium from occluded coronary arteries. Dysrhythmias, particularly ventricular fibrillation, are one of the major contributing factors that result in sudden cardiac death.

Post-MI complications are related to the location of the MI, the extent of the MI (subendocardial vs transmural), the physiological condition of the individual prior to the MI, and the immediacy of therapeutic intervention to treat the occluded arteries (McCance &Huether, 2014). The most common complication post MI are abnormal heart rhythms, or dysrhythmias, caused by hypoxia, lactic acidosis, and electrolyte abnormalities to name a few. After a MI, the heart undergoes functional changes such as decreased cardiac contractility, left ventricular compliance alteration, decreased stroke volume, decreased ejection fraction, increased left ventricular end-diastolic pressure (LVEDP), and SA or AV node malfunction, which can lead to heart failure (McCance &Huether, 2014). Another common complication of acute MIs is inflammation of the pericardium, termed pericarditis. Patients often experience chest pain 2-3 days after an MI that worsens upon respiratory effort and can be verified with auscultation of a pericardial friction rub (McCance &Huether, 2014). 

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