WEEK four response

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). 

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 mightthe 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).

 

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