NURS 6501N-38 Week4 Discussion Solution

NURS 6501N-38 Week4 Discussion Solution

NURS 6501N-38 Week4 Discussion Solution

Myocardial Infraction

The heart is a fist-sized organ in the center of our chest known to cause life-threatening conditions.  My favorite Cardiologist Dr. S.L. Wiggins (personal communication, n.d.) always quotes, “when your heart is having trouble you need to either call in a plumber or an electrician.”  Dr. Wiggins is referring to either blockage in the coronary arteries or issues with the electrical conduction system of the heart.  Sadly, the Centers for Disease Control and Prevention (CDC, 2015) report every 43 seconds a US citizen has an MI totaling approximately 735,000 individuals each year.  This discussion concerns the pathophysiology of myocardial infarction (MI), individual behaviors impacting the incidence of MI and the effect of dyslipidemia in MI.

NURS 6501N-38 Week4 Discussion Solution

Pathophysiology

Myocardial infarction (MI), or heart attack to most individuals, occurs when blood flow through coronary arteries is suddenly completely occluded, resulting in myocardial tissue ischemia or myocyte necrosis and death (Huether, & McCance, 2017).  The occluding blockage is usually due to ulceration or rupture and thrombosis of unstable plaque from atherosclerosis and is a mixture of fat, proteins, cholesterol, calcium and white blood cells (Huether, & McCance, 2017).  Other causes of ischemia and possible infraction are due to decreased blood flow and oxygen, such as anemia, coronary spam, dysrhythmia, hypotension, and hypoxemia (Huether, & McCance, 2017).  Typically, occlusion or decreased blood flow occurs in one of the three coronary arteries or off a major branch of the coronary arteries.

In as little time as 8-10 seconds, tissue ischemia can occur due to lack of oxygenated, nutrient rich blood flow causing an anaerobic process to take over resulting in an acidotic state leaving the myocardium vulnerable to damaging effects and increased risk of future heart failure (Huether, & McCance, 2017).  The early stage of ischemia is reversible when blood flow is restored (Huether, & McCance, 2017).  However, it is important to acknowledge in unstable angina plaque is complicated and MI with tissue death is highly possible.

The myocardial cells deprived of oxygen and nutrients lose contractility, diminishing the pumping action of the heart (Huether, & McCance, 2017).  Catecholamine’s from the sympathetic nervous system such as epinephrine and norepinephrine are released causing ectopy, dysrhythmias, and heart failure (Huether, & McCance, 2017).  Inflammatory responses also contribute to myocardial tissue injury.  Angiotensin II is secreted as well, contributing to damage by 1. increasing the workload of the myocardial tissue through peripheral vasoconstriction and fluid retention, 2. causing structural changes in the myocardium from remolding, 3. promotes catecholamine release (Huether, & McCance, 2017).

Myocardial cells begin apoptosis and cause tissue necrosis this leads to the secretion of troponins and creatine phosphokinase-MB (CPK-MB), detectable in serologic tests (Huether, & McCance, 2017).  Within 20-40 minutes’ tissue ischemia becomes irreversible and revascularization to distal tissue needs immediate attention to decrease long-term effects.  However, revascularization can exacerbate the ischemic injury, due to the release of toxic oxygen free radicals, calcium flux, and pH changes (Huether, & McCance, 2017).

When revascularization ensues before complete distal tissue necrosis, the infraction only involves the myocardium directly beneath the endocardium resulting in a subendocardial infarction (Huether, & McCance, 2017).  A subendocardial infarction is clinically classified as a non-ST elevation MI (NSTEMI), and usually presents on an electrocardiogram (ECG) as ST segment depression and T wave inversion (Huether, & McCance, 2017).  After 3-6 hours’ tissue necrosis extends the width of the entire wall resulting in a transmural infarction, clinically classified as an ST elevation MI (STEMI) and presenting on an ECG as ST segment elevation (Huether, & McCance, 2017).  NSTEMI or STEMI both result in myocardial functional and structural changes, which may not be apparent for several hours or days.  A temporary change is myocardial stunning which can contribute to dysrhythmias, heart failure and shock (Huether, & McCance, 2017).  Lasting functional impairment depends on infarction site and size of the lesion.

NURS 6501N-38 Week4 Discussion Solution

Behavior

Many factors are present in MI and are similar to any risk factor present in cardiovascular diseases.  Genetics, family history, advanced age, male gender or postmenopausal women (Huether, & McCance, 2017).  However, an individual’s behavior is the risk factor this section focus.  Personal behaviors such as tobacco and alcohol consumption, poor diet choices, obesity, sedentary lifestyle are all modifiable risk factors that can considerably reduce the risk for coronary artery disease (CAD), atherosclerosis and MI (AHA, 2016).  The CDC validates individuals with an understanding of heart disease, decreased individual participation in risky behaviors, reducing the overall possibility for CAD (Hurtado et al., 2014).  The Million Hearts educational initiative is government sponsored and designed to improve the cardiovascular health of the United States “by preventing 1 million heart attacks and strokes by 2017” (CDC Grand Rounds: The Million Hearts Initiative, 2012).  If preventive measures and healthy lifestyles are adopted earlier in life, individual’s health outcomes could be better in later in life (AHA, 2016).

Effects of Dyslipidemia

Dyslipidemia or abnormal levels of serum lipoproteins, such as cholesterol, lipids, phospholipids, and triglycerides (Huether, & McCance, 2017).  A diet high in cholesterol and fats leads to elevated bloodstream levels, causing migration of lipoproteins into vessel walls, oxidation, and phagocytosis resulting in the buildup of plaque seen in atherosclerosis (Huether, & McCance, 2017).  This plaque is what hardens, narrows the lumens of the coronary arteries and can sometimes rupture, thrombosis and cause an MI (Huether, & McCance, 2017.

NURS 6501N-38 Week4 Discussion Solution

References

American Heart Association (AHA) (2016.) Family history and heart disease, stroke.

Retrieved from http://www.heart.org/HEARTORG/Conditions/More/MyHeartandStroke

News/Family-History-and-Heart-Disease-Stroke_UCM_442849_Article.jsp#.

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Centers for Disease Control and Prevention. (2015). Heart attack. Retrieved from https://www.cdc.gov/heartdisease/heart_attack.htm

CDC Grand Rounds: The Million Hearts Initiative. (2012). MMWR: Morbidity & Mortality

            Weekly Report, 61(50), 1017-1021.

Huether, S. E., & McCance, K. L. (2017). Understanding pathophysiology (6th ed.). St. Louis, MO: Mosby.

Hurtado M, Spinner JR, Yang M, Evensen C, Windham A, Ortiz G, Tracy, R, Ivy, ED. (2014).

Knowledge and Behavioral Effects in Cardiovascular Health: Community Health Worker

Health Disparities Initiative, 2007–2010. Preventing Chronic Disease 2014;11:130250.

DOI: http://dx.doi.org/10.5888/pcd11.130250

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