Identify 4 risk factors that make Mrs Gray a likely candidate for ischaemic heart disease. Explain how each of these risk factors can contribute to the development of ischaemic heart disease.
Ischaemic heart disease also known as coronary artery disease is characterised by loss of oxygen and nutrients to myocardium due to insufficient coronary blood flow (Copstead & Banasik, 2010). In United States, about 250,000 people die every year due to ischaemic heart disease (McCann, 2009). Risk factors of ischaemic heart disease are categorised as modifiable and non-modifiable risk factors. In the case of Mrs. Judy Gray, the four major risk factors that make her a candidate for ischaemic heart disease are:
Non-modifiable risk factors:
Advanced age and women post menopausal- Mrs. Gray is 55 years old and she is post menopausal. According to McCance, Huether, Brashers, and Rote (2010), aging and post menopausal women are major risk factors of ischemic heart disease. Due to degenerative changes in the heart and blood vessels, persons aged 40 and above are at risk to develop coronary artery disease. Post menopausal women are also at risk due to decreased oestrogen level, decreased HDL (high density lipoprotein), and increased LDL (low density lipoprotein). These contribute to the development of atherosclerosis, which is the main cause of coronary artery disease (Copstead & Banasik, 2010).
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Family History- Mrs. Gray's father had a coronary artery bypass at the age of 57. Her aunt and uncle died in their 30's due to unexplained heart failure. According to McCann (2009), that research evidence confirmed that 250 genes are link to heart diseases and coronary artery disease. Some genes linked to coronary artery disease are low-density lipoprotein (LDL) receptor and apolipoprotein B-100. A mutation of low-density lipoprotein (LDL) receptor contribute to familial hypercholesterolemia and apolipoprotein B-100 causes LDL to stay longer in the plasma that result to very high LDL levels (McCann, 2009).
Modifiable risk factors:
c.) Hypertension- Mrs. Gray has a history of hypertension. According to Phibbs (2007), a person with hypertension increases the risk of coronary artery disease about 200%. Due to abnormally high pressure within the vessel, the cells in the lining of the coronary arteries are often damaged. The damaged endothelial lining speeds up the narrowing of the arteries. Cells begin to degenerate and form masses of fat called atheromas. These atheromas cause a blockage to the flow of blood through the vessels resulting to atherosclerosis (Hurst, 2008).
d.) Hypercholesterolemia- the cholesterol level of Mrs. Gray was 4.5 mmol/L; however, the ratio of her good cholesterol (HDL) to bad cholesterol (LDL) was lower than desirable meaning she has high level of LDL(bad cholesterol) . High level of LDL damages endothelium and causes accumulation of fatty plaques on endothelial lining and proliferation of smooth muscle cells that contribute to the development of coronary artery disease (Copstead & Banasik, 2010).
2.) Discuss the pathogenesis of myocardial infarction. Relate your discussion to Mrs Gray.
Mrs. Gray has developed myocardial infarction due to predisposing factors such as aging, post menopausal, family history of heart disease and hypertension and hypercholesterolemia. These risk factors contribute to the development of atherosclerosis which is the major cause of myocardial infarction. Normally, the coronary arteries supply blood flow sufficient to the myocardium to meet oxygen demand (McCance et al., 2010). When the endothelial cell layer of the coronary arteries are injured due to predisposing factors, the white blood cells, platelets, lipids and fibrins converge at the damaged site. Hence, causing the resident macrophages or foam cells to cluster at the injured lining and absorb oxidised cholesterol which consequently form into a mass of fat or atheroma. This atheroma narrows the arterial lumen (Turer & Hill, 2010). Due to gradual narrowing of arterial lumen, the collateral circulation develops which try to compensate myocardial perfusion distal to the obstruction (Port & Matfin, 2009). Then myocardial metabolism shift from aerobic to anaerobic that result to the increased lactic acid production which activate the nerve ending, thus causing pain and referred pain to Mrs. Gray. Then myocardial cells die due to insufficient oxygen that causes decrease in myocardial contractility, cardiac output and decrease arterial pressure. Hypoperfusion stimulates baroreceptors which cause stimulation of sympathetic receptors. The release of epinephrine and nor epinephrine increases the heart rate, peripheral vasoconstriction and myocardial oxygen demand. Then ventricular arrhythmias develop with elevated cardiac troponin, CK-MB, and lactate dehydrogenase. Due to spontaneous depolarisation and repolarisation of myocardial cells, the electrical conduction system is affected by injury, infarct and ischemia. Left ventricle impair its ability to pump blood due to extensive damage, causing blood to back up into the left atrium and finally in the pulmonary veins and capillaries of Mrs. Gray (McCann, 2005).
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3.) Explain the underlying pathophysiology of both ST elevation in Mrs Gray's ECG recording and the altered levels of Troponin. Discuss the relevance of these results in the diagnosis and treatment of Mrs Gray's condition.
Mrs. Gray had chest pain and her electrocardiogram (ECG) result shows ST segment elevation. This indicates that there is a reduced blood supply due to 100% occlusion of the anterior descending coronary artery that causes myocardial ischemia and cell injury (McCann, 2005). ST segment elevation leads to appropriate treatment to Mrs. Gray which includes BalIoon angioplasty and stent. In fact, ischaemic death of myocardial tissue is the main cause of the ST-segment elevation on the ECG reading of Mrs. Gray (Cohen, Roubin, & Kuepper, 2007). Within several minutes of myocardial infarction changes of cell structures occur like mitochondrial swelling and glycogen depletion. This will be reversible if blood flow is restored immediately, however, irreversible necrosis occur when there is severe ischemia in 20 to 40 minutes. ST elevation myocardial infarction (STEMI) causes multiple structural changes in the cardiac function of Mrs. Gray. This includes progressive changes in ventricular size, shape and thickness, early wall thinning, healing, hypertrophy and dilation of both infarcted and non-infarcted areas (Porth & Matfin, 2009).
Blood test was drawn from Mrs. Gray 2 hours post onset of symptoms and revealed Troponin T at 0.2 mcg/L. Normal range of Troponin within first 3 hours post onset is 0 to 0.2 mcg/L (Wood, Froelicher, Motser & Bridges, 2005). After 6 hours, it was repeated and revealed abnormally high level of Troponin T at 1.1 mcg/L. Cardiac Troponins are the most specific laboratory test to detect myocardial infarction (Bukkapatman, Robinson, Turnipseed, Tancredi, Amsterdam, Srivatsa, 2010 ). Normally, Troponin I and Troponin T are present in myocardium and become elevated within 3 hours after the onset of symptoms of myocardial infarction (Porth & Matfin, 2009).Due to myocardial cell death, troponin becomes elevated. Myocardial cell contains isoforms, a cardiac protein. These isoforms become elevated when there is leakage from fatally injured cells that have lost plasma membrane integrity (Copstead & Banasik, 2010).
4.) Describe the actions of GTN and morphine and explain why these 2 drugs were given to Mrs Gray.
Mrs. Gray experienced chest pain, when the ambulance officers arrived, they gave Nitrolingual Pump Spray (GTN) under her tongue.GTN is a form of nitrates which is the drug of choice for preventing and relieving acute angina (McCann, 2005). Nitrates have direct relaxing effect on vascular smooth muscle and causes vasodilation (Lehne, 2007). Nitrate acts by dilating blood vessel so that less blood will returns in the heart. This will reduce the volume of blood in the ventricle at the end of diastole or the preload. By decreasing the preload, nitrates reduce the ventricular wall tension and ventricular size resulting to reduce heart's workload and oxygen demand of the heart (Lehne, 2007).
Since Mrs. Gray's chest pain was not relieve with GTN, she was given morphine 2.5 mg via intravenously. Morphine is narcotic agonist that reduces the chest pain by binding opioid receptors within the peripheral nervous system and central nervous system (Schrefer, 2005). Morphine acts by mimicking the effects of endomorphines and produces therapeutic effects of analgesia. It also acts by dilating veins in the periphery and reducing cardiac preload and afterload (McCann, 2005).
5.) Explain the mechanism of action of any 2 of the drugs Mrs Gray was prescribed on discharge. Discuss the patient education you will give to Mrs Gray in relation to these drugs.
Upon discharge Mrs. Gray was prescribed Betaloc 2.5 mg daily. Bataloc is beta-adrenergic antagonist 1 that is known for long term prevention of angina. Beta-adrenergic antagonist acts by blocking beta-1 receptor in the heart, preventing norepinephrine and epinephrine from inhibiting beta receptor site (McCann, 2005). By blocking beta receptor, Betaloc decreases heart rate, decreases myocardial contractility, decreases oxygen demand of the heart and reduces myocardial ischemia severity to Mrs. Gray (Lehne, 2007). Instruct Mrs. Gray that before taking Betaloc, assess first her pulse, check for the quality and irregularity and withhold the drug if bradycardia is present. Ask her to take the drug with meal to prevent gastro intestinal upset. Ask Mrs. Gray to observe for the side effects of the drug which includes diarrhoea, nausea, vomiting, fatigue, and decreased sexual function. Instruct her to take blood pressure frequently while taking the drug to monitor signs of hypotension and shortness of breath. And if she missed a dose, take the next schedule dose and never double the dose (Schrefer, 2005).
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Another drug that was prescribed to Mrs. Gray is Crestor 5 mg once daily. Since the ratio of cholesterol level of HDL(good cholesterol) to LDL (bad cholesterol) of Mrs. Gray was lower than desirable meaning the more LDL in her plasma and less HDL, the greater risk of developing coronary heart disease (Lehne, 2007). High level of LDL contributes to the development of coronary heart disease, in contrast, high level of HDL reduces the risk of coronary heart disease (Lehne, 2007). Crestor (Rosuvastatin) is a form of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors or also known as statin that lowers the cholesterol level associated with LDL (Lehne, 2007). Crestor (Rosuvastatin) acts by inhibiting the hepatic HMG-CoA reductase, an enzyme that is responsible for the conversion of HMG-CoA to mevalonate . In response to the inhibition of cholesterol synthesis, the heptocytes causes to synthesis more LDL receptor, removing more LDL (bad cholesterol) from the blood (Lehne, 2007). Ask Mrs. Gray to monitor her cholesterol and triglyceride level regularly to check for the therapeutic response of the drug. Tell her that headache, diarrhoea, nausea, dyspepsia and epigastric distress are the occasional side effects of the drug. Instruct her that cholesterol-lowering diet is very important as part of her treatment (Schrefer, 2005).