Reference no: EM133948285
Overview
Coronary artery disease (CAD) is a type of blood vessel disease associated with atherosclerosis. Endothelial injury and inflammation play central roles in the development of atherosclerosis. Once endothelial injury has occurred, lipoproteins (carrier proteins within the bloodstream) transport cholesterol and other lipids into the arterial intima. Over time, the deposition of cholesterol and lipids causes the formation of fibrous plaque, resulting in narrowing of the vessel lumen and a reduction in coronary artery blood flow. The final stage of plaque development results in a complicated lesion that can rupture, attract platelets, and cause the formation of a thrombus. The thrombus may adhere to the wall of the artery, leading to further narrowing or total occlusion of the artery. CAD develops slowly over many years, and clinical manifestations are not apparent in the early stages of the disease process. However, there are associated risk factors that can identify persons at risk for CAD. Interventions can then be prescribed to modify these risk factors and reduce the onset and progression of the disease.
Chronic stable angina, a clinical manifestation of CAD, refers to chest pain that occurs intermittently over a long period with the same pattern of onset, duration, and intensity of symptoms. It is transient (reversible) chest pain that occurs when the heart muscle becomes ischemic during exertion or increased cardiac activity. It subsides when the precipitating factor is resolved and/or when nitroglycerin is provided, and no permanent injury to cardiac cells occurs.
When ischemia is prolonged and not immediately reversible, acute coronary syndrome (ACS) develops and includes the spectrum of unstable angina (UA), non-ST-segment-elevation myocardial infarction (NSTEMI), and ST-segment-elevation myocardial infarction (STEMI). The patient presenting with unstable angina is at high risk for developing an MI and thus must be treated aggressively. Myocardial infarction occurs as a result of sustained ischemia, causing irreversible cell death (necrosis) of the myocardium. Contractile function of the heart stops in the areas of myocardial necrosis, and the degree of altered function depends on the area of the heart involved and the size of the infarction.
Case Study
G.G. is a 62-year-old white male with a 15-year history of CAD and hypertension. He had an anterolateral MI 2 years ago. He also has a history of hyperlipidemia, type 2 diabetes mellitus, and chronic renal insufficiency. His father died of sudden cardiac death at age 44, and his mother died while undergoing a coronary artery bypass graft (CABG) at age 68. His hypertension is treated with hydrochlorothiazide and verapamil (Calan), and he takes metformin (Glucophage) for control of his diabetes and atorvastatin for his high cholesterol. He is a current cigarette smoker with a 45 pack-year smoking history and drinks a beer almost daily. He is 5'10" tall, weighs 209 pounds, and does not regularly exercise. He tries to watch what he eats, but he travels a lot as a computer consultant, and it is difficult to maintain a healthy, diabetic diet when he is out of town.
Questions
1. Identify relevant assessment data for a patient with ACS.
2. Evaluate results of diagnostic studies for a patient with ACS.
3. Prioritize nursing interventions for a patient with acute chest pain.
4. Develop a nursing care plan for a patient with ACS.
5. Describe the appropriate treatment for a patient with complications of ACS.
6. Formulate an individualized teaching plan for a patient with ACS.