Critical Analysis of Cardiac Artery Disease
Coronary artery disease (CAD) happens when the arteries that supply blood to the heart muscle become hardened and narrowed. This hardening and narrowing of arteries occurs because of two factors called plaque deposition and atherosclerosis. Plaque is made up of fat, cholesterol, calcium and other substances found in the blood. When plaque builds in the arteries, the condition is called atherosclerosis (Cotran et al, 2000).
Prolonged hypertension is one risk factor for development of CAD. When high pressure blood continues to flow through arteries and veins, it causes thickening of the arteries and veins which result in deposition of hard component like cholesterol and fatty acid deposit in the wall of arteries thus resulting in atherosclerosis.
The continued development of atherosclerosis involves an inflammatory response that begins with injury to the vascular endothelium. The presence of inflammation has multiple effects on the arterial wall including the attraction of inflammatory cells (including macrophages). The macrophages infiltrate the injured vascular endothelium and ingest lipids, which turns them into the foam cells. Activated macrophages release biochemical substances that can further damage the endothelium, attracting platelets and initiating clotting. Smooth muscle cells within the vessel wall subsequently proliferate and form a fibrous cap over a core filled with lipid and inflammatory infiltrate. These deposits called atheromas or plaques protrude into the lumen of the vessel, narrowing it and obstructing blood flow. If the fibrous cap of the plaque is thick and the lipid pool remains relatively stable, it can resist the stress from blood flow and vessel movement. If the cap is thin and inflammation is ongoing, the lipid core may grow, causing it to rupture and cause hemorrhage into the plaque. A rupture plaque is a focus for thrombus formation. The thrombus may then obstruct blood flow (Smeltzer et al, 2006).
Mrs. Suleena Devi was admitted to hospital crying with chest pain. It is the vital symptom of coronary artery disease. Sharp pain is commonly felt retrosternally and may radiate to the left or more rarely the right arm to the throat, jaw and teeth or through to the back and pain called angina. Angina develops when the epicardial arteries are stenosed by atherosclerosis (Mohan, 2008). The obstructed blood flow due to thrombus leads to inadequate supply of oxygen- rich blood to the heart muscles further resulting in ischemia. Ischemia causes the muscles to release acidic substances not removed by the slowly moving coronary blood flow. The high concentrations of acidic substances then stimulate pain nerve endings in the cardiac muscle, sending pain impulses through sensory afferent nerve fibers into the central nervous system (Guyton and Hall, 2006). Tablet Nitroglycerine (vasodilator) 5mg sublingually was ordered to relieve her from the chest pain and to improve coronary perfusion. Moreover, this drug may reverse myocardial ischemia by increasing and redistributing coronary blood flow (Katzung, 2001).
On admission, the patient was suffering from tachycardia. Her pulse was 120/min. Tachycardia means increased heart rate than normal (Kasper, 2005). Patient had previous history of blood pressure that increased stiffness/resistance in the peripheral arteries throughout the tissues of the body. This resistance causes the heart muscle to work harder to pump the blood through these blood vessels. The increased workload, due to the narrowing and hardening of the arteries, can put a strain on the heart which can lead to tachycardia (Goldman and Ausiello, 2007). Aspirin is an anticoagulant drug that decreases platelet aggregation and inhibits thrombus formation. It also inhibits prostaglandins synthesis action which prevents formation of the platelet aggregating substance thromboxanes A2. Prostaglandins are local hormones produced in the body and thromboxanes are responsible the aggregation of platelets that form blood clots (Tripathi, 2000).
Electrocardiography shows S T segment elevation. It occurs when thrombus forms on a ruptured atheromatous plaque and occludes an epicardial coronary artery and abnormal Q wave occurs due to narrowing of arteries (Goodman and Gillman, 2001).
Overall management was good. Mrs. Suleena Devi was treated symptomatically and discharged in satisfactory condition.
