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MED SURG II EXAM #1
Endocarditis, Atherosclerosis, Angina, CAD, MI
| Question | Answer |
|---|---|
| Angina Pectoris | Occurs from the need for oxygen exceeds the supply. Can be caused by physical exertion, exposure to cold, eating a heavy meal, and stress. |
| Stable Angina | Predictable and consistent pain that occurs on exertion and is relieved by rest or nitroglycerin |
| Unstable Angina | Symptoms increase in frequency and severity. May not be relieved with rest of nitroglycerin |
| Intractable Angina | Severe incapacitating chest pain |
| Variant Angina | Pain at rest with reversible ST segment elevation. thought to be caused by coronary artery vasospasm |
| Angina Pectoris Clinical Manifestations | Can be mild from indigestion, to choking, or heavy sensation in the upper chest. Ranges from minor discomfort to agonizing pain. may have a feeling of impending death. Pain felt deep in the chest behind the sternum, poorly localized pain that may radiate to the neck, jaw, shoulders, and inner asects of arms. Weakness and numbness in the arms, wrists, and hands, SOB, diaphoresis, palpitations, dizziness, and nausea or vomiting |
| Angina Nursing Management | Have the patient stop activities, place them in semi-fowler positions to reduce oxygen requirements. Assess if the pain is similar to past experiences, monitor ECG and vital signs. Give nitroglycerin, oxygen therapy |
| Atherosclerosis | Stenosis of the lumen, obstruction by thrombosis, aneurysm, ulceration, and an accumulation of lipids, calcium, blood, carbohydrates, and fibrous tissue, referred to as plaques. |
| Fatty Streak Lesions | Yellow and smooth, protruding slightly into the lumen of the artery and are composed of elongated smooth muscle cells. Seen in all people, even infants. Do not usually cause clinical symptoms |
| Fibrous Plaque Lesions | Composed of smooth muscle cells, collagen fibers, plasma components, and lipids. They are yellow and protrude to varioius degrees into the arterial lumen, sometimes completely obstructing it. Predominantly in the abdominal aorta and the coronary, popliteal, and carotid arteries. |
| Atherolsclerosis Risk Factors | Nicotine, diabetes, obesity, stress, sedentary lifestyle, hypertension, hyperlipidemia, elevated C-Reactive Protein, stress, hyperhomocysteinemia, increasing age, and genetics |
| Atherosclerosis Management | Reducing lipid levels through statins, bile acid sequestrnats, nictonic acid, fibric acid inhibitors, and cholesterol absorption inhibitors. |
| Atherosclerosis Nursing Management | Enhance arterial blood supply to a body part by positioning the body part below the heart. |
| Acute Coronary Syndrome | Emergent situation characterized by an acute onset of myocardial ischemia that results in myocardial death if interventions are not started immediately. Chest pain is sudden and continues despire rest and medication is the presenting symptom. It includes unstable angina, NSTEMI, and STEMI |
| Myocardial Infarction | Diagnosed with a 12-lead ECG, and should be obtained within 10 minutes from arrival in the ED. Expected T wave inversion, and ST Segment Eversion, with the development of an abnormal Q wave that develops within 1-3 days. |
| STEMI | Patient has ECG evidence of acute MI with characteristic changes in two continuous 12-lead ECG. In this type of MI, there is significant damage to the myocardium |
| NSTEMI | The patient has elevated biomarkers, but no definite ECG evidence of an MI. Less damage may be done to the myocardium |
| The main cardiomarkers | Troponin, Creatine Kinase, and Myoglobin |
| Troponin | Protein found in myocardial cells and regulates the myocardial contractile process. I and T are specific for cardiac muscles and are used as the most reliable critical markers for myocardial infarction. three levels will be obtained as they do not rise for a few hours, but they remain elevated for as long as 2 weeks. |
| Creatine Kinase MB | Found in many cardiac cells, therefore it increases when there has been myocardial damage to these cells. Elevated levels are an indication of an acute MI. The levels increase within a few hours, and peak within 24 hours |
| Myoglobin | A heme protein that transports ocygen. Levels start to increase 1-3 hours after infarction, and peaks within 12 hours after the onset of symptoms. The increase is not specific to an acute cardiac event, however negative results can be used to rule out an acute MI |
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