Thrombolysis in Critical Care Term Paper

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How do you diagnose acute myocardial infarction in the patient with chest pain? A rule-out diagnosis should be considered in any patient presenting to the accident and emergency department with complaint of chest pain. High risk findings include chest pain, known history of coronary artery disease, radiation of the pain to left arm or neck, pain which lasts more than one hour, and diaphoresis. Lower risk findings include a sharp pain, lasting longer than 48 hours and pain which can be fully reproduced with palpation over the area (American College of Cardiology, 2000). It is also important to remember that 23% of patients presenting to accident and emergency with gastro-intestinal symptoms such as indigestion or burning substernal pain are found to be experiencing myocardial infarction. In addition to the pain, AMI is diagnosed in the setting of any of the following: 1) ST-segment elevation in two or more contiguous leads (greater than or equal to 1mm in limb leads or greater than or equal to 2 mm in precordial leads) or new or presumably new left bundle branch block (LBBB) or ST-segment depression greater than or equal to 2 mm in V1 or V2 leads, 2) T-wave inversion or ST segment depression in any lead persisting for greater than 24 hours that is unrelieved by nitroglycerine. (National Guideline Clearinghouse, 2004). It can often times be difficult to make the diagnosis of AMI in the absence of ST-segment elevation, but clinical suspicion should remain high until the diagnosis is definitely ruled out.(DeBono, Hopkins, 1994) Most AMI are attributed to thromboses, that are clots which occlude one of the coronary arteries. These clots often form in an artery which has been previously narrowed from changes related to atherosclerosis. The atherosclerotic plaque inside the arterial wall sometimes cracks and triggers the thrombus formation. This clot in turn will disrupt the flow of blood and oxygen to the myocardium, leading to the death of myocardial cells from anoxia. This "dead area" then loses its ability to effectively contract, and the remaining, undamaged myocardium must then compensate for the dead tissue to contract the heart. It is difficult to estimate the prevalence of AMI. In the United States alone, as many as 200,000 to 300,000 people die each year before medical help is even sought. However, in 2002 approximately 1 million patients visited American hospitals with AMI (Institute for Clinical Systems Improvement).

The definitive diagnosis of AMI is best obtained by following a standard chest pain protocol. Most accident and emergency wards have these in place. It is standard to initially obtain a 12 lead electrocardiogram (ECG) and begin cardiac monitoring. Patient's routine laboratory studies include electrolytes, blood urea nitrogen (BUN), complete blood count (CBC) and markers for myocardial injury (Creatinine Kinase isoenzyme-myocardial (CK-MB) or troponin). Normal serial CK values rule out an acute infarction but are negative in the setting of acute unstable angina. A slight rise in CK-MB or troponin indicates myocardial injury but is not specific for ischemic syndromes. Troponin assay is highly sensitive for identifying acute coronary syndromes. Troponin has longer half life in the system than CK-MB but is less specific for the identification of infarction as opposed to repeated episodes of myocardial ischemia. As the total CK greater than two times the upper ranges of normal is indicative of infarction it can be used as an adjunct in diagnosis ischemia vs. infarction and also in determining the relative efficacy of reperfusion. Serum troponin may take up to six hours to become diagnostically sensitive enough (Dougan, 2001).

When the clinician has been able to rule out all other obvious diagnoses and the working diagnosis comes back to true AMI, there are several treatment options available. Two potential algorithms exist which have been approved by the American Heart association. The well-managed accident and emergency department will have clinical protocols in place to ensure each AMI patient receives the most comprehensive and appropriate treatment for his or her case. (Institute for Clinical Systems Improvement, 2002). In emergency management of AMI, once ECG evidence and clinical history present a working diagnosis, the patient should be placed on supplemental oxygen. Intravenous access should be established at two or three sights, especially if the clinician plans to use thrombolysis. Rapid volume expansion with normal saline as the fluid of choice may be indicated, with care taken for patients at risk for rapid decompensation for congestive heart failure (i.e., history of left ventricular dysfunction, poor ejection fraction). The patient should receive either intravenous or sublingual nitrates to lower blood pressure if needed, or to potentially relieve chest pain. It is also appropriate to administer analgesics or anxiolytics. Morphine sulfate would be the drug of choice at a dose rate of 2-5 mg IV every 5-10 minutes as needed. Benzodiazepines may also be used, as indicated in a selected patient population. The patient's vital signs must be carefully monitored and the consideration must be made to administer thrombolytic therapy within the first 30-60 minutes of therapy. Acute adjunctive medications must also be used, depending on vital signs, rhythms and the patient history. First, antiplatelet medication may be considered. Aspirin at 81, 160 or 325 mg or 300 mg clopidogrel (Plavix) with 81 mg Aspirin should be given as soon as possible to all patients even in the rule out diagnosis of acute MI. The first dose should be chewed to improve bioavailability. Acute aspirin therapy should of course be withheld from those patients who report true anaphylactic allergy. History of remote gastrointestinal bleed or stomach irritation with salicylates is not an absolute contraindication for rapid administration of aspirin.

If the patient is to receive early intervention with angiogram, many clinicians will prefer to avoid early use of clopidogrel and other medical therapies, especially in the setting of non-ST segment elevation AMI. In these cases it may be preferable to wait until it is clear that surgical revascularization is not clinically indicated (American College of Cardiology/American Heart Association, 2002). If clopidogrel is given and coronary artery bypass graft surgery is planned, clopidogrel should be held for five days before surgery owing to the risk of perioperative bleeding. Beta-blockers are shown in large scale clinical trials to reduce infarction mortality and should be considered. The dosing would be something like metroprolol, 5 mg IV every five minutes for three doses followed by 25 to 50 mg every six hours for forty eight hours. Patients who have a systolic blood pressure less than 100 mm Hg, heart rate less than 60 beats per minute, history of reactive airway disease and heart block greater than first degree all posses relative contraindications to beta blocker therapy. Beta blockers may cause bronchospasm in asthmatics. If a clinician is concerned about the use of a beta-blocker in patients with relative contraindication, then a longer acting beta blocker, like intravenous esmolol may be used. (Harrison's Textbook of Internal Medicine, 2003).

Nitrate medication is commonly used in management of AMI, although the mortality benefit has not been clearly demonstrated. The sublingual and intravenous forms of nitrates may be helpful as previously mentioned in reducing chest pain symptoms and in the acute treatment of congestive heart failure and hypertension. Because nitrates can cause hypotension and/or bradycardia, especially in patients with inferior myocardial infarction, at least one IV site should be established prior to nitroglycerin use. In the treatment of ventricular arrhythmia associated with AMI, Amiodarone is currently the drug of choice. No other anti-arrythmics are indicated for the treatment of AMI. Calcium channel blockers may be used in patients in who there are contraindications for beta blockers, but are contraindicated themselves for patients who have a reduced ejection fraction of congestive heart failure

The electrocardiographic findings specific to AMI have been discussed previously, but special attention must be paid to the finding of left bundle branch block. Left bundle branch block occurs when the transmission of cardiac electrical impulses are delayed or fail to conduct along the rapidly conducting fibers of the main left bundle branch or in both the left anterior and posterior fascicles of the myocardium. The left ventricle depolarizes slowly via cell-to-cell conduction spreading from the right to left ventricle. This results in a characteristic ECG pattern of prolonged QRS, absent Q. wave in leads I, AVL and V6. A prominent QS pattern is seen in lead V1 with or without a small initial R. wave. A tall, wide and often notched R. wave is seen in leads I, AVL and V6. A tall R. wave is seen in lead V6 (Goodacre, 2003)

Thrombolysis should be administered within 30-60 minutes of arrival to definitive care. As mentioned previously, acute myocardial infarction occurs when a clot occludes one or more of the coronary arteries, which may have been previously narrowed by atherosclerotic changes. In the damaged vessel, platelets are activated to clump at the defect site. Fibrin fibers settle out of the blood on top of the platelets. Fibrin fibers act as net, trapping red blood cells as they flow by.… [END OF PREVIEW] . . . READ MORE

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