TREATMENT Initial Therapy Goal is to relieve pain, minimize extent of infarcted tissue, and prevent/treat arrhythmias and mechanical complications.Aspirin (160–325 mg chewed at presentation, then 160–325 mg po qd) should be administered immediately. 121-2), thrombolysis should be initiated as quickly as possible (ideally within 30 min) in the emergency room or coronary care unit (CCU); pts treated within 3 h of initial symptoms benefit the most.In pts with contraindications to thrombolytic therapy (Fig.

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121 ACUTE MYOCARDIAL INFARCTION Harrison’s Manual of Medicine 121 ACUTE MYOCARDIAL INFARCTION Complications Ventricular Tachycardia Secondary Prevention Bibliography Early recognition and immediate treatment of acute MI are essential; diagnosis is based on characteristic history, ECG, and evolution of cardiac enzymes. 2) but more intense and persistent (30 min); not fully relieved by rest or nitroglycerin, often accompanied by nausea, sweating, apprehension. PHYSICAL EXAMINATION Pallor, diaphoresis, tachycardia, S4, dyskinetic cardiac impulse may be present. Jugular venous distention is common in right ventricular infarction.

ECG Q-wave MI ST elevation, followed by T-wave inversion, then Q- wave development (Chap. Non-Q-wave MI ST depression followed by persistent ST-T-wave changes without Q-wave development. CARDIAC ENZYMES Time course is important for diagnosis; creatine phosphokinase (CK) level should be checked every 8 h for first day: CK rises within 4–8 h, peaks at 24 h, returns to normal by 48–72 h.

For Q-wave MI (ST-segment elevation MI), early thrombolytic therapy with streptokinase, reteplase (r PA), or tissue plasminogen activator (t PA) can reduce infarct size and mortality and limit LV dysfunction. Complications include bleeding, reperfusion arrhythmias, and, in the case of streptokinase, allergic reactions.

Anticoagulation with heparin [60 U/kg, then 12 (U/kg)/h] is begun concurrently with the thrombolytic agent (Fig. Subsequent coronary arteriography is reserved for pts with recurrent angina or positive exercise test prior to discharge.

Cardiac-specific troponin T and troponin I are highly specific for myocardial injury and are the preferred biochemical markers for acute MI. NONINVASIVE IMAGING TECHNIQUES Useful when diagnosis of MI is not clear.

Echocardiography detects infarct-associated regional wall motion abnormalities (but cannot distinguish acute MI from a previous myocardial scar).Adequate beta blockade should be established; when that is not possible or contraindications exist, a calcium antagonist can be considered. Pain control: (a) Morphine sulfate 2–4 mg IV q5–10 min until pain is relieved or side effects develop [nausea, vomiting, respiratory depression (treat with naloxone 0.4–1.2 mg IV), hypotension (if bradycardic, treat with atropine 0.5 mg IV; otherwise use careful volume infusion)]; (b) nitroglycerin 0.3 mg SL if systolic bp 100 mm Hg; for refractory pain: IV nitroglycerin (begin at 10 µg/min, titrate upward to maximum of 200 µg/min, monitoring bp closely); (c) b-adrenergic antagonists (see below). Oxygen 2–4 L/min by nasal cannula (maintain O2 saturation 90%). Table 121-2 Indications for Swan-Ganz Catheter in Acute Myocardial Infarction BRADYARRHYTHMIAS AND AV BLOCK (See Chap.Pts at high risk should be triaged to cardiac catheterization with plans for revascularization if clinically suitable; pts who are clinically stable can be treated more conservatively with continued observation in the hospital and consideration of a stress test to screen for any provocable myocardial ischemia. 115) In inferior MI, usually represent heightened vagal tone or discrete AV nodal ischemia.If CHF improves on parenteral vasodilator therapy, oral therapy follows with ACE inhibitor (e.g., captopril, enalapril, or lisinopril–Chap.124) or the combination of nitrates plus hydralazine (Chap. CARDIOGENIC SHOCK Severe LV failure with hypotension (bp 2 weeks after initial infarct; aneurysm is confirmed by echocardiography and by left ventriculography.Pts treated after 12 h should receive the initial medical therapy noted above and, on an individual basis, may be candidates for ACE inhibitors (particularly if LV function is impaired). Begin aspirin and antithrombin therapy: either low-molecular-weight heparin (e.g., enoxaparin 1 mg/kg SC q12h) or IV heparin [60 U/kg followed by 12(U/ kg)/h, then adjust to maintain PTT at 2 × control).