Chapter 21 Marini Acute Coronary Syndromes

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CHAPTER 21 • Acute Coronary Syndromes

5 days. Complications generally fall into one of two categories—electrical or mechanical. Because spe- cialized coronary care units are able to immediately detect and treat arrhythmias, mechanical complica- tions have assumed relatively greater importance. Electrical Complications A detailed discussion of arrhythmias, heart block, and the use of cardiac pacing is presented in Chapter 4. Tachyarrhythmias occur very com- monly within the first 3 days after MI as a result of the electrical instability caused by ischemic or dying cells. Fortunately, most early tachyarrhyth- mias are self-limited. These early arrhythmias have little prognostic import if they receive appropriate treatment when symptomatic. A major change in the philosophy of caring for patients with MI has occurred in the practice of tachyarrhythmia treat- ment. Whereas essentially all patients with MI once received prophylactic antiarrhythmic therapy (lido- caine) to suppress ventricular tachyarrhythmias, the use of routine arrhythmia prophylaxis is inadvisable. Amiodarone is now favored (over lidocaine) in those with sustained symptomatic VT and in those who have survived VF. Although effective in suppressing ventricular tachyarrhythmias and even succeeding at times when amiodarone fails, lidocaine infusion increases risk of asystole. Premature Ventricular Contractions PVCs occur in almost all patients with MI, but their incidence declines rapidly with time. (Baseline rates are usually restored within 24 to 72 hours.) Isolated unifocal PVCs are of little importance. However, in the setting of acute infarction, consideration should be given to treating PVCs if they are frequent and precipitate angina or hemodynamic instability. Besides myocardial reperfusion, use of β -blockers and correction of electrolyte imbalances (keeping potassium >4 mmol/L and magnesium >2 mmol/L) will help a great deal. Intravenous followed by oral amiodarone may be used if the patient continues to have troublesome ventricular arrhythmias. Although expensive, intravenous amiodarone has replaced lidocaine as the drug of choice for ventricular arrhythmias because of its effectiveness and safety profile. Lidocaine should probably be reserved for young patients with good pump function and for those unusual patients refractory to amiodarone. For patients with hepatic disease, poor LV function,

and high-grade AV block and for elderly patients, the risks of lidocaine usually exceed the benefits. In the skillfully monitored critical care unit, the development of early VT or VF is of little impor- tance because it is corrected rapidly by electrical cardioversion. Ventricular Tachycardia For patients with acute ischemia, sustained VT occurs commonly within the first 48 hours and usually needs suppression. If the patient becomes hemodynamically unstable during an episode of VT, immediate DC cardioversion should be performed. If the rate is less than 150/min and patient remains relatively stable, antiarrhythmic therapy should be tried. Amiodarone is the drug of choice for control, initially given as a 150- or 300-mg bolus, followed by an infusion of 1 mg/min for 6 hour and 0.5 mg/min for 18 hours. Oral amiodarone is usually overlapped with intravenous form of the medication and should be continued for 3 to 6 months. Lidocaine infusion can also be used in this situation. It is given in bolus of 75 mg intravenously, followed by 50 mg every 5 minutes × 3 (for a total of 225 mg). Bolus doses of this agent rapidly achieve therapeutic concentrations. It is important to use lean body weight in calculating lidocaine doses to avoid toxicity. After loading, a con- tinuous infusion of 1 to 2 mg/min is used for contin- ued control. Because lidocaine is eliminated by the liver, patients with hepatic disease, CHF with pas- sive hepatic congestion, and advanced age can have a reduced rate of clearance. In such patients, the load- ing dose should be lowered to 75 to 125 mg and the infusion rate to 0.5 to 1 mg/min. Toxicity usually is manifest as either a CNS alteration (e.g., agitation, somnolence, seizures, confusion, muscle twitching) or cardiac effect (hypotension, bradycardia, sinus arrest). Plasma lidocaine levels probably should be monitored on a daily basis in patients at highest risk for lidocaine toxicity and should be spot-checked in all patients who exhibit CNS alterations compatible with lidocaine toxicity. For patients who are refrac- tory to the effects of lidocaine in therapeutic doses, procainamide is given in an intravenous infusion at a dose of 20 mg/min loading dose until arrhythmia is suppressed, a total of 17 mg/kg is administered, hypotension occurs, or if QRS duration increases beyond 50%. Following the bolus, it is continued as an infusion at a dose of 1 to 4 mg/min. Procainamide can induce torsades de pointes in patients with hypokalemia, hypomagnesemia, LV dysfunction, and