Chapter 21 Marini Acute Coronary Syndromes

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SECTION II • Medical and Surgical Crises

renal failure. Continuous monitoring of BP and ECG is necessary during its infusion. Prompt myocardial reperfusion, β -blocker ther- apy, and correction of electrolyte and metabolic abnormalities are vital in restoring electrical stabil- ity in these patients. One particular form of VT, IVR, deserves spe- cial mention. Usually self-limited, IVR is a series of wide QRS complexes of ventricular origin. When IVR occurs at a rate of 60 to 100 beats/min, it is termed “accelerated.” This rhythm most commonly occurs after reperfusion of ischemic myocardium or as an escape mechanism for patients with high- grade AV block. If perfusion is adequate, no treat- ment is indicated. Indeed, suppression may cause asystole. VT that occurs within the first 48 hours has little impact on the patient’s eventual outcome. However, that, which occurs after that time win- dow, usually arises from LV dysfunction and carries increased risk of mortality. These patients must be revascularized to the extent possible and considered for defibrillator implantation. Ventricular Fibrillation VF occurs in up to 10% of all cases of MI and is responsible for 65% of all deaths. Most deaths occur in the prehospital phase of care, usually within the first hour of ischemia. An additional 15% to 20% of patients suffer VF after hospitalization. If applied promptly, DC cardioversion can correct more than 50% of episodes of acute VF due to AMI. Defibrillation is successful in less than 25% if applied after 4 minutes of onset of VF. VF carries little prognostic import if defibrillation is successful and if the disturbance occurs as an isolated electri- cal event early in the course of an MI (within first 24 to 48 hours). Like VT, VF occurring after the first 48 hours of an AMI usually occurs in the setting of poor LV systolic function and carries a poor long- term prognosis and must be considered for implant- able cardioverter–defibrillators (ICD). Reversible factors increasing the risk of VF should be addressed promptly, and these include ongoing ischemia, elec- trolyte imbalances, anemia, hypoxemia, excessive catecholamine stimulation, or presence of pulmo- nary artery catheters or pacemakers in the heart. For refractory or recurrent VF, intravenous amio- darone or lidocaine is usually advisable after the initial resuscitation. Intravenous procainamide can be given in rare situations where the arrhythmia is

refractory to lidocaine or amiodarone. Magnesium sulfate (1 to 2 g intravenously) has been advocated as a safe, prophylactic antiarrhythmic agent, par- ticularly appropriate for patients with polymorphic VT or hypomagnesemia. Although magnesium is almost certainly safe in patients with normal renal function, commonly used doses are of questionable efficacy. Bradycardia Bradyarrhythmias occur more commonly in inferior and posterior MIs because of intense vagal stimu- lation and a higher incidence of sinoatrial (SA) and AV nodal ischemia resulting from occlusion of the right or circumflex coronary arteries. AV block and use of pacemakers are described in detail in Chapter 4. Bundle-branch blocks and infranodal high-grade AV blocks that occur in the setting of an anterior MI carry poor prognosis because of the extent of myocardial damage and usually need per- manent pacing if the patient survives. Acute right bundle-branch block (RBBB) occurs in about 5% of acute infarctions and is associated with increased mortality. Transcutaneous or transvenous pacing may be needed if there is symptomatic bradycardia. Acute LBBB, which complicates 1% to 5% of acute infarcts, is associated with a 25% rate of in-hospi- tal mortality and pacing may be needed in these patients as well. AF is not uncommon and is usually of acute onset. Acute and rapid AF can precipitate heart failure. The patient must be anticoagulated with IV heparin or enoxaparin (1 mg/kg SQ b.i.d.). Initially, the ventricular rate can be controlled with beta- blockers or calcium channel blockers. The patient should be cardioverted with IV amiodarone or by electrical means in situations of acute AF. Mechanical (Structural) Complications (Fig. 21-7) Pericarditis/Tamponade Post-MI pericarditis can be divided conveniently into two distinct types: acute early pericarditis and delayed pericarditis (Dressler syndrome). The pain of pericarditis may be distinguished from that of continued or recurrent myocardial ischemia by its failure to radiate to distant sites, its poor response to antianginal therapy, the presence of a friction rub, and its sharp, pleuritic, or positional nature.