Chapter 21 Marini Acute Coronary Syndromes

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CHAPTER 21 • Acute Coronary Syndromes

risk of symptomatic coronary disease for as long as 1 to 2 years. β -Blockers present significant risk for patients with seriously impaired left ventricular function and tendencies for congestive failure and shock and should not be used until hemodynamic stability is achieved. Nonetheless, given its proven benefits, it is curious that so few patients with MI uncomplicated by overt systolic dysfunction receive β -blocker therapy. Possibly, concerns over the potential side effects of therapy or lack of enthu- siasm over a “low-tech” treatment are responsible. Metoprolol and carvedilol are frequently selected as oral agents. (Suggested dosing regimens are listed in Table 21-2.) Absolute contraindica- tions to β -blockade include known drug hypersen- sitivity, severe active bronchospasm, type I or type II second-degree atrioventricular (AV) block, com- plete heart block, sinus bradycardia (pulse <60), hypotension (systolic blood pressure <100 mm Hg), or overt LV failure (i.e., cardiogenic shock or pul- monary edema). Relative contraindications include insulin-dependent diabetes, concurrent use of a calcium channel antagonist, a history of obstructive lung disease, bibasilar rales, heart rates approxi- mating 60 beats/min, systolic blood pressure near 100 mm Hg, and evidence for pulmonary venous hypertension (e.g., a wedge pressure higher than 20 mm Hg). If the blood pressure is marginal or if the history or physical examination suggests that the patient is prone to complications of β -blocker therapy, a short-acting intravenous agent such as esmolol (0.5 mg/kg load followed by 0.05 mg/kg/min Table 21-2.  b -Blocker Regimens Atenolol IV load: 5 mg repeated once after 10 minutes if pulse rate >60 Oral maintenance: 50 mg b.i.d or 100 mg daily Metoprolol IV load: 5 mg every 5 minutes, to a total dose of 15 mg Oral maintenance: 50–100 mg b.i.d Carvedilol IV load: 2.5 mg Oral maintenance: 12.5–25 mg b.i.d Propranolol IV load 0.1 mg/kg up to three times at 15-minutes intervals (hold for pulse <50–60) Oral maintenance: 10–80 mg p.o. every 6 hours

infusion) can be tried and terminated rapidly should adverse response occur. Insulin Infusion Hyperglycemia is quite common in patients with complicated AMI, as is the case with most acutely ill intensive care unit (ICU) patients. Influential trials have suggested that such patients benefit from aggressive control of blood glucose levels by insulin infusion. Although the wisdom of doing so is debated, current recommendations are to start all STEMI patients with a complicated course and those who exhibit sustained hyperglycemia on an insulin infusion, targeting blood sugars 100 to 140 mg/dL. Magnesium Infusion Clinical trials have not demonstrated benefit from routine infusion of magnesium in STEMI patients. However, hypomagnesemia occurs in 30% to 40% of patients with AMI and should be corrected with intravenous and/or enteral therapies. The level is kept greater than 2 mmol/L to minimize risk of poly- morphic ventricular tachycardia (VT) and ventricu- lar fibrillation (VF). Eighty-five to ninety percent of patients who sustain an AMI have coronary thrombosis. Fibrinolytics have been shown to limit infarct size, improve LV function, and reduce the mortality of certain patients with AMI by dissolving an intra- coronary clot and restoring myocardial blood flow. The thrombolytic agents available for clinical use are (1) streptokinase (SK), (2) tissue plasmino- gen activator (t-PA or alteplase), (3) recombinant plasminogen activator (r-PA or Retavase), and (4) TNK-tPA (tenecteplase). All four agents accelerate conversion of plasminogen to plasmin, an enzyme that attacks fibrin and breaks down fibrin-rich or red clot. SK binds to plasminogen to form an activator complex. TNK-tPA and t-PA are fibrin- specific agents that act on clot-bound plasmino- gen and, therefore, do not cause a systemic “lytic” state. SK and to some extent r-PA cause a systemic lytic state. This systemic action usually produces a hypercoagulable state by reducing circulating lev- els of fibrinogen and most clotting proteins, like Reperfusion Therapies (Fig. 21-6) Fibrinolytic Therapy M echanism of A ction and C hoice of A gent