Chapter 21 Marini Acute Coronary Syndromes

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SECTION II • Medical and Surgical Crises

FIGURE 21-3. Steps in balloon angioplasty with intracoronary stent deployment.

ACS but are contraindicated in acute heart failure, coronary artery spasm, or severe bronchospasm. Selective β -blocking agents such as carvedilol may be used cautiously in patients with modestly impaired ejection fractions and tachycardia, but, in general, should be withheld until stability is achieved. Increasing Myocardial Oxygen Supply The most important treatments under this category are the strategies for myocardial revascularization, which include percutaneous coronary angioplasty, coronary stenting, and coronary artery bypass sur- gery (dealt with later in this chapter). Myocardial oxygen supply can also be increased simply by boosting hemoglobin saturation or elevating hemo- globin concentration to levels higher than 9 g/dL, in severely anemic patients. Pharmacotherapy is also necessary to optimize myocardial perfusion. Nitroglycerin (NTG) is used commonly and may be administered sublingually, orally, transcutaneously, or intravenously. (For unstable patients, the intravenous route is most eas- ily regulated and reliable.) In addition to dilating coronary vessels, NTG also decreases wall tension of the LV by reducing preload and, to a lesser extent, afterload. Acting through these mechanisms, NTG also reduces the risks of life-threatening arrhythmias in acute ischemia. Nitrates are effective both for classical and variant angina because of their direct coronary vasodilating properties. NTG is titrated to relieve chest pain or to reduce blood pressure by 10% to 20%. Usually, intravenous doses of 0.7 to 2.0 μ g/kg/min suffice. Intravenous NTG usually

is begun at 5 to 15 μ g/min and titrated upward as necessary in increments of 5 μ g/min every 5 minutes up to a maximum dose of 200 μ g/min. Headache is a common side effect but usually responds to simple oral analgesics. When the dose is excessive or the patient is dehydrated, hypo- tension and reflex tachycardia result from NTG- induced vasodilation. These adverse effects usually can be offset by volume expansion or α -agonist therapy. Because ethanol is used as a vehicle for NTG infusions, violent adverse reactions may occur in those rare patients taking Antabuse. Obviously, use of high doses of NTG for prolonged periods may also produce alcohol intoxication. Within 48 to 72 hours of initiating NTG therapy, tolerance is often observed, necessitating higher infusion rates. Seldom seen problems induced by NTG therapy include increased intraocular and intracranial (IC) pressures and methemoglobinemia. Coronary spasm, a major contributor to myocar- dial ischemia provoked by the irritating products of plaque rupture, may be ameliorated by nitrates or calcium channel blockers. Blockers of slow calcium channels (e.g., nifedipine, nicardipine, and amlo- dipine) can be rapidly effective in reversing coro- nary spasm. In UA, these drugs should be viewed as adjuncts to nitrate, β -blocker, and antithrombotic therapy. Because calcium antagonists have vasodi- lating, negative inotropic, and positive chronotropic actions, they may not always be well tolerated. If coronary vasodilating effects predominate, myo- cardial oxygen supply–demand balances benefits. Conversely, if systemic vasodilation, hypotension, and reflex tachycardia predominate, myocardial