What are the pharmacologic alternatives for treating myocardial ischemia in this patient?

What are the pharmacologic alternatives for treating myocardial ischemia in this patient?

Nitroglycerin and other nitrates exert their anti-anginal effects by dilating epicardial coronary arteries and decreasing left ventricular end-diastolic pressure due to systemic venodilation. Nitrates also cause mild arterial vasodilatation and may decrease the pressure work of the myocardium on that basis. The limiting factor of nitrate therapy is that large doses cause hypotension, which would lower myocardial oxygen supply, and reflex tachycardia may occur.

β-Adrenergic blocking drugs slow the heart rate, which has two beneficial effects on myocardial ischemia. First, the duration of diastole increases and improves coronary perfusion. Second, myocardial oxygen consumption is decreased. β-Adrenergic blockers also decrease myocardial contractility, and this also decreases myocardial oxygen consumption. Propranolol and metoprolol have been used for many years for intraoperative β-adrenergic blockade. Esmolol, a short-acting intravenous β-adrenergic blocker, has become increasingly popular among anesthesiologists because of its relative cardiac (β₁ receptor) selectivity and favorable pharmacokinetics.

Calcium-channel entry blockers are an important component of the medical therapy for patients with CAD. Their role as intraoperative agents for the management of myocardial ischemia is less clear. There is even some evidence that preoperative calcium-channel entry blocker therapy may increase the incidence of intraoperative myocardial ischemia.

Phenylephrine, a “pure” α-adrenergic agonist, is the agent of choice for the treatment of hypotension in myocardial ischemia because it increases diastolic pressure with no change (or a slight decrease) in heart rate. Drugs with β-adrenergic effects, such as ephedrine, dobutamine, and dopamine, would increase the heart rate, increase myocardial contractility, and decrease diastolic arterial pressure. All these β-adrenergic actions are undesirable during myocardial ischemia.

Clonidine is an α₂-adrenergic agonist, which is available only for the enteral route of application in the United States. Dexmedetomidine is a more selective α₂-adrenergic agonist than clonidine that can be intravenously adminis-tered. This class of drugs decreases sympathetic outflow from the central nervous system and plasma norepineph-rine concentrations. α₂-Adrenergic agonists ameliorate episodes of “breakthrough hypertension” that occur with surgical stimulation and postoperative stresses, attenuate increases in heart rate, and reduce myocardial oxygen demand. α₂-Adrenergic agonists potentiate anesthetic agents, can be used as sedatives, and decrease postoperative pain medication requirements. Thus, their role in the peri-operative treatment for patients with CAD seems to be very favorable. A review of recently published studies on the efficacy of α₂-adrenergic agonists in the perioperative treatment of cardiac risk patients indicates reduced risk of perioperative myocardial ischemia, but the incidence of myocardial infarction or death did not change. The exact role of this class of drugs in the cardiac risk patient has yet to be defined.