the pharmacologic alternatives for treating myocardial ischemia in this
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
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.