Mechanism of Action/Pharmacology
Reduced rate of Phase 4 (precedes the sharp upstroke in Phase 0) depolarization
Has a methylester group and is hydrolyzed by red cell esterases (half-life 9 minutes)
Hemodynamic Effects
Decreases heart rate, contractility, and sometimes blood pressure. Note that beta blockers do not always decrease blood pressure, especially during acute administration, although esmolol is more likely than propranolol. Decreases myocardial work and usually increasing coronary blood flow (improved by a relative increase in diastolic time, potentially worsened if diastolic pressure gradients are decreased) improve the myocardial supply:demand ratio
Systemic
Unlike non-selective beta-blockers, esmolol does not block B2 receptors and thus is more likely to cause hypotension
Pulmonic
Because it is highly B1-selective, esmolol appears to be safe in patients with pulmonary disease
Cardiac
Clinical Use
Hemodynamic Control
Loaded at 0.5 mg/kg followed by an infusion of 50-300 ucg/kg/min. Used for blood pressure and heart rate control (especially in atrial fibrillation).
Alternative to Opioids
It has been well documented that even a single dose of fentanyl with induction can increase the incidence of PONV, increase post-operative opioid consumption, and delay PACU discharge [Sukhani R. Anesth Analg 83: 975, 1996]. In light of this, alternative agents may warrant consideration for control of hemodynamic changes, in particular the sympathetic response to noxious stimuli under general anesthesia – interestingly, two randomized controlled trials have show comparable or even favorable outcomes when esmolol is used in lieu of opioids to control sympathetic nervous system responses to noxious stimuli under general anesthesia [Coloma M et al. Anesth Analg 92: 352, 2001; Collard V et al. Anesth Analg 105: 1255, 2007]
