Propranolol nonselectively blocks β1- and β2-receptors. Arterial blood pressure is lowered by several mechanisms, including decreased myo-cardial contractility, lowered heart rate, and diminished renin release. Cardiac output and myo-cardial oxygen demand are reduced. Propranolol is particularly useful during myocardial ischemia related to increased blood pressure and heart rate. Impedance of ventricular ejection is benefi-cial in patients with obstructive cardiomyopathy and aortic aneurysm. Propranolol slows atrio-ventricular conduction and stabilizes myocardial membranes, although the latter effect may not be significant at clinical doses. Propranolol is particu-larly effective in slowing the ventricular response to supraventricular tachycardia, and it occasionally controls recurrent ventricular tachycardia or fibril-lation caused by myocardial ischemia. Propranolol blocks the β-adrenergic effects of thyrotoxicosis and pheochromocytoma.
Side effects of propranolol include broncho-spasm (β2-antagonism), congestive heart failure, bradycardia, and atrioventricular heart block (β1-antagonism). Propranolol may worsen the myocar-dial depression of volatile anesthetics (eg, halothane) or unmask the negative inotropic characteristics of indirect cardiac stimulants (eg, isoflurane). Concomitant administration of propranolol and verapamil (a calcium channel blocker) can synergis-tically depress heart rate, contractility, and atrioven-tricular node conduction.
Propranolol is extensively protein bound and is cleared by hepatic metabolism. Its elimination half-life of 100 min is quite long compared with that of esmolol.
Individual dosage requirements of propranolol depend on baseline sympathetic tone. Generally, propranolol is titrated to the desired effect, beginning with 0.5 mg and progressing by 0.5-mg increments every 3–5 min. Total doses rarely exceed 0.15 mg/kg. Propranolol is supplied in 1-mL ampules containing 1 mg.