Beta Blockers



Propranolol will be discussed as a prototype beta-adrenergic receptor blocker. Differences in the pharmacokinetics, beta-adrenergic receptor selectivity, and antagonist/agonist actions have been discussed in Chapter 7.
Propranolol slows the sinus nodal discharge rate and lengthens AV nodal conduction time (PR interval increases) and refractoriness. These, ef­fects may be marked if the heart rate or AV con­duction is particularly dependent on sympathetic tone or if sinus or AV nodal dysfunction is pres­ent. There is no effect on refractoriness or con­duction in the His-Purkinje system at usual doses, and the QRS complex and QT interval do not change. It appears that the beta-blocking activity of propranolol is responsible for its antiar­rhythmic effects, since a local anesthetic (or quinidine-like) effect of propranolol is present only at doses ten times those causing the beta-blocking effect. There is variability in serum concentra­tions from patient to patient, and the appropriate dose is determined by the patient’s physiological response, such as changes in resting heart rate or prevention of an increase in heart rate with ex­ercise. If one beta blocker is ineffective against arrhythmias, the other beta blockers are usually also ineffective.
Propranolol is used most commonly to treat su­praventricular tachyarrhythmias. Sinus tachycar­dia due to thyrotoxicosis, anxiety, and exercise may be slowed by propranolol. Propranolol does not usually terminate atrial flutter or fibrillation but may, by itself or combined with digitalis, con­trol the ventricular response by prolonging AV nodal conduction time or refractoriness. Re-en­trant supraventricular tachycardias using the AV node as one limb of the pathway (e.g., AV nodal re-entrant tachycardia and reciprocating tachy­cardias associated with the Wolff-Parkinson-White syndrome) may be prevented by propran­olol alone or combined with other drugs. Pro­pranolol is useful in treating ventricular arrhyth­mias associated with the prolonged QT syndrome and mitral valve prolapse. It usually does not pre­vent chronic recurrent ventricular tachycardia in patients with ischemic heart disease if the tachy­arrhythmia occurs without acute ischemia.