In addition to class III actions, sotalol (Betapace) pos-sesses β-adrenoceptor blocking properties. The - blocking effects are most evident at low doses, with ac-tion potential prolongation predominating at higher doses. The D-isomer of sotalol, which is devoid of β-blocking action, may increase mortality in post-infarcted patients.
Pacemaker activity in the sinoatrial node is de-creased because of β-adrenoceptor blockade and a re-moval of sympathoadrenal influences on spontaneous diastolic depolarization. Sotalol increases the refractory period of atrial muscle.
Sotalol decreases conduction velocity and prolongs the ERP in the A-V node, an action held in common with other β1-adrenoceptor blocking agents.
The actions of sotalol on the delayed rectifier potas-sium current prolong the ERP in His-Purkinje tissue. As with other members of class III, the electrophysiologi-cal action of sotalol is characterized by prolongation of repolarization and an increase in the ERP of ventricu-lar muscle.
Administration of sotalol is associated with dose- and concentration-dependent slowing of the heart rate and prolongation of the PR interval. The QRS duration is not affected with plasma concentrations within the ther-apeutic range. The corrected QT interval is prolonged as a result of the increase in the ERP of ventricular my-ocardium.
The hemodynamic effects of sotalol are related to its β- adrenoceptor antagonist activity. Accordingly, de-creases in resting heart rate and in exercise-induced tachycardia are seen in patients receiving sotalol. A modest reduction in systolic pressure and in cardiac output may occur. The reduction in cardiac output is a consequence of lowering the heart rate, since stroke volume is unaffected by sotalol treatment. In patients with normal ventricular function, cardiac output is maintained despite the decrease in heart rate because of the simultaneous increase in the stroke volume.
The pharmacokinetic characteristics of sotalol:
Oral bioavailability : 50%o
Onset of action : 0.5 hours
Peak response : 1–2 hours
Duration of action : 12–24 hours
Plasma half-life : 4 hours
Primary route of metabolism: Hepatic (80%)
Primary route of excretion : Renal (20% unchanged); 40% metabolite
Therapeutic serum : 1–4 : μg /mLconcentration
Sotalol possesses a broad spectrum of antiarrhythmic ef-fects in ventricular and supraventricular arrhythmias. It has value in the management of patients with paroxys- mal supraventricular arrhythmias, in terminating the reentrant arrhythmia in which the atrioventricular node serves as the reentrant pathway, and possibly in termi-nating supraventricular tachyarrhythmias associated with an accessory pathway.
Side effects of sotalol include those attributed to both β-adrenoceptor blockade and proarrhythmic effects. This arrhythmia is a serious threat, as it may lead to ven-tricular fibrillation. Adverse effects attributable to its - blocker activity include fatigue, dyspnea, chest pain, headache, nausea, and vomiting.
The contraindications that apply to other β-adrenocep-tor blocking agents also apply to sotalol. In addition, hy-pokalemia and drugs known to prolong the QT interval may be contraindicated, as they enhance the possibility of proarrhythmic events.
Drugs with inherent QT interval–prolonging activity (i.e., thiazide diuretics and terfenadine) may enhance the class III effects of sotalol.
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