This chapter reviews the pharmacology of selected antiarrhythmics and antihypertensives (β-blockers and calcium channel blockers) used in the ED. Discussion of additional antihypertensives can be found in chapter 57, "Systemic Hypertension."
Antiarrhythmic medications treat cardiac rhythm abnormalities by modifying autonomic function or myocardial ion channels, leading to changes in conduction velocity or duration of the effective refractory period.1 Failure to reduce mortality has been a criticism of many agents in this class of drugs.2,3,4,5 In general, electrical cardioversion is preferable to pharmacologic conversion in patients who are hemodynamically unstable. The majority of antiarrhythmics are organized based on the Vaughan-Williams classification system (Classes I to IV) (Table 19-1). Other medications used to treat arrhythmias include digoxin, atropine, adenosine, magnesium, and isoproterenol.
TABLE 19-1Vaughan-Williams Classification of Antiarrhythmic Medications |Favorite Table|Download (.pdf) TABLE 19-1 Vaughan-Williams Classification of Antiarrhythmic Medications
|Action ||Class ||Example Medications |
|Sodium channel blockers ||Class Ia ||Disopyramide, quinidine, procainamide |
|Class Ib ||Lidocaine, mexiletine, phenytoin, |
|Class Ic ||Flecainide, propafenone |
|β-Blockers ||Class II ||Esmolol, labetalol, metoprolol, propranolol |
|Potassium channel blockers ||Class III ||Amiodarone, dronedarone, dofetilide*, ibutilide, sotalol†, vernakalant‡ |
|Calcium channel blockers ||Class IV ||Diltiazem, verapamil |
|Unclassified agents# || ||Adenosine, atropine, digoxin, isoproterenol, magnesium |
CLASS I ANTIARRHYTHMICS: FAST SODIUM CHANNEL BLOCKERS
Class I agents block fast sodium channels (INa) and are further subcategorized based on their degree of blockade into Classes Ia (moderate blockade), Ib (weak blockage), and Ic (strong blockade). Sodium channel blockers increase the excitability threshold, requiring more sodium channels to open in order to overcome the potassium current and generate an action potential. This effect increases refractoriness and can be useful in terminating reentry currents. In addition, some Class I agents block potassium channels (IK) and exhibit antimuscarinic effects.
Class Ia antiarrhythmics block open sodium channels and have a slow dissociation from their target, causing an increase in the refractory period. The use of these agents is limited by their side effect profile and proarrhythmic nature. Quinidine and disopyramide are Class Ia agents but are not discussed here because they are infrequently used in the ED. Quinidine can cause torsades de pointes. Disopyramide is used orally in patients with hypertrophic cardiomyopathy due to its negative inotropic properties; however, its association with heart failure and hypotension and its anticholinergic effects, including urinary retention, limit its use.
Procainamide is a Class Ia agent that increases the refractory period, decreases automaticity and conduction, and prolongs cardiac action potentials through ...