This chapter reviews common antiarrhythmic and antihypertensive medications administered in the ED. Acute medical conditions presenting with systemic hypertension and the specific recommended antihypertensive agents are presented 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 Long-term use of these agents to prevent arrhythmias has not been proven to reduce mortality2-5; however, this chapter focuses on medications used for acute pharmacologic conversion or rate control of common arrhythmias. 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). This chapter also discusses the emergency applications of atropine, adenosine, magnesium, and isoproterenol.
TABLE 19-1Vaughan-Williams Classification of Antiarrhythmic Medications ||Download (.pdf) TABLE 19-1 Vaughan-Williams Classification of Antiarrhythmic Medications
|Action ||Class ||Selected Example Medications |
|Sodium channel blockers ||Class Ia ||Procainamide |
|Class Ib ||Lidocaine |
|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, nicardipine |
CLASS I ANTIARRHYTHMICS: FAST SODIUM CHANNEL BLOCKERS
Class I agents block fast sodium channels and are further categorized based on their degree of blockade into classes Ia (moderate blockade), Ib (weak blockade), and Ic (strong blockade). They 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 the refractory period and can be useful in terminating reentry currents. In addition, some class I agents block potassium channels and exhibit antimuscarinic effects.
Procainamide increases the refractory period, decreases automaticity and conduction, and prolongs cardiac action potentials through intermediate blockade of open sodium and potassium channels. N-Acetylprocainamide, the active metabolite of procainamide, lacks sodium channel effects but does block potassium channels, which can lead to QT prolongation.
TABLE 19-2Procainamide Pharmacokinetics (Adults) ||Download (.pdf) TABLE 19-2 Procainamide Pharmacokinetics (Adults)
|Distribution ||Metabolism ||Excretion ||Half-Life ||Onset/Duration of Action |
|2 L/kg || |
Hepatic and renal
Active metabolite: NAPA (renal elimination)
|Urine, feces || |
Procainamide: 2.5–4.7 h NAPA: 6–8 h (prolonged with renal impairment)
Onset (IV): immediate
Duration: 3–6 h
Procainamide is indicated for life-threatening ventricular arrhythmias and supraventricular arrhythmias. Although it can be used to treat supraventricular tachycardia, the proarrhythmic nature of ...