Drugs affecting cardiac rhythm

Research output: Chapter in Book/Report/Conference proceedingChapter


• Antiarrhythmics restore normal rhythm and rate by varied mechanisms. • All drugs given to treat an arrhythmia also may cause an arrhythmia. • Class I drugs block the infl ux of sodium in the myocardial membrane. They are local anesthetics or membrane stabilizing agents that depress phase 0 of the action potential. • Quinidine, a Class I antiarrhythmic, is used for treating atrial fi brillation and fl utter. Quinidine depresses myocardial excitability, conduction velocity, and contractility. The effective refractory period is prolonged, increasing conduction time. Re-entry phenomenon is therefore prevented. Quinidine also exerts an indirect anticholinergic effect; it decreases vagal tone and may promote conduction in the AV junction. • Potassium enhances the effect of quinidine, and hypokalemia reduces the effectiveness. • Class IB antiarrhythmics depress phase 0 of the action potential, but not as much as Class IA drugs. They also suppress automaticity. Like quinidine, these drugs may also cause arrhythmias, in addition to treating them. Unlike quinidine, they are used primarily with ventricular arrhythmias, and they may shorten the action potential duration. Lidocaine is a Class IB drug; it may be used with all acute ventricular arrhythmias that occur in association with cardiac surgery or acute MI. • Class IC antiarrhythmics also depress phase 0 but markedly so. In addition, they have a slight effect on repolarization and decrease conduction substantially. They have been found to increase mortality signifi cantly when used in patients who have had an MI. • All Class I antiarrhythmics have the potential to increase mortality; none have been proved to decrease mortality. • Class II antiarrhythmics block the beta-1 and beta-2 adrenergic receptors and stabilize the cardiac cell membranes. They depress phase 4 depolarization. • Propranolol, a beta blocker and Class II antiarrhythmic, is used to treat supraventricular, ventricular, and tachyarrhythmias secondary to digoxin toxicity or arising from excessive catecholamine action during anesthesia. • Propranolol slows the sinus heart rate, depresses AV conduction, decreases cardiac output, reduces systolic and diastolic blood pressure at rest and on exercise, and reduces supine and standing blood pressure. • Class II antiarrhythmics are the only antiarrhythmics that have been shown to decrease mortality. • Class III drugs slow heart action by prolonging the action potential or myocardial repolarization (prolonged phase 3). • Amiodarone, a Class III antiarrhythmic, is used to treat life-threatening ventricular arrhythmias. It also has actions from other classifi cations. These diverse actions of amiodarone are why the drug is being considered as potentially appropriate for treating atrial fi brillation as well. • Amiodarone has unusual pharmacokinetic and pharmacodynamic properties. These unique effects include incomplete bioavailability, distribution to multiple tissue sites, extreme lipid solubility, biotransformation to an active metabolite, and extremely slow elimination of amiodarone and its metabolite. These effects may be attributable to genetic variations, although this possibility is not yet confi rmed. Because of these unique effects, the effect on patients is variable. • Adverse effects of amiodarone can be serious and potentially fatal. The patient needs to be monitored closely while on amiodarone therapy. • Class IV drugs alter the action potential, decrease AV conduction, and prolong repolarization by inhibiting the infl ux of calcium in cardiac muscle cells. A few calcium channel blocker drugs are in this class. • Verapamil, a calcium channel blocker and Class IV antiarrhythmic, controls ventricular rate in chronic atrial fl utter or fi brillation (used in conjunction with digoxin). It is also used prophylactically for repetitive paroxysmal SVT. IV verapamil is used to treat SVT. • Verapamil also is used in treating angina (including Prinzmetal angina) and hypertension. • Sodium polystyrene sulfonate is a potassium-removing resin used in treating hyperkalemia. Because hyperkalemia may lead to cardiac arrhythmias, this drug prevents arrhythmias from occurring. • Sodium polystyrene sulfonate is given orally or as an enema. • Although sodium polystyrene sulfonate is in the GI tract, sodium ions are exchanged for potassium ions, which are then excreted in the stool. Onset is slow and unpredictable. Therefore, if the serum potassium level is quite elevated, other mechanisms of lowering the potassium level should be used.

Original languageEnglish (US)
Title of host publicationDrug Therapy in Nursing
PublisherWolters Kluwer Health Adis (ESP)
Number of pages30
ISBN (Electronic)9781469819174
ISBN (Print)9781451187663
StatePublished - Nov 7 2012

ASJC Scopus subject areas

  • Nursing(all)


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