Effect of drugs on defibrillation capacity

Anna Legreid Dopp, John Miller, James E. Tisdale

Research output: Contribution to journalArticle

27 Citations (Scopus)

Abstract

Over 300 000 people die of sudden cardiac death (SCD) in the US annually. Implantable cardioverter-defibrillators (ICDs) have been shown to be more effective than antiarrhythmic drugs for the prevention of SCD in specific susceptible populations. Many patients in whom ICDs have been implanted receive concomitant therapy with antiarrhythmic drugs, for the purpose of reducing the frequency of appropriate and inappropriate defibrillation shocks. Drugs may influence defibrillation capacity and therefore influence the function of ICDs. The objective of this article is to review and update the literature regarding the effects of drugs on defibrillation capacity. A literature search was performed using PubMed (1966 to December 2007) to identify clinical studies, case reports and animal studies describing the effects of drugs on defibrillation capacity. Search terms included: antiarrhythmic drugs; cardiovascular drugs; amiodarone; sotalol; flecainide; propafenone; dofetilide; ibutilide; β-blockers; lidocaine; procainamide; N-acetylprocainamide; mexiletine; disopyramide; moricizine; calcium channel blockers; defibrillation threshold; defibrillation energy requirements; defibrillation energy changes; defibrillation efficacy; implantable cardioverter defibrillators; and external defibrillators. Evidence from clinical studies indicates that amiodarone may increase defibrillation threshold (DFT). In addition, some data indicate that drugs including lidocaine, mexiletine, moracizine (moricizine), verapamil, venlafaxine and anaesthetic agents may increase DFT. In contrast, agents including sotalol, dofetilide and β-adrenergic receptor antagonists (β-blockers) may reduce DFT. Propafenone and procainamide appear to have minimal effect on DFT. For those antiarrhythmic drugs with both sodium and potassium channel blockade (e.g. amiodarone), the effect of sodium channel blockade predominates, resulting in an increase in DFT. Numerous drugs may affect defibrillation capacity. These effects must be considered when managing patients who have an ICD and require concomitant pharmacotherapy.

Original languageEnglish
Pages (from-to)607-630
Number of pages24
JournalDrugs
Volume68
Issue number5
DOIs
StatePublished - 2008

Fingerprint

Implantable cardioverter defibrillators
Implantable Defibrillators
Moricizine
Anti-Arrhythmia Agents
Amiodarone
Propafenone
Mexiletine
Sotalol
Procainamide
Pharmaceutical Preparations
Sodium Channels
Sudden Cardiac Death
Lidocaine
Acecainide
Defibrillators
Flecainide
Disopyramide
Drug therapy
Cardiovascular Agents
Adrenergic Antagonists

Keywords

  • Acecainide, therapeutic use
  • Amiodarone, therapeutic use
  • Anaesthetics, therapeutic use
  • Beta adrenergic receptor antagonists, therapeutic use
  • Defibrillation
  • Defibrillators
  • Digoxin, therapeutic use
  • Disopyramide, therapeutic use

ASJC Scopus subject areas

  • Toxicology
  • Health, Toxicology and Mutagenesis

Cite this

Effect of drugs on defibrillation capacity. / Dopp, Anna Legreid; Miller, John; Tisdale, James E.

In: Drugs, Vol. 68, No. 5, 2008, p. 607-630.

Research output: Contribution to journalArticle

Dopp, Anna Legreid ; Miller, John ; Tisdale, James E. / Effect of drugs on defibrillation capacity. In: Drugs. 2008 ; Vol. 68, No. 5. pp. 607-630.
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