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Drugs for Arrhythmias

By

L. Brent Mitchell

, MD, Libin Cardiovascular Institute of Alberta, University of Calgary

Last full review/revision Jan 2021
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Topic Resources

The need for treatment of arrhythmias Overview of Arrhythmias The normal heart beats in a regular, coordinated way because electrical impulses generated and spread by myocytes with unique electrical properties trigger a sequence of organized myocardial... read more Overview of Arrhythmias depends on the symptoms and the seriousness of the arrhythmia. Treatment is directed at causes. If necessary, direct antiarrhythmic therapy, including antiarrhythmic drugs, cardioversion-defibrillation Direct-Current (DC) Cardioversion-Defibrillation The need for treatment of arrhythmias depends on the symptoms and the seriousness of the arrhythmia. Treatment is directed at causes. If necessary, direct antiarrhythmic therapy, including antiarrhythmic... read more , implantable cardioverter-defibrillators Implantable Cardioverter-Defibrillators (ICD) The need for treatment of arrhythmias depends on the symptoms and the seriousness of the arrhythmia. Treatment is directed at causes. If necessary, direct antiarrhythmic therapy, including antiarrhythmic... read more Implantable Cardioverter-Defibrillators (ICD) (ICDs), pacemakers Cardiac Pacemakers The need for treatment of arrhythmias depends on the symptoms and the seriousness of the arrhythmia. Treatment is directed at causes. If necessary, direct antiarrhythmic therapy, including antiarrhythmic... read more Cardiac Pacemakers (and a special form of pacing, cardiac resynchronization therapy Cardiac Resynchronization Therapy (CRT) The need for treatment of arrhythmias depends on the symptoms and the seriousness of the arrhythmia. Treatment is directed at causes. If necessary, direct antiarrhythmic therapy, including antiarrhythmic... read more ), catheter ablation Ablation for Cardiac Arrhythmia The need for treatment of arrhythmias depends on the symptoms and the seriousness of the arrhythmia. Treatment is directed at causes. If necessary, direct antiarrhythmic therapy, including antiarrhythmic... read more , surgery Surgery for cardiac arrhythmias The normal heart beats in a regular, coordinated way because electrical impulses generated and spread by myocytes with unique electrical properties trigger a sequence of organized myocardial... read more Surgery for cardiac arrhythmias , or a combination, is used.

Digoxin, adenosine, and ivabradine were not included in the original Vaughan Williams classification. Digoxin shortens atrial and ventricular refractory periods and is vagotonic, thereby prolonging AV nodal conduction and AV nodal refractory periods. Adenosine slows or blocks AV nodal conduction and can terminate tachyarrhythmias that rely upon AV nodal conduction for their perpetuation. Ivabradine inhibits the SA node funny current and slows SA node rate. More inclusive updates to the Vaughan Williams classification have been proposed (1 Antiarrhythmic drug reference The need for treatment of arrhythmias depends on the symptoms and the seriousness of the arrhythmia. Treatment is directed at causes. If necessary, direct antiarrhythmic therapy, including antiarrhythmic... read more ).

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Antiarrhythmic drug reference

  • 1. Lei M, Wu L, Terrar DA, Huang CLH: Modernized classification of cardiac antiarrhythmic drugs. Circulation 138(17):1879–1896, 2018. doi: 10.1161/CIRCULATIONAHA.118.035455

Class I Antiarrhythmic Drugs

Class I antiarrhythmic drugs are

  • Sodium channel blockers (membrane-stabilizing drugs), which block fast sodium channels, slowing conduction in fast-channel tissues (working atrial and ventricular myocytes, His-Purkinje system)

In the electrocardiogram (ECG), this effect may be reflected as widening of the P wave, widening of the QRS complex, prolongation of the PR interval, or a combination.

Class I drugs are subdivided based on the kinetics of the sodium channel effects:

  • Class Ib drugs have fast kinetics.

  • Class Ic drugs have slow kinetics.

  • Class Ia drugs have intermediate kinetics.

The kinetics of sodium channel blockade determine the heart rates at which their electrophysiologic effects become manifest. Because class Ib drugs have fast kinetics, they express their electrophysiologic effects only at fast heart rates. Thus, an ECG obtained during normal rhythm at normal rates usually shows no evidence of fast-channel tissue conduction slowing. Class Ib drugs are not very potent antiarrhythmics and have minimal effects on atrial tissue.

Class Ic drugs have slow kinetics, so they express their electrophysiologic effects at all heart rates. Thus, an ECG obtained during normal rhythm at normal heart rates usually shows fast-channel tissue conduction slowing. Class Ic drugs are more potent antiarrhythmics.

Class Ia drugs have intermediate kinetics, so their fast-channel tissue conduction slowing effects may or may not be evident on an ECG obtained during normal rhythm at normal rates. Class Ia drugs also block repolarizing potassium channels, prolonging the refractory periods of fast-channel tissues. On the ECG, this effect is reflected as QT-interval prolongation even at normal rates. Class Ib drugs and class Ic drugs do not block potassium channels directly.

The primary indications are supraventricular tachycardia (SVT) for class Ia and Ic drugs and ventricular tachycardia (VTs) for all class I drugs.

Adverse effects of class I drugs include proarrhythmia, a drug-related arrhythmia worse than the arrhythmia being treated, which is the most worrisome adverse effect. All class I drugs may worsen VTs. Class I drugs also tend to depress ventricular contractility. Because these adverse effects are more likely to occur in patients with a structural heart disorder, class I drugs are not generally recommended for such patients. Thus, these drugs are usually used only in patients who do not have a structural heart disorder or in patients who have a structural heart disorder but who have no other therapeutic alternatives. There are other adverse effects of class I drugs that are specific to the subclass or individual drug.

Class Ia antiarrhythmic drugs

Class Ia drugs have kinetics that are intermediate between the fast kinetics of class Ib and the slow kinetics of class Ic. Their fast-channel tissue conduction slowing effects may or may not be evident on an ECG obtained during normal rhythm at normal rates. Class Ia drugs block repolarizing potassium channels, prolonging the refractory periods of fast-channel tissues. On the ECG, this effect is reflected as QT-interval prolongation even at normal rates.

Class Ia drugs are used for suppression of atrial premature beats Atrial premature beats Various rhythms result from supraventricular foci (usually in the atria). Diagnosis is by electrocardiography. Many are asymptomatic and require no treatment. (See also Overview of Arrhythmias... read more Atrial premature beats , ventricular premature beats Ventricular Premature Beats (VPB) Ventricular premature beats (VPB) are single ventricular impulses caused by reentry within the ventricle or abnormal automaticity of ventricular cells. They are extremely common in both healthy... read more Ventricular Premature Beats (VPB) , supraventricular tachycardia Reentrant Supraventricular Tachycardias (SVT) including Wolff-Parkinson-White Syndrome Reentrant supraventricular tachycardias (SVT) involve reentrant pathways with a component above the bifurcation of the His bundle. Patients have sudden episodes of palpitations that begin and... read more , ventricular tachycardia Ventricular Tachycardia (VT) Ventricular tachycardia is ≥ 3 consecutive ventricular beats at a rate ≥ 120 beats/minute. Symptoms depend on duration and vary from none to palpitations to hemodynamic collapse and death. Diagnosis... read more , atrial fibrillation Atrial Fibrillation Atrial fibrillation is a rapid, irregularly irregular atrial rhythm. Symptoms include palpitations and sometimes weakness, effort intolerance, dyspnea, and presyncope. Atrial thrombi may form... read more , atrial flutter Atrial Flutter Atrial flutter is a rapid regular atrial rhythm due to an atrial macroreentrant circuit. Symptoms include palpitations and sometimes weakness, effort intolerance, dyspnea, and presyncope. Atrial... read more , and ventricular fibrillation Ventricular Fibrillation (VF) Ventricular fibrillation causes uncoordinated quivering of the ventricle with no useful contractions. It causes immediate syncope and death within minutes. Treatment is with cardiopulmonary... read more Ventricular Fibrillation (VF) . The primary indications are supraventricular and ventricular tachycardias.

Class Ia drugs may cause torsades de pointes ventricular tachycardia. Class Ia drugs may organize and slow atrial tachyarrhythmias enough to permit 1:1 AV conduction with marked acceleration of the ventricular response rate.

Class Ib antiarrhythmic drugs

Class Ic antiarrhythmic drugs

Class Ic drugs have slow kinetics; they express their electrophysiologic effects at all heart rates. Thus, an ECG obtained during normal rhythm at normal heart rates usually shows fast-channel tissue conduction slowing. Class Ic drugs are more potent antiarrhythmics than either class Ia or class Ib drugs. Class Ic drugs do not block potassium channels directly.

Class Ic drugs may organize and slow atrial tachyarrhythmias enough to permit 1:1 AV conduction with marked acceleration of the ventricular response rate.

Class Ic drugs are used for suppression of atrial premature beats Atrial premature beats Various rhythms result from supraventricular foci (usually in the atria). Diagnosis is by electrocardiography. Many are asymptomatic and require no treatment. (See also Overview of Arrhythmias... read more Atrial premature beats , ventricular premature beats Ventricular Premature Beats (VPB) Ventricular premature beats (VPB) are single ventricular impulses caused by reentry within the ventricle or abnormal automaticity of ventricular cells. They are extremely common in both healthy... read more Ventricular Premature Beats (VPB) , supraventricular tachycardia Reentrant Supraventricular Tachycardias (SVT) including Wolff-Parkinson-White Syndrome Reentrant supraventricular tachycardias (SVT) involve reentrant pathways with a component above the bifurcation of the His bundle. Patients have sudden episodes of palpitations that begin and... read more , ventricular tachycardias Ventricular Tachycardia (VT) Ventricular tachycardia is ≥ 3 consecutive ventricular beats at a rate ≥ 120 beats/minute. Symptoms depend on duration and vary from none to palpitations to hemodynamic collapse and death. Diagnosis... read more , atrial fibrillation Atrial Fibrillation Atrial fibrillation is a rapid, irregularly irregular atrial rhythm. Symptoms include palpitations and sometimes weakness, effort intolerance, dyspnea, and presyncope. Atrial thrombi may form... read more , atrial flutter Atrial Flutter Atrial flutter is a rapid regular atrial rhythm due to an atrial macroreentrant circuit. Symptoms include palpitations and sometimes weakness, effort intolerance, dyspnea, and presyncope. Atrial... read more , and ventricular fibrillation Ventricular Fibrillation (VF) Ventricular fibrillation causes uncoordinated quivering of the ventricle with no useful contractions. It causes immediate syncope and death within minutes. Treatment is with cardiopulmonary... read more Ventricular Fibrillation (VF) .

Class II Antiarrhythmic Drugs

Class II antiarrhythmic drugs are

  • Beta-blockers

Beta-blockers affect predominantly slow-channel tissues (sinoatrial and atrioventricular nodes), where they decrease rate of automaticity, slow conduction velocity, and prolong refractoriness. Thus, heart rate is slowed, the PR interval is lengthened, and the AV node transmits rapid atrial depolarizations at a lower frequency.

Class II drugs are used primarily to treat supraventricular tachycardias Reentrant Supraventricular Tachycardias (SVT) including Wolff-Parkinson-White Syndrome Reentrant supraventricular tachycardias (SVT) involve reentrant pathways with a component above the bifurcation of the His bundle. Patients have sudden episodes of palpitations that begin and... read more , including sinus tachycardia, AV nodal reentry, atrial fibrillation Atrial Fibrillation Atrial fibrillation is a rapid, irregularly irregular atrial rhythm. Symptoms include palpitations and sometimes weakness, effort intolerance, dyspnea, and presyncope. Atrial thrombi may form... read more , and atrial flutter Atrial Flutter Atrial flutter is a rapid regular atrial rhythm due to an atrial macroreentrant circuit. Symptoms include palpitations and sometimes weakness, effort intolerance, dyspnea, and presyncope. Atrial... read more . These drugs are also used to treat ventricular tachycardia Ventricular Tachycardia (VT) Ventricular tachycardia is ≥ 3 consecutive ventricular beats at a rate ≥ 120 beats/minute. Symptoms depend on duration and vary from none to palpitations to hemodynamic collapse and death. Diagnosis... read more to raise the threshold for ventricular fibrillation Ventricular Fibrillation (VF) Ventricular fibrillation causes uncoordinated quivering of the ventricle with no useful contractions. It causes immediate syncope and death within minutes. Treatment is with cardiopulmonary... read more Ventricular Fibrillation (VF) and reduce the ventricular proarrhythmic effects of beta-adrenoceptor stimulation.

Beta-blockers are generally well tolerated; adverse effects include lassitude, sleep disturbance, and gastrointestinal upset. These drugs are contraindicated in patients with asthma.

Class III Antiarrhythmic Drugs

Class III drugs are

  • Membrane stabilizing drugs, primarily potassium channel blockers

Class III drugs prolong action potential duration and refractoriness in slow- and fast-channel tissues. Thus, the capacity of all cardiac tissues to transmit impulses at high frequencies is reduced, but conduction velocity is not significantly affected. Because the action potential is prolonged, rate of automaticity is reduced. The predominant effect on the ECG is QT-interval prolongation.

Class IV Antiarrhythmic Drugs

Class IV drugs are

  • Nondihydropyridine calcium channel blockers

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