Pharmacologic cardioversion (pharmacologic cardioversion) is the use of medications in certain cardiac arrhythmias to return them to sinus rhythm (normal heart rhythm). Note: According to one study, immediate cardioversion is not necessarily required in patients who visit a hospital emergency department because of symptomatic atrial fibrillation. It was shown that a wait-and-see approach (“Wait and See” strategy) and drug frequency control resulted in an equally good outcome: after 48 hours, 150 of 218 patients (69%) in the “Wait and See” group had sinus rhythm; after 4 weeks, 193 of 212 patients (91%) in the “Wait And See” group versus 202 of 215 patients (94%) in the early cardioversion group had sinus rhythm. The difference between the groups was not significant. Therefore, for the authors, there is no reason to immediately cardiovert all patients with less than 36 hours of AF. However, attention should be directed toward risk assessment of stroke and into initiation of oral anticoagulation.
Indications (areas of application)
- Atrial fibrillation (VHF)
- Atrial flutter
- Ventricular tachycardia
The following comments relate exclusively to the indication of atrial fibrillation. In the case of pharmacological cardioversion, it remains to mention that the success rate (about 70%) is lower than that of electrical cardioversion (about 90%) and that it does not act immediately. However, one advantage is that the patient does not need anesthesia and it is easy to perform by taking a tablet (or i.v. administration, if necessary).
Before cardioversion
- Exclusion of thrombi – before performing cardioversion, it is essential to check that no thrombi (blood clots) have formed during the presence of atrial fibrillation, because after cardioversion has been performed, the resumption of mechanical activity of the atria may dislodge them and cause emboli (vascular occlusions).
- In atrial fibrillation (AF) that has been present for less than 48 hours, prior transesophageal echocardiography (TEE; ultrasound examination in which an endoscope (device used for endoscopy) with a built-in transducer is inserted into the esophagus) to rule out thrombi (blood clots) may not be necessary, if necessary.
- In contrast to acute AF, prior transesophageal echocardiography (TEE) must be performed to exclude thrombi if AF has been present for more than 48 hours. If thrombi are detected, cardioversion should not be performed until they are resolved by effective anticoagulation (blood clotting). Note: If thrombus is detected, repeat TEE should be performed after at least 3 weeks of anticoagulation before cardioversion (IIaC).
- Thromboprophylaxis:
- Regardless of CHA2DS2-VASc score, subsequent effective anticoagulation for at least 4 weeks is recommended for any pharmacologic and/or electrical cardioversion of atrial fibrillation/flutter (IB)This may be waived: Drug-induced cardioversion using antiarrhythmic drug therapy as “pill-in-the-pocket” therapy in patients with low CHA2DS2-VASc score.
- Laboratory testing – Two laboratory parameters are of great importance in predicting the success of electrocardioversion. Both hypokalemia (potassium deficiency) and hyperthyroidism (hyperthyroidism) should be excluded before the procedure is performed.
The procedure and modes of action
Pharmacological cardioversion is performed only in hemodynamically stable patients – that is, with good cardiovascular function. Effective antiarrhythmic agents for drug or pharmacologic cardioversion in atrial fibrillation are class IA, IC, and III agents (see table below):
- Rapid-acting agents are flecainide and propafenone. Cardioversion rates of 40-70% are possible with these agents. Both agents can also be used in the “pill in the pocket” concept, i.e., a short-term dose increase is made by the patient during an attack. However, the first dose must be taken once beforehand in the hospital under monitoring. This therapy strategy requires that the patient is reliably aware of the occurrence of atrial fibrillation.Contraindication: The “pill in the pocket” concept must not be used if the duration of the episode of atrial fibrillation is unclear, as thrombi (blood clots) may have formed in the atrium due to the atrial fibrillation.
- With vernakalant (class III antiarrhythmic agent), conversion rates of 62% are observed in atrial fibrillation that persisted for less than 72 hours. The time from onset of drug administration to conversion to sinus rhythm was a median of 10 minutes. The drug may be used only in atrial fibrillation – with a duration ≤ 7 days.
- Cardioversion rates of 50-70% are achieved with ibutilide, a class III antiarrhythmic agent (this drug is not available in Germany).
- Amiodarone is used in patients with structurally predamaged hearts and impaired left ventricular function (does not act negatively inotropic/”affecting the contractility of the heart“), but shows delayed conversion of atrial fibrillation to sinus rhythm.
After cardioversion
Thromboprophylaxis:
- In the presence of atrial fibrillation (AF) that has been present for less than 48 hours and a CHA2DS2-VASc score (score for estimating the risk of apoplexy) of 0, four weeks of anticoagulation (anticoagulant) can be omitted because thrombus formation usually cannot occur within two days. Furthermore, in such a case, no prior transesophageal echocardiography (TEE; ultrasound examination in which an endoscope (device for reflection) with a built-in transducer is inserted into the esophagus) is indicated.
- Regardless of CHA2DS2-VASc score, subsequent effective anticoagulation for at least 4 weeks is recommended for any pharmacological and/or electrical cardioversion of atrial fibrillation/flutter (IB)This may be waived: Drug-induced cardioversion using antiarrhythmic drug therapy as “pill-in-the-pocket” therapy in patients with low CHA2DS2-VASc score.
Results of drug-induced cardioversion.
- Normalization of sinus rhythm occurred in 52% of cases by an antiarrhythmic drug in weight-dependent doses within an average of 23 minutes.
- More adverse events occurred with radioversion by medication. However, these were mostly not serious,
- At 2 weeks, 95% of patients were in sinus rhythm after drug cardioversion; 92% of patients after electrical cardioversion).
- Note: Attempted pharmacological cardioversion was with intravenous procainamide (15 mg/kg over 30 min). It cannot be excluded that the above results are not transferable to other antiarrhythmic agents.
If pharmacologic or electrical cardioversion is not an option, the therapeutic goal is pharmacologic rate control (eg, with beta-blockers, Ca-channel blockers (eg, verapamil), class III antiarrhythmics, or cardiac glycosides).
Overview of Antiarrhythmic Drugs
Antiarrhythmics are drugs used to terminate cardiac arrhythmias when they occur. Four classes of antiarrhythmic drugs are distinguished according to the principle of action (after Vaughan Williams).
| Class | Agents | Mechanism of action |
| Ia | Ajmaline quinidine disopyramide prajmaline procainamide | Inhibition of rapid sodium influx into the cell and slow reactivation → conduction delay |
| Ib | Aprindine lidocaine phenytoin tocainide | Inhibition of rapid sodium influx and rapid reactivation → conduction enhancement (by shortening the action potential). |
| Ic | Flecainide lorcainide propafenone | Inhibition of rapid sodium influx and slow reactivation → conduction delay |
| II | Atenolol bisoprolol metoprolol propranolol | Competitive inhibition of ß-receptors → excitability ↓ |
| III | Amiodarone Ibutilide (not approved in Germany) Sotalol Vernakalant | Inhibition of potassium efflux → action potential ↑ |
| IV | Diltiazem verapamil | Inhibition of calcium efflux → conduction delay |
| Non-classified | Adenosine | Inhibition of excitation conduction |
| Magnesium | Calcium antagonist |
Legend
- Class I – Sodium channel blockers
- Class II – Beta blockers
- Class III – Potassium channel blockers
- Class IV – Calcium channel blockers
- In addition, there are also the agents adenosine or digitalis, which can not be divided into the above classes.
Side effects result from the respective side effect spectrum of the prescribed drugs. In any case, it may come to the triggering of further cardiac arrhythmias.
