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PekkaRaatikainen

Management of Acute Atrial Fibrillation

For prevention of atrial fibrillation, see Prevention of Atrial Fibrillation.

Essentials

  • In the treatment of acute atrial fibrillation (AF), the choice between rhythm control and rate control as the treatment approach is made on an individual basis (see Treatment Approach for Atrial Fibrillation: Rate Control or Rhythm Control?). At the same it must be ensured that anticoagulation treatment is implemented according to recommendations.
  • As a common rule in frequently recurring AF, it is worthwhile to omit cardioversion and to concentrate on rate control if it is not possible to intensify preventive therapy.

Ventricular rate control Drugs for Ventricular Rate Control in Atrial Fibrillation, Intravenous Digoxin for Controlling Heart Rate in Atrial Fibrillation

  • Unless an immediate restoration of sinus rhythm is necessary, the initial treatment of AF should aim to slow the ventricular rate to below 100/min.
    • Response is achieved quickly with intravenous administration of an agent that depresses atrioventricular (AV) conduction.
    • In 50-70 % of cases, sinus rhythm is restored spontaneously within 24-48 hours with no further intervention required.
  • The drug of first choice is usually a beta blocker. They are safe in coronary heart disease and, with correct dosage, also in heart failure. They are also suitable for use in primary care.
  • Calcium-channel blockers (verapamil and diltiazem) are well tolerated in lone AF, but they must not be used in heart failure.
  • Digoxin is less effective than beta blockers and calcium-channel blockers, and the onset of its action is slower. In severe heart failure (e.g. pulmonary oedema Acute Heart Failure and Pulmonary Oedema), however, it does not lower blood pressure as do beta blockers or calcium-channel blockers.
  • Amiodarone may sometimes be used in specialist units to control the rate of ventricular response to AF. Its advantages include little negative inotropic effect and low risk of proarrhythmia, which make it suitable for the treatment of postoperative, critically ill and haemodynamically otherwise unstable patients.
  • Dronedarone is contraindicated for rate control in permanent AF.
  • The safest treatment option of AF associated with WPW syndrome is electrical cardioversion. If this is not possible, the patient may be given flecainide or amiodarone. These drugs also depress conduction over the accessory pathway.
    • Calcium-channel blockers, digoxin and beta blockers favour preferential conduction over the accessory pathway, which is why they must not be used in patients with pre-excited atrial fibrillation.
  • A summary of drugs used for ventricular rate control and cardioversion in acute AF is given in table T1.

Dosage of drugs in the management of acute AF. Intravenous administration is recommended in urgent cases.

DrugDosage
Ventricular rate control
Beta blockersMetoprolol5 mg by slow intravenous injection, may be repeated 2-3 times at 5 minute intervals
Esmolol1)Initially 10-50 mg by rapid intravenous injection, subsequent infusion 1-4 mg/min according to heart rate and blood pressure
Calcium-channel blockersVerapamil2.5-5 mg by slow intravenous injection, may be repeated if necessary up to a total dose of 10 mg
Other drugsDigoxin0.25 mg by slow intravenous injection, may be repeated 2-3 times at 1-2 hour intervals (maximum dose 1 mg/24 h)
Amiodarone1)Initially 150-300 mg by intravenous infusion over 10-60 minutes, subsequent infusion 1 200-1 800 mg/24 hours
Cardioversion
Class IC drugsFlecainide1-2 mg/kg (max 150 mg) by intravenous infusion over 10-30 minutes or 300 mg by mouth as a single dose
Class III drugsAmiodarone1)Initially 150-300 mg by intravenous infusion over 10-60 minutes, subsequent infusion 1 200-1 800 mg/24 hours
Ibutilide1)1 mg by intravenous infusion over 10 minutes, may be repeated once after 10 minutes
Other drugsVernakalant1)3 mg/kg (max 339 mg) by intravenous infusion over 10 minutes, after 15 minutes if needed 2 mg/kg (max 226 mg) by intravenous infusion over 10 minutes
1) Usually used in specialized care only.
Cardioversion Restoration of Sinus Rhythm in Atrial Fibrillation
  • Cardioversion is associated with a considerable risk of embolism. Therefore, its need must always be carefully considered; see Treatment Approach for Atrial Fibrillation: Rate Control or Rhythm Control?.
    • In low-symptomatic patients who are elderly or otherwise belong to a high-risk group, cardioversion can usually be omitted and the treatment concentrated on optimizing rate control and anticoagulation.
    • On the other hand, if acute AF causes haemodynamic collapse, electrical cardioversion must be carried out without delay even if anticoagulation were not at therapeutic level or the patient had just eaten.
  • Contraindications to cardioversion
    • The duration of AF is unknown or it has been present for more than 48 hours, if anticoagulation therapy has not been implemented according to recommendations and intracardiac thrombi have not been excluded by transoesophageal echocardiography (TOE) or computed tomography.
    • Electrolyte disturbance (hypokalaemia) and digitalis intoxication
    • Severe sinus node dysfunction unless the patient has an implanted pacemaker
    • If the rhythm alternates between sinus rhythm and AF, electrical cardioversion is contraindicated, but antiarrhythmic agents can be used.
  • If AF is caused by a treatable underlying cause, e.g. acute myocardial infarction, heart failure, myocarditis, thyroid dysfunction or an acute pulmonary disease, the treatment is initially targeted at the underlying cause, and cardioversion is only considered after that.

Electrical cardioversion

  • Electrical cardioversion involves the restoration of sinus rhythm through a delivery of a direct-current electrical shock, which is synchronised to the QRS wave, under light anaesthesia.
    • Carrying out elective cardioversion, see Electrical Cardioversion
    • In acute atrial fibrillation, sinus rhythm is restored in over 90% of cases, depending on the duration of the arrhythmia and other related factors.
  • Electrical cardioversion is more effective than pharmacological cardioversion and poses only a low risk of proarrhythmia. It does, however, always require anaesthesia.
  • If sinus rhythm is not restored even after the maximum amount of energy has been applied, and restoration of sinus rhythm is considered important, a specialist physician should be consulted as it may be appropriate to administer intravenous antiarrhythmic agents (ibutilide) and repeat the cardioversion attempt during the same anaesthesia.
    • Another management strategy involves the initiation of antiarrhythmic medication by mouth, followed by a new cardioversion attempt when the effect of the medication has stabilised. This will take 1-4 weeks depending on the chosen drug (anticoagulation has to be within therapeutic range).

Pharmacological cardioversion

  • Pharmacological cardioversion does not require anaesthesia or fasting which makes it easier to carry out than electrical cardioversion.
  • Beta blockers, calcium-channel blockers and digoxin are ineffective for cardioversion of AF but they do offer symptom relief through controlling ventricular response rate.
  • Class IC antiarrhythmic drug flecainide is effective for the pharmacological cardioversion of acute AF.
    • It is also well suited for use in primary care, particularly by oral administration.
    • In order to avoid paradoxal acceleration of the ventricular rate it must not be used in cardioversion of atrial flutter. In atrial fibrillation it is recommended that the patient is given a beta blocker, or another drug that depresses AV conduction, prior to the administration of flecainide.
  • The use of flecainide for cardioversion of AF is contraindicated if the patient has been diagnosed with
    • myocardial infarction, systolic heart failure (left ventricular ejection fraction < 50%) or some other severe structural heart disease
    • sinus node dysfunction, second or third degree AV block (pacemaker not implanted)
    • wide QRS complex (bundle branch block)
    • Brugada syndrome or if
    • the arrhythmia is associated with acute coronary syndrome or worsening of heart failure.
  • Vernakalant has the advantage of rapid onset of action. It can be used in mild heart diseases but it is contraindicated if the patient has
    • severe cardiac failure (NYHA III-IV)
    • severe aortic valve stenosis
    • history of an acute coronary syndrome within the previous month
    • systolic blood pressure less than 100 mmHg
    • long QT interval (uncorrected QT > 440 ms), severe bradycardia, sinus node dysfunction, or second or third degree AV block with no pacemaker
  • The most common adverse effects of vernakalant include transient taste disturbances, paraesthesias, nausea and sneezing.
    • Proarrhythmia is rare because the action is mainly directed at the atrial electrical activity, and the QT interval is not significantly prolonged.
    • Also other severe adverse effects are rare, but due to the risk of hypotonia it is important to monitor blood pressure.
  • The efficacy of amiodarone for pharmacological cardioversion of acute AF is variable, and its onset of action is slower that that of other drugs used for cardioversion of AF.
  • Ibutilide has the asset of being well effective in atrial flutter, but it carries a risk of torsade de pointes VT and its use should, therefore, be limited to specialist physicians with expertise in arrhythmia management.
  • Another management approach involves the patient taking antiarrhythmic medication himself/herself as soon as the arrhythmia occurs (”pill in the pocket”). Before this type of therapy is begun a specialist should be consulted, and an initial successful conversion trial should be undertaken in a hospital using the intended antiarrhythmic drug. Suitable product for this purpose is flecainide (300 mg p.o.).
  • The procedure of pharmacological cardioversion of AF is presented in table T2.

How to carry out pharmacological cardioversion of AF

1.Ensure the availability of adequate monitoring equipment (e.g. ECG surveillance, blood pressure recording) and facilities to manage possible proarrhythmia (defibrillator).
2.Attach the patient to an ECG monitor.
3.Place an intravenous line and start infusion with e.g. physiological saline solution.
4.Slow ventricular rate by administering a beta blocker (or a calcium-channel blocker / digoxin).
5.Administer the antiarrhythmic drug.
  • Flecainide 1-2 mg/kg (max 150 mg) by intravenous infusion over 30 minutes or 300 mg as a single oral dose
  • Vernakalant 3 mg/kg (max 339 mg) by intravenous infusion over 10 minutes, another dose if needed after 15 minutes 2 mg/kg (max 226 mg) by intravenous infusion over 10 minutes
  • Do not use Class IC drugs or vernakalant for cardioversion of atrial flutter.
  • Ibutilide is effective also in atrial flutter, but its use warrants many precautions and continuous monitoring due to the risk of proarrhythmia.
  • Should any proarrhythmic effects, or any changes suggestive of such effects (e.g. increased QRS duration or prolongation of QT interval), become evident the administration of the drug must be stopped immediately.
6.Stop the infusion as soon as sinus rhythm is restored. Depending on the agent used, continue ECG monitoring for at least 3-4 hours after which the patient may be discharged home if fully recovered.
7.If the administration of the antiarrhythmic agent does not restore sinus rhythm, it is safer to refer the patient for electrical cardioversion than attempting pharmacological cardioversion with another agent.

Anticoagulation during cardioversion of AF

  • Acute AF (duration < 48 hours) may also be associated with a significant risk of thrombosis.
    • The risk of trombosis is at its highest during the first days after the cardioversion.
    • When assessing the risk of thrombosis and the need of anticoagulant therapy, the (modified) CHA2DS2-VASc score is used (picture ).
    • In high-risk patients (CHA2DS2-VASc ≥ 2) Indications for and Implementation of Anticoagulant Therapy in Atrial Fibrillation, an anticoagulant is always administered already before cardioversion. If warfarin is used, the patient is initially given low-molecular-weight heparin (LMWH) (dose adjusted to the body weight, see local sources for dosage) which is continued until INR is within therapeutic range. If direct anticoagulants are used, there is no need for LMWH.
    • In patients at low or moderate risk (CHA2DS2-VASc ≤ 1) Indications for and Implementation of Anticoagulant Therapy in Atrial Fibrillation, sinus rhythm may be restored without preceding anticoagulation if the duration of arrhythmia is < 12 h. In other cases, a direct anticoagulant or low-molecular-weight heparin and warfarin are started before cardioversion like in high-risk patients.
  • In patients with AF that is of unknown duration or has lasted for more than 48 hours, a prerequisite for cardioversion to be undertaken is that
    • warfarin therapy has been within therapeutic range (INR ≥ 2) for at least 3 weeks or
    • the patient has taken a direct anticoagulant (dabigatran, apixaban, edoxaban, rivaroxaban) at a therapeutic dose uninterrupted for at least 3 weeks or
    • no intracardiac thrombi are identified by transoesophageal echocardiography (TOE).
  • Anticoagulation therapy after cardioversion
  • The guidelines for cardioversion of atrial flutter are the same as those given for atrial fibrillation.

Transoesophageal echocardiogram (TOE) in cardioversion of AF

  • If the duration of AF is unclear or it has lasted for more than 48 hours and the patient is not on anticoagulant therapy or it has not been at therapeutic level, patients with severe symptoms can be referred for urgent transoesophageal echocardiogram (TOE).
    • A direct anticoagulant, or warfarin with LMWH, is started already before cardioversion similarly to high-risk patients with acute AF.
  • If no intracardiac thrombi are detected by TOE, cardioversion can be performed right away.
    • After cardioversion, anticoagulant therapy is continued for at least 4 weeks or permanently depending on other factors predisposing the patient to thrombi.
  • The advantage of TOE-guided cardioversion is rapid improvement of symptoms. Moreover, it may increase the chances of successful cardioversion as the therapeutic delay is shortened.

Evidence Summaries ⬆