Recommendations
Urgent
Assess haemodynamic status immediately.[1][3]
Regardless of the duration of onset of the patient’s arrhythmia, do not delay emergency synchronised direct current (DC) cardioversion in the following groups as their condition may be life-threatening:[1][3][32]
Features of haemodynamic instability
Symptoms of acute myocardial ischaemia
Suspected or confirmed serious precipitating illness requiring hospital care
Atrial fibrillation (AF) alongside a pre-excitation syndrome such as Wolff-Parkinson-White syndrome
Signs or symptoms of acute stroke.
For any patient who is haemodynamically compromised:
Urgently admit to an acute medical unit[32]
Call for anaesthetic support to sedate the patient before DC cardioversion[1]
Seek senior and/or specialist review; this should not delay urgent DC cardioversion[1][3]
Check the patient’s oral anticoagulation status as soon as possible.[1] In patients not already on therapeutic anticoagulation, immediately start anticoagulation pre-cardioversion[1]
Consider intravenous amiodarone for acute control of heart rate, if needed.[1]
Follow the integrated Atrial fibrillation Better Care (ABC) pathway for holistic management of any patient with AF:[1][63]
Anticoagulation/ Avoid stroke
Better symptom management
Cardiovascular and comorbidity optimisation (including lifestyle changes).
In all patients, prioritise calculating stroke risk using the CHA2DS2-VASc score.[1][3][34] [ Atrial Fibrillation CHA(2)DS(2)-VASc Score for Stroke Risk Opens in new window ]
Consider oral anticoagulation for stroke prevention in men with a CHA2DS2-VASc score of 1 or more and women with a score of 2 or more.[1][3] In these groups, continue anticoagulation long-term.[1]
Guidelines from the European Society of Cardiology (ESC) give an additional, stronger recommendation for higher CHA2DS2-VASc scores; the ESC recommends commencing oral anticoagulation in AF patients with a CHA2DS2-VASc score of 2 or more in men and 3 or more in women.[1]
If you are considering anticoagulation, use the ORBIT score or the HAS-BLED score to:[1][3][34][36] [ ORBIT Bleeding Risk Score Opens in new window ] [ HAS-BLED Bleeding Risk Score Opens in new window ]
Assess the risk of a major bleed
Identify (and subsequently manage) modifiable risk factors for bleeding
Flag the ‘high bleeding risk’ patients for early review and follow-up.
Guidelines from the European Society of Cardiology recommend use of the HAS-BLED score.[1] The National Institute for Health and Care Excellence (NICE) recommends use of ORBIT over HAS-BLED where possible.[3] In practice, either HAS-BLED or ORBIT is acceptable.
Do not use bleeding risk scores to exclude anticoagulant treatment.[64]
Bleeding risk is dynamic and requires regular re-assessment, and should not be based on a single one-off assessment.[65]
When indicated, start anticoagulation as soon as possible.
Assess and manage acute presentation with AF-related stroke in accordance with the acute stroke pathway. See Ischaemic stroke and Stroke due to spontaneous intracerebral haemorrhage.
If an underlying cause for AF is identified, manage (where possible) or refer, as appropriate. Always use your clinical judgement and local policies and guidelines to determine urgency.
Key Recommendations
In any patient without life-threatening haemodynamic instability:
Start rate control (e.g., beta-blocker, rate-limiting calcium-channel blocker)[1]
If the patient still has symptoms after their rate has been controlled or rate control has not been achieved, consider rhythm control (steps 2, 3, and 4)
Check the patient's oral anticoagulation status[1]
If the patient is already on therapeutic anticoagulation:
Check international normalised ratio (INR), if possible, in patients taking warfarin before electrical cardioversion to confirm good anticoagulant adherence
Proceed with cardioversion (either immediate or delayed for possible spontaneous cardioversion)[1]
If the patient is not on anticoagulation, start anticoagulation pre-cardioversion as soon as possible.[1] Choose an appropriate anticoagulant for the patient in line with your hospital protocols
Check the duration of AF and consider options for rhythm control to further reduce symptoms[1]
If the onset of the arrhythmia is less than 48 hours, consider early cardioversion in selected patients[1]
In patients with AF duration 24 to 48 hours who are undergoing cardioversion, initiate oral anticoagulation for at least 4 weeks after cardioversion.[1] Use a direct oral anticoagulant in preference to a vitamin K antagonist.[1] This is an optional step for those with AF onset definitely less than 24 hours[1]
Urgently assess for features of haemodynamic instability.[1][3] These patients may need emergency electrical cardioversion; see Emergency management of haemodynamically unstable patients below.
Although controlling symptoms by minimising circulatory instability or insufficiency is central to any approach taken, reducing stroke risk and preventing complications is paramount in the management strategy.[3][32]
Follow the integrated Atrial fibrillation Better Care (ABC) pathway for holistic management of any patient with AF:[1][63]
Anticoagulation/ Avoid stroke
Better symptom management
Cardiovascular and comorbidity optimisation (including lifestyle changes).
Use the modified European Heart Rhythm Association (EHRA) symptom scale to quantify the patient’s symptom status before, and after initiation of, treatment.[1]
The EHRA symptom scale evaluates the effect of six symptoms (palpitations, fatigue, dizziness, dyspnoea, chest pain, and anxiety) during AF on the patient’s daily activity, ranging from none to symptom frequency or severity that leads to a discontinuation of daily activities.[44]
Carefully consider whether the patient should be admitted to hospital, either via direct admission if they present to the accident and emergency department or following urgent referral from the community.
In practice, if the patient meets all of the following criteria, they may be suitable for outpatient rate control and anticoagulation (depending on their risk of stroke):
Able to tolerate symptoms
Haemodynamically stable
No serious precipitating illness
Able to adhere to medication and appointments (if known).
Consult senior colleagues if you are unsure.
In practice, even if you decide to manage the patient as an outpatient, refer to a cardiologist specialising in arrhythmia care services (ideally within 4-6 weeks) for longer-term management options. The specialist may offer direct current (DC) cardioversion with or without interventional catheter ablation.
Integrated management of any patient with AF relies on a co-ordinated multidisciplinary team with the patient and their family/carers at the centre of the approach.[1]
In hospital: indications for immediate admission
In practice, arrange admission for any patient with any one of:
Features of life-threatening haemodynamic instability
Hypotension (systolic blood pressure <90 mmHg) or other signs of shock
Chest pain or evidence of myocardial ischaemia on ECG
Signs of reduced cerebral perfusion (reduced conscious level/Glasgow Coma Scale, syncope)
Signs of heart failure
Symptoms of acute myocardial ischaemia
Chest pain or evidence of myocardial ischaemia on ECG
Suspected or confirmed serious precipitating illness requiring hospital care
For example, pulmonary emboli, severe pneumonia, severe pericarditis
AF alongside a pre-excitation syndrome such as Wolff-Parkinson-White syndrome
Patients with Wolff-Parkinson-White syndrome and AF are at risk of fast ventricular rates resulting from rapid conduction of atrial electrical activity to the ventricles via the accessory pathway, and at increased risk of ventricular fibrillation and sudden death[1]
See Wolff-Parkinson-White syndrome
Signs or symptoms of acute stroke
Pronounced tachycardia.
These patients may need emergency electrical cardioversion. See Emergency management of haemodynamically unstable patients below.
In the community: indications for urgent referral to hospital
Arrange immediate transfer to hospital, via a blue-light ambulance, for any patient with any one of:
Features of life-threatening haemodynamic instability
Hypotension (systolic blood pressure <90 mmHg) or other signs of shock
Chest pain or evidence of myocardial ischaemia on ECG
Signs of reduced cerebral perfusion (reduced conscious level/Glasgow Coma Scale, syncope)
Signs of heart failure
Persistent tachycardia
Symptoms of acute cardiac ischaemia
Chest pain or evidence of myocardial ischaemia on ECG
Suspected or confirmed serious precipitating illness requiring hospital care
For example, pulmonary emboli, severe pneumonia, severe pericarditis
AF alongside a pre-excitation syndrome such as Wolff-Parkinson-White syndrome
Signs or symptoms of acute stroke
Pronounced tachycardia.
This recommendation is based on clinical experience.
These patients may need emergency electrical cardioversion. See Emergency management of haemodynamically unstable patients below.
If the patient is haemodynamically unstable, prioritise stabilisation as detailed in this section. Once the patient is stable, work through the integrated Atrial fibrillation Better Care (ABC) pathway; see A - Anticoagulation and stroke prevention, B - Better symptom management, and C - Cardiovascular and comorbidity optimisation below.[1][63]
Rhythm control
Identify any patient with uncontrolled fast AF who has features of:[1][3]
Acute or worsening haemodynamic instability[1]
Syncope, owing to global reduction in blood flow to the brain
Acute pulmonary oedema
Ongoing myocardial ischaemia; typical ischaemic chest pain and/or evidence of myocardial ischaemia on 12-lead ECG
Symptomatic hypotension; systolic blood pressure <90 mmHg
Cardiogenic shock; see Shock
Heart failure
Pulmonary oedema and/or raised jugular venous pressure
Evidence of ventricular pre-excitation on ECG with rapid antegrade conduction, as seen in people with Wolff-Parkinson-White syndrome
Patients with Wolff-Parkinson-White syndrome and AF are at risk of fast ventricular rates resulting from rapid conduction of atrial electrical activity to the ventricles via the accessory pathway, and at increased risk of ventricular fibrillation and sudden death[1]
Do not delay emergency synchronised direct current (DC) cardioversion in these groups, regardless of the duration of onset of the patient’s arrhythmia, as their condition may be life-threatening.
Electrical cardioversion quickly and effectively converts AF to sinus rhythm.[1]
Electrical cardioversion restores sinus rhythm quicker and more effectively than pharmacological cardioversion and is associated with shorter hospital stays.[66]
Do not use pharmacological cardioversion in haemodynamically compromised patients.[1]
Urgently admit to an acute medical unit.[32]
Call for anaesthetic support to sedate the patient before DC cardioversion.[1] This will usually be with a short-acting general anaesthetic.
Seek senior and/or specialist review; this should not delay urgent DC cardioversion.[1][3] Further treatment should only be initiated by a specialist.
Record and store an ECG rhythm strip during and immediately after shock delivery.
Continuously monitor the patient’s blood pressure and oximetry during the procedure.[1][67]
Practical tip
Ensure the defibrillator is synchronised and that it remains synchronised between shocks.
If initial attempts at DC cardioversion fail, ensure there is good skin-to-electrode contact with the pads in the anteroposterior position.
Anticoagulation
Check the patient’s oral anticoagulation status as soon as possible.[1] In patients not already on therapeutic anticoagulation, immediately start anticoagulation pre-cardioversion. Use a low molecular weight heparin (LMWH), such as enoxaparin, or unfractionated heparin.[3] After cardioversion, transition patients who are started on a LMWH or unfractionated heparin to a direct oral anticoagulant (DOAC), such as rivaroxaban, apixaban, edoxaban, or dabigatran, or warfarin when appropriate.[1]
This is important to prevent potential thromboembolic complications and should be given in a timely manner even in haemodynamically unstable patients.[1]
In patients with AF duration of more than 24 hours who are undergoing cardioversion, initiate oral anticoagulation for at least 4 weeks after cardioversion.[1] Use a DOAC in preference to a vitamin K antagonist.[1]
This is an optional step for those with AF onset definitely less than 24 hours.[1]
Beyond 4 weeks, base decisions about long-term anticoagulation on associated stroke risk factors, as per the patient’s CHA2DS2-VASc score.[1][3][34] [ Atrial Fibrillation CHA(2)DS(2)-VASc Score for Stroke Risk Opens in new window ] See Anticoagulation and stroke prevention below.
Be aware that some patients may develop sinus bradycardia after successful DC cardioversion. Ensure there are provisions for the use of intravenous atropine or isoprenaline or temporary transcutaneous pacing to manage post-cardioversion bradycardia until the patient stabilises.[1]
Rate control
Bear in mind that rhythm control is often unsuccessful in critically ill patients and those with severely impaired ventricular systolic function, because AF is often precipitated/exacerbated by increased sympathetic tone, inotropes, and vasopressors.[1] In these patients, work to identify and correct precipitating factors and secondary causes and optimise background treatment.[1]
Consider intravenous amiodarone for acute control of heart rate in these patients.[1] Only do this with advice from a specialist.
Do not use rate control drugs in people with AF with a pre-excitation syndrome such as Wolff-Parkinson-White syndrome.[1] In practice, seek advice from a specialist or senior colleague to determine suitable alternatives. See Wolff-Parkinson-White syndrome.
These drugs accelerate conduction down the accessory pathway to the ventricle putting the patient at risk of life-threatening arrhythmias, such as ventricular fibrillation and sudden death.[1]
AF is the second most common arrhythmia in Wolff-Parkinson-White syndrome, occurring in approximately one third of patients.[1]
Atrial activity predominantly conducts down the accessory pathway, causing ventricular pre-excitation.
The ECG will show a fast, broad QRS irregular rhythm with delta waves.
[Figure caption and citation for the preceding image starts]: Atrial fibrillation with Wolff-Parkinson-White syndromeFrom the collections of Arti N. Shah and Bharat K. Kantharia [Citation ends].
If the patient is haemodynamically compromised do not delay emergency synchronised direct current (DC) cardioversion, because their condition may be life-threatening.[1][3] Go straight to Emergency management of haemodynamically unstable patients above.
Once the patient is stable, prioritise anticoagulation and stroke prevention, a critical aspect of management in AF, in line with the integrated Atrial fibrillation Better Care (ABC) pathway for holistic management of any patient with AF.[1][63]
Overall, AF increases the risk of stroke fivefold, but this risk is not homogeneous, depending on the presence of specific stroke risk factors/modifiers.[1]
Stroke risk
Use the CHA2DS2-VASc score to calculate stroke risk in all patients presenting with AF.[1][3][34] [ Atrial Fibrillation CHA(2)DS(2)-VASc Score for Stroke Risk Opens in new window ]
Consider oral anticoagulation for stroke prevention in men with a CHA2DS2-VASc score of 1 or more and women with a score of 2 or more.[1][3] In these groups, continue anticoagulation long-term.[1]
Guidelines from the European Society of Cardiology (ESC) give an additional, stronger recommendation for higher CHA2DS2-VASc scores; the ESC recommends commencing oral anticoagulation in AF patients with a CHA2DS2-VASc score of 2 or more in men and 3 or more in women.[1]
Ensure any patient, regardless of their CHA2DS2-VASc score, who is going to have non-emergency cardioversion has been maintained on therapeutic anticoagulation for a minimum of 3 weeks before commencing cardioversion.[1][3] For choice of pre-cardioversion anticoagulant, see B - Better symptom management below.
In patients with AF duration of more than 24 hours who are undergoing cardioversion, continue anticoagulation for at least 4 weeks after cardioversion.[1] This is an optional step for those with AF onset definitely less than 24 hours.[1]
Beyond 4 weeks, base decisions about long-term anticoagulation on associated stroke risk factors, as per the patient’s CHA2DS2-VASc score.[1][3][34]
Bleeding risk
If you are considering anticoagulation, use either the ORBIT score or the HAS-BLED score to:[1][3][34][36] [ ORBIT Bleeding Risk Score Opens in new window ] [ HAS-BLED Bleeding Risk Score Opens in new window ]
Assess the risk of a major bleed
Identify (and subsequently manage) modifiable risk factors for bleeding, such as uncontrolled hypertension, harmful alcohol consumption, labile international normalised ratio (INR; if the patient is on warfarin), concurrent use of medication (including antiplatelets, selective serotonin reuptake inhibitors, and non-steroidal anti-inflammatory drugs), and reversible causes of anaemia
Flag the ‘high bleeding risk’ patients for early (4 weeks as opposed to 4-6 months) review and follow-up.
Guidelines from the European Society of Cardiology recommend use of the HAS-BLED score.[1] The National Institute for Health and Care Excellence (NICE) recommends use of ORBIT over HAS-BLED where possible.[3] In practice, either HAS-BLED or ORBIT is acceptable.
Do not use bleeding risk scores to exclude anticoagulant treatment; a high score should not rule out anticoagulation.[64]
Bleeding risk is dynamic and requires regular re-assessment; it should not be based on a single one-off assessment.[65]
Practical tip
A history of falls is not an independent predictor of bleeding on oral anticoagulants. A modelling study estimated that a patient would need to fall 295 times per year for the benefits of ischaemic stroke reduction with oral anticoagulants to be outweighed by the potential for serious bleeding.[1]
Practical tip
Follow your local protocol when choosing a bleeding risk score. 2020 guidelines from the European Society of Cardiology recommend use of the HAS-BLED score.[1] NICE recommends preferential use of the ORBIT score in its 2021 guideline.[3] However, subsequently published data show no advantage of ORBIT over HAS-BLED, even in patients taking direct oral anticoagulants, and suggest that in some circumstances ORBIT performs worse.[68][69][70] The use of either score is reasonable, and the choice of bleeding risk score is less important than failure to consider anticoagulation at all.
Choice of anticoagulant
When indicated by the CHA2DS2-VASc score, start oral anticoagulation as soon as possible.[1] [ Atrial Fibrillation CHA(2)DS(2)-VASc Score for Stroke Risk Opens in new window ]
Use a direct oral anticoagulant (DOAC) in preference to a vitamin K antagonist.[1][3]
Discuss the options for anticoagulation with the patient and base the choice on their clinical features and preferences.[1][3]
Before starting anticoagulation treatment, specifically discuss the potential risks and benefits with the patient, as part of the shared decision-making process, explaining that:[3]
For most people the benefit of anticoagulation outweighs the bleeding risk
For people with an increased risk of bleeding the benefit of anticoagulation may not always outweigh the bleeding risk, and careful monitoring of bleeding risk is important.
If using a DOAC, choose one of apixaban, edoxaban, rivaroxaban or dabigatran.[1] The choice of DOAC should be tailored to the person's clinical needs and preferences.[3]
DOACs have non-inferior efficacy and are possibly safer, particularly in terms of major bleeding, compared with warfarin.[71] [
]
[Evidence A] Unlike warfarin, DOACs don’t require laboratory anticoagulation monitoring.[72][73]
If using warfarin, start the patient on a parenteral anticoagulant, such as unfractionated heparin or a low molecular weight heparin, at the same time. Ensure INR is in the range of 2.0 to 3.0 before ceasing the parenteral anticoagulant.[1][3][32] Ensure follow-up to maintain the patient’s time in therapeutic range (TTR) >65%.[3] This approach is in line with recommendations from the National Institute for Health and Care Excellence and reflects common practice in the UK. Bear in mind, however, that guidelines from the ESC recommend maintaining TTR >70%.[1]
Do not offer aspirin monotherapy solely for stroke prevention to people with AF.[3]
A specialist may consider non-drug options in the presence of absolute contraindications to oral anticoagulants, including:[1]
Active serious bleeding (where the source should be identified and treated)
Associated comorbidities (e.g., severe thrombocytopenia <50 platelets/microlitre, severe anaemia under investigation, etc.)
A recent high-risk bleeding event such as intracranial haemorrhage.
If the patient is haemodynamically compromised do not delay emergency synchronised direct current (DC) cardioversion, regardless of the duration of onset of their arrhythmia, because their condition may be life-threatening.[1][3] Go straight to Emergency management of haemodynamically unstable patients above.
In any patient without life-threatening haemodynamic instability:
Start rate control (e.g., beta-blocker, rate-limiting calcium-channel blocker).[1] In practice, do this while initially assessing the patient
If the patient still has symptoms after their rate has been controlled or rate control has not been achieved, consider rhythm control (steps 2, 3, and 4)
Check the patient's oral anticoagulation status[1]
If the patient is already on therapeutic anticoagulation:
Check international normalised ratio (INR), if possible, in patients already taking warfarin before electrical cardioversion to confirm good anticoagulant adherence, with the INR within therapeutic range for 3 weeks prior to cardioversion. In patients already taking a direct oral anticoagulant (DOAC), confirm they have been on an appropriate dose with good adherence to treatment for 3 weeks before cardioversion
Proceed with cardioversion (either immediate or delayed for possible spontaneous cardioversion)[1]
If the patient is not on anticoagulation, assess bleeding risk using the ORBIT score or the HAS-BLED score, and then start anticoagulation pre-cardioversion as soon as possible[3] [ ORBIT Bleeding Risk Score Opens in new window ] [ HAS-BLED Bleeding Risk Score Opens in new window ]
Choose an appropriate anticoagulant for the patient in line with your hospital protocols
Guidelines from the European Society of Cardiology recommend using a DOAC such as rivaroxaban, apixaban, edoxaban, or dabigatran; or a low molecular weight heparin (LMWH), such as enoxaparin; or unfractionated heparin.[1] The choice of DOAC should be tailored to the person's clinical needs and preferences.[3]
Guidelines from the National Institute for Health and Care Excellence in the UK recommend using a LMWH or unfractionated heparin at initial presentation in this group[3]
Transition patients who are started on a LMWH or unfractionated heparin to a DOAC, such as rivaroxaban, apixaban, edoxaban, or dabigatran, or warfarin, when appropriate[1]
Check the duration of AF and consider options for rhythm control to further reduce symptoms[1]
If the onset of the arrhythmia is definitely less than 48 hours, consider early cardioversion in selected patients[1]
Beyond 4 weeks, long-term anticoagulation depends on associated stroke risk factors, as per the patient’s CHA2DS2-VASc score.[1][3][34] [ Atrial Fibrillation CHA(2)DS(2)-VASc Score for Stroke Risk Opens in new window ] See Anticoagulation and stroke prevention above.
Practical tip
In patients with onset of the arrhythmia definitely less than 48 hours: use early rhythm control, rather than delayed rhythm control or rate control alone, if it is feasible within the treatment setting and appropriate to patient characteristics, clinical presentation, and preferences. This may result in earlier symptom relief for the patient.
Rate control
Use rate control to slow the patient’s heart rate in the presence of tachycardia.[1][2][3]
Rate control is often sufficient to improve AF-related symptoms.[1]
Bear in mind that there is very little in the way of robust evidence to inform the best type and intensity of rate control treatment.[1]
Use atrioventricular nodal blocking drugs – either a standard beta-blocker (that is, a beta-blocker other than sotalol) such as bisoprolol, metoprolol, esmolol, or carvedilol, or a rate-limiting non-dihydropyridine calcium-channel blocker (diltiazem or verapamil) – as initial monotherapy.[1][3] Base the choice of drug on the person's symptoms, heart rate, comorbidities, and preferences when considering drug treatment.[3]
These are preferred first-line options as they have rapid onset of action and are effective for high sympathetic tone.[74][75][76][77][78]
Bear in mind that rate-limiting calcium-channel blockers are contraindicated in patients with heart failure with reduced ejection fraction (a common comorbidity).
Alternative drugs are available. Seek advice from a specialist on the best option for your individual patient.
Consider digoxin monotherapy if the patient is sedentary (they do no or very little physical exercise) or if other rate-limiting drugs are not appropriate because of comorbidities or patient preferences.[3] In practice, this is also a good option for older patients.
If monotherapy does not control symptoms, and if continuing symptoms are thought to be due to poor ventricular rate control, consider combination therapy with any two of the following:[3]
A beta-blocker
Diltiazem
Bear in mind that this is contraindicated in people with heart failure with reduced ejection fraction.[1] See Acute heart failure
Digoxin.
Do not offer amiodarone for long-term rate control.[3] The National Institute for Health and Care Excellence (NICE) recommends against use of long-term amiodarone (longer than 12 months) due to lack of evidence and the risk of serious side effects.[3] Amiodarone is usually only indicated for rate control in critically ill patients and those with severely impaired ventricular systolic function under the advice of a specialist.[1] See Emergency management of haemodynamically unstable patients above.
Practical tip
In stable patients, oral therapy is reasonable. If the patient is stable but you wish to achieve more rapid rate control, intravenous administration is a better choice than oral. Intravenous administration is also useful for observation of acute adverse effects (as infusion can be discontinued promptly) and therefore appropriate dose titration.
Do not use rate control drugs in people with AF with a pre-excitation syndrome such as Wolff-Parkinson-White syndrome.[1] In practice, seek advice from a specialist or senior colleague to determine suitable alternatives. See Wolff-Parkinson-White syndrome.
These drugs accelerate conduction down the accessory pathway to the ventricle putting the patient at risk of life-threatening arrhythmias, such as ventricular fibrillation and sudden death.[1]
Rhythm control
Consider either pharmacological or electrical cardioversion depending on clinical circumstances, patient preferences, and resources, to reduce symptoms.[1][3]
Electrical cardioversion restores sinus rhythm quicker and more effectively than pharmacological cardioversion and is associated with shorter hospital stays.[1][66] Pharmacological cardioversion, however, does not require fasting or sedation.
Electrical cardioversion is achieved with synchronised DC cardioversion; pharmacological cardioversion uses an anti-arrhythmic drug, selected according to the patient’s history and condition.[1]
In haemodynamically stable patients, the decision to use electrical or pharmacological cardioversion will depend on local expertise, facilities and drugs available, the availability of a suitable clinician to administer sedation if electric cardioversion is selected, and patient preference.
Start immediate anticoagulation before elective electrical or pharmacological cardioversion.[1] Use a DOAC, or a LMWH, or unfractionated heparin according to local protocols. Transition patients who are started on a LMWH or unfractionated heparin to warfarin when appropriate. Continue for a minimum of 3 weeks before commencing cardioversion.[1][3]
Cardioversion carries an inherent risk of stroke in non-anticoagulated patients, which is reduced substantially by administering anticoagulation.[1]
Initiate oral anticoagulation in all patients with AF duration of more than 24 hours for at least 4 weeks after cardioversion.[1] Use a DOAC in preference to a vitamin K antagonist.[1]
This is an optional step for those with AF onset definitely less than 24 hours.[1]
Beyond 4 weeks, long-term anticoagulation depends on associated stroke risk factors, as per the patient’s CHA2DS2-VASc score.[1][3][34] [ Atrial Fibrillation CHA(2)DS(2)-VASc Score for Stroke Risk Opens in new window ] See Anticoagulation and stroke prevention above.
Electrical cardioversion
Seek anaesthetic support to sedate the patient before DC cardioversion.[1]
Intravenous sedation should not be administered in the fed state as this increases the risk of aspiration. The anaesthetist will also be able to advise how long the patient should be fasting for safe sedation.
Record and store an ECG rhythm strip during and immediately after shock delivery.
Continuously monitor the patient’s blood pressure and oximetry during the procedure.[1][67]
Bear in mind that some patients may develop sinus bradycardia after successful DC cardioversion. Ensure there are provisions for the use of intravenous atropine or isoprenaline or temporary transcutaneous pacing to manage post-cardioversion bradycardia until the patient stabilises.[1]
Practical tip
Ensure the defibrillator is synchronised and that it remains synchronised between shocks.
If initial attempts at DC cardioversion fail, ensure there is good skin-to-electrode contact with the pads in the anteroposterior position.
Pharmacological cardioversion
Bear in mind that pharmacological cardioversion requires continuous medical supervision and ECG monitoring, regardless of the drug used, to detect a pro-arrhythmic event.[79]
In practice, this will usually be undertaken in a cardiac monitoring bed (e.g., in the cardiac care unit or a resuscitation bed in the accident and emergency department).
Use an anti-arrhythmic drug, selected according to the patient’s history and the overall clinical picture.[1][3] The National Institute for Health and Care Excellence in the UK recommends offering:[3]
A choice of flecainide or amiodarone to people with no evidence of structural or ischaemic heart disease
or
Amiodarone to people with evidence of structural heart disease
You will need a large-bore cannula for amiodarone.
Other anti-arrhythmics used outside of the UK include:[1]
Vernakalant – although available in the UK, it is rarely used
Ibutilide – not available in the UK.
Seek specialist opinion from a cardiologist if you are unsure about which drug to use.
Do not use sotalol.[3]
If using a class 1C anti-arrhythmic (e.g., flecainide), co-prescribe an atrioventricular (AV) nodal blocking agent (e.g., a rate-limiting calcium-channel blocker or beta-blocker) if the patient is not already taking an AV nodal blocking agent. This is to prevent accelerated ventricular responses.[1]
Using a sodium-channel blocker such as flecainide without an AV nodal blocking agent can convert to a slower atrial flutter rhythm, which allows the AV node to conduct in a 1:1 fashion and paradoxically results in faster ventricular response.[1]
Although this can occur in the acute situation of pharmacological cardioversion it is more important when considering these drugs for longer-term management to prevent recurrent AF.
Bear in mind that flecainide can only be used in the absence of structural heart disease/past ischaemic heart disease.
If in doubt, seek specialist cardiology advice.
If the patient is haemodynamically compromised do not delay emergency synchronised direct current (DC) cardioversion, regardless of the duration of onset of their arrhythmia, because their condition may be life-threatening.[1][3] Go straight to Emergency management of haemodynamically unstable patients above.
Once the patient is stable and you have worked through ‘A’ and ‘B’ of the integrated Atrial fibrillation Better Care (ABC) pathway (see sections above), manage underlying causes and ensure the patient receives advice about lifestyle and comorbidities.[1][63]
Manage any underlying causes
Identify and manage risk factors and concomitant conditions.[1] Correct treatable causes of AF where possible, or refer, as appropriate.[1][32] Use local policies and guidelines alongside your clinical judgement to determine urgency.
In practice, refer to a cardiologist, any patient:
Who is young and has suspected underlying structural heart disease
With a pre-excitation syndrome such as Wolff-Parkinson-White syndrome.[53] See Wolff-Parkinson-White syndrome
With valvular heart disease associated with AF
With suspected heart failure.
Practical tip
Signs of stroke or heart failure may be subtle in some instances.
Discharge and follow-up
Identify unhealthy lifestyle factors and give the patient advice on these to help prevent recurrence.[1] Focus, where relevant, on the following factors.
Physical activity: encourage the patient to undertake moderate-intensity exercise and remain physically active.[1] Advise the patient to avoid excessive endurance exercise (e.g., marathons and long-distance triathlons), especially if they are over 50 years old.[1]
Weight loss with comprehensive management of concomitant cardiovascular risk factors: maintaining a healthy weight may reduce blood pressure, dyslipidaemia, and risk of developing type 2 diabetes mellitus, therefore improving the patient’s overall cardiovascular risk profile.[1]
Alcohol intake reduction: regular heavier alcohol consumption (>14 units/week) is associated with an increased risk of AF.[23] Alcohol abstinence has been shown to reduce arrhythmia recurrence in regular drinkers with AF.[1]
Work with the patient to identify strategies for comprehensive risk-factor modification and interventions targeting underlying conditions that may apply, in particular:[1]
Hypertension
Heart failure
Coronary artery disease
Diabetes mellitus
Obstructive sleep apnoea
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