Recommendations

Key Recommendations

Organise emergency electrical cardioversion for any patient with features of haemodynamic instability, which include:[5][20] 

  • Shock – see our topic  Shock

  • Syncope

  • Myocardial ischaemia – see our topics ST-elevation myocardial infarction and Non ST-elevation myocardial infarction

  • Acute, severe heart failure (characterised by acute pulmonary oedema or raised jugular venous pressure) – see our topic Acute heart failure.

If the patient is haemodynamically stable and presents acutely, use a rate control strategy or a rhythm control strategy (using cardioversion, either electrical or pharmacological).[23]  Drug treatment is often ineffective in controlling the rate in patients with atrial flutter. For most patients, therefore, the aim of treatment is to restore sinus rhythm.

  • In practice, start a rate control drug if the patient is tachycardic while you are initially assessing them, before deciding whether to use a rate control or rhythm control strategy.

  • Electrical cardioversion is generally preferred over pharmacological cardioversion, because anti-arrhythmic drugs are usually not effective in patients with atrial flutter.[5]

In the absence of evidence for choice of initial management strategy in patients with atrial flutter, use a similar approach to atrial fibrillation:

  • Either a rate control or rhythm control strategy if the onset of atrial flutter is definitely <48 hours[23] 

  • A rate control strategy if the onset of atrial flutter is >48 hours, or uncertain[23] 

  • Consider a longer-term rhythm control strategy for these patients using transoesophageal-guided or conventional cardioversion.[23]

Prioritise identification and treatment of any underlying cause; in about 60% of patients, atrial flutter occurs as part of an acute medical illness, and will resolve when this is treated.[6] 

Refer the patient to an electrophysiologist for electrophysiological studies and consideration of catheter ablation.[5] 

If the patient has new-onset atrial flutter and is receiving no, or subtherapeutic, anticoagulation, start initial parenteral anticoagulation and continue this until you have made a full assessment for long-term anticoagulation.[23] This should not delay urgent cardioversion, however. 

Discuss the patient with a senior colleague and/or a cardiologist when considering long-term anticoagulation in order to weigh up the risks and benefits.

  • In general, the anticoagulation strategy for atrial flutter should follow the  same approach as for atrial fibrillation (AF), particularly if the patient is undergoing cardioversion or has concomitant AF.[5][23][24]

  • Use the CHA 2DS 2-VASc score and a bleeding risk score when assessing the patient. [ Atrial Fibrillation CHA(2)DS(2)-VASc Score for Stroke Risk Opens in new window ]

  • If anticoagulation is suitable for the patient, use a direct oral anticoagulant first-line, unless the patient is already taking warfarin.[23]

Full recommendations

Urgently identify any patient with features of haemodynamic instability, which include:[5][20] 

  • Shock – see our topic Shock

  • Syncope

  • Myocardial ischaemia – see our topics ST-elevation myocardial infarction and Non ST-elevation myocardial infarction

  • Acute, severe heart failure (characterised by acute pulmonary oedema or raised jugular venous pressure) – see our topic Acute heart failure.

Supportive measures

While assessing the patient, start resuscitation measures. However, do not delay emergency synchronised direct current (DC) cardioversion in a haemodynamically unstable patient, because their condition may be life-threatening. See Electrical cardioversion below.

  • Monitor controlled oxygen therapy. An upper SpO 2 limit of 96% is reasonable when administering supplemental oxygen to most patients with acute illness who are not at risk of hypercapnia.

    • Evidence suggests that liberal use of supplemental oxygen (target SpO 2 >96%) in acutely ill adults is associated with higher mortality than more conservative oxygen therapy.[25]

    • A lower target SpO 2 of 88% to 92% is appropriate if the patient is at risk of hypercapnic respiratory failure.[26]

  • Monitor the ECG and blood pressure.[20]

  • Obtain intravenous access.[20]

  • Identify and treat any reversible causes (e.g., electrolyte abnormalities).[20]

Emergency electrical cardioversion

Organise immediate synchronised DC cardioversion.[5][20]

  • Call for anaesthetic support to ensure any conscious patient has sedation or general anaesthesia.[20]

  • Seek senior and/or specialist review and consider pre-cardioversion anticoagulation; this should not delay urgent cardioversion, however. See Anticoagulation below. 

  • Electrical cardioversion is achieved with synchronised DC cardioversion. Give up to three shocks.[20]

    • For the initial shock, use 70 to 120 J of energy.[20]

    • Give subsequent shocks using stepwise increases in energy.[20]

  • If cardioversion has not terminated the atrial flutter after three shocks, further treatment should only be initiated by a specialist.[20]


Electrical (direct current) cardioversion animated demonstration
Electrical (direct current) cardioversion animated demonstration

How to perform electrical (direct current) cardioversion using a defibrillator.


There are two different management strategies for the patient with atrial flutter who is haemodynamically stable and presents acutely; a rate control strategy and a rhythm control strategy (using electrical or pharmacological cardioversion).[5][23]

  • In practice, start a rate control drug if the patient is tachycardic while you are initially assessing them, before deciding whether to use a rate control or rhythm control strategy.

  • Drug treatment is often ineffective in controlling the rate in patients with atrial flutter. For most patients, therefore, the aim of treatment is to restore sinus rhythm.

  • Electrical cardioversion is preferred over pharmacological cardioversion, because anti-arrhythmic drugs are usually not effective in patients with atrial flutter.[5] 

In the absence of evidence for choice of initial management strategy in patients with atrial flutter, use a similar approach to atrial fibrillation:

  • Either a rate control or rhythm control strategy if the onset of atrial flutter is definitely <48 hours.[23] 

  • A rate control strategy if the onset of atrial flutter is >48 hours, or uncertain[23] 

    • Consider a longer-term rhythm control strategy for these patients using transoesophageal-guided or conventional cardioversion.[23] 

In addition, always use your clinical judgement when choosing the type of strategy; a rhythm control strategy may be preferred if the patient would be suitable for ablation.[5] 

Seek advice from a senior colleague or a specialist if you are unsure.

Rate control

Start rate control using an atrioventricular (AV) nodal blocking drug (e.g., a beta-blocker or a non-dihydropyridine calcium-channel blocker).[5][23] In practice, do this if the patient is tachycardic while you are initially assessing them. 

  • Base your choice of drug on the patient’s symptoms, heart rate, comorbidities, and preferences.[23] Seek specialist input about choice of drug if you are unsure. 

  • Non-dihydropyridine calcium-channel blockers include verapamil and diltiazem. However, these are contraindicated if the patient has hypotension or heart failure with reduced ejection fraction.[5] 

  • Beta-blockers are contraindicated if the patient has decompensated heart failure.[5] 

  • Digoxin is also an option.[37] In practice, it may convert atrial flutter to atrial fibrillation, which can be easier to manage. See our topic  Atrial fibrillation.

Do not use rate control drugs in people with atrial flutter with a pre-excitation syndrome such as Wolff-Parkinson-White syndrome.[38] In practice, seek advice from a specialist or a senior colleague to determine suitable alternatives. See our topic  Wolff-Parkinson-White syndrome.

Rate control may be difficult to achieve in practice.[5] 

  • Drug treatment is often ineffective in controlling the rate in patients with atrial flutter. For most patients, therefore, the aim of treatment is to restore sinus rhythm.

More info: Rate control

Adequate rate control is more difficult with atrial flutter than with atrial fibrillation. However, most randomised controlled trials of AV nodal blocking agents generally do not report data for atrial flutter alone, but rather combined groups of patients with atrial fibrillation and/or flutter.[2] 

Treatment of underlying cause

Prioritise treating any underlying cause you identify, because atrial flutter may resolve once the cause is treated.[6] In about 60% of patients, atrial flutter occurs as part of an acute medical illness.[6] 

Correct any electrolyte imbalances, although these are generally not the sole cause of atrial flutter.

Rhythm control: elective electrical cardioversion

Organise elective electrical cardioversion if a rhythm control strategy is suitable. Electrical cardioversion may also be used if atrial flutter persists despite rate control and treatment of the underlying cause (or in the absence of a reversible cause).[5][23]

  • Electrical cardioversion is achieved with synchronised direct current cardioversion.

  • Atrial flutter is extremely responsive to electrical cardioversion.[2] The success rate for electrical cardioversion, using 5 to 50 J of energy, is 95% to 100%.[39][40][41] Lower amounts of energy are most successful with biphasic rather than monophasic waveforms. 

Before elective cardioversion:

  • Organise echocardiography.[23]  

    • In general, this should be with transthoracic echocardiography. However, transoesophageal echocardiography is equally effective if the onset of atrial flutter is >48 hours.[23] 

  • Seek senior/specialist advice to consider pre-cardioversion anticoagulation. See Anticoagulation below.

In general, continue rate control drugs before electrical cardioversion and discontinue them when sinus rhythm is restored.

  • However, they may be continued in certain patients to prevent rapid ventricular rate in case of recurrence; consider decreasing the dose after cardioversion if there is bradycardia or hypotension.

High-rate atrial pacing may be considered by a specialist if electrical cardioversion has failed and the patient has an implantable cardioverter defibrillator or permanent pacemaker.[5] However, this is rarely used in practice. 

Rhythm control: pharmacological cardioversion

Be aware that anti-arrhythmic drugs are generally not effective in re-establishing sinus rhythm; in practice, electrical cardioversion is preferred.[5] 

However, consider pharmacological cardioversion if:

  • Atrial flutter persists despite treatment of any underlying cause, rate control, and electrical cardioversion[5][23]

  • Electrical cardioversion is unavailable or not acceptable to the patient.[5][23] 

Pharmacological cardioversion should only be used:

  • If the patient has a normal QT interval, and no permanent pacemaker or implantable cardioverter defibrillator[5] 

  • In hospital under specialist supervision.

Pharmacological cardioversion uses an anti-arrhythmic drug, selected according to the patient’s history and condition.[23] Options include:[23] 

  • Flecainide or amiodarone if the patient has no evidence of structural or ischaemic heart disease

  • Amiodarone if the patient has evidence of structural heart disease

  • Ibutilide (although this is not available in the UK).[5] 

Before cardioversion:

  • Organise echocardiography[23]

    • In general, this should be with transthoracic echocardiography. However, transoesophageal echocardiography is equally effective if the onset of atrial flutter is >48 hours[23] 

  • Seek senior/specialist advice to consider pre-cardioversion anticoagulation. See Anticoagulation below

  • Co-prescribe an AV nodal blocking drug if you are giving a class IC anti-arrhythmic drug (e.g., flecainide) to prevent slowing of the atrial rate, which may result in 1:1 AV conduction and a potentially life-threatening ventricular rate.[5] 

Monitor the ECG continuously during pharmacological cardioversion.

  • The major risk associated with pharmacological cardioversion is torsade de pointes. Patients with reduced left ventricular ejection fraction are at the highest risk.

More info: Effectiveness/risks of pharmacological cardioversion

Pharmacological cardioversion is less effective than synchronised cardioversion, with potential for being pro-arrhythmic. The success rate is 38% to 76% for conversion of atrial flutter to sinus rhythm, with the mean time to conversion reported to be 30 minutes in those who respond. Ventricular pro-arrhythmia, specifically sustained polymorphic ventricular tachycardia, occurs at a rate of 1.2% to 1.7%.[42][43][44][45] For this reason, these drugs should not be given to those with severe structural heart disease and prolonged QT interval.

Catheter ablation

Refer the patient to an electrophysiologist for electrophysiology studies and catheter ablation. Catheter ablation should be considered in all patients after the first episode of atrial flutter.[5] The European Society of Cardiology recommends ablation for any patient with:[5] 

  • Atrial flutter that is refractory to pharmacological rate control, or a contraindication to pharmacological rate control

  • Symptomatic, recurrent, cavotricuspid-isthmus (CTI)-dependent atrial flutter

  • Symptomatic, recurrent episodes of non-CTI-dependent flutter at experienced catheter ablation centres

  • Persistent atrial flutter or atrial flutter associated with depressed left ventricular systolic function due to tachycardiomyopathy.

More info: Catheter ablation

Catheter ablation is effective at maintaining sinus rhythm in typical atrial flutter in which the CTI is a necessary part of the arrhythmic circuit. This invasive technique involves a femoral venous approach. An ablation catheter is placed at the isthmus between the inferior vena cava and the tricuspid annulus using either fluoroscopic guidance or a 3-dimensional electroanatomic mapping system. Radiofrequency energy is then applied to create a line of ablation from the tricuspid annulus to the inferior vena cava. The success rate for treatment of typical atrial flutter is high and has been reported at 92% for the first procedure and 97% for multiple procedures.[46][47][48] Atypical flutter is more difficult to ablate, particularly when associated with congenital heart disease. In such situations, referral to an experienced centre should be be considered.

Drug treatment

If catheter ablation is not feasible or the patient would prefer drug therapy, rate control ± rhythm control is a second-line option.

Long-term rate control 

Give long-term rate control if catheter ablation is not feasible or the patient would prefer drug therapy.[5] However, be aware that  drug treatment is often ineffective in controlling the rate in patients with atrial flutter. 

For most patients, therefore, the aim of treatment is to restore sinus rhythm.

  • Use an atrioventricular (AV) nodal blocking drug (e.g., a beta-blocker, a non-dihydropyridine calcium-channel blocker).[5] 

  • Base your choice of drug on the patient’s symptoms, heart rate, comorbidities, and preferences.[23]

Do not use rate control drugs in people with atrial flutter with a pre-excitation syndrome such as Wolff-Parkinson-White syndrome.[38] In practice, seek advice from a specialist or a senior colleague to determine suitable alternatives. See our topic  Wolff-Parkinson-White syndrome.

Long-term anti-arrhythmic therapy

Consider anti-arrhythmic therapy to maintain sinus rhythm if atrial flutter persists despite rate control.[5] 

  • Use amiodarone if the patient has heart failure or structural heart disease.[5] 

  • Do not give a class 1c anti-arrhythmic drug (e.g., flecainide or propafenone):

    • To a patient with known ischaemic or structural heart disease[23]

    • Without co-prescribing an AV nodal blocking drug because of the risk of slowing of the atrial rate, which may result in 1:1 AV conduction and a potentially life-threatening ventricular rate.[5] 

More info: Risks of class IC anti-arrhythmic drugs

Class IC anti-arrhythmic drugs should not be used without co-prescription of an AV-nodal blocking drug because of the risk of slowing of the atrial rate, which may result in 1:1 AV conduction.[2][5][8] For example, atrial flutter with a rate of 300 bpm that conducts 2:1 will result in a ventricular rate of 150 beats per minute (bpm). An anti-arrhythmic drug that slows the flutter rate to 200 bpm might allow 1:1 AV nodal conduction in the absence of AV nodal blockers, thus resulting in a potentially clinically dangerous ventricular rate of 200 bpm.

Initial/pre-cardioversion anticoagulation

If the patient has new-onset atrial flutter and is receiving no, or subtherapeutic, anticoagulation, start initial parenteral anticoagulation and continue this until you have made a full assessment.[23] This should not delay urgent cardioversion, however. 

  • Choose an appropriate anticoagulant for the patient in line with your hospital protocols. Unfractionated heparin or a low molecular weight heparin (LMWH) such as enoxaparin are options.[23]

  • Transition patients who are started on unfractionated heparin or an LMWH to a direct oral anticoagulant (DOAC; e.g., rivaroxaban, apixaban, edoxaban, or dabigatran), or warfarin, when appropriate, and after assessment of stroke and bleeding risk.[23] See  Long-term anticoagulation strategy below.

Long-term anticoagulation strategy

Discuss the patient with a senior colleague and/or a cardiologist when considering long-term anticoagulation in order to weigh up the risks and benefits.

  • In general, the anticoagulation strategy for atrial flutter should follow the same approach as for atrial fibrillation (AF), particularly if the patient is undergoing cardioversion or has concomitant AF.[5][23][24]

  • In the UK, the National Institute for Health and Care Excellence recommends using the CHA 2DS 2-VASc score to calculate stroke risk in all patients presenting with atrial flutter.[23] [ Atrial Fibrillation CHA(2)DS(2)-VASc Score for Stroke Risk Opens in new window ] Although thrombo-embolic risk is lower in atrial flutter than in AF, it is still significant.[5] 

  • If anticoagulation is being considered, use a bleeding risk score to assess the patient’s risk of bleeding.[23] 

    • NICE recommends using the ORBIT score to assess bleeding risk, but other bleeding risk scores (such as HAS-BLED) may still be used depending on your local protocol. [ HAS-BLED Bleeding Risk Score Opens in new window ]

    • Use a bleeding risk score to:[23][38][49]

      • 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), and concurrent use of aspirin or a non-steroidal anti-inflammatory drug

      • Flag the ‘high bleeding risk’ patients for early review and follow-up.

  • If long-term anticoagulation is suitable for the patient, start a DOAC using any one of apixaban, dabigatran, edoxaban, or rivaroxaban.[23] 

    • If a DOAC is contraindicated, not tolerated, or unsuitable for the patient, use warfarin.[23] 

    • If the patient is already taking warfarin and their INR is stable, continue warfarin and discuss the option of switching to a DOAC at their next routine appointment, while taking into account the time the amount of time their INR is in therapeutic range.[23] 

More info: Risk of embolisation

Observational studies have demonstrated a 1.7% to 7% risk of embolisation during cardioversion from atrial flutter.[50] The incidence of thrombus or echo-dense material in the atria in patients with atrial flutter who are not anticoagulated ranges from 0% to 34% and increases with atrial flutter duration more than 48 hours.[51] Atrial mechanical stunning has also been documented to persist for several weeks after cardioversion.[52] 

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