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Atrial Flutter

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Atrial flutter has many clinical aspects that are similar to atrial fibrillation but they are different in terms of mechanism and management.1 Some patients have both atrial flutter and atrial fibrillation and both arrhythmias are associated with a risk of thrombus formation and thromboembolism. Atrial flutter can be divided into 2 types:2

  • Type I: is described well both anatomically and electrically and is always being interrupted by rapid atrial pacing, with atrial rates from 240-350 beats per minute.
  • Type II: is not fully characterised as atrial flutter and is associated with atrial rates above 350 beats per minute.
Epidemiology
  • Atrial flutter is much less common than atrial fibrillation.
  • Although the exact incidence is not known, it is a common arrhythmia estimated to be present in approximately 10% of patients presenting with a supraventricular tachycardia.3
  • The prevalence increases with age.
  • Atrial flutter is more common in men.
  • Common during the first week after open heart surgery.
Causes
Presentation

May be asymptomatic but is generally not as well tolerated as atrial fibrillation and most often presents with palpitations.

  • May present with ECG findings of atrial flutter.
  • Mild symptoms include palpitations, irregular heart beat, fatigue, dyspnoea, chest pain, dizziness.
  • Syncope.
  • Heart failure.
  • Thromboembolism with transient ischaemic attacks or stroke.
  • Pulse may be irregular or regular, but is usually rapid. Arteriovenous conduction is usually 2:1, making the ventricular rate approximately 150 beats per minute. 1:1 AV conduction may lead to haemodynamic collapse. Carotid massage may decrease the ventricular rate.
  • Atrial flutter waves may be present in the jugular venous pulse.
  • May be associated with signs of underlying causes, e.g. thyrotoxicosis, alcoholism, pericarditis, valvular dysfunction or septal heart defects.
  • Heart failure, hypotension and respiratory distress may be present.
Differential diagnosis
  • Supraventricular tachyarrhythmias
  • Atrial fibrillation
  • Wolff-Parkinson-White syndrome
Investigations

Further assessment is focused on identifying any specific underlying cause and an assessment of cardiac function:

  • Electrocardiogram:
    • The common form of type I atrial flutter has saw-tooth flutter waves, best seen in leads II, III, and aVF, with atrial rates of 240-340. A 12-lead ECG may be necessary for the diagnosis of atrial flutter.4
    • The ventricular response may be regular or irregular.
    • Variable AV conduction also can be seen (commonly present with 2:1 or 3:1 AV conduction).
    • May be normal if paroxysmal and between episodes of atrial flutter. Ambulatory ECG monitoring and event recorders may be required.
  • Investigations for associated causes: chest x-ray, thyroid function tests, full blood count, ESR, renal function and electrolytes, liver function tests and coagulation screen (pre-warfarin).
  • Echocardiogram:
    • To evaluate underlying cardiac function, structural abnormalities, evidence of coronary artery disease or pericardial fluid.
    • If immediate cardioversion is considered, it is also used to detect any thrombus formation.
Associated diseases
  • Episodes of atrial flutter and atrial fibrillation often occur in the same patient.
  • Atrial fibrillation occasionally occurs when atrial flutter deteriorates into multiple small re-entrant wavelets.
Management

Treatment is usually cardioversion or ventricular rate control with medications. The preferred therapy for recurrent or persistent atrial flutter is now considered to be radiofrequency and cryotherapy catheter ablation.5,6

  • Treatment of underlying conditions, e.g. hyperthyroidism, alcoholism, obesity. After the initial episode is terminated and the underlying disease is treated, the patient may not need any further intervention except avoidance of the precipitating factor (e.g. alcohol, caffeine).
  • If haemodynamically unstable: urgent rate control or cardioversion is required.
  • Adequate anticoagulation has been shown to decrease thromboembolic complications in patients with persistent or paroxysmal atrial flutter and in patients who are undergoing cardioversion. Patients with atrial flutter are anticoagulated in the same way as for atrial fibrillation (see article on Atrial Fibrillation for details of NICE guidance).

Electrical cardioversion

  • External electrical cardioversion is safe and effective. The success rate is higher than 95%.2
  • If the atrial flutter has persisted for more than 48 hours then adequate anticoagulation is required before cardioversion to avoid the complication of emboli.

Pharmacological cardioversion

  • Intravenous amiodarone, sotalol, flecainide or propafenone may be used to restore sinus rhythm.
  • One study reported no significant difference in efficacy between amiodarone and sotalol for the restoration of sinus rhythm in patients with atrial flutter of less than a 24-hour duration.4
  • Ibutilide and dofetilide, which are able to achieve very rapid cardioversion, are not currently available in the UK.

Ventricular rate control

  • Rate control is usually more difficult for atrial flutter than for atrial fibrillation. However rate control is less likely than rhythm control to make the arrhythmia worse.
  • Ventricular rate control can be achieved with drugs that block the AV node. Calcium channel blockers (e.g. verapamil, diltiazem), beta-blockers and amiodarone can be used.
  • Diltiazem is contraindicated in AF associated with an accessory bypass tract such as in WPW syndrome or short PR syndrome.
  • Sotalol should not be used for rate control as it is associated with an increase in ventricular arrhythmias.
  • The ventricular rate at rest can sometimes be controlled with digoxin but digoxin does not usually adequately controls heart rate during exertion.

Antiarrhythmic agents

  • The use of antiarrhythmic drugs in atrial flutter is similar to that of atrial fibrillation.
  • The most effective drugs are the class III antiarrhythmic agents, dofetilide or ibutilide. Alternative class III agents include amiodarone and sotalol, which are the most commonly used antiarrhythmic agents for the prevention of recurrences of atrial flutter.
  • Second-line treatment to control rhythm are the class Ic antiarrhythmics flecainide or propafenone Class Ic agents should only be considered for patients with no structural heart disease.1

Catheter radiofrequency ablation

  • Catheter ablation is suggested as the first-line therapy in patients with atrial flutter and normal or mildly enlarged left atrial size. The success rate of radiofrequency catheter ablation for atrial flutter is 90-95%.
  • It has been shown to have a higher success rate, better quality of life, lower occurrence of atrial fibrillation and less need for hospital readmission when compared with drug treatment.
  • Type I atrial flutter is amenable to cure with catheter ablation. Type II flutter is potentially curable with catheter-based techniques but is more difficult.

Pacemaker

  • In some situations, e.g. after cardiac surgery, overdrive atrial pacing may be required for acute control of atrial flutter.
  • Atrial overdrive pacing can be performed invasively or via a trans-oesophageal electrode to pace the left atrium, with a success rate of approximately 50%.3

Prevention of thromboembolism

  • Patients with atrial flutter should be given antithrombotic therapy in the same manner as those with atrial fibrillation (see separate article on Atrial Fibrillation for details).4
  • Adequate anticoagulation has been shown to decrease thromboembolic complications in patients with chronic atrial flutter and in patients undergoing cardioversion.
  • Long-term anticoagulation is therefore advised for patients with persistent or paroxysmal atrial flutter.
  • After successful catheter ablation, anticoagulation can be stopped 4 to 6 weeks later if sinus rhythm is still present.
  • It is recommended that cardioversion of atrial flutter presents similar risks to cardioversion of atrial fibrillation and therefore requires similar anticoagulation, i.e. when atrial flutter persists for more than 48 hours, 3 weeks of anticoagulation is required before attempting cardioversion to sinus rhythm and anticoagulation should be continued for at least 4 weeks after cardioversion.4
Surgical

In patients who have atrial flutter and need cardiac surgery, creation of a cryothermal lesion can be curative for atrial flutter and may also prevent an incisional reentrant arrhythmia.

Complications
  • Heart failure; acute atrial flutter can impair cardiac function, lower blood pressure, and initiate myocardial ischaemia.3
  • Thromboembolism (transient ischaemic attacks and stroke). Systemic embolism is less commonly associated with atrial flutter than atrial fibrillation, but is still a significant risk. The risk of stroke in patients with atrial flutter is increased by about 40% (compared to 60% for patients with atrial fibrillation).
  • Tachycardia-induced cardiomyopathy.
  • Persistent untreated atrial flutter can become chronic atrial fibrillation.
Prognosis
  • Atrial flutter leads to an increased overall mortality.
  • Often converts within one week to normal sinus rhythm or atrial fibrillation but can occasionally persist for weeks or months.
Prevention
  • Effective prevention and management of potential causes, e.g. hypertension, obesity, excessive alcohol intake, hyperthyroidism and obstructive sleep apnoea.

Document references
  1. New Zealand Guidelines Group; The management of people with atrial fibrillation and flutter. May 2005.
  2. Rosenthal L, McManus DD; Atrial Fibrillation. eMedicine, November 2008.
  3. Wellens HJ; Contemporary management of atrial flutter. Circulation. 2002 Aug 6;106(6):649-52.
  4. The management of atrial fibrillation, NICE Clinical Guideline (Jun 2006)
  5. Sawhney NS, Feld GK; Diagnosis and management of typical atrial flutter. Med Clin North Am. 2008 Jan;92(1):65-85, x. [abstract]
  6. Andrew P, Montenero AS; Atrial flutter: a focus on treatment options for a common supraventricular tachyarrhythmia. J Cardiovasc Med (Hagerstown). 2007 Aug;8(8):558-67. [abstract]
Acknowledgements EMIS is grateful to Dr Colin Tidy for writing this article. The final copy has passed scrutiny by the independent Mentor GP reviewing team. ©EMIS 2009.
Document ID: 233
Document Version: 23
Document Reference: bgp24978
Last Updated: 6 Apr 2009
Planned Review: 6 Apr 2011

The authors and editors of this article are employed to create accurate and up to date content reflecting reliable research evidence, guidance and best clinical practice. They are free from any commercial conflicts of interest. Find out more about updating.

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