> Table of Contents > Atrial Fibrillation and Atrial Flutter
Atrial Fibrillation and Atrial Flutter
Youhua Zhang, MD, PhD
Bianca Lee, DO, MS
image BASICS
This topic covers both atrial fibrillation (AFib) and atrial flutter (AFlut).
  • AFib: Paroxysmal or continuous supraventricular tachyarrhythmia characterized by rapid, uncoordinated atrial electrical activity and an irregularly irregular ventricular response. In most patients, the ventricular rate is rapid because the atrioventricular (AV) node is bombarded with very frequent atrial electrical impulses (400 to 600 bpm).
  • AFlut: Paroxysmal or continuous supraventricular tachyarrhythmia with rapid but organized atrial electrical activity. The atrial rate is typically between 250 and 350 bpm and is often manifested as “sawtooth” flutter (F) waves on the ECG, particularly in the inferior leads and V1. AFlut commonly occurs with 2:1 or 3:1 AV block, so the ventricular response may be regular and typically at a rate of ˜150 bpm.
  • AFib and AFlut are related arrhythmias, sometimes seen in the same patient. Distinguishing the two is important, as there may be implications for management.
  • Clinical classifications:
    • Paroxysmal: self-terminating episodes, usually <7 days
    • Persistent: sustained >7 days, usually requiring pharmacologic or DC cardioversion to restore sinus rhythm
    • Permanent: Sinus rhythm cannot be restored or maintained. It is a shared decision between patient and clinician as to when to cease further attempts to restore and/or maintain sinus rhythm.
  • Lone AFib occurs in patients <60 years (with possible genetic predisposition) who have no clinical or echocardiographic evidence of cardiovascular disease, including hypertension (HTN).
  • Incidence/prevalence increases significantly with age.
  • Young patients with AFib, particularly lone AFib, are most commonly males.
  • AFib: from <0.1%/year <40 years to >1.5%/year >80 years
  • Lifetime risk: 25% for those ≥40 years
  • AFlut is less common.
  • Estimated at 0.4-1% in general population, with 2.7 million patients in America
  • Increase with age, up to 8% in those ≥80 years
  • Cardiac: HTN, ischemic heart disease, heart failure, valvular heart disease, cardiomyopathy, pericarditis, and infiltrative heart disease
  • Pulmonary: pulmonary embolism (PE), chronic obstructive pulmonary disease (COPD), obstructive sleep apnea, pneumonia
  • Ingestion: ethanol, caffeine
  • Endocrine: hyperthyroidism, diabetes
  • Obesity
  • Postoperative: cardiac, pulmonary, or esophageal
  • Idiopathic: lone AFib
  • Patients with paroxysmal episodes are usually associated with premature atrial beats and/or bursts of tachycardia, originating in pulmonary vein ostia or other sites.
  • Many patients with AFib are thought to have some degree of atrial fibrosis or scarring. This is often subclinical and usually not detectable with current cardiac imaging techniques but plays an important role in the pathogenesis of the arrhythmia.
  • Autonomic (vagal and sympathetic) tone may play a role in triggering the arrhythmia.
  • The presence of AFib is associated with electrical and structural remodeling processes that promote arrhythmia maintenance in the atria, termed “AFib begets AFib.”
Familial forms are rare but do exist. There are ongoing efforts to identify the genetic underpinnings of such cases.
Age, HTN, and obesity are the most important risk factors for both AFib and AFlut.
Adequate control of HTN may prevent development of AFib due to hypertensive heart disease and is the most significant modifiable risk factor for AFib. Weight reduction may decrease the risk of AFib in obese patients. Ethanol consumption may trigger AFib in some.
HTN and other cardiac diseases
  • AFib: irregularly irregular heart rate and pulse, frequently tachycardiac, pulse deficit
  • AFlut: similar to AFib but may have regular pulse
  • Multifocal atrial tachycardia
  • Sinus tachycardia with frequent atrial premature beats
  • Paroxysmal supraventricular tachycardia (Wolff-Parkinson-White [WPW], atrioventricular nodal reentry tachycardia [AVNRT])
  • AFib: The ECG is diagnostic, with findings of low-amplitude fibrillatory waves without discrete P waves and an irregularly irregular pattern of QRS complexes. There is often tachycardia in the absence of heart rate-controlling medications (1).
  • AFlut: The ECG is again diagnostic. Saw-tooth flutter waves are the classic sign, generally best seen in the inferior leads, although ventricular rate may need to be slowed to see the waves. QRS complexes may be regular or irregular; there is usually tachycardia (1).
  • Ambulatory rhythm monitoring (e.g., telemetry, Holter monitoring, event recorders) is helpful in diagnosing paroxysmal AFib or AFlut and monitoring for recurrence (1)[C].
Initial Tests (lab, imaging)
TSH, electrolytes, CBC, 2-D transthoracic echocardiogram, PT/INR (if anticoagulation is contemplated); digoxin level (if appropriate)
Follow-Up Tests & Special Considerations
  • Occasional Holter monitoring and/or exercise stress testing to assess for adequacy of rate and/or rhythm control
  • Chest x-ray (CXR) for cardiopulmonary disease
  • ECG for signs of cardiac hypertrophy, ischemia, and/or other arrhythmias
  • Transesophageal echocardiogram to detect left atrial appendage thrombus if cardioversion is planned
  • Sleep study may be useful if sleep apnea is suspected.
Test Interpretation
  • Atrial dilatation and fibrosis
  • Atrial thrombus, especially in atrial appendage
  • Valvular/rheumatic disease
  • Cardiomyopathy
  • Two primary issues in the management of AFib and/or AFlut:
    • Decisions on heart rate control (control ventricular rate while allowing AFib to continue) or rhythm control (terminate AFib and restore normal sinus rhythm)
    • Anticoagulation therapy to prevent thromboembolism (primarily stroke)
  • Anticoagulation guidelines (the same for AFib and AFlut) (1,2)[C]:
  • CHA2DS2VASc scoring (CHF [1 point], HTN [1 point], Age ≥75 [2 points], DM [1 point], prior Stroke or TIA [2 points]), Vascular disease (1 point), Age 65 to 74 years (1 point), female Sex category (1 point) (1,2,3). CHA2DS2VASc is the recommended stroke risk assessment for patients with nonvalvular AFib (1)[B].
    • In patients with nonvalvular AFib and a CHA2DS2VASc score of 0, antithrombotic therapy may be omitted (1)[B].
    • In patients with nonvalvular AFib and a CHA2DS2VASc score of 1, no antithrombotic therapy or oral anticoagulant or aspirin is recommended (1)[C].
    • Unless contraindicated, patients with nonvalvular AFib with any high-risk factors for stroke (prior transient ischemic attack [TIA]/cerebrovascular accident [CVA]/thromboembolism) or a CHA2DS2VASc score ≥2 should receive oral anticoagulants. The following oral anticoagulants include warfarin maintaining an INR of 2.0 to 3.0 (1,3)[A], dabigatran (1)[B], rivaroxaban (1)[B], or apixaban (1)[B]. Patients with mechanical valves should maintain an INR of 2.0 to 3.0 or 2.5 to 3.5 dependent on the type and location of the prosthesis (1)[B]. For patients with AFib and mitral stenosis, a target INR range of 2.0 to 3.0 is recommended (2)[B].
    • Dabigatran (Pradaxa), a direct thrombin inhibitor, and apixaban (Eliquis) and rivaroxaban (Xarelto), factor Xa inhibitors, have recently been approved as alternatives to warfarin for the prevention of first and recurrent stroke in patients with nonvalvular AFib (1,3)[B]. The selection of an

      antithrombotic should be individualized (1)[B]; consider the risks of each agent, cost, patient preference, and tolerability (1)[C].
      • ALERT: Renal function should be evaluated prior to initiation of direct thrombin or factor Xa inhibitors (1)[B]. Dosing of such agents may in fact need individualized adjustment.
      • ALERT: Direct thrombin inhibitor dabigatran should not be used in patients with AF and a mechanical heart valve (1)[B].
    • Anticoagulation recommendations are independent of AFib pattern (paroxysmal, persistent, and permanent) (1,2)[B] although ongoing efforts to better understand who may be at greater and lesser risk of thromboembolism continue.
  • Four classes of medications are available to achieve ventricular rate control: β-blockers (i.e., metoprolol), nondihydropyridine calcium channel blockers (i.e., verapamil, diltiazem), digoxin, and amiodarone. Optimal target for ventricular rate has not been firmly established, but there is evidence that aggressive control of the ventricular rate (<80 bpm) offers no benefit beyond more modest rate control (i.e., resting heart rate <110 bpm) (1,4)[B].
  • Preventing rapid ventricular response (RVR) rates using AV nodal blocking medications is also often effective at controlling a patient's symptoms associated with AFib or AFlut. Patients in whom rate control cannot be achieved or who continue to have persistent symptoms despite reasonable heart rate control may require attempts at restoration of sinus rhythm.
  • Of note, ventricular rate control can often be difficult to achieve in AFlut due to the more organized nature of the atrial electrical activity. For this reason, conversion to sinus rhythm is often the preferred strategy, and catheter ablation is also considered as a first-line treatment in recurrent AFlut (1).
  • Restoration of sinus rhythm using electrical or pharmacologic cardioversion may significantly reduce the symptom burden of AFib or AFlut in many patients and may also be useful for controlling ventricular rate. Cardioversion does not impact the long-term risk/benefit ratio of anticoagulation:
    • Cardioversion is most often performed electrically, but may also be achieved using antiarrhythmic drug therapy in some instances, by experienced clinicians (1)[A].
    • If duration of AF is >48 hours or unknown, anticoagulate for ≥3 weeks before cardioversion to reduce the risk of stroke. Alternatively, once anticoagulation is established, a transesophageal echo may be performed to exclude the presence of left atrial thrombus, allowing cardioversion to proceed. After cardioversion, anticoagulation should be continued for ≥4 weeks in all patients in whom duration of AFib/AFlut is >48 hours, as the postcardioversion period is a time of increased stroke risk (1,2)[B].
  • Randomized clinical trials (AFFIRM and RACE) comparing the outcomes of rate versus rhythm control found no difference in morbidity, mortality, and stroke rates in patients assigned to one therapy or the other (1).
  • Chronic PO antiarrhythmic therapy to suppress AFib recurrence is available for appropriately selected patients. Expert consultation is recommended owing to the complexities of safe antiarrhythmic drug selection.
Management of AFib or AFlut refractory to standard medical therapy (i.e., unable to achieve adequate rate control with medication or development of significant bradycardia with treatment) may require the use of more aggressive treatments. These may include pacemaker implantation (to allow for more intensive pharmacologic blocking of the AV node) or an ablation procedure. AFlut in particular is often very amenable to ablation; thus, consideration should be given to early expert referral in appropriate patients. Antiarrhythmic drug therapy can often be very effective but should be prescribed by experienced practitioners.
  • Electrophysiologic study and ablation may be considered for patients with either AFib or AFlut. In the case of AFlut, ablation is often a relatively straightforward procedure generally viewed as a first-line therapy due to its high rate of success in appropriate candidates. Ablation of AFib is a much more complex procedure with a more variable success rate; it continues to evolve. Thus, it is typically reserved for drug refractory patients.
  • Cardiac surgery (e.g., the maze procedure, ligation of the left atrial appendage) may be considered in patients planning to undergo cardiac surgery for other reasons. Surgical therapy in isolation is rarely indicated for AFib or AFlut.
Admission Criteria/Initial Stabilization
  • Patients with significant symptoms, RVR, AFib/AFlut triggered by an acute process (e.g., MI, CHF, PE), or in whom antiarrhythmic therapy is being started likely require admission to the hospital for a period of stabilization.
  • Outpatient management is reasonable for low-risk patients with controlled ventricular rates.
  • Acute therapy for symptomatic or hemodynamically compromised patients with AFib or AFlut:
    • IV β- or nondihydropyridine calcium channel blockers for control of ventricular rate. Once hemodynamically stable, oral medications may be administered (1)[B].
  • Commonly used therapies in the acute setting include (1):
    • Metoprolol tartrate: 2.5-5.0 mg IV bolus over 2 minutes; up to 3 doses
    • Diltiazem: 0.25 mg/kg IV bolus over 2 minutes, then 5 to 15 mg/hr
    • Some patients will be far more responsive to one class of agents than another. For this reason, if rate control is difficult to achieve, switching drug classes may be useful.
  • Urgent cardioversion should be performed in hemodynamically unstable patients (1)[B]. It is somewhat unusual for AFib or AFlut alone to cause marked hemodynamic insult; thus, the possibility of a concurrent process should be considered in this setting.
  • Consider the initiation of PO anticoagulation therapy. Inpatients may be “bridged” with IV or SC heparin or SQ low-molecular-weight heparin (LMWH) while waiting for warfarin to become effective (1)[C].
Discharge Criteria
Adequate rate or rhythm control without symptoms; long-term plan for anticoagulation established
Many patients may benefit from elective expert consultation. In patients with no significant symptoms, if ventricular rate control or sinus rhythm is easily achieved and the choice of thromboembolic prevention is clear, management in a primary care setting may be appropriate.
Patient Monitoring
Adequate anticoagulation levels (if warfarin is employed) should be determined at least weekly during initiation and monthly when stable (1)[A]. Ventricular rate control should be assessed on a regular basis.
Patients on warfarin should attempt to consume a stable amount of vitamin K.
Anticoagulation reduces the annual embolic stroke rate from ˜5-6% per year to 1-2% for most patients. AFib and AFlut may increase morbidity and mortality, but the overall prognosis is a function of underlying heart disease and adherence with therapy. Reported risk of anticoagulation varies but lies between 1% and 4% per year for major hemorrhage.
1. January CT, Wann LS, Alpert JS, et al. 2014 AHA/ACC/HRS guideline for the management of patients with atrial fibrillation: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society. Circulation. 2014;130(23):2071-2104.
2. You JJ, Singer DE, Howard PA, et al. Antithrombotic therapy for atrial fibrillation: antithrombotic therapy and prevention of thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest. 2012;141(2 Suppl):e531S-e575S.
3. Furie KL, Goldstein LB, Albers GW, et al. Oral antithrombotic agents for the prevention of stroke in nonvalvular atrial fibrillation: a science advisory for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2012;43(12):3442-3453.
4. Wann LS, Curtis AB, January CT, et al. 2011 ACCF/AHA/HRS focused update on the management of patients with atrial fibrillation (updating the 2006 guideline): a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. 2011;123(1):104-123.
  • I48.91 Unspecified atrial fibrillation
  • I48.92 Unspecified atrial flutter
  • I48.0 Paroxysmal atrial fibrillation
Clinical Pearls
  • Primary decision in persistent AFib is whether to strive for rate control or rhythm control. Younger patients often do better with a rhythm control strategy, whereas older patients often do well with rate control. Decision is complex.
  • Anticoagulation recommendations are based on the risk of thromboembolism irrespective of the AFib pattern.