Atrial Flutter

Atrial flutter is a regular supraventricular tachycardia characterized by an atrial heart rate between 240/min and 340/min (typically 300/min), atrioventricular (AV) node conduction block, and a “sawtooth” pattern on an electrocardiogram (ECG). There are many cardiac and non-cardiac causes, but patients will usually have underlying structural heart disease. Symptoms include palpitations, shortness of breath, chest pain, dizziness, and nausea. Management is similar to atrial fibrillation, with a focus on rhythm control and preventing systemic embolization.

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Overview

Epidemiology

  • More common in the elderly
  • Uncommon in patients without underlying structural heart disease (higher incidence with left atrial enlargement, or with left ventricular or biventricular heart failure)
  • Less common than atrial fibrillation
  • 2.5 times more prevalent in men than in women

Etiology

  • Cardiac causes:
    • Structural diseases:
      • Coronary artery disease and myocardial infarction
      • Congestive heart failure
      • Valvular disease
      • Hypertensive heart disease
      • Cardiomyopathy
      • Post-cardiac surgery (such as bypass surgery) or ablation
    • Congenital heart defects:
      • Ebstein’s anomaly
      • Atrial septal defect
      • Tetralogy of Fallot
    • Inflammatory diseases:
      • Pericarditis
      • Myocarditis
    • Conduction system abnormalities:
      • Sinus node dysfunction
  • Pulmonary causes:
    • Chronic obstructive pulmonary disease
    • Pulmonary embolism
    • Obstructive sleep apnea
  • Other causes:
    • Electrolyte imbalance
    • Acute illness (e.g., sepsis, shock)
    • Hyperthyroidism
    • Obesity
    • Antiarrhythmic drug initiation
    • Digitalis toxicity (rare)

Pathophysiology

Atrial flutter is caused by a macroreentrant electrical loop (reentrant circuit covers a large area of the atrium):

  • Leads to an atrial heart rate between 240/min and 340/min
  • Atrioventricular node conduction block results in a lower ratio of ventricular to atrial beats.
    • Atrioventricular node cannot conduct at the same rate as the atrial activity.
    • Usually seen as a 2:1 ratio if the patient is not on AV nodal blocking medications
    • Leads to an average ventricular heart rate of approximately 150/min
  • Usually converts back into sinus rhythm or deteriorates into atrial fibrillation

Typical atrial flutter:

  • Circuit originates in the right atrium.
  • Involves the cavotricuspid isthmus (region in the right atrium between the opening of the inferior vena cava and the tricuspid valve):
    • Usually a counterclockwise circuit
    • Clockwise circuit = reverse typical atrial flutter
Typical atrial flutter

Image shows the macroreentrant circuits in typical atrial flutter. Notice that the cavotricuspid isthmus is involved in typical atrial flutter.

Image by Lecturio.

Atypical atrial flutter:

  • Originates in any region of the right or left atria, usually around scar tissue (scar tissue may be from intrinsic heart disease or iatrogenic from a cardiac procedure)
  • No involvement of the cavotricuspid isthmus
Atypical atrial flutter

Image shows the macroreentrant circuits in atypical atrial flutter. Notice that the atypical flutter is focused around an area of scar tissue.

Image by Lecturio.

Clinical Presentation

Symptoms

  • Atrial flutter may be asymptomatic or present with: 
    • Palpitations 
    • Light-headedness
    • Syncope
    • Shortness of breath
    • Chest pain
    • Fatigue
    • Nausea
    • Anxiety
  • Patients may present with conditions resulting from atrial flutter (see table in “Complications”).

Physical exam

  • Tachycardia, usually with a regular pulse
  • Hypotension
  • Diaphoresis
  • Indicators of an underlying cause:
    • Heart murmur → valvular disease 
    • Pericardial rub → pericarditis 
    • Exophthalmos → hyperthyroidism 
    • Prolonged expiration or wheeze → COPD

Complications

ComplicationPossible symptomsExam findings
Cardiac:
  • Long-term tachycardia can cause cardiac structural changes.
  • Increased oxygen demand of the myocardium
Congestive heart failure
  • Dyspnea
  • Cough
  • Orthopnea
  • Edema
  • Jugular venous distension
  • Crackles
  • S3 gallop
  • Lower extremity pitting edema
Myocardial ischemia
  • Chest pressure
  • Dyspnea
  • Dizziness
  • Generally non-specific
  • Diaphoresis
Thromboembolic:
  • Mechanism not completely understood
  • May be related to intermittent periods of atrial fibrillation, resulting in stasis of blood and thrombus formation
Stroke/transient ischemic attack (TIA)
  • Dysarthria
  • Weakness
  • Numbness
  • Vision changes
Focal deficits on neurologic exam
Splenic infarct
  • Left upper abdominal pain
  • Nausea and vomiting
  • Left shoulder pain
  • Left upper quadrant tenderness
  • Left flank tenderness
  • Fever
Bowel infarct
  • Intense abdominal pain
  • Postprandial pain
  • Nausea and vomiting
  • Abdominal tenderness
  • Abdominal distension
  • Absent bowel sounds
  • Peritoneal signs
Renal infarct
  • Flank or abdominal pain
  • Nausea and vomiting
  • Flank tenderness
  • Elevated blood pressure
  • Fever

Diagnosis

Diagnostic tests

  • Electrocardiogram: 
    • Atrial rate of approximately 300/min (range from 240 to 340/min)
    • Typical P waves are replaced by “sawtooth” flutter waves (F waves).
    • Narrow QRS complexes
    • Consistent ratio between atrial and ventricular rates (usually a ventricular rate of approximately 150/min in 2:1 conduction)
    • May give clues to underlying cardiac disease or complications:
      • Evidence of left ventricular hypertrophy
      • Rate-related myocardial ischemia (ST depressions that resolve with improvement in heart rate)
      • Myocardial infarction
  • Holter monitoring:
    • Portable device that continuously records cardiac activity (usually worn for 2448 hours)
    • Not required for diagnosis, but can catch transient events if symptoms are non-specific or short-lived
    • Identify triggering events
    • Detect other associated arrhythmias

Further workup

  • Transthoracic echocardiogram: 
    • Evaluate for structural disease, such as atrial dilation or valvular disease
    • Look for wall motion abnormalities
    • Assess ventricular systolic function
  • Transesophageal echocardiogram:
    • Examine for intracardiac thrombus
    • Important evaluation prior to cardioversion to minimize risk of thromboembolism
  • Exercise stress testing:
    • Evaluate for associated ischemic heart disease
    • Can reproduce exercise-induced atrial flutter
  • Other tests to search for an underlying cause:
    • Serum electrolytes → electrolyte imbalance
    • B-type natriuretic peptide (BNP) → heart failure
    • Troponins → myocardial ischemia
    • Thyroid-stimulating hormone (TSH) → screen for hyperthyroidism
    • WBCs → sepsis
    • Digoxin level → digitalis toxicity
  • CT pulmonary angiography → pulmonary embolism

Management

Acute management

  • Hemodynamically unstable patients → immediate cardioversion 
  • Hemodynamically stable patients → ventricular rate control with:  
    • Non-dihydropyridine calcium channel blockers (verapamil, diltiazem)
    • Beta blockers (metoprolol)
    • Digoxin may be used in some patients with concurrent systolic heart failure. 
  • Identify and treat reversible causes (e.g., hyperthyroidism, sepsis, electrolyte abnormalities).

Long-term management

  • Similar to treatments for atrial fibrillation, but focus is on rhythm control
  • Cardioversion to normal sinus rhythm:  
    • Consider if a patient does not spontaneously convert.
    • Radiofrequency catheter ablation (definitive treatment):
      • Generally has a high rate of success, low rate of complications
      • Reduced rate of recurrence compared to synchronized cardioversion
      • Preferred in most patients, except those with reversible causes of atrial flutter 
    • Synchronized cardioversion:
      • May be considered if no prior episodes of atrial flutter
    • Pharmacologic cardioversion:
      • Ibutilide (new, drug of choice)
      • Other common choices: amiodarone, flecainide, sotalol
  • Prevention of systemic embolization:
    • The approach is similar to atrial fibrillation. 
    • If atrial flutter persists > 48 hours, or the onset is unknown: 
      • 3–4 weeks of anticoagulation prior to cardioversion
      • Continue anticoagulation 4 weeks post-procedure due to atrial “stunning” (temporary reduction in atrial contractile function).
    • If there is recurrence, long-term anticoagulation may be required. 
    • Risk stratification using the CHA2DS2-VASc scoring system (table below) should be completed:
      • Score of 0: no anticoagulation required
      • Score of 1 (unless the 1 point comes from the “female sex”): low-risk, but may benefit from anticoagulation 
      • Score of ≥ 2: strong candidate for anticoagulation
    • Options include:
      • Heparin or enoxaparin (usually only used in an acute, inpatient setting)
      • Warfarin (maintain an international normalized ratio (INR) of 2–3)
      • Novel oral anticoagulants (dabigatran, apixaban, and rivaroxaban)
Table: Cha2DS2-VASc score (assesses thromboembolic risk and the risk for stroke in patients with AF)
CCongestive heart failure1
HHypertension1
AAge (≥ 75 years)2
DDiabetes mellitus1
SStroke, TIA, or thromboembolism2
VVascular disease1
AAge 65–74 years1
ScSex category (female)1

Differential Diagnosis

  • Atrial fibrillation: the most common form of supraventricular arrhythmia. Symptoms are highly variable, but include palpitations, syncope, shortness of breath, or chest pain. Atrial fibrillation is diagnosed with an irregularly irregular rhythm without visible P waves on an ECG, which differentiates it from atrial flutter. Treatment focuses on rate or rhythm control, as well as anticoagulation to reduce thromboembolic risk.
  • Multifocal atrial tachycardia: an atrial tachyarrhythmia due to pacemaker activity from multiple atrial locations. Multifocal atrial tachycardia is seen in elderly patients with chronic pulmonary conditions, and symptoms typically relate to the respiratory illness. Diagnosis is made by ECG, where ≥ 3 P wave morphologies are identified. This distinguishes multifocal atrial tachycardia from the uniform, “sawtooth” pattern of atrial flutter. Treatment includes rate or rhythm control.
  • Paroxysmal supraventricular tachycardia: often due to a reentry pathway. Patients may have abrupt onset of chest pain, shortness of breath, or dizziness. An ECG shows narrow QRS complexes with a rate between 150/min and 240/min. The fast rate and lack of flutter waves differentiates paroxysmal supraventricular tachycardia from atrial flutter. Treatment depends on hemodynamics and the type of SVT, but may include vagal maneuvers, adenosine, and cardioversion.
  • Sinus tachycardia: due to increased SA node activity as a physiologic response to a stressor. Sinus tachycardia may be normal and asymptomatic, or due to an active disease process. Symptoms are usually related to the underlying cause. An ECG will show a heart rate > 100/min, narrow QRS complexes, and regular P waves (which differentiates sinus tachycardia from atrial flutter). Treatment focuses on the precipitating disease.

References

  1. Phang, R., Prutkin, J.M., & Ganz, L.I. (2019). Overview of atrial flutter. In Zimetbaum, P.J. (Ed.), UpToDate. Retrieved October 19, 2020, from https://www.uptodate.com/contents/overview-of-atrial-flutter
  2. Prutkin, J.M. (2019). Atrial flutter: Maintenance of sinus rhythm. In Knight, B.P. (Ed.), UpToDate. Retrieved October 19, 2020, from https://www.uptodate.com/contents/atrial-flutter-maintenance-of-sinus-rhythm
  3. Manning, W.J., & Prutkin, J.M. (2019). Embolic risk and the role of anticoagulation in atrial flutter. In Knight, B.P., Kasner, S.E. (Eds.), UpToDate. Retrieved October 19, 2020, from https://www.uptodate.com/contents/embolic-risk-and-the-role-of-anticoagulation-in-atrial-flutter
  4. Rodriguez Ziccardi, M., Goyal, A., & Maani, C.V. (2020). Atrial flutter. In: StatPearls. Retrieved October 19, 2020, from https://www.ncbi.nlm.nih.gov/books/NBK540985/
  5. Kasper, D.L., Fauci, A.S., Longo, D.L., Bruanwald, E., Hauser, S. L., & Jameson, J.L. (2007). Harrison’s principles of internal medicine (16th edition). New York: McGraw Hill Education.

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