Atrial Flutter

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

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

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

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 24–48 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)

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.