Atrial Flutter

Description

Atrial flutter (AFL) is a paroxysmal, regular, macro re-entrant arrhythmia most often occurring in patients with structural heart disease. The re-entrant circuit is classically confined to the right atrium with typical rates from 240 to 320 beats per minute (bpm).
Ventricular rate is determined by AV node conduction; thus a 2:1 AV block results in a ventricular rate of 120–160 bpm. Rapid AV node conduction is responsible for hemodynamic deterioration and AFL-related fatalities.
AFL is usually short-lived and closely related to atrial fibrillation (AF). If present for a prolonged period, AFL usually evolves to AF.

Epidemiology

Incidence

Incidence of ~1% in the general population
Incidence >5% in patients >80 years old

Prevalence

Uncertain since AFL is rarely a chronic condition

Morbidity/Mortality

Based on the integrity of the myocardial conduction system, ventricular function, age at presentation, duration of arrhythmia, and presence of other coexisting diseases.
Associated with a 1.7-fold increase in mortality over a mean period of 3.6 years. The risk is higher if AFL coexists with AF.

Etiology/Risk Factors

Male gender: AFL ~5-fold more common in men.
Cardiac procedures:
- Pericarditis following cardiac surgery can lead to atrial inflammation and AFL.
- Myocardial scar formation following atrial ablation procedures can instigate AFL.
Cardiovascular diseases:
- Structural heart disease leading to right atrial enlargement (valvular heart disease, pulmonary embolism, or cardiomyopathy).
- Slowing of cardiac conduction (fibrosis or antiarrhythmic agents).
Other disease: Chronic obstructive pulmonary disease (COPD), thyrotoxicosis, and chronic alcoholism.
Iatrogenic: Digitalis toxicity.

Physiology/Pathophysiology

AFL describes a class of re-entrant arrhythmias localized to the atria.
- Typical AFL (isthmus-dependent, Type I): Right atrial re-entrant circuit that travels around the tricuspid valve either counterclockwise or clockwise.
  - The flutter wave circuit is bounded by the caval veins, crista terminalis, and the Eustachian ridge (the "isthmus" of slow conduction).
  - The direction of the re-entry circuit determines polarity of typical "sawtooth" flutter waves (T_a). The T_a waves, which reflect atrial repolarization, are positive in the inferior leads with counterclockwise re-entry. Clockwise re-entry results in negative T_a deflection in the inferior leads. If discernable, P’ waves (atrial depolarization) have reverse polarity in the same leads.
  - Cycle length of 200–400 ms depends on atrial size and the presence of antiarrhythmic drugs.
- Atypical AFL (non-isthmus dependent, Type II): Right or left atrial re-entrant circuits that travel around a region of atrial scarring.
  - Atrial scar secondary to myocardial disease, surgical procedure, or extensive radiofrequency atrial ablation.
  - Difficult to treat: Ablation, cardioversion, and pharmacologic interventions are often unsuccessful.
AV conduction ratio (1:1, 2:1, 4:1, 6:1) influences the physiologic consequences of AFL.
- 1:1 AV node conduction results in a rapid ventricular rate and hemodynamic compromise.
  - Occurs in the setting of accessory pathways or exogenous catecholamines.
  - Rapid ventricular rate may lead to myocardial ischemia, malignant ventricular arrhythmias, and death.
- 2:1 AV node conduction results in a fixed and regular ventricular rate.
- Variable AV block produces an irregular ventricular rhythm.
  - Occurs with nodal disease, increased vagal tone, and in the presence of nodal blocking agents.
AFL and AF have similar pathophysiology and coexist in many patients.
- ~50% of patients with AFL will develop AF over a 5-year period.
- The arrhythmia-related "remodeling" caused by one arrhythmia AFL leads to progression of the other AF. "Remodeling" is characterized by structural (increased atrial size), electrical (shortening of atrial refractory period), and ultrastructural (promoting atrial fibrosis) changes.

Pediatric Considerations

AFL with atrial rates of 400–600 bpm and 2:1 conduction is common in neonates. Termination of the arrhythmia can be accomplished with transesophageal pacing or external synchronized cardioversion.

Mustard, Senning, or Fontan cardiac procedures dramatically increase the risk for development of AFL.

Anesthetic GOALS/GUIDING Principles

The underlying medical condition or inciting event should be optimized.
Control the ventricular rate to enhance ventricular filling and sufficient stroke volume.
- Calcium channel blockers or beta-blockers can be used to increase AV conduction block and slow ventricular rate.
- Carotid sinus massage may increase the AV conduction ratio and temporarily slow the ventricular rate.
Conversion to sinus rhythm via synchronized cardioversion:
- Monophasic shocks in the following sequence: 100 J, 200 J, 300 J, 360 J.
- If AFL duration is >48 hours, confirmation via transesophageal electrocardiography (TEE) to confirm the absence of atrial thrombus and/or anticoagulation must precede cardioversion.
Anticoagulation is typically via heparin or warfarin.
- Patients with AFL are at similar risk of stroke as patients with AF and should be anticoagulated if AFL lasts >48 hours.

Symptoms

The hemodynamic consequences of AFL depend on the flutter rate, AV conduction ratio, ventricular rate, and presence of ventricular dysfunction.
Symptoms depend on the ventricular rate.
- Increased ventricular rates (1:1 or 2:1 AV conduction) are often perceived as palpitations, chest discomfort, or dizziness.
- Decreased ventricular rates (8:1 AV conduction) may manifest as fatigue and exercise intolerance.

History

Evaluation of risk factors: Open heart surgery, cardiac valvular disease, myocardial ischemia, pulmonary embolism, COPD, hyperthyroidism, and/or digitalis toxicity.
History of AFL: Duration, current management, and previous treatment.
Presence of coexisting diseases: Pharmacologic management depends on myocardial function.

Signs/Physical Exam

Tachycardia with regular, usually fixed, ventricular rate of 140–160 bpm. Irregularly irregular pulse is rare, but may occur if AV conduction ratio is variable.
Rapid, rippling flutter waves may be seen in the jugular venous pulse with an AV conduction ratio of 4:1 but not with 2:1 ratio.
Cardiac decompensation leads to dyspnea, hypoxemia, rales, and crackles.

Previous radiofrequency ablation
- AFL ablation has a >90% long-term success rate. Best results are seen with isthmus-dependent AFL, normal right atrial size, and no history of AF.

Medications

Rate control: Amiodarone, diltiazem, verapamil, or beta-adrenergic blockers slow down AV conduction and control the ventricular rate.
- Amiodarone, diltiazem, and digoxin are preferred in the presence of impaired myocardial function.
- Beta-blockers are effective in the setting of increased sympathetic tone and thyrotoxicosis.
- Vagolytic effects of class I antiarrhythmic drugs administered for AFL may result in reduction of atrial rate to 18000 bpm, consequential 1:1 AV nodal conduction, and resultant increase of ventricular rate. Thus, AV blocking drugs should be administered before the administration of class I antiarrhythmic drugs.
Convert rhythm: Ibutilide, amiodarone, dofetilide, sotalol, flecainide, propafenone, procainamide, and disopyramide have variable success (50–60%) in terminating AFL.
Approximately 15% of patients treated with class IC antiarrhythmic agents or amiodarone for AF will develop AFL. This led to the development of a "hybrid" management strategy of antiarrhythmic drugs to treat AF with subsequent ablation to treat AFL.

Diagnostic Tests & Interpretation

Labs/Studies

Labs: Electrolytes, cardiac enzymes, digoxin level, and thyroid function tests.
ECG: Atrial rate ranges from 240 to 340 bpm, "sawtooth" pattern in the inferior leads, and regular ventricular response with a discernable and consistent relationship between flutter waves and QRS complexes.
- Flutter waves can be obscured by the T waves. Infusion of adenosine or vagal maneuvers will briefly stop or decrease AV conduction, allowing recognition of the flutter waves.
- In the setting of an accessory pathway, the ECG pattern is indistinguishable from ventricular tachycardia, even with 2:1 conduction.
- Atrial rate of >340 bpm may be seen with atypical AFL.
Echocardiogram: Evaluate atrial size and ventricular function
- TEE is used to evaluate for the presence of atrial thrombus prior to synchronized cardioversion in patients with AFL lasting longer than 48 hours.

Circumstances to delay/Conditions

Uncontrolled ventricular rate, myocardial ischemia, or cardiac decompensation.
Synchronized cardioversion in hemodynamically unstable patients.

PREOPERATIVE PREPARATION

Premedications

Anxiolytics can decrease sympathetic output.
Rate control: Calcium channel blockers or beta-adrenergic blockers can be titrated to effect.

INTRAOPERATIVE CARE

Choice of Anesthesia

Insufficient evidence to suggest that either general or regional anesthesia is preferred for patients with AFL.

Monitors

Standard ASA monitors including ECG with ST segment analysis.
Arterial catheter for close monitoring of blood pressure or frequent blood gas evaluation.
Central venous catheter for infusion of vasopressors or transvenous pacing.
Pulmonary artery catheter for evaluation of cardiac output or mixed venous oxygenation, if indicated.
Transesophageal echocardiography, if indicated.

Induction/Airway Management

Risk of hemodynamic instability
- Vasodilation and myocardial depression from induction agents (propofol and thiopental).
- Sympathetic stimulation from laryngoscopy.
- Dexmedetomidine is associated with prolonged hypotension and increased AV nodal blockade.
Avoid pharmacologic agents associated with sympathetic activation (ketamine) or vagolytic effects (pancuronium).

Maintenance

Use of either volatile anesthetic or total intravenous anesthetic is acceptable.
Conservative fluid management in the setting of reduced myocardial function.
Intraoperative occurrence may be treated with rate control medications, vagal maneuvers, or cardioversion if the patient is hemodynamically unstable.

Extubation/Emergence

Avoid sympathetic stimulation.
Ensure adequate analgesia.
Balance reversal of neuromuscular block (excessive anticholinergics can provoke AFL); consider slow titration to reduce incidence.

Bed Acuity

ICU with hemodynamically unstable or poorly controlled AFL

Medications/Lab Studies/Consults

Medications: Rate control agents and anticoagulation as indicated.
Labs: Electrolytes, digoxin level, cardiac enzymes, and thyroid function tests.

Complications

Systemic thromboembolism
Coronary and/or cerebral ischemia secondary to hemodynamic insufficiency
Tachycardia-induced cardiomyopathy
Sinus bradycardia following administration of AV nodal blocking agents

Lee KW , Yang Y , Scheinman MM. Atrial flutter: A review of its history, mechanism, clinical features, and current therapy. Curr Probl Cardiol. 2005;30:121–168.
Nattel S , Singh BN. Evolution, mechanisms, and classification of antiarrhythmic drugs: Focus on class III actions. Am J Cardiol. 1999;84:11R–19R.
Van Gelder IC , Hagens VE , Bosker HA , et al. Pharmacologic versus direct-current electrical cardioversion of atrial flutter and fibrillation. Am J Cardiol. 1999;84:147R–151R.

See Also (Topic, Algorithm, Electronic Media Element)

Atrial Fibrillation
Electrical Cardioversion
Wolff–parkinson–white

ICD9

427.32 Atrial flutter

ICD10

I48.3 Typical atrial flutter
I48.4 Atypical atrial flutter
I48.92 Unspecified atrial flutter

Atrial flutter (AFL) commonly occurs in patients after open heart surgery and those with underlying cardiac disease.
ECG manifestations include flutter waves with variable AV conduction.
Ventricular rate control is achieved with beta-blockers or calcium channel blockers.
Hemodynamically unstable patients require immediate synchronized cardioversion.

Mirsad Dupanovic , MD

Svjetlana Tisma-Dupanovic , MD

section name header

Basics ⬇

Incidence

Prevalence

Morbidity/Mortality

Pediatric Considerations

Diagnosis ⬆ ⬇

History

Signs/Physical Exam

Labs/Studies

Treatment ⬆ ⬇

Premedications

Choice of Anesthesia

Monitors

Induction/Airway Management

Maintenance

Extubation/Emergence

Follow-Up ⬆ ⬇

References ⬆ ⬇

Additional Reading ⬆ ⬇

Codes ⬆ ⬇

Clinical Pearls ⬆ ⬇

Author(s) ⬆

section name header

Basics ⬇

Incidence

Prevalence

Morbidity/Mortality

Pediatric Considerations

Diagnosis ⬆ ⬇

History

Signs/Physical Exam

Labs/Studies

Treatment ⬆ ⬇

Premedications

Special Concerns for Informed Consent

Choice of Anesthesia

Monitors

Induction/Airway Management

Maintenance

Extubation/Emergence

Follow-Up ⬆ ⬇

References ⬆ ⬇

Additional Reading ⬆ ⬇

Codes ⬆ ⬇

Clinical Pearls ⬆ ⬇

Author(s) ⬆