Atrial Flutter

Atrial
Fibrillation,fibrillation,AF,Heart,ECG,Atrial
Fibrillation,cardiac,heart,Atrial Fibrillation,ECG,AF,ECG,Cardiac
muscle,AF,ECG,Atrial Fibrillation,AF,ECG,AF,ECG,Cardiac
muscle,AF,ECG,Atrial Fibrillation,AF
Background

Atrial
flutter has many clinical aspects that are similar to atrial
fibrillation (ie, underlying disease, predisposing factors,
complications, medical management). However, the underlying mechanism of
atrial flutter makes it amenable to cure this arrhythmia with
percutaneous catheter-based techniques. Some patients have both atrial flutter and atrial fibrillation.
The elimination of atrial flutter has been noted to reduce or eliminate
episodes of atrial fibrillation. Left untreated, persistent atrial
flutter can degenerate into chronic atrial fibrillation. Uncommon forms
of atrial flutter have been noted during long-term follow-up in as many
as 26% of patients with surgical correction of congenital cardiac
anomalies.
Next Section: Pathophysiology

Pathophysiology
In
most studies, approximately 30% of patients have no underlying cardiac
disease, 30% have coronary artery heart disease, and 30% have
hypertensive heart disease. Other conditions are also associated with
atrial flutter, including cardiomyopathy, hypoxia, chronic obstructive
pulmonary disease, thyrotoxicosis, pheochromocytoma, electrolyte
imbalance, and alcohol consumption.

Animal models have been used
to demonstrate that an anatomical block (surgically created) or a
functional block of conduction between the superior vena cava and
inferior vena cava, similar to the crista terminalis in the human right
atrium, is key to initiating and maintaining the arrhythmia. In
humans, the most common form of atrial flutter (type I [classic])
involves a single reentrant circuit with circus activation in the right
atrium around the tricuspid valve annulus (most often in a
counterclockwise direction), with an area of slow conduction located
between the tricuspid valve annulus and the coronary sinus ostium
(subeustachian isthmus).



Twelve-lead ECG of type I atrial flutter. Note negative sawtooth pattern of flutter waves in leads II, III, and aVF. A 3D electroanatomic map of type I atrial flutter:The
3-dimensional electroanatomic map of type I atrial flutter. The colors
progress from blue to red to white and represent relative conduction
time in the right atrium (early to late). An ablation line (red dots)
has been created on the tricuspid ridge extending to the inferior vena
cava. This interrupts the flutter circuit.RAA: right atrial appendage;
CSO: coronary sinus os; IVC: inferior vena cava; TV: tricuspid valve
annulus. The crista terminalis acts as
another anatomic conduction barrier, similar to the line of conduction
block between the 2 venae cavae required in the animal model. The
orifices of both venae cavae, the eustachian ridge, the coronary sinus
orifice, and the tricuspid annulus complete the barrier for the reentry
circuit. Atrial flutter is often referred to as isthmus-dependent
flutter. Usually the rhythm is due to reentry, there is an excitable
gap, and the rhythm can be entrained.


The
anatomy of classic counterclockwise atrial flutter. This demonstrates
an oblique view of the right atrium and shows some of the crucial
structures. The isthmus of tissue responsible for atrial flutter is seen
anterior to the orifice of the coronary sinus. The Eustachian ridge is
part of the crista terminalis that separates the roughened part of the
right atrium from the smooth septal part of the right atrium. Classic
counterclockwise atrial flutter has caudocranial activation (ie,
counterclockwise around the tricuspid valve annulus when viewed in the
left antero-oblique fluoroscopic view) of the atrial septum.


Classic
counterclockwise atrial flutter. This 3-dimensional electroanatomic map
of the tricuspid value and right atrial show the activation pattern
displayed in color format. Red is early and blue is late relative to a
fixed point in time. Activation travels in a counterclockwise direction.
Classic atrial flutter can also have the
opposite activation sequence (ie, clockwise activation around the
tricuspid valve annulus). Clockwise atrial flutter is much less common.
This arrhythmia is still considered type I, isthmus-dependent, clockwise
flutter.Type II (atypical) atrial flutters are less extensively
studied and electroanatomically characterized. Atypical atrial flutters
may originate from the right atrium (surgical scars [ie, incisional
reentry]) or from the left atrium (pulmonary veins [ie, focal reentry]
or mitral annulus).


Atypical LA flutter. Left
atrial flutter is common after incomplete left atrial ablation
procedures and may result in faster ventricular rates than seen during
atrial fibrillation. Thus, tricuspid isthmus dependency is not a
prerequisite for atrial flutter. Often, the atrial rate is faster
(340-350 bpm) in atypical flutter and the arrhythmia can not be
entrained.
Previous
Next Section: Pathophysiology
Epidemiology

Frequency

United States
Atrial
flutter is much less common than atrial fibrillation. From 1985-1990,
of patients admitted to US hospitals with a diagnosis of
supraventricular tachycardia, 77% had atrial fibrillation and 10% had
atrial flutter. Based on a study of patients referred for tertiary care
centers, the incidence of atrial flutter in the United States is
estimated at 200,000 new cases per year.^[1] Mortality/Morbidity

Prognosis
depends on the patient's underlying medical condition. Any atrial
arrhythmia can cause a tachycardia-induced cardiomyopathy. Intervening
to control the ventricular response rate or to return the patient to
sinus rhythm is important. Thrombus in the left atrium has been
described in patients with atrial flutter (0-21%). Thromboembolic
complications have also been described. Due to conduction
properties of the atrioventricular node, many people with atrial flutter
will have a faster ventricular response (than those with atrial
fibrillation). Heart rate is often more difficult to control with atrial
flutter than with atrial fibrillation.
Sex

Atrial
flutter is associated with a male predominance. In a study of 100
patients with atrial flutter, 75% were men. In another study performed
at a tertiary care study, atrial flutter was 2.5 times more common in
men.
Age

Patients with atrial flutter, as with atrial
fibrillation, tend to be older adults. In one study, the average age was
64 years (range 27-86 y).

Atrial Flutter Clinical Presentation

History

The severity of symptoms and the patient's underlying cardiac condition dictate the initial management approach. The most common symptom is palpitations. Other symptoms include fatigue, dyspnea, and chest pain.

• Address
  symptoms of other noncardiac conditions (eg, hyperthyroidism, pulmonary
  disease) or cardiac conditions associated with atrial flutter that may
  be reversible.
  
• The most common symptom is palpitations. Other symptoms include fatigue, dyspnea, and chest pain.
  
• Assessing
  the onset of symptoms/palpitations is critical. Atrial flutter (of a
  duration >48 h) requires anticoagulation with warfarin or
  transesophageal echo to rule out thrombus in the left atrium prior to
  cardioversion to sinus rhythm. Thus, the duration of the episode and the
  onset of atrial fibrillation or flutter may affect the timing of
  cardioversion and the need to address anticoagulation.
  
• Precipitating causes and modes of termination of the arrhythmia.
  
• Previous response to pharmacologic therapy.
  
• Often,
  atrial flutter is not as well tolerated as atrial fibrillation. This
  may be due to the rapid and difficult-to-control ventricular response,
  especially with minimal exertion.
  
• Atrial
  flutter can cause hypotension, angina, congestive heart failure, and
  rarely syncope due to rapid ventricular response in the setting of
  compromised left ventricular function.
  

Physical

• The
  general appearance and vital signs of the patient are important when
  determining the urgency with which to restore sinus rhythm. Thus, the
  initial cardiopulmonary evaluation and monitoring for signs of cardiac
  or pulmonary failure help guide initial management.
  
• Evaluate the vitals with a close eye on heart rate, blood pressure, and oxygen saturation.
  
• Palpate the neck/thyroid gland for goiter.
  
• Evaluate the neck for jugular venous distention.
  
• Auscultate the lungs for rales/crackles.
  
• Auscultate/palpate the heart for extra heart sounds and murmurs, and palpate the point of maximum impulse.
  
• Examine the extremities to access for lower extremity edema/perfusion.
  

Causes

• Atrial
  flutter is most often associated with left ventricular dysfunction,
  rheumatic heart disease, congenital heart disease, and postcardiac
  surgery.
  
• Thyroid disease, obesity, pericarditis,
  pulmonary disease, and pulmonary embolism have been associated with
  atrial fibrillation and atrial flutter. Rarely, mitral valve prolapse
  has been associated with atrial flutter.
  
• Rarely, atrial flutter can be associated with an acute myocardial infarction.
  
• Postcardiac surgery, atrial flutter may be reentrant as a result of natural barriers, atrial incisions, and scar.
  
• Some patients develop atypical left atrial flutter after pulmonary vein isolation for atrial fibrillation.
  
• Atrial Flutter Differential Diagnoses
  
• Differentials
  
• Atrial Fibrillation
  
• Atrial Tachycardia
  
• Atrial Flutter Workup
  
• Laboratory Studies
  
• The
  history and physical examination findings guide laboratory studies.
  Asymptomatic hyperthyroidism, especially in elderly patients, can
  manifest with atrial fibrillation or flutter; therefore, obtain thyroid
  function tests. Hyperthyroidism is a rare cause of atrial flutter and
  should be excluded with blood testing.
  
• Serum electrolytes and pulmonary function tests may be indicated based on the history.
  
• Electrocardiography is essential in making the diagnosis.
  
  
  
  • The
    common form of type I atrial flutter has sawtooth flutter (F) waves,
    best seen in leads II, III, and aVF, with atrial rates of 240-340 bpm
    and without an isoelectric interval between these F waves.
    
  • The ventricular response may be regular or irregular.
    
  • The ventricular rate is a fixed mathematical relationship of flutter waves and the resulting QRS complexes.
    
  • Variable
    AV conduction can also be seen (commonly present with 2:1 or 3:1 AV
    conduction). With 1:1 AV conduction, hemodynamic collapse may occur.
    
  • Morphology
    of the flutter wave can predict findings in the electrophysiology
    laboratory. A negative flutter wave in the inferior limb leads and a
    positive flutter wave in V₁ are highly predictive of a
    counterclockwise circuit; however, with positive flutter waves in the
    inferior limb leads and negative flutter waves in V₁,
    differentiating between clockwise type I atrial flutter and atypical
    forms of non–isthmus-dependent intra-atrial
    
  • 
    
  • reentry is difficult.
    
  • 
    
  • 
    
  • Twelve-lead ECG of type I atrial flutter. Note negative sawtooth pattern of flutter waves in leads II, III, and aVF.
    
  • Imaging Studies
    
    
    
    • Transthoracic
      echocardiography should be performed to evaluate for structural
      abnormalities and left ventricular systolic function. It also can detect
      valvular abnormalities, left ventricular hypertrophy, and pericardial
      disease.
      
    • Transesophageal echocardiography is the preferred technique to detect thrombus in the left atrium.
      
    • Chest radiograph may be useful in evaluation of lung disease and the pulmonary vasculature.
      
    • Procedures
      
      See Medical Care for information regarding radiofrequency ablation and electrical cardioversion.
      
    • Atrial Flutter Treatment & Management
      
    • Medical Care
      
      General
      goals for the treatment of symptomatic atrial flutter are similar to
      those for atrial fibrillation and include (1) control of the ventricular
      rate, (2) restoration of sinus rhythm, (3) prevention and decreased
      frequency or duration of recurrent episodes, (4) prevention of
      thromboembolic complications, and (5) minimization of adverse effects
      from therapy. However, these goals can be modified for each patient. In
      an acute setting with pending hemodynamic collapse, follow the adult
      advanced cardiac life support algorithms for managing atrial
      fibrillation and flutter. Consider immediate electrical cardioversion
      for patients who are hemodynamically unstable.The main difference
      between atrial fibrillation and atrial flutter is that most cases of
      atrial flutter can be cured with radiofrequency ablation. In all
      available studies, catheter ablation is superior to rate control and
      rhythm control strategies with antiarrhythmic drugs.
      
    • Ventricular rate control
      
      Ventricular
      rate control is a priority because it may alleviate symptoms. Rate
      control is typically more difficult for atrial flutter than for atrial
      fibrillation.
      
      
      
      • Calcium channel blockers and beta-blockers
        
        
        
        • Ventricular
          rate control can be achieved with drugs that block the AV node.
          Intravenous calcium channel blockers (eg, verapamil, diltiazem) or
          beta-blockers can be used, followed by initiation of oral agents.
          
        • Hypotension and negative inotropic effects are concerns with the use of these medications.
          
        • A
          history of Wolff-Parkinson-White syndrome or evidence of ventricular
          preexcitation should be determined because agents that act exclusively
          at the level of the AV node may enhance accessory pathway conduction.
          
        
        </li>
        
      • Vagal maneuvers: These can be helpful in determining the underlying atrial rhythm if flutter waves are not seen well.
        
      • Intravenous
        adenosine: This drug, administered as an intravenous push followed with
        an intravenous bolus with flush, can also be helpful in making the
        diagnosis of atrial flutter by transiently blocking the AV node.
        
      Restoration of sinus rhythm
      
      After
      determining the patient's needs for anticoagulation and ventricular
      rate control, the issue of restoration of the sinus rhythm can be safely
      addressed.
      
      
      
      • Radiofrequency ablation
        
        
        
        • Radiofrequency
          ablation is often used as first-line therapy to permanently restore
          sinus rhythm. This procedure is often performed electively, rather than
          in the acute setting, to restore sinus rhythm.
          
        • For patients
          with recurrent symptomatic atrial flutter that is proven to be
          isthmus-dependent in the electrophysiologic laboratory, expect a success
          rate of higher than 95% with current technology.
          
        • Catheter ablation has been shown to significantly improve the quality of life in patients with atrial flutter.
          
        • The
          frequency of hospital admissions and emergency department visits and
          the number of antiarrhythmic drugs administered are decreased
          significantly after ablation.
          
        • Activity capacity significantly improves in patients with preexisting LV dysfunction.
          
        • Type
          I atrial flutters (tricuspid valve isthmus dependent): Catheter
          ablation is typically an outpatient procedure. The procedure involves
          moderate sedation and accessing the femoral veins for catheter
          insertion. The diagnosis of atrial flutter is confirmed using pacing
          maneuvers and ablation is performed typically at 6:00 on the tricuspid
          valve isthmus. A line of block is required to interrupt the circuit.
          (see image below). Postablation pacing maneuvers can confirm that the
          substrate required for the circuit has been modified. Recurrence is less
          than 5%. Postprocedure anticoagulation with warfarin is usually
          continued for 4-6 weeks.
          
        • Classic
          counterclockwise atrial flutter. This 3-dimensional electroanatomic map
          of the tricuspid value and right atrial show the activation pattern
          displayed in color format. Red is early and blue is late relative to a
          fixed point in time. Activation travels in a counterclockwise direction.
          
        • Type II atrial flutters
          (non—isthmus dependent): These circuits are amenable to catheter
          ablation, especially in centers with advanced mapping systems. The
          ablation procedure is similar but may involve additional mapping of the
          left atrium (via a trans-septal puncture). Success depends on localizing
          the circuit and creating a line of block that includes an electrically
          inert anatomic structure (ie, the mitral valve annulus). While success
          should approach 95%, recurrence is more common and may also require the
          use of antiarrhythmic agents for suppression.
          
        
        </li>
        
      • Electrical cardioversion
        
        
        
        • The success rate of electrical cardioversion is higher than 95%.
          
        • Factors
          to consider include synchronization of shocks to R waves, adequate
          sedation, and electrode position (apex anterior, apex posterior,
          anteroposterior).
          
        • Atrial flutter generally requires less energy for conversion than atrial fibrillation, and as few as 50 joules may be necessary.
          
        • If
          cardioversion is not successful with one electrode configuration,
          switching may improve success. A second set of electrodes can be used
          with tandem or simultaneous shocks.
          
        • Biphasic external waveform may be more effective in restoring sinus rhythm.
          
        • A
          few points to remember about the cardioversion technique include a wide
          electrode separation in the right anterior and left posterior position
          (sandwiching the atria) (the more traditional location of pad location
          [anterior and apical] will also work), the application of pressure on
          paddles or electrodes to reduce thoracic impedance, and the placement of
          electrode patches under or lateral to the breasts in women.
          
        • Risius
          et al found that in external electrical cardioversion of atrial
          flutter, anterior-lateral electrode positioning yields results superior
          to those achieved with anterior-posterior positioning. In a randomized
          trial, 96 patients (72 of them men), received sequential biphasic
          waveform shocks using a step-up protocol consisting of 50, 75, 100, 150,
          or 200 J. Compared with anterior-posterior positioning,
          anterior-lateral positioning resulted in successful cardioversion with
          less mean energy (65 +/- 13 vs 77 +/- 13 J, P = 0.001) and fewer mean shocks (1.48 +/- 1.01 vs 1.96 +/- 1.00, P
          = 0.001). In addition, cardioversion occurred with the first 50 J shock
          in 73% of patients when anterior-lateral positioning was used, versus
          36% with the anterior-posterior electrode position (P = 0.001).^[2]
          
        
        </li>
        
      • Pharmacological cardioversion
        
        
        
        
        • Flecainide^[3] is only effective in approximately 10% of patients.
          
        • Dofetilide^[4] is effective in 70-80% of patients. This drug should be initiated in an inpatient setting.
          
        • Ibutilide^{[5, 6, 7, 8]} is
          effective, converting recent-onset atrial flutter to sinus rhythm in
          63% of patients with a single infusion. This is the only agent available
          intravenously in the United States that can be used for cardioversion.
          This drug must be given in a monitored setting due to risk of QT
          prolongation and torsade de pointes. The patient should be monitored
          with continuous ECG monitoring for at least 4 hours after the infusion.
          
        • Large
          single oral doses of type IC antiarrhythmic agents, such as propafenone
          (450-600 mg) or flecainide (200-300 mg), have also been shown to be
          effective in converting recent-onset atrial fibrillation to sinus
          rhythm. Their use in atrial flutter can be assumed to have at least
          equal success.
          
        • Combination of the above treatments:
          Antiarrhythmic medication prior to electrical cardioversion has been
          shown to improve the rate of conversion to sinus rhythm.
          
        </li>
        
      Prevention (decrease frequency or duration of recurrence episodes)
      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 (eg, alcohol, caffeine). For
      atrial fibrillation, approximately 30% of patients remain in sinus
      rhythm at 1 year without antiarrhythmic therapy.
      
      
      
      • Antiarrhythmic agents
        
        
        
        • For more information on the use of antiarrhythmic agents, see Atrial Fibrillation.
          Data on the use of antiarrhythmic agents specifically for atrial
          flutter are limited. Most studies of antiarrhythmics agents and atrial
          fibrillation include some patients with atrial flutter (10-20%).
          
        • In
          general, the use of antiarrhythmic drugs in atrial flutter is similar
          to that of atrial fibrillation; however, with a high success rate and
          low complication rate, the use of radiofrequency ablation in atrial
          flutter makes this procedure a favorable option compared with lifelong
          antiarrhythmic drug therapy because fatal proarrhythmic events (even in
          healthy hearts) and organ toxicity may occur.
          
        • In general,
          antiarrhythmics used to treat atrial fibrillation have been shown
          effective in fibrillation or flutter during a 6 to 12 month follow-up.
          Considering the characteristic adverse effects of each antiarrhythmic
          agent, some guidelines are available regarding the choice of medication
          when taking into account the underlying cardiac pathology.
          
        • For patients without structural heart disease, class IC agents can be used safely.
          
        • For patients with LV hypertrophy without ischemia or conduction delay, class III agents, specifically amiodarone, can be used.
          
        • For patients with ischemic heart disease, sotalol or amiodarone can be used. Avoid class IC agents.
          
        • For
          patients with significant systolic dysfunction, amiodarone can be used,
          dofetilide may be used, and class IC agents should be avoided.
          
        
        </li>
        
      • Surgery:
        In patients who have atrial flutter and need cardiac surgery,
        modification of the atrial incision and creation of a cryothermal
        lesion, similar to the lesion created during radiofrequency catheter
        ablation, can be curative for atrial flutter and may prevent an
        incisional reentrant arrhythmia.
        
      Prevention of complications
      
      
      
      
      • Thromboembolic
        
        
        
        • Patients
          with atrial flutter are at increased risk of thromboembolic
          complications compared with the general population. The anticoagulation
          strategy used for atrial fibrillation is also recommended for atrial
          flutter.
          
        • In general, when atrial flutter persists for more than
          48 hours, 4 weeks of adequate anticoagulation or TEE is needed before
          attempting cardioversion to sinus rhythm.
          
        • Thromboembolic
          complications occur spontaneously after cardioversion or ablation, and
          postconversion anticoagulation is recommended for a minimum of 4 weeks.
          
        • Use
          long-term anticoagulation for patients with persistent or paroxysmal
          atrial flutter. As with atrial fibrillation, keep the international
          normalized ratio (INR) at 2-3 to optimize the therapeutic effect and
          minimize the risk of bleeding.
          
        • Unlike atrial fibrillation,
          atrial flutter has a regular pattern of atrial contraction. TEE data
          have demonstrated an organized sawtooth pattern of the left atrial
          appendage flow with alternating filling and emptying wavelets. No
          difference in the left atrial appendage function is observed compared
          with patients in sinus rhythm. Patients with both atrial flutter and
          atrial fibrillation have significantly decreased left atrial appendage
          function, more spontaneous echo contrast, and larger left atria and
          accompanying appendages.
          
        • Patients with atrial flutter and
          episodes of atrial fibrillation are at higher risk of thromboembolic
          events; however, determining whether episodes of atrial fibrillation are
          associated with episodes of atrial flutter is difficult.
          
        • A
          large retrospective review of patients in chronic atrial flutter
          revealed a 14% occurrence rate of thromboembolic events over 4.5 years,
          with half of these events being ischemic stroke. In another large cohort
          of patients with atrial flutter, the occurrence rate of embolic
          complications in patients with chronic or recurrent atrial flutter was
          12%. For stroke, this risk is estimated at approximately one third of
          patients with nonrheumatic atrial fibrillation. Males with hypertension,
          structural heart disease, LV dysfunction, and diabetes may be at higher
          risk of thromboembolic complications. Interestingly, associated atrial
          fibrillation did not significantly increase the risk of the embolic
          complications.
          
        • Other reports have demonstrated thrombus in the
          left atrium appendage of patients with atrial flutter (as many as 43%).
          Most studies of non–anticoagulated patients with atrial flutter report a
          rate of 10-15% for patients with thrombus in the left atrium or left
          atrial appendage. Spontaneous echo contrast associated with increased
          risk of thromboembolism was found in 6-43% of patients with atrial
          flutter.
          
        • The CHA2DS2-VASc score includes congestive heart
          failure, hypertension, age 65-74 years, diabetes, previous stroke,
          vascular disease, and sex category. This score has been shown to perform
          well at predicting patients at high-risk and patients categorized at
          low risk for thromboembolism.^[9]
          
        • Postcardioversion
          thromboembolic events can complicate as many as 7.3% of procedures in
          patients who are not anticoagulated. These events occur within 3 days
          after the cardioversion; almost all occur within 10 days after the
          cardioversion^[10] .
          
        • In atrial fibrillation, postcardioversion stunning of the left atrial appendage is thought to contribute to thrombogenicity.^[11] This
          phenomenon may last as long as 4 weeks in patients with atrial
          fibrillation and may be related to how long patients have been in
          arrhythmia.
          
        • Stunning of the left atrial appendage also occurs
          following conversion from atrial flutter to sinus rhythm (electrical or
          spontaneous), although to a lesser degree. Left atrial and left atrial
          appendage function decrease immediately after conversion, and, in one
          study, spontaneous echo contrast was noted to develop within 5 minutes
          after conversion in 43% of patients. This is thought to be the source of
          emboli in patients whose TEE findings revealed no evidence of thrombus
          but who had a thromboembolic event after cardioversion.
          
        • In a
          study comparing left atrial appendage function before and after catheter
          ablation (immediate, 1 d, 1 wk, and 6 wk) of persistent atrial flutter,
          a significant increase in atrial standstill, decrease in left atrial
          appendage function, and new spontaneous echo contrast occurred after
          ablation. One patient formed a new left atrial appendage thrombus after
          ablation. Evidence of atrial stunning significantly improved after 1
          week. Anticoagulation for at least 1 week is advocated after ablation of
          an atrial flutter that persists for more than 2 days.
          
        • Adequate anticoagulation, as recommend by the American College of Chest Physicians,
          has been shown to decrease thromboembolic complications in patients
          with chronic atrial flutter and in patients undergoing cardioversion.
          
        
        </li>
        
      • Cardiomyopathy:
        Termination of long-standing atrial flutter with a rapid ventricular
        response has been reported to improve LV systolic function in patients
        without other known causes of dilated cardiomyopathy.
        
      Minimizing adverse effects of antiarrhythmic therapy
      
      Because
      atrial flutter is a nonfatal arrhythmia, carefully assess the risks and
      benefits of drug therapy, especially with antiarrhythmic agents. Always
      consider catheter-based ablation as first-line therapy prior to
      starting an antiarrhythmic agent. A few points to remember that will
      help minimize the adverse effects include the following:
      
      
      
      • Avoidance
        of precipitating factor(s) or therapy of the underlying problem may be
        all that is needed to prevent recurrent episodes.
        
      • Of
        antiarrhythmic agents, amiodarone is effective and is associated with a
        low proarrhythmic risk but may adversely affect multiple organs,
        including the skin, liver, lungs, and thyroid. Thus, sotalol would seem a
        reasonable choice of antiarrhythmic drug therapy for atrial flutter.
        Per guidelines, sotalol should be initiated in the inpatient setting.
        
      • Radiofrequency
        ablation is currently the preferred therapeutic choice. Although many
        patients who were treated with radiofrequency ablation subsequently
        developed atrial fibrillation after long-term follow-up (56% in one
        study), this procedure still represents a safe alternative to
        antiarrhythmic agents.
        
      
      Next Section: Consultations
      Consultations
      In
      general, consult a cardiologist and/or electrophysiologist because the
      use of antiarrhythmic drugs may be harmful and radiofrequency ablation
      may eliminate atrial flutter.
      Previous
      Next Section: Consultations
      Diet
      Any dietary recommendations should be appropriate for the underlying heart disease and other comorbidities (eg, diabetes).
      </li>
      
    • 
      Atrial Flutter Medication
      
      
    • Medication Summary
      Medications
      are usually used in the acute setting or in people who are not
      candidates for radiofrequency ablation. Agents can be used to control
      the ventricular rate, terminate acute episodes, prevent or decrease the
      frequency or duration of recurrent episodes, and prevent complications.
      Various categories of drugs are used to treat atrial flutter. Drug
      initiation in an outpatient setting is generally accepted in patients
      without underlying structural heart disease who are in sinus rhythm. In
      addition, many specialists initiate outpatient drug therapy in patients
      with therapeutically anticoagulated atrial flutter who are awaiting
      outpatient electrical cardioversion in the near future. Certain
      medications, such as initiation of sotalol and dofetilide, by guidelines
      should be administered in an inpatient setting as they can prolong the
      QT interval and be proarrhythmic. Regardless, close patient follow-up is
      mandated, with frequent ECG monitoring or transtelephonic monitoring
      for potential signs of proarrhythmia.
      Next Section: Atrioventricular nodal conduction blockers
      Atrioventricular nodal conduction blockers
      
      Class Summary
      Used
      to slow ventricular response by slowing AV nodal conduction during
      atrial fibrillation or flutter. Also indicated for use in conjunction
      with class IA and IC antiarrhythmics, which slow atrial
      fibrillation/flutter rate and may cause more rapid ventricular response.
      View full drug information
      Metoprolol (Lopressor)
      Selective
      beta1-adrenergic receptor blocker that decreases automaticity of
      contractions. During IV administration, carefully monitor BP, heart
      rate, and ECG. View full drug information
      Atenolol (Tenormin)
      Selectively blocks beta-1 receptors with little or no effect on beta-2 receptors.View full drug information
      Esmolol (Brevibloc)
      Excellent
      for use in patients at risk for experiencing complications from
      beta-blockade, particularly those with reactive airway disease,
      mild-to-moderate LV dysfunction, and/or peripheral vascular disease.
      Short half-life of 8 min allows titration to desired effect and quick
      discontinuation if needed.
      Previous
      Next Section: Atrioventricular nodal conduction blockers
      Calcium channel blockers (nondihydropyridine)
      
      Class Summary
      
      Effective for rate control.View full drug information
      Verapamil (Calan)
      Calcium
      channel blocker. Only nondihydropyridines are effective for rate
      control. During depolarization, inhibits calcium ions from entering slow
      channels and voltage-sensitive areas of vascular smooth muscle and
      myocardium. View full drug information
      Diltiazem (Cardizem)
      Only
      nondihydropyridines are effective for rate control. During
      depolarization, inhibits calcium ions from entering slow channels and
      voltage-sensitive areas of vascular smooth muscle and myocardium.
      Previous
      Next Section: Atrioventricular nodal conduction blockers
      Cardiac glycosides
      
      Class Summary
      
      AV nodal blocking agents.View full drug information
      Digoxin (Lanoxin)
      
      
      Slows
      sinus node and AV node via vagomimetic effect and not very effective if
      sympathetic tone is increased. Generally not recommended unless
      depressed LV function is present.
      Previous
      Next Section: Atrioventricular nodal conduction blockers
      Antiarrhythmics, class IC
      
      Class Summary
      
      For
      use in patients with atrial flutter and SVT without structural heart
      disease. Use in conjunction with AV nodal blocking agents when
      administered to patients in atrial flutter because conversion to atrial
      flutter with 1:1 conduction (producing fast ventricular rates) is noted.
      View full drug information
      Propafenone (Rythmol)
      
      Treats
      life-threatening arrhythmias. Possibly works by reducing spontaneous
      automaticity and prolonging refractory period. Indicated for patients
      with AF and SVT without structural heart disease. Use in conjunction
      with AV nodal blocking agents when administered to patients in AF
      because conversion to AFL with 1:1 conduction (producing fast
      ventricular rates) is noted. View full drug information
      Flecainide (Tambocor)
      Treats
      life-threatening ventricular arrhythmias. Causes prolongation of
      refractory periods and decreases action potential without affecting
      duration. Blocks sodium channels, producing a dose-related decrease in
      intracardiac conduction in all parts of heart, with greatest effect on
      the His-Purkinje system (HV conduction). Effects on AV nodal conduction
      time and intra-atrial conduction times, although present, are less
      pronounced than on ventricular conduction velocity. Use in conjunction
      with AV nodal blocking agents when administered to patients in AF
      because conversion to AFL with 1:1 conduction (producing fast
      ventricular rates) is noted.
      Previous
      Next Section: Atrioventricular nodal conduction blockers
      Antiarrhythmics, class III
      
      Class Summary
      
      Class
      III drugs widely used in maintenance of sinus rhythm in patients with
      atrial flutter. Drugs may include amiodarone (Cordarone), sotalol
      (Betapace), ibutilide (Corvert), and dofetilide (Tikosyn). View full drug information
      Amiodarone (Cordarone)
      May
      inhibit AV conduction and sinus node function. Prolong action potential
      and refractory period in myocardium and inhibit adrenergic stimulation.Prior to administration, control ventricular rate and CHF (if present) with digoxin or calcium channel blockers.View full drug information
      Sotalol (Betapace)
      
      Class
      III antiarrhythmic agent, which blocks K+ channels, prolongs action
      potential duration (APD), and lengthens QT interval. Noncardiac
      selective beta-adrenergic blocker. Sotalol is shown to be effective in
      the maintenance of sinus rhythm, even in patients with underlying
      structural heart disease. View full drug information
      Ibutilide (Corvert)
      
      Newer
      class III antiarrhythmic agent that may work by increasing action
      potential duration and thereby changing atrial cycle length variability.
      Mean time to conversion is 30 min. Two thirds of patients who converted
      were in sinus rhythm at 24 h. Ventricular arrhythmias occurred in 9.6%
      of patients and mostly were PVCs. The incidence of torsades de pointes
      was < 2%. View full drug information
      Dofetilide (Tikosyn)
      Recently
      approved by FDA for maintenance of sinus rhythm. Increases monophasic
      action potential duration, primarily due to delayed repolarization.
      Terminates induced re-entrant tachyarrhythmias (eg, atrial
      fibrillation/flutter, ventricular tachycardia) and prevents their
      reinduction.Has no effect on cardiac output, cardiac index,
      stroke volume index, or systemic vascular resistance in patients with
      ventricular tachycardia, mild to moderate CHF, angina, and either normal
      or reduced LVEF. No evidence of negative inotropic effect.
      Previous
      Next Section: Atrioventricular nodal conduction blockers
      Antiarrhythmic agent, miscellaneous
      Class Summary
      
      Dronedarone is an antiarrhythmic agent with properties belonging to all 4 Vaughn-Williams antiarrhythmic classes.View full drug information
      Dronedarone (Multaq)
      Blocks
      sodium channels, blocks beta1-adrenergic site, and alters adenyl
      cyclase generation (ie, negative inotropic effects); blocks potassium
      channels (eg, hERG) and therefore prolongs cardiac repolarization.In
      a multinational clinical trial (n >4600), dronedarone reduced
      cardiovascular hospitalization or death from any cause by 24% compared
      with placebo.Indicated to reduce risk for cardiovascular
      hospitalization in patients with paroxysmal or persistent atrial
      fibrillation (AF) or atrial flutter (AFL), with a recent episode of
      AF/AFL and associated cardiovascular risk factors (ie, age >70 y,
      hypertension, diabetes, history of CVA, LAD >50 mm or LVEF < 40%)
      who are in sinus rhythm or who will be cardioverted.
      Previous
      Next Section: Atrioventricular nodal conduction blockers
      Anticoagulants
      
      Class Summary
      
      Used to prevent thromboembolic complications.View full drug information
      Heparin
      
      
      Augments
      activity of antithrombin III and prevents conversion of fibrinogen to
      fibrin. Does not actively lyse but is able to inhibit further
      thrombogenesis. Prevents reaccumulation of clot after spontaneous
      fibrinolysis. Most data are related to use of unfractionated heparin.
      Low–molecular-weight heparin probably as effective but awaits results
      from clinical studies. View full drug information
      Warfarin (Coumadin)
      
      
      Interferes
      with hepatic synthesis of vitamin K–dependent coagulation factors. Used
      for prophylaxis and treatment of venous thrombosis, pulmonary embolism,
      and thromboembolic disorders.Tailor dose to maintain INR of 2-3.
      
    • Atrial Flutter Follow-up
      
    • Further Inpatient Care
      
      
      
      • Consider
        catheter-based ablation as first-line therapy in patients with type I
        typical atrial flutter if they are reasonable candidates. Ablation is
        usually done as an elective procedure; however, it can be done when the
        patient is in atrial flutter as well.
        
      • Given the high success rate and low complication rate, radiofrequency ablation is superior to medical therapy.
        
      • For
        atrial flutter of less than 48 hours in duration, attempt cardioversion
        as soon as possible. Postconversion anticoagulation is usually
        unnecessary, although data from TEE studies indicate that postconversion
        anticoagulation a reasonable option.
        
      • For episodes
        of atrial flutter of uncertain duration or greater than 48 hours, begin
        anticoagulation therapy. If cardioversion is needed sooner,
        anticoagulate patients with intravenous heparin and perform TEE as close
        to the time of cardioversion as possible. Patients still require
        anticoagulation for at least 4 weeks after cardioversion.
        
      • If
        thrombus is observed or suspected based on TEE findings, delay
        cardioversion. Rate control and therapeutic anticoagulation is required
        for a minimum of 4 weeks.
        
      • In patients who are not
        candidates for catheter-based ablation, rate and rhythm control
        strategies should be considered. The risk of proarrhythmia is probably
        greatest during the first 24-48 hours after the initiation of
        antiarrhythmics and drugs such as ibutilide, sotalol, and dofetilide
        should be initiated in an inpatient setting. Pause-dependent torsades de pointes can occur after conversion to sinus rhythm.
        
      Further Outpatient Care
      
      Closely
      monitor the patient's anticoagulation therapy, with a target INR of
      2-3. Take special care when additional medications (including
      antibiotics) are added because they may cause dramatic alterations in
      INR values.
      Previous
      Next Section: Further Outpatient Care
      Inpatient & Outpatient Medications
      
      
      
      
      • Anticoagulant
        therapy (ie, heparin and/or warfarin) is indicated, especially when the
        onset of atrial flutter is of more than 48 hours' duration or is
        uncertain.
        
        
        
        • Patients need to maintain a therapeutic INR for 3
          weeks prior to conversion and for at least 4 weeks after conversion to
          sinus rhythm.
          
        • Long-term anticoagulation is recommended for patients with chronic atrial flutter.
          
        • Anticoagulants are used to decrease thromboembolic complications.
          
        
        </li>
        
      • Preferred
        medications that slow AV node conduction include beta-blockers (eg,
        atenolol, metoprolol, propranolol) and calcium channel blockers (eg,
        verapamil, diltiazem).
        
        
        
        • These medications are used to control ventricular rates.
          
        • Also
          use these medications in patients who are taking class IA or IC
          antiarrhythmic drugs (to prevent rapid ventricular response, which can
          occur when the atrial rate is slowed).
          
        
        </li>
        
      • Antiarrhythmic drugs are indicated for the termination of acute episodes or the prevention of recurrent episodes.
        
        
        
        • For atrial flutter, electrical cardioversion is effective and usually requires less energy than for atrial fibrillation.
          
        • Catheter ablation offers a potential cure and is safer long-term use of an antiarrhythmic agent.
          
        </li>
        
      Complications
      
      The
      major potential complication with atrial flutter (or atrial
      fibrillation) is neurologic insult, either transient ischemic attack or
      stroke. This risk can be minimized with proper anticoagulation. Consider
      patients with common type I atrial flutter for catheter ablation to
      eliminate the need for long-term anticoagulation and antiarrhythmic
      medications.
      Previous
      Next Section: Further Outpatient Care
      
      Prognosis
      
      
      
      
      • Atrial
        flutter itself is not considered a life-threatening arrhythmia;
        however, uncontrolled ventricular rates can lead to impaired ventricular
        function. Additionally, patients with Wolff-Parkinson-White syndrome
        can develop life-threatening ventricular responses. Consider these
        patients for catheter ablation of their accessory bypass tract. Data
        from the Framingham study suggest that patients with atrial fibrillation
        do not live as long as patients without atrial fibrillation (ie,
        controls). No data are available on atrial flutter.
        
      • The
        prognosis for patients with Type I atrial flutter who undergo catheter
        ablation is excellent, with a very low recurrence rate. The picture is
        not as clear for patients with both atrial flutter and atrial
        fibrillation. Some reports have documented fewer episodes of atrial
        fibrillation after successful flutter ablation, while others have not.
        Atrial fibrillation is thought to possibly be more responsive to
        antiarrhythmic agents after atrial flutter has been eliminated.
        
      • Numerous
        reports indicate that patients with atrial fibrillation who are given
        class IC antiarrhythmic agents may convert to atrial flutter with faster
        ventricular rates. Thus, patients receiving type IC agents (flecainide)
        should also receive an AV nodal blocking drug such as a beta-blocker or
        calcium channel blocker.
        
      
      Previous
      Next Section: Further Outpatient Care
      Patient Education
      
      
      
      
      • Patient education regarding medications and diet is important.
        
      • Patients
        taking warfarin should avoid major changes in their diet unless
        consulting with their providers. Recall that warfarin inhibits vitamin K
        synthesis and that sources of vitamin K are green leafy vegetables. A
        sudden change to a diet high in vitamin K may increase the requirements
        for warfarin.
        
      </li>
      
    </li>
    
  </li>