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 Atrial Flutter

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john



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PostSubject: Atrial Flutter    Wed Jun 08, 2011 1:21 pm

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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).

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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>

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