The initial ECG (see Figure 1) reveals a tachycardic rhythm that is regular and consistent with

clockwise typical atrial flutter with a 2:1 atrioventricular conduction block [1]; this is consistent with
congestive heart failure. Atrial flutter is a relatively common atrial tachyarrhythmia and is the most
significant of the atrial tachyarrhythmias, after sinus tachycardia and atrial fibrillation. Atrial flutter is
defined by the presence of stable, uniform atrial activation, which is seen on ECG as flutter waves
(most evident in lead II; see Figure 1), and has traditionally been characterized as a macroreentrant
arrhythmia, with atrial rates ranging from 240 to 400 bpm[1] (though the rate is most commonly
around 300 bpm). Depending on the ventricular rate, the rhythm can interfere with cardiac output,
leading to heart failure or atrial thrombus formation. Thrombus places the patient at risk for possible
systemic embolization and stroke. Atrial flutter usually includes an atrioventricular (AV) block, with
the rhythm commonly conducted at a 2:1 or 4:1 ratio; less commonly, a ratio of 3:1 or 5:1 is seen. [1]

The pathophysiology of atrial flutter includes multiple reentrant or ectopic atrial waveforms reaching
the AV node. There are 2 forms of atrial flutter, referred to as type I and type II. Type I, also called
typical, common, or isthmus-dependent atrial flutter, involves a reentrant circuit that encircles the
tricuspid annulus of the right atrium, with rates that average 240-340 bpm. The depolarizing impulse
can travel in a "counterclockwise" fashion around the tricuspid annulus, resulting in negative flutter
waves in the inferior leads, or it can travel in a "clockwise" fashion, resulting in positive flutter waves
in the inferior leads. Type II atrial flutter, also known as atypical aflutter, is less common and
remains uncharacterized except for unusually high rates of
340-440 beats/min.[1,2] The exact etiology of atrial flutter is unknown, but it has been found to occur
in patients with a variety of conditions, such as heart failure, pericarditis, valvular disease,
pulmonary embolism, chronic obstructive pulmonary disease, and hyperthyroidism, as well as
following most types of cardiac surgery. It is estimated that 200,000 new cases of atrial flutter are
diagnosed each year in the United States. The condition tends to be more common in elderly men
and in patients with the above mentioned comorbidities; however, it can also occur in patients
without identifiable risk factors.[1]

After addressing the need for immediate cardioversion in patients with atrial flutter who may be
hemodynamically unstable,[1] the general goals for pharmacotherapy include ventricular rate control,
conversion to a normal sinus rhythm (NSR), prevention of recurrent episodes, minimization of the
risk of thromboembolic complications, and minimization of any adverse effects from pharmacologic
therapy.[2] Ventricular rate control can alleviate the symptoms associated with a rapid ventricular
response. Two classes of medications are routinely used: calcium channel blockers (eg. diltiazem)
and beta-blockers (eg. metoprolol). Both classes of medications work by blocking conduction of the
atrial tachydysrhythmia through the AV node. The potential for hypotension associated with the
negative inotropic effects of these drugs should be considered when they are used to treat atrial
flutter.

After controlling the ventricular rate, the safety of attempting restoration of an NSR must be
established; addressing the need for anticoagulation therapy for the prevention of thromboembolic
phenomenon should be the first consideration. The success rate of direct current (DC) synchronized
cardioversion is >95% for returning the heart to an NSR; however, as with atrial fibrillation, the
success rate of sinus rhythm maintenance after 1 year of DC cardioversion without the aid of
antiarrhythmic pharmacotherapy varies from 20 to 50%. Atrial flutter generally requires less energy
for conversion than atrial fibrillation; in many cases, conversion is achieved with as little as 50
joules. Pharmacologic cardioversion is an alternative to electrical cardioversion, and it offers several
choices with regard to specific medications. Procainamide is effective in 0-13% of patients;
flecainide, in approximately 10% of patients; and dofetilide, in approximately 70-80% of patients.
Ibutilide can convert recent-onset atrial flutter to an NSR in 63% of patients with a single infusion.
Large, single oral doses of type IC antiarrhythmic agents, such as propafenone
(450-600 mg) or flecainide (200-300 mg), have been shown to be effective in converting recent-
onset atrial fibrillation to an NSR as well.[2] Oral amiodarone during the loading period (>1 mo) has
been shown to convert 18% of cases of atrial fibrillation or flutter to an NSR. Intravenous
amiodarone is also effective in converting an atrial flutter to an NSR, and it slows the ventricular rate
in patients with a rapid ventricular response. A final option is atrial overdrive pacing, which can be
performed invasively or through the use of a transesophageal electrode to pace the left atrium; this
therapy has a success rate of approximately 50%.[2] A combination of DC cardioversion and
antiarrhythmic therapy is most commonly used to effectively restore an NSR and maintain sinus
rhythm.[1,2]

After the initial episode of atrial flutter has terminated and any underlying precipitating factors have
been treated, some patients may not need any further intervention, except for avoidance of the
precipitating factor (eg, alcohol, caffeine); however, as mentioned above, approximately 30% of
patients remain in sinus rhythm at 1 year without antiarrhythmic therapy, requiring some sort of
maintenance therapy. The guidelines regarding the use of antiarrhythmic agents in atrial flutter are
similar to those for using antiarrhythmic agents in atrial fibrillation. In addition, radiofrequency
ablation has a high success rate and low complication rate for treating atrial flutter, and in some
cases, it may be a more favorable option when compared with lifelong antiarrhythmic drug therapy
because of adverse reactions that can include fatal proarrhythmic events and organ toxicity.
Antiarrhythmics used to treat atrial fibrillation have been shown to be effective in treating fibrillation
or flutter during a 6- to 12-month follow-up; the specific characteristics and the adverse effects of
each antiarrhythmic agent should be considered when selecting which pharmacologic agent to use.
Generally speaking, class IC agents may be used in patients without structural
heart disease[3]; however, for patients with left ventricular hypertrophy with or without ischemia or
conduction delay, class III agents (specifically, sotalol or amiodarone) are the drugs of choice. For
patients with significant systolic dysfunction, dofetilide can be an effective option provided that there
is no evidence of renal dysfunction.[1,2]
There is an increased risk of thromboembolic complications for patients who have been in atrial
flutter for more than 48 hours, which may result from episodic atrial fibrillation leading to impaired
left atrial appendage function and subsequent thrombus formation. The same anticoagulation
strategy used in patients with atrial fibrillation may be applied to patients with atrial flutter. [2] Some
reports have demonstrated thrombus in the left atrium appendage in as many as 43% of patients
with atrial flutter, with postcardioversion thromboembolic events occurring in up to 7% of patients
who were not anticoagulated. These events, if not occurring immediately after cardioversion,
typically occur at about 3 days following cardioversion, with almost all cases occurring within 10
days after restoration of an NSR. Stunning of the left atrial appendage is thought to contribute to
thrombogenicity and may play a role for as long as 4 weeks following cardioversion. This is believed
to be the source of emboli in patients who have had a thromboembolic event after cardioversion
despite no evidence of thrombus found on transesophageal electrocardiography (TEE).
Anticoagulation is also recommended for at least 1 week after any ablation of an atrial flutter that
persists for more than 48 hours. Adequate anticoagulation, as recommended 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. [2]

The patient in this case was placed on noninvasive positive pressure ventilation for her pulmonary
edema and treated with intravenous diltiazem for the rapid ventricular response to the underlying
2:1 atrial flutter rhythm. Administration of diltiazem resulted in conversion to a variable block that
was mainly 4:1, resulting in a heart rate of around 80 bpm. Additional intravenous pharmacologic
therapy with furosemide, nitroglycerin, and morphine sulfate was administered for her congestive
heart failure. Heparin was administered as an anticoagulant for the atrial flutter. After several hours,
the patient improved notably and was in no evident respiratory distress. The initial examination of
cardiac enzymes was unremarkable, and she was admitted to a cardiac unit on a monitored floor for
further management of her congestive heart failure, evaluation for possible myocardial ischemia,
and workup for her atrial flutter. She continued to improve with intravenous diuretic therapy; on
hospital day 2, she underwent a TEE that did not reveal structural heart disease or thrombus in the
left atrium. She was DC cardioverted successfully (see ECG in Figure 2) and discharged on
warfarin therapy with follow-up.