Patients with atrial flutter can be asymptomatic or present with symptoms as palpitations, lightheadedness, fatigue, and shortness of breath especially in the presence of rapid ventricular conduction.

Decreased exercise tolerance is another symptom that can be present during patient evaluation.

During the rapid ventricular rate, hypotension, syncope and near syncope can occur in susceptible patients with high ventricular rates.

Some patients remain asymptomatic until they develop acutely decompensated heart failure, tachycardia-induced cardiomyopathy, and embolic stroke.

The physical exam in patients with atrial flutter will show regular or irregularly regular peripheral pulse (due to variable conduction from the atrioventricular node), jugular venous distension, respiratory sounds with crackles in lung fields, tachycardia, abdominal distention, and lower extremities edema when congestion occurs. 

Initial evaluation of the underlying rhythm is necessary, and determination of possible etiology or trigger is crucial.

Electrocardiogram:

Electrocardiogram generally shows flutter waves with the absence of an isoelectric line between QRS complexes, with an atrial wave around 300 beats per minute with ventricular conduction that can be 2 to 1, 3 to 1 or 4 to 1 or with variable conduction due to Wenckebach phenomenon.

In inferior leads, typical flutter waves resemble a picket fence or sawtooth because the P waves are negative due to the direction of the vector.

Typical atrial flutter with counterclockwise activation will show inferior leads with negative flutter waves with low amplitude in lead I and upright flutter wave in aVL.[9]

Echocardiogram

Echocardiography for the evaluation of atrial flutter bases its value on the determination of underlying structural heart disease. Presence of dilated atrial chambers is a sign of chronicity and also fibrosis of the atrium that could make the circuit persist and more challenging to control.[13]

Assessment of left ventricular ejection fraction can be the cause or consequence of underlying atrial flutter because the persistence of tachycardia can generate tachycardia induced-cardiomyopathy or the cardiomyopathy and volume status can trigger the atrial flutter. 

Evaluation for atrial or ventricular thrombus is also important, especially when desiring cardioversion to sinus rhythm. A transesophageal echocardiogram is the modality of choice because it can visualize the atrial appendage where atrial thrombus is more frequently present.[14]

Laboratory evaluation

An initial determination of atrial flutter triggers is necessary. Laboratory evaluation of electrolytes disturbance, abnormal thyroid function, infection, anemia, hypoxia. Correction of these abnormalities can improve symptoms and decrease the threshold of development of atrial flutter and rapid ventricular response.

Pulmonary function test might be necessary for this set of patients; there is a correlation between lung disease and presence the atrial arrhythmias including atrial flutter. Management of the underlying lung condition can improve the control of the atrial flutter.

Treatment management should focus on the following aspects:

1. Rhythm control
2. Rate control
3. Anticoagulation due to embolization risk

1. Rhythm control

Maintenance of the sinus rhythm or conversion of the sinus rhythm is essential. 

Persistence of atrial flutter, can cause chronic remodeling of the atrium and make it more difficult to manage the rate and the conversion or maintenance of sinus rhythm.

There are different ways to achieve sinus rhythm: with electrical cardioversion, pharmacological cardioversion and ultimately with catheter ablation.

The rhythm strategy divides into acute and long term management.

In the acute setting, in patients with atrial flutter who are hemodynamically unstable, synchronized cardioversion is indicated for the conversion of sinus rhythm to stabilize the patient.[15]

In stable patients, pharmacological cardioversion is achievable with different antiarrhythmics.  Antiarrhythmic drugs like amiodarone, class IA (procainamide, quinidine, and disopyramide) and IC drugs (flecainide and propafenone), calcium channel blockers (verapamil, diltiazem), and beta-blockers (metoprolol, carvedilol, esmolol) are some of the choices for pharmacological cardioversion.[16]

Despite the multiple pharmacological options the control and conversion of atrial flutter to sinus rhythm is difficult. The mechanisms by which antiarrhythmic drugs maintain sinus rhythm is by prevention of premature beats that usually start the activation of the tachycardia circuit by a reentrant or an ectopic beat. 

In the presence of a new diagnosis of atrial flutter, one should start the patient on anticoagulation. In the absence of intracardiac thrombus, electrical cardioversion in stable patients can be considered, especially to prevent persistence of the arrhythmia and further fibrosis that will perpetuate the presence of atrial flutter and more difficult to control or to convert to sinus rhythm.[17]

In patients who have a contraindication to these drugs or do not tolerate them may consider catheter ablation of the atrial flutter circuit.[18]

Radiofrequency catheter ablation of the CTI is the standard treatment for typical atrial flutter with a success rate of 95% with few complications post-procedure.[19] The procedure consists placement of intracardiac catheters into the coronary sinus, the atrium, and an ablation catheter. The anatomical target for the CTI is found through a mapping and entrapment technique. After this, the linear lesion is made by the ablation catheter with the use of radiofrequency energy. At the end of the ablation when the line is complete, verification bidirectional conduction block and absence of atrial flutter is done to confirm ablation is complete.  In the rare cases of medication and ablation failure, atrioventricular nodal ablation with the placement of a pacemaker might be indicated to prevent atrial to ventricular conduction of rapid atrial flutter.

2. Rate control

Rate control is achievable with the use of atrioventricular nodal agents as calcium channel blockers (first line) or beta blockers.[20] Digoxin is another option for rate control but needs to be used carefully due to its side effects and toxicity.

Combination of these agents is an option.

Adequate control of the atrial flutter through AV nodal agents is difficult because atrial flutter continuously fires at the same rate to the AV node. 

The heart rate goal should be below 110 beats per minute.[21] This was determined after the RACE II trial (Rate Control Efficacy in Permanent Atrial Fibrillation: a Comparison between Lenient versus Strict Rate Control II). This study compared strict heart rate control of <80 bpm versus <110bpm, this study showed that very stringed heart rate control is not necessary and more lenient control reduces polypharmacy and fewer side effects and less outpatient visits. This study was in patients with atrial flutter but can extrapolate to the rate control of atrial flutter.

In patients who are intolerant of medications or have significant bradycardia due to rate control measures, a catheter ablation is an option.

3. Anticoagulation due to the risk of embolic events:

Patients with atrial flutter have a similar risk of strokes as those with atrial fibrillation.[22]

Use of a scoring system to determine the annual risk of stroke must be used such as the CHADS2-Vasc.[23] This scoring system helps to risk stratify the patient according to their risk of developing embolic strokes due to atrial flutter or atrial fibrillation. The presence of congestive heart failure, systemic hypertension, diabetes, female sex, age between 65 to 74 years and a history of the peripheral vascular disease score as one point for each comorbidity that is present. 

Age more than 75 years old and a history of stroke are two additional points each.

The presence of one point can give the patient an annual risk of 1.3% of embolic stroke per year when two points the risk is 2.2%. In patients with two or more points, the use of anticoagulation is a strong recommendation. In patients with one point, one may use either aspirin or full anticoagulation.

• Atrial fibrillation: mostly irregular, no evidence of organized atrial activity in the electrocardiogram, absence of P waves
• Multifocal atrial tachycardia: multiple P waves morphology due to the presence of several atrial pacers
• Atrial tachycardia with variable conduction: the isoelectric line between QRS complexes

Prognosis of patients with typical atrial flutter undergoing catheter ablation is good with a recurrence rate of less than 5%.

Persistence of atrial flutter can generate tachycardia induce cardiomyopathy that is hard to control causing multiple hospitalizations due to decompensation.

The most common complication of atrial flutter is the increased risk of embolic stroke and disability related to this event.

Hemodynamically instability is also possible especially in patients with a rapid ventricular response.

Chronicity and poor control of atrial flutter can generate tachycardia induce cardiomyopathy and also can produce hard to control heart failure.

The complications secondary to the use of antiarrhythmic drugs are related to the type of drug and underlying mechanism of the drug. 

Atrial flutter ablation complications also depend on the side of the origin of the atrial flutter. Right-sided atrial flutter is related to fewer complication rates than left-sided atrial flutter ablation, and this is due to the need for creating a transeptal communication during the procedure to reach the left atrium foci of arrhythmia and perform the ablation. The transseptal puncture produces transient communication between the left and right chambers of the heart. There is also increasing the risk of embolic strokes with left-sided atrial flutter ablation when compared with right side procedures. 

There is no cure for atrial flutter and the disorder is known to be associated with a high risk of a stroke and other embolic phenomena; this the management of atrial flutter is best done by an interprofessional team including physicians, specialists, pharmacist, and a cardiac specialty nurse is recommended. While the cardiologist may initiate the initial treatment, the majority of patients are followed by the primary provider or nurse practitioner. These patients need life-long follow up because there is a risk of an embolic stroke. If the disorder receives inadequate therapy, it leads to a poor quality of life.

The primary care providers, pharmacists, and nurse practitioners should enforce medication compliance. Those patients on warfarin should have a dietary consult because a sudden change in the consumption of green leafy vegetables can affect the INR. The hematology nurse and pharmacist should monitor the INR but the dose adjustment of warfarin should be done by the clinician.

At each clinic visit, an ECG should be performed and the patient examined for any embolic phenomenon. To improve outcomes, open communication between members of the interprofessional team is essential.

Outcomes

Despite advances in treatment, recurrence and multiple admission to the hospital are very common.