Atrial flutter


Atrial flutter

A rhythm that starts in the atrial chambers of the heart.

It is usually associated with a fast heart rate and is classified as a type of supraventricular tachycardia.

Atrial flutter is caused by a re-entrant rhythm, that usually occurs along the cavo-tricuspid isthmus of the right atrium though atrial flutter can originate from the left atrium as well.

It is typically initiated by a premature electrical impulse arising in the atria.

It is propagated due to differences in refractory periods of atrial tissue.

The electrical activity that moves in a localized self-perpetuating loop, which usually lasts about 200 milliseconds for the complete circuit.

For each cycle around the loop, an electric impulse results and propagates through the atria.

It is the second most common pathologic supraventricular tachycardia.

Its prevalence rate is less than one-tenth of the most common supraventricular tachycardia, atrial fibrillation.

Characterized by a sudden-onset of regular abnormal heart rhythm on an electrocardiogram in which the heart rate is fast.

Symptoms may include: heart beating too fast, too hard, or skipping beats, chest discomfort, difficulty breathing, light-headedness, or loss of consciousness.

Occurs typically in individuals with cardiovascular diseases and diabetes mellitus.

The incidence of atrial flutter has been estimated at 88 cases per 100,000 person-years.

Its incidence is significantly lower, about 5 cases/100,000 person-years in patients younger than age 50 and is far more common (587 cases/100,000 person-years) in those over 80 years of age.

May occur spontaneously in people with otherwise normal hearts.

Can sometimes be asymptomatic.

Its presence is often marked by characteristic palpitations.

Can often degenerate into atrial fibrillation.

Rarely persists for months to years.

Leads to poor contraction of the atrial chambers of the heart,and pooling of the blood in the heart.

It can lead to the formation of blood clots in the heart which pose a significant risk of embolization and stroke.

A supraventricular tachycardia with a ventricular heart rate of 150 beats per minute is suggestive of atrial flutter.

Intravenous adenosine can help differentiate between atrial flutter and other forms of supraventricular tachycardia.

Acute management requires slowing the heart rate with medications such as beta blockers or calcium channel blockers, if chest pain, syncope are absent and normotension is present.

If chest pain, loss of consciousness, or unstable atrial flutter with hypotension is present an urgent electrical shock to the heart to restore a normal heart rhythm is necessary.

Long-term use of anticoagulants reduces the risk of blood clot formation in the heart and resultant strokes.

Antiarrhythmic drugs such as ibutilide can effectively control atrial flutter about 80% of the time.

Atrial flutter recurs 70–90% of the time despite continued use of antiarrhythmic drugs.

It is treated more definitively with catheter ablation.

It is usually well tolerated initially, but people with other underlying heart disease or poor exercise tolerance may rapidly develop symptoms.

Symptoms include: shortness of breath, chest pain, lightheadedness or dizziness, nausea, nervousness and feelings of impending doom.

In the presence of prolonged atrial flutter with fast heart rates it may lead to ventricular decompensation with heart failure: with exertional breathlessness, nocturnal dyspnea, and edema of the legs.

Overall mortality of atrial fibrillation and atrial flutter conditions appears to be very similar.

The rapid heart rates in atrial flutter may produce symptoms in patients with pre-existing heart disease as it can lead to inadequate blood flow to the heart muscle and even precipitate a heart attack.

Rarely, atrial flutter associated with a fast heart rate that persists can lead to a tachycardia-induced cardiomyopathy.

With atrial flutter there is little effective contraction of the atria and pooling of blood in the atria.

With such stasis formation of a thrombus within the heart can occur.

A thrombus is most likely to form in the atrial appendage, that can embolize with the potentially devastating consequence of a stroke.

Sudden death is not directly associated with atrial flutter, but in patients with a pre-existing accessory conduction pathway, the accessory pathway may conduct activity from the atria to the ventricles at a rate that the AV node would usually block leading to a ventricular rate of 300 beats/minute with a 1:1 conduction.

A 1:1 flutter with time may degenerate into ventricular fibrillation, causing hemodynamic collapse and death.

Atrial flutter significance is dependent on the heart rate of the affected person.

Heart rate is a measure of the ventricular rather than atrial activity.

Atrial impulses are conducted to the ventricles through the atrio-ventricular node (AV node).

In a person with atrial flutter, the atrial chambers of the heart contracting at a rate of 280–300 beats per minute whereas the ventricular chambers of the heart typically beat at a rate of 140–150 beats per minute.

The AV node exerts a protective effect on heart rate, due to its longer refractory period , by blocking atrial impulses in excess of about 180 beats/minute, for the example of a resting heart rate.

This AV node block is dependent on the age of the patient

If the flutter rate is 300/minute only half of these impulses will be conducted, giving a ventricular rate of 150/minute, or a 2:1 heart block.

The addition of rate-controlling drugs or conduction system disease can increase the block rate substantially.

It is recognized on an electrocardiogram by presence of characteristic “flutter waves” at a regular rate of 200 to 300 beats per minute.

Such flutter waves may not be evident on an ECG in atypical forms of atrial flutter.

Flutter waves may be symmetrical, resembling p-waves, or may be asymmetrical with a “sawtooth” pattern.

A Lewis lead ECG may be helpful in revealing flutter waves.

There are two types of atrial flutter, classified as the common type I and rarer type II.

Rarely, a patient may manifest both types, however, they can manifest only one type at a time.

Type I atrial flutter, known as common atrial flutter or typical atrial flutter, has an atrial rate of 240 to 340 beats/minute.

The reentrant loop circles the right atrium, passing through the cavo-tricuspid isthmus.

The cavo-tricuspid isthmus is a body of fibrous tissue in the lower atrium between the inferior vena cava, and the tricuspid valve.

Type I flutter can be divided into counterclockwise atrial flutter and clockwise atrial flutter subtypes depending on the direction of current passing through the loop.

Counterclockwise atrial flutter, also known as cephalad-directed atrial flutter, is more common.

Counterclockwise atrial flutter waves are inverted in ECG leads II, III, and aVF.

In clockwise atrial flutter, thus the flutter waves are upright in II, III, and aVF.

Type II, atypical, atrial flutter follows a significantly different re-entry pathway to type I flutter.

Type II, atypical, atrial flutter is typically faster than type I atrial flutter, usually 340–440 beats/minute.

Type II atypical atrial flutter rarely occurs in people who have not undergone previous heart surgery or previous catheter ablation procedures.

Left atrial flutter is considered atypical and is common after incomplete left atrial ablation procedures.

Atypical atrial flutter originating from the right atrium and heart’s septum have also been described.

Atrial flutter is managed the same as atrial fibrillation.

Most patients with atrial flutter usually require some form of anticoagulation or antiplatelet agent.

Both rhythms can be associated with dangerously fast heart rates and thus require medication to control the heart rate and/or rhythm control with class III antiarrhythmics.

Atrial flutter is more resistant to correction with medications than atrial fibrillation.

Class III antiarrhythmic agent ibutilide is an effective treatment for atrial flutter, but rates of recurrence after treatment are quite high (70–90%).

Atrial flutter is more sensitive to electrical direct current cardioversion than atrial fibrillation.

Cardio version with a shock of only 20 to 50 Joules commonly being enough to cause a return to a normal heart rhythm.

Catheter ablation is considered to be a first-line treatment method for many people with typical atrial flutter due to its high rate of success of greater than 90% and low incidence of complications.

It is performed in a cardiac electrophysiology lab at the site of the cavotricuspid isthmus that crosses the path of the circuit that causes atrial flutter.

Ablation eliminates conduction through the isthmus and prevents reentry, and recurrence of the atrial flutter.

Atrial fibrillation often occurs in about 30% of patients within 5 years, after catheter ablation for atrial flutter.[1]

Like atrial fibrillation is an independent predictor of 2-3 fold increased mortality.

A supraventricular tachycardia.

Much less common than atrial fibrillation with an estimated 200,000 new cases per year.

Atrial flutter is the second most common pathologic supraventricular tachycardia and as a result of reentry circuit around the tricuspid valve in the right atrium.

Atypical atrial flutter occurs primarily in persons who have undergone cardiac surgery or cardiac ablation.

In typical atrial flutter, a macro reentrant circuit conducts flutter waves in a counterclockwise direction around the tricuspid annulus and through the cavotricuspid isthmus, which is in the area between the tricuspid anulus and the inferior vena cava.

The cycle of depolarization result in a characteristic sawtooth flutter pattern in the inferior EKG leads II, III, and aVF.

Diagnosis is based on EKG findings, which demonstrates atrial complexes of constant morphology with a saw tooth baseline pattern.

Initially, there is a slowly downsloping segment of the flutter wave as it passes through the cavotricuspid isthmus followed by a rapidly ascending segment.

In lead V1, and anterior lead, typical flutter waves are upright because of their anterior and superior vector through the right atrium.

Ventricular rate is often close to 150 bpm as the atrioventricular node conduction reaches a ratio of 2:1,

Atrial flutter is in organized regular rhythm generally characterized by an atrial rate of 280-300 bpm and with 2:1 conduction in the AV node resulting in a ventricular rate of 140-150 beats per minute.

Heart rate of 150 suggestive of atrial flutter supraventriculat tachyarrhythmia, and in patients with atrioventricular node disease or who are taking atrioventricular node blocking medications the rate may be slower than 140-150 beats per minute.

Male predominance in one study of 100 patients and 2.5 times more common in another series.

Has many similarities to atrial fibrillation in regard to underlying disease, predisposing factors, complications, and medical management.

Patients can be both atrial flutter and atrial fibrillation.

Eliminating atrial flutter reduces or eliminates episodes of atrial fibrillation.

Left untreated can deteriorate into chronic atrial fibrillation.

Associated with surgically corrected congenital cardiac abnormalities.

Approximately-30% of patients have no cardiac disease.

Often tolerated less well than atrial fibrillation, and is related to its rapid rate and difficulty in controlling ventricular response.

Class 1C antiarrhythmic drugs can organize atrial fibrillation into atrial flutter, and may result in a flutter with the rate that is relatively slow.

Typically atrial flutter rate of 300 beats per minute is associated with a ventricular response rate of 100 beats per minute and is normally associated with three flutter waves per QRS complex (AV conduction ratio 3:1) .

30% of patients have coronary artery disease and 30% have hypertensive heart disease.

Associated with cardiomyopathy, hypoxia, chronic obstructive pulmonary disease, thyrotoxicosis, electrolyte abnormalities, alcohol consumption and pheochromocytoma.

Clinically may go unnoticed, but most often its onset is manifested by palpitations in the chest, which clear when the process is resolved or the rate is controlled.

Initially may be well tolerated, but in patients with underlying heart disease or poor exercise tolerance it may rapidly cause shortness of breath, chest pain, lightheadedness, dizziness, nausea, anxiety of impending doom.

Prolonged flutter may lead to heart failure.

Most common form is type I, classic type, involving a single reentrant circuit with circus activation in the right atrium around the tricuspid valve annulus.

There is an area of slow conduction between the tricuspid valve annulus and the coronary sinus ostium.

Electrocardiogram shows a regular rapid rate of 250-350/min arrhythmia originating in the atria with a rapid succession of identical back to back depolarization waves, giving a saw tooth pattern.

In lead V1, an anterior lead, typical flutter waves are upright because of their anterior and superior vector to the right atrium.

Typical counterclockwise atrial flutter with the familiar sawtooth EKG pattern accounts for about 90% of atrial flutters seen in practice.

Not all atrial beats are transmitted to the ventricles because of the AV node is in a refractory period.

Classic atrial flutter is counterclockwise with caudocranial activation of the atrial septum.

Type II, atypical, atrial flutter may originate from the right atrium or from the left atrium.

Left atrial flutter is common after incomplete left atrial obliteration with resultant faster ventricular rates than seen with atrial fibrillation.

Can lead to a tachycardia induced cardiomyopathy and controlling ventricular rate or returning to a sinus rhythm is important.

May be associated with thromboembolism.

Many with atrial flutter have a faster ventricular rate than those with atrial fibrillation, related to conduction properties of the atrioventricular node.

It is often more difficult to control the heart rate of atrial flutter than with atrial fibrillation.

Attention must be given to non cardiac conditions such as hyperthyroidism, pulmonary disease or cardiac processes that can be corrected with resolution of the process.

Duration of greater than 48 hours anticoagulation is required with warfarin or a Trans esophageal echocardiogram needs to be done to rule out laft atrial thrombus before cardio version to a sinus rhythm.

Atrial flutter can mimic an acute myocardial infarction pattern by deforming the ST segments, especially in the inferior leads.

Atrial flutter can resemble ST segment elevation or depression depending on where the flutter waves fall within the ST segment.

Medications such as beta-blockers and calcium channel blockers can be used to slow heart rate.

Antiarrhythmics may be prescribed to prevent the heart from beating in an abnormal rhythm.

Anticoagulants may help prevent blood clots from forming in the heart.

When medication is unsuccessful, cardiac ablation can control heart rate and rhythm by destroying the abnormal circuit causing atrial flutter.

An anatomically guided procedure directed to isthmuses at the lower part of the right atrium.

Ablation is possible during sinus rhythm.

Type 1 AFl is defined as AFl with atrial rate range between 240 and 340 bpm.

This type of AFl is associated with predominantly negative F waves in the inferior ECG leads.

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