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Atrial flutter
Classification & external resources

ICD-10	I48.
ICD-9	427.32
DiseasesDB	1072
MedlinePlus	000184
eMedicine	med/185

Atrial flutter is a rhythmic, fast rhythm that occurs in the atria of the heart. This rhythm occurs most often in individuals with organic heart disease (ie: pericarditis, coronary artery disease, and cardiomyopathy).

Atrial flutter is typically not a stable rhythm, and frequently degenerates to atrial fibrillation. However, it may persist for months to years.

Contents 1 Symptoms 2 Mechanism of action 3 Types of atrial flutter 3.1 Type I flutter 3.1.1 Counterclockwise atrial flutter 3.1.2 Clockwise atrial flutter 3.2 Type II flutter 4 Complications 4.1 Clot formation 4.2 Sudden death 5 Treatment 5.1 Ablation 5.2 Rate control 6 References 7 External Links 8 See also

While atrial flutter can sometimes go unnoticed by sufferers, its onset is often marked by characteristic sensations of rapid thumping and palpitations in the chest; such sensations usually last for the entire duration of the episode. Atrial flutter may also be accompanied by shortness of breath, lightheadedness or dizziness, nausea and, in some patients, by nervousness and feelings of impending doom.

Atrial flutter is caused by a reentrant rhythm in either the right or left atrium. Typically initiated by a premature electrical impulse arising in the atria, atrial flutter is initiated due to differences in refractory periods of atrial tissue. This creates a loop of reentry moving along the atrium. Recent studies have shown that patients with typical atrial flutter demonstrate longer refractory periods in the lower right atrial tissue.

There are two types of atrial flutter, known as type I and type II.¹ Most individuals with atrial flutter will manifest only one of these types of atrial flutter. Rarely someone may manifest both types of flutter; however, they can only manifest one type at a time.

Type I atrial flutter, also known as common atrial flutter or typical atrial flutter, has an atrial rate of 240 to 350 beats/minute. However, this rate may be slowed by antiarrhythmic agents.

Type I flutter can be entrained by rapid atrial beating. This means that the re-entrant rhythm of the flutter can be broken if a stimulus enters the re-entrant cycle at just the right point, breaking the cycle and thereby terminating the atrial flutter. While this can be performed with a pacemaker, it is performed almost exclusively in the electrophysiology lab by pacing the atrium at a rate just above the rate of the atrial flutter. While entrainment may break atrial flutter and cause the individual to revert to a normal sinus rhythm, the rapid atrial pacing may cause the individual to go into atrial fibrillation. Type I atrial flutter is increasingly easy to cure in the electrophysiology lab due to its dependence on a fixed anatomic structure known as the isthmus. The isthmus is a body of fibrous tissue that makes up a portion of the reentrant loop. Catheter ablation of the isthmus prevents reentry, and terminates atrial flutter if successful.

Type I flutter has two subtypes, known as counterclockwise atrial flutter and clockwise atrial flutter.

Counterclockwise atrial flutter (known as cephalad-directed atrial flutter) is more commonly seen than clockwise atrial flutter. The flutter waves in this rhythm are inverted in II, III, and aVF.

Clockwise atrial flutter is less common than counterclockwise atrial flutter. The flutter waves are upright in II, III, and aVF in this rhythm.

Type II flutter is faster than type I flutter, and usually is 340–430 beats/minute.

Unlike type I flutter, the rhythm of type II flutter cannot be entrained by rapid atrial pacing.

In atrial flutter, as in atrial fibrillation, there is no effective contraction of the atria. In individuals with structural heart disease, this causes stasis of blood in the atria. The stasis of blood leads to formation of thrombus material (clots) within the heart. In the left side of the heart, thrombus is most likely for form in the left atrial appendage. This is important because, since the left side of the heart supplies blood to the entire body, any thrombus material that dislodges from the left side of the heart can potentially embolize to the brain, causing a stroke. Of course, the thrombus material can also embolize to any other portion of the body.

Sudden death is not directly associated with atrial flutter. However, in individuals with a pre-existing accessory conduction pathway, such as the bundle of Kent in Wolff-Parkinson-White syndrome, the accessory pathway may conduct activity from the atria to the ventricles much faster than the AV node. In this case, the atrial rate of 300 beats/minute will lead to a ventricular rate of 300 beats/minute. If the ventricles are unable to sustain such high ventricular rates, 1:1 flutter may degenerate into ventricular fibrillation, causing hemodynamic collapse and death.

In general, atrial flutter should be treated the same as atrial fibrillation. Both rhythms do not provide effective contraction of the atria. Because of this, there is stasis of blood in the atria. This stasis of blood leads to the potential formation of thrombus material in the atria. Therefore, individuals with atrial flutter require some form of anticoagulation or anti-platelet agent.

In addition to the treatments available to individuals in atrial fibrillation, there are a couple of treatment considerations that are particular to individuals with atrial flutter.

Because of the reentrant nature of atrial flutter, it is possible to ablate the circuit that causes atrial flutter. This is done in the electrophysiology lab by causing a ridge of scar tissue that crosses the path of the circuit that causes atrial flutter. Ablation of the isthmus, as discussed above, is a common treatment for typical atrial flutter.

Control of the ventricular rate in atrial flutter may be more difficult than if the individual was in atrial fibrillation. This is because of properties of the AV node. In atrial fibrillation, the AV node is typically bombarded with signals from the atria at rates in excess of 400 beats/minute. This causes a high degree of block within the AV node, with many signals partially penetrating the node and blocking at the lower levels of the AV node. This phenomenon is known as concealed conduction. The AV node has decremental properties, such that it will permit more electrical signals to pass through at lower frequences. Therefore, in atrial flutter, on the other hand, the AV node receives signals very rhythmically at a rate of about 300/minute compared to > 400/minute in fibrillation. Since the atrial flutter is an organized rhythm of the atria, the block at the AV node will be consistently at the same level, and paradoxically a higher number of impulses will get through per minute.

1. Chou's Electrocardiography in Clinical Practice, Fifth Edition, Surawicz & Knilans, ISBN 0-7216-8697-4
2. Electrophysiologic Testing, Richard N. Fogoros, Blackwell Science, ISBN 0-632-04325-3

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