Atrial flutter

Atrial flutter (AFL) is an abnormal heart rhythm thatoccurs in the atria of the heart.[1] When it first oc-curs, it is usually associated with a fast heart rate ortachycardia (beats over 100 per minute),[2] and falls intothe category of supra-ventricular tachycardias. While thisrhythm occurs most often in individuals with cardiovas-cular disease (e.g. hypertension, coronary artery disease,and cardiomyopathy) and diabetes, it may occur sponta-neously in people with otherwise normal hearts. It is typi-cally not a stable rhythm, and frequently degenerates intoatrial fibrillation (AF). However, it does rarely persist formonths to years.Atrial flutter was first identified as an independentmedicalcondition in 1920 by the British physician Sir ThomasLewis (1881–1945) and colleagues.[3]

1 Signs and symptoms

While atrial flutter can sometimes go unnoticed, its on-set is often marked by characteristic sensations of regularpalpitations. Such sensations usually last until the episoderesolves, or until the heart rate is controlled.Atrial flutter is usually well tolerated initially (a high heartrate is for most people just a normal response to exercise),however, people with other underlying heart disease orpoor exercise tolerance may rapidly develop symptoms,which can include shortness of breath, chest pains, light-headedness or dizziness, nausea and, in some patients,nervousness and feelings of impending doom.Prolonged fast flutter may lead to decompensation withloss of normal heart function (heart failure). This maymanifest as effort intolerance (exertional breathlessness),nocturnal breathlessness, or swelling of the legs or ab-domen.Atrial flutter is recognized on an electrocardiogram bypresence of characteristic flutter waves at a regular rate of240 to 440 beats per minute. Individual flutter waves maybe symmetrical, resembling p-waves, or may be asym-metrical with a “sawtooth” shape, rising gradually andfalling abruptly or vice versa. If atrial flutter is suspectedclinically but is not clearly evident on ECG, acquiring aLewis lead ECGmay be helpful in revealing flutter waves.

2 Pathophysiology

Atrial flutter is caused by a reentrant rhythm in eitherthe right or left atrium. Typically initiated by a prema-ture electrical impulse arising in the atria, atrial flutteris propagated due to differences in refractory periods ofatrial tissue. This creates electrical activity that moves ina localized self-perpetuating loop. For each cycle aroundthe loop, there results an electric impulse that propagatesthrough the atria.The impact and symptoms of atrial flutter depend on theheart rate of the patient. Heart rate is a measure of theventricular rather than atrial activity. Impulses from theatria are conducted to the ventricles through the atrio-ventricular node. Due primarily to its longer refractoryperiod, the AV node exerts a protective effect on heartrate by blocking atrial impulses in excess of about 180beats/minute, for the example of a resting heart rate.(This block is dependent on the age of the patient, andcan be calculated roughly by subtracting patient age from220). If the flutter rate is 300/minute only half of theseimpulses will be conducted, giving a ventricular rate of150/minute, or a 2:1 heart block. The addition of rate-controlling drugs or conduction system disease can in-crease this block substantially (see image below).

3 Classification

There are two types of atrial flutter, the common type Iand rarer type II.[4]Most individuals with atrial flutter willmanifest only one of these. Rarely someonemaymanifestboth types; however, they can only manifest one type at atime.

3.1 Type I

Type I atrial flutter, also known as common atrial flut-ter or typical atrial flutter, has an atrial rate of 240 to340 beats/minute. However, this rate may be slowed byantiarrhythmic agents.The reentrant loop circles the right atrium, passingthrough the cavo-tricuspid isthmus - a body of fibrous tis-sue in the lower atrium between the inferior vena cava,and the tricuspid valve. Type I flutter is further dividedinto two subtypes, known as counterclockwise atrialflutter and clockwise atrial flutter depending on the di-rection of current passing through the loop.

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2 5 COMPLICATIONS

Type I atrial flutter, counterclockwise rotation with 3:1 and 4:1AV nodal block.

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

• The re-entry loop cycles in the opposite direction inclockwise atrial flutter, thus the flutter waves are up-right in II, III, and aVF.

Catheter ablation of the isthmus is a procedure usuallyavailable in the electrophysiology laboratory. Eliminatingconduction through the isthmus prevents reentry, and ifsuccessful, prevents the recurrence of the atrial flutter.

3.2 Type II

Type II flutter follows a significantly different re-entrypathway to type I flutter, and is typically faster, usually340-440 beats/minute.[5] Left atrial flutter is common af-ter incomplete left atrial ablation procedures.

4 Management

In general, atrial flutter should be managed the same asatrial fibrillation. Because both rhythms can lead to theformation of thrombus in the atria, individuals with atrialflutter usually require some form of anticoagulation oranti-platelet agent. Both rhythms can be associated withdangerously fast heart rate and thus require medicationfor rate and or rhythm control. Additionally, there aresome specific considerations particular to treatment ofatrial flutter.

4.1 Cardioversion

Atrial flutter is considerably more sensitive to electricaldirect-current cardioversion than atrial fibrillation, andusually requires a lower energy shock. 20-50J is com-monly enough to revert to sinus rhythm. Conversely, it

is relatively resistant to chemical cardioversion, and oftendeteriorates into atrial fibrillation prior to spontaneous re-turn to sinus rhythm. Exact placement of the pads doesnot appear important.[6]

4.2 Ablation

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

5 Complications

Although often regarded as a relatively benign rhythmproblem, atrial flutter shares the same complications asthe related condition atrial fibrillation. There is paucityof published data directly comparing the two, but overallmortality in these conditions appears to be very similar.[7]

5.1 Rate related

Rapid heart rates may produce significant symptoms inpatients with pre-existing heart disease. Even in patientswhose hearts are normal to start with, prolonged tachy-cardia tends to produce ventricular decompensation andheart failure.

5.2 Clot formation

Because there is little if any effective contraction of theatria there is stasis (pooling) of blood in the atria. Stasisof blood in susceptible individuals can lead to formationof thrombus (blood clots) within the heart. Thrombus ismost likely to form in the atrial appendages. Clot in theleft atrial appendage is particularly important since theleft side of the heart supplies blood to the entire body.Thus, any thrombus material that dislodges from this sideof the heart can embolize to the brain, with the potentiallydevastating consequence of a stroke. Thrombus materialcan of course embolize to any other portion of the body,though usually with a less severe outcome.

5.3 Sudden cardiac death

Sudden death is not directly associated with atrial flut-ter. However, in individuals with a pre-existing accessoryconduction pathway, such as the bundle of Kent inWolff-Parkinson-White syndrome, the accessory pathway mayconduct activity from the atria to the ventricles at a ratethat the AV node would usually block. Bypassing the AV

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node, the atrial rate of 300 beats/minute leads to a ven-tricular rate of 300 beats/minute (1:1 conduction). Evenif the ventricles are able to sustain a cardiac output atsuch a high rates, 1:1 flutter with time may degenerateinto ventricular fibrillation, causing hemodynamic col-lapse and death.

6 References[1] Atrial flutter at Mount Sinai Hospital

[2] "atrial flutter" at Dorland’s Medical Dictionary

[3] Lewis T, Feil HS, Stroud WD (1920). “Observationsupon flutter, fibrillation, II: the nature of auricular flutter”.Heart 7: 191.

[4] Surawicz, Borys; Knilans, Timothy K.; Chou, Te-Chuan(2001). Chou’s electrocardiography in clinical practice:adult and pediatric. Philadelphia: Saunders. ISBN 0-7216-8697-4.

[5] “Atrial Flutter: Overview - eMedicine Cardiology”.Archived from the original on 26 February 2009. Re-trieved 2009-03-06.

[6] Kirkland, S; Stiell, I; AlShawabkeh, T; Campbell, S; Dick-inson, G; Rowe, BH (July 2014). “The efficacy of padplacement for electrical cardioversion of atrial fibrilla-tion/flutter: a systematic review.”. Academic emergencymedicine : official journal of the Society for AcademicEmergency Medicine 21 (7): 717–26. PMID 25117151.

[7] Vidaillet H, Granada JF, Chyou PH, Maassen K, Ortiz M,Pulido JN, et al., “A Population-Based Study of Mortal-ity among Patients with Atrial Fibrillation or Flutter” TheAmerican Journal of Medicine 2002 Oct 1;113(5):365-70.PMID 12401530. doi:10.1016/S0002-9343(02)01253-6

4 7 TEXT AND IMAGE SOURCES, CONTRIBUTORS, AND LICENSES

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