What is theAtrial flutter
Atrial flutter (AFL) is an abnormal heart rhythm that occurs
in the atria of the heart.
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When it first occurs, it is usually associated
with a fast heart rate or tachycardia (beats over 100 per minute),
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and falls into the category of supra-ventricular
tachycardias. While this rhythm occurs most often in individuals with
cardiovascular disease (e.g. hypertension, coronary artery disease, and
cardiomyopathy) and diabetes, it may occur spontaneously in people with
otherwise normal hearts. It is typically not a stable rhythm, and frequently
degenerates into atrial fibrillation (AF). However, it does rarely persist for
months to years.
Atrial flutter was first identified as an independent
medical condition in 1920 by the British physician Sir Thomas Lewis (1881–1945) and colleagues.[3]
There are two types of atrial flutter, the common type I and
rarer type II.Most individuals with atrial flutter will manifest only one of
these. Rarely someone may manifest both types; however, they can only manifest
one type at a time.
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Type I
Type I atrial flutter, counterclockwise rotation with 3:1
and 4:1 AV nodal block.
Type I atrial flutter, also known as common atrial flutter
or typical atrial flutter, has an atrial rate of 240 to 340 beats/minute.
However, this rate may be slowed by antiarrhythmic agents.
The reentrant loop circles the right atrium, passing through
the cavo-tricuspid isthmus - a body of fibrous tissue in the lower atrium
between the inferior vena cava, and the tricuspid valve. Type I flutter is
further divided into two subtypes, known as counterclockwise atrial flutter and
clockwise atrial flutter depending on the direction of current passing through
the loop.
Counterclockwise
atrial flutter (known as cephalad-directed atrial flutter) is more commonly
seen. The flutter waves in this rhythm are inverted in ECG leads II, III, and
aVF.
The re-entry loop
cycles in the opposite direction in clockwise atrial flutter, thus the flutter
waves are upright in II, III, and aVF.
Catheter ablation of the isthmus is a procedure usually
available in the electrophysiology laboratory. Eliminating conduction through
the isthmus prevents reentry, and if successful, prevents the recurrence of the
atrial flutter.
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Type II
Type II flutter follows a significantly different re-entry
pathway to type I flutter, and is typically faster, usually 340-440
beats/minute. Left atrial flutter is common after incomplete left atrial
ablation procedures.
Management
In general, atrial flutter should be managed the same as
atrial fibrillation. Because both rhythms can lead to the formation of thrombus
in the atria, individuals with atrial flutter usually require some form of
anticoagulation or anti-platelet agent. Both rhythms can be associated with
dangerously fast heart rate and thus require medication for rate and or rhythm
control. Additionally, there are some specific considerations particular to
treatment of atrial flutter.
Cardioversion
Atrial flutter is considerably more sensitive to electrical
direct-current cardioversion than atrial fibrillation, and usually requires a
lower energy shock. 20-50J is commonly enough to revert to sinus rhythm.
Conversely, it is relatively resistant to chemical cardioversion, and often
deteriorates into atrial fibrillation prior to spontaneous return to sinus
rhythm.
Ablation
Because of the reentrant nature of atrial flutter, it is
often 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.
Complications
Although often regarded as a relatively benign rhythm
problem, atrial flutter shares the same complications as the related condition
atrial fibrillation. There is paucity of published data directly comparing the
two, but overall mortality in these conditions appears to be very similar.[6]
Rate related
Rapid heart rates may produce significant symptoms in
patients with pre-existing heart disease. Even in patients whose hearts are
normal to start with, prolonged tachycardia tends to produce ventricular
decompensation and heart failure.
Clot formation
Because there is little if any effective contraction of the
atria there is stasis (pooling) of blood in the atria. Stasis of blood in
susceptible individuals can lead to formation of thrombus (blood clots) within
the heart. Thrombus is most likely to form in the atrial appendages. Clot in
the left atrial appendage is particularly important since the left side of the
heart supplies blood to the entire body. Thus, any thrombus material that
dislodges from this side of the heart can embolize to the brain, with the
potentially devastating consequence of a stroke. Thrombus material can of
course embolize to any other portion of the body, though usually with a less
severe outcome.
Sudden cardiac death
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 at a rate that the AV
node would usually block. Bypassing the AV node, the atrial rate of 300
beats/minute leads to a ventricular rate of 300 beats/minute (1:1 conduction).
Even if the ventricles are able to sustain a cardiac output at such a high
rates, 1:1 flutter with time may degenerate into ventricular fibrillation,
causing hemodynamic collapse and death.
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