Atrial Flutter - ECG From Basics To Essentials Step by Step

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244

ATRIAL FLUTTER 1

Atrial flutter (AFL) is a very fast atrial rhythm (240–300 bpm). The atrial flutter rate may
be slower (even < 200 bpm) in the presence of pharmacologic therapy or marked con-
duction delay within the atria. The atrial rhythm is regular and organized. Occasionally it
may coexist with atrial fibrillation and is then called atrial flutter-fibrillation.
The common type of AFL is a macro-reentrant phenomenon in the right atrium in con-
trast to atrial fibrillation which is never sustained by macro-reentry.
There are two types of common flutter: anticlockwise and clockwise. They both engage
the same macro-reentrant pathway in the right atrium but in opposite directions. The
anticlockwise form constitutes about 90% of all atrial flutters and is by far more common
than the clockwise form of common atrial flutter (AFL).

Schematic representation of reentry circuits


Anticlockwise Clockwise

SVC SVC PV

RA
RA
IVC IVC

CS CS

time time

negative flutter waves in the positive flutter waves in the


inferior leads (leads II, III, aVF) inferior leads (leads II, III, aVF)
CS = coronary sinus ; IVC = inferior vena cava ; SVC = superior vena cava ; PV = pulmonary veins

Reentry
All reentrant processes must have an area of slow conduction for sustaining an arrhythmia.
In common AFL the area of slow conduction is in the lower part of the right atrium.
In anticlockwise AFL the depolarization front emerges from the site of slow conduction and
passes along the posterior wall of the right atrium, then upwards along the atrial septum and
then it travels inferiorly along the anterior and lateral wall of the right atrium to its destination
point of origin where it reengages the same macro-reentrant pathway in a self-perpetuating
fashion.
Clockwise (inverse or reverse) AFL takes the identical depolarization pathway but in the
opposite direction.
Common AFL can be cured by catheter ablation of the area or slow conduction in the lower
right atrium (cavotricuspid isthmus between the tricuspid ori ce and the inferior vena cava).
This type of atrial utter is called isthmus dependent.
ECG of the typical AFL
There is a typical sawtooth appearance without isoelectric segments and without P waves.
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The utter waves called “F waves” are inverted in the inferior leads (II, III, aVF) because the
activation moves from the inferior to the superior part of the heart. The F waves are positive in
lead V1. The positive part of the F wave (craniocaudal) lasts longer and is less visible than the
negative portion (inferior to superior). There are no isoelectric segments in the inferior leads.
This pattern is highly predictive of anticlockwise atrial utter.
In clockwise AFL, the utter waves are reversed (i.e. positive) in the inferior leads and
negative in V1. The pattern of clockwise AFL may be impossible to differentiate from that of
atypical AFL.

I
V1
II V2

III V3

aVR V4

aVL
V5
aVF
V6

Atrial utter with varying AV block 2:1, 4:1, etc.


(The atrial rate is 300 bpm and the ventricular rate varies from 150 bpm to 75 bpm)

R R R R R

time

200ms 200ms

AV

V 2/1 4/1 2/1 4/1 4/1


R R R R R
400ms 800ms 800ms

3:1 and 5:1 blocks are possible but are rare.


The diagram shows how the atrial impulses achieve varying degrees of penetration into the AV node
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ATRIAL FLUTTER 2

Diagnosis
The diagnosis is usually easy. A common mistake is to call AFL sinus tachycardia at a
rate of 150 bpm. It is an important clinical rule that a narrow QRS tachycardia at a rate
close to 150 bpm should be considered as being AFL until proven otherwise. With this
concept one can then look for the “hidden” F waves on the T wave. AFL must be
differentiated from other forms of supraventricular tachycardia. Carotid sinus
massage often causes a higher degree of AV block such as 4:1 AV block whereupon
the atrial utter waves are easily recognizable. With the common types of reentrant
supraventricular tachycardia, carotid sinus massage may either terminate the
tachycardia or have no effect. Multifocal atrial tachycardia and atrial tachycardia with
AV block (atrial rate usually < 240 bpm) must be ruled out. If the QRS complex is wide
(functional or stable bundle branch block), AFL at a rate of 150 bpm may mimic
ventricular tachycardia. Artifacts from tremor (as in Parkinson’s disease) may closely
resemble AFL. The ECG should then be taken at the highest points on the extremities.

Atrial flutter rate slowed due to the effect of antiarrhythmic drug

The atrial rate is 220 bpm (slower than classic AFL) and the ventricular rate is 110 bpm.
It is important not to mistake this arrhythmia for sinus tachycardia.
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Atrial flutter (300 bpm) with 2:1 ventricular response (150 bpm)

There is mostly 2:1 AV block. The average irregular ventricular rate is about 150 bpm.
Note that in AFL with 2:1 block the ventricular rate is almost never perfectly regular.
Some atrial impulses are blocked in the AV node. They may travel along the AV node
and are then blocked at various levels within the node while others traverse the AV node
successfully. The atrial impulses blocked in the body of the AV node in uence the con-
duction of subsequent atrial impulses with resultant variations in AV conduction that
cause obvious or subtle irregularity of the ventricular rate.

Effect of Carotid Sinus Massage (CSM) on atrial flutter.


CSM slows the ventricular rate by producing high grade AV block

The ECG suggests anticlockwise AFL at a rate of 250 bpm


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ATRIAL FLUTTER 3

Ventricular rate

The ventricular rate is usually 150 bpm because of 2:1 AV block (i.e. 2 atrial
impulses and 1 ventricular impulse). This is a functional AV block (the tollbooth
effect as a safety or protective mechanism) because the normal AV node can
conduct the atrial impulses on a 1:1 fashion (300 bpm) only in exceptional
circumstances. Such a 1:1 conduction is rare but may occur in patients with an
accessory pathway that bypasses the AV node (no protective mechanism as in the
AV node) or in states of excessive catecholamine (adrenaline) stimulation or even
exercise. Some antiarrhythmic agents can also precipitate 1:1 AV conduction. With
medication with drugs that block AV nodal function the degree of functional block
may increase to 4:1 AV block or periods of 2:1 AV block may occur with periods of
4:1 block. Conduction ratios of 3:1 or 5:1 are unusual. The ventricular rate may be
slow if the patient already has partial or complete AV block.

The tracing shows atrial utter at a rate of about 300 bpm and varying degrees of AV block.
Anticlockwise AFL is ruled out by the pattern in lead II where the F waves are positive. This
is compatible with clockwise AFL but a nonisthmus-dependent AFL cannot be ruled out.
Atrial flutter with complete AV block 249

The escape ventricular rate is 33 bpm

Atypical Atrial Flutter


Atypical AFL may occur in many parts of the heart especially the left atrium. AFL may
also revolve around a scar from previous cardiac surgery or occur after catheter
ablation in the left atrium as for atrial brillation. These utters produce electrocar-
diographic patterns that usually do not resemble those of common AFL in the right
atrium. Indeed, left AFL is often fast, 340–350 bpm, obviously not isthmus-
dependent and behaves like atrial brillation. Finding the origin and mechanism of
these atypical utters requires an invasive electrophysiologic study.

LOWER LOOP UPPER LOOP


REENTRY TACHYCARDIA REENTRY TACHYCARDIA

SVC

SVC

IVC
IVC
CS
A B

INCISIONAL (SCAR) MACRO-REENTRY TACHY-


REENTRY TACHYCARDIA CARDIA in the LEFT ATRIUM

SVC

IVC PV

CS
C D
250
ATRIAL FLUTTER 4

Antiarrhythmic drugs, especially ecainide or propafenone (class 1C), may slow the utter to 200
+/- 20 bpm. A slower atrial rate can change the usual 2:1 AV block (e.g. when the atrial rate is 300
bpm and the ventricular rate is 150 bpm) to 1:1 AV conduction which seems to be a paradoxical
response as far as the ventricular rate is concerned. 1:1 AV conduction may occur if AV nodal
blocking drugs are not administered together with antiarrhythmic agents. A 1:1 AV response may be
blocked by the administration of AV nodal suppressing agents that delay AV nodal conduction.
1:1 AV conduction of ordinary atrial utter is rare. The ventricular rate approaches 300 bpm and
causes aberrant ventricular conduction thereby mimicking ventricular tachycardia. The com-
monest cause of 1:1 AV conduction is an accessory pathway (with a short refractory period) as in
the Wolff-Parkinson-White syndrome. Other patients with an AV node capable of rapid conduction
(due to a bypass tract across part or all of the AV node) may develop 1:1 atrial utter especially in
response to increased sympathetic tone as with exercise. Such patients may have short PR
interval in sinus rhythm. Rapid AV conduction may also occur in hyperthyroidism. Very fast
ventricular rates close to 300 bpm may lead to syncope, hemodynamic collapse and ventricular
brillation.
Coronary Care Unit 251
Keep quiet
It’s simple. I saw the monitor
display a rate of 150 and then
I looked at the patient. As he
was in no distress, I made the
diagnosis of atrial flutter with
2:1 AV block. I ruled out sinus
tachycardia at a rate of 150 in
which case the patient would
have been in distress and ob-
viously very sick. On the other
hand, atrial flutter with 2:1 AV
block and a ventricular rate of
150 (or close to it) may be inter-
How did you make the diagnosis preted as sinus tachycardia.
of atrial flutter from the end of the Remember if an atrial deflec-
bed where you could not possibly tion occurs in the middle of an
see the monitored ECG ? RR interval, there is probably
another atrial deflection buried
inside the QRS complex.

It is important to remember that the ventricular rate in atrial flutter varies slightly. This
is because the atrial impulses achieve varying degrees of penetration in the AV node
before being blocked thereby creating different levels of refractoriness which will
influence AV conduction of subsequent beats. Therefore an absolutely regular ven-
tricular rate may represent a separate AV regular junctional rhythm as in digitalis
toxicity.

On the other side the ECG shows 1:1 atrial utter at a rate of 215 bpm in a patient taking ecainide. At
this fast ventricular rate the QRS complex is different from the one at a slower rate on the right. The
altered QRS morphology is caused by aberrant ventricular conduction at a fast rate. On this page the
ECG shows atrial utter at a rate of 210–215 bpm with 2:1 AV block (ventricular rate of approximately
107 bpm) after administration of an agent that attenuated AV nodal conduction.

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