One wave circles the right atrium near 300 times a minute. The baseline becomes a sawtooth, and the AV node conducts every second, third or fourth wave.
On the trace
The tracing above is untreated typical flutter with 2:1 conduction. Turn on the Normal switch under the tracing to draw a normal ECG in grey behind it. Every grey beat has a P wave. No trace beat has one.
- Measure the ventricular rate. 150 per minute, regular, R-R 400 ms. A regular, narrow rhythm at 150 is flutter until you prove it is not.
- Look at the baseline in II, III and aVF. It is never flat. A sawtooth runs under the whole strip, about 2.5 mm from peak to trough.
- Look at one wave in II. A slow fall of about 90 ms, then a steep rise to a sharp peak and a quick fall, about 50 ms each. At 2:1 every second peak lands on the T, so the T looks narrow and peaked.
- Look at V1 and V2. Upright flutter waves with flat segments between them, about 2 mm.
- Measure the flutter cycle. One wave every 200 ms: 300 per minute. The waves do not stop for the QRS.
- Count the flutter waves for each QRS. Two. One is hidden in the QRS. The other lands on the T. That is 2:1, and it is why the sawtooth is easy to miss.
- Measure the QRS. 96 ms, narrow, with a normal axis of 59°.
- Look for the T. It is buried in the flutter waves: you cannot measure the QT. The readout shows a dash for the QT and QTc.
How to recognise it
| Feature | Value | On this tracing |
|---|---|---|
| Atrial rate | 250 to 350 per minute in typical flutter | 300 |
| Flutter waves | A continuous sawtooth in II, III and aVF, its slow limb falling; upright in V1 and V2 | 2.5 mm in II, 2 mm in V2 |
| P waves | Absent | None |
| Conduction ratio | 2:1 untreated; 4:1 or variable (2:1 to 4:1) with AV node block | 2:1 |
| Ventricular rate | The atrial rate divided by the ratio | 150 |
| QRS | Narrow, unless there is a bundle branch block or aberrancy | 96 ms |
The 2015 ACC/AHA/HRS and 2019 ESC guidelines describe typical flutter by these features.
Mechanism
One wave of activation turns round the tricuspid valve in the right atrium. In typical flutter it goes up the septum and down the free wall (counter-clockwise, seen from below). Each lap passes through the cavotricuspid isthmus, where conduction is slow. One lap takes about 200 ms.
The wave never meets tissue it has just left, because the circuit is longer than the wavelength. There is always an excitable gap ahead of it. The atria are never at rest, so there is no P wave and no flat baseline.
The AV node cannot follow 300 waves a minute. Its refractory period sets how many waves it blocks between the waves it conducts. The ratio is always a whole number, so the ventricular rate is 300 divided by 1, 2, 3 or 4.
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Why 2:1 untreated
The AV node meets the flutter waves at two levels. Its upper level is refractory for about 280 ms. That is longer than one flutter cycle (200 ms) and shorter than two (400 ms). So it passes every second wave: 2:1.
AV nodal drugs act mainly on the lower level. As they depress it, it starts to block some of the waves the upper level passes. First it blocks one now and then, so the ratio changes between 2:1 and 4:1. Then it blocks every second one: 4:1. That is why even ratios are much more common than odd ones.
Reading the wave
Each part of the flutter wave in II is a part of the lap. The slow fall is the wave in the cavotricuspid isthmus. The steep part is the wave going up the septum and across to the left atrium. The rise is the wave coming down the free wall of the right atrium.
Unmasking the sawtooth
A vagal manoeuvre or adenosine blocks the AV node for a few seconds. The QRS complexes move apart and the flutter waves appear between them. The flutter does not stop, because its circuit does not use the AV node.
Clockwise flutter
The same circuit can turn the other way. The sawtooth then rises slowly in II, III and aVF, and the flutter waves are negative in V1. It is treated in the same way.
Class IC drugs and 1:1
Flecainide and propafenone slow conduction in the atria, so the flutter becomes slower. A slower flutter can fall into a range the AV node can follow 1:1, especially with exercise. Give an AV nodal blocker with these drugs. The 1:1 form beside the title shows this.
Variable block can look like atrial fibrillation
Variable block gives an irregular, narrow rhythm, often at about 100 per minute. That is what most readers expect of atrial fibrillation. Look at the baseline: flutter waves repeat exactly, and the R-R intervals are whole numbers of flutter cycles. The AV node can also go through Wenckebach cycles of its own, which makes groups of beats that repeat. Group beating in an irregular, narrow rhythm also points away from atrial fibrillation.
The difference changes the treatment. Typical flutter is cured by a line of ablation across the cavotricuspid isthmus. Atrial fibrillation needs pulmonary vein isolation. A patient with the wrong diagnosis gets the wrong procedure.
The drugs
- Class IA and IC drugs (for example flecainide) seldom convert flutter, and a class IC drug can cause 1:1 conduction (above).
- Ibutilide or dofetilide given IV converts about half to three quarters of patients within an hour. They prolong the QT and can cause torsades.
- In randomised trials, isthmus ablation keeps patients in sinus rhythm better than antiarrhythmic drugs.
Flutter and atrial fibrillation
Many patients with flutter also have, or later develop, atrial fibrillation. New typical flutter makes atrial fibrillation about five times more likely over ten years. After isthmus ablation, about a quarter of patients who never had atrial fibrillation develop it. Without treatment, flutter comes back in about half of patients within five years. The stroke risk is the same as in atrial fibrillation, and anticoagulation follows the same rules, whatever the rhythm is today.
Clinical impact
Rate control is harder than in atrial fibrillation. An AV nodal drug moves the rhythm from one whole-number ratio to the next, not smoothly.
Management
Unstable: synchronised cardioversion
Flutter usually converts with low energy, because the circuit is organised. Cardioversion is a reasonable first choice in a stable patient too.
Expose the rhythm when the diagnosis is not clear
Use a vagal manoeuvre or adenosine. The block shows the flutter waves. It does not stop the flutter.
Control the rate
Give a beta-blocker, diltiazem or verapamil. Rate control is often difficult. Ibutilide or dofetilide can convert flutter, but monitor the QT.
Ablate the isthmus, and assess the stroke risk
Catheter ablation of the cavotricuspid isthmus cures most typical flutter. Decide anticoagulation by the same score as for atrial fibrillation.
Differential
Also regular and narrow, often at 150 to 200. There is no activity between the QRS complexes. Adenosine usually stops them. It does not stop flutter.
Discrete P waves with a flat baseline between them, because one focus fires and then stops. A flutter circuit never stops.
A baseline that never repeats, and an irregularly irregular rhythm. Flutter waves repeat exactly, and the R-R intervals are whole numbers of flutter cycles.
A P wave before each QRS, upright in II, with a flat baseline after the T. The rate changes gradually, and seldom stays at exactly 150.
References
- 2015 ACC/AHA/HRS Guideline for the Management of Adult Patients With Supraventricular Tachycardia — Circulation, 2016
- 2019 ESC Guidelines for the management of patients with supraventricular tachycardia — European Heart Journal, 2020
- 2023 ACC/AHA/ACCP/HRS Guideline for the Diagnosis and Management of Atrial Fibrillation — Circulation, 2024