Atrial flutter

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Atrial flutter produces organised, rapid atrial depolarisation. AV nodal conduction determines the ventricular rate, so the surface rhythm may be regular with fixed block or irregular when the block varies.

The immediate decision is stability. Electrical cardioversion is highly effective and is preferred when life-threatening adverse features are present; a stable patient can undergo rate control and planned rhythm management.

Stroke prevention must be considered separately from symptom relief. Coexistent or future AF is common, and anticoagulation decisions should be based on validated risk assessment and the cardioversion timeline rather than perceived ablation success alone.

Key points

Typical flutter is a macro-re-entrant atrial rhythm, usually circulating around the tricuspid annulus through the cavotricuspid isthmus.
An atrial rate near 300/min with 2:1 AV conduction often produces a very regular ventricular rate near 150/min.
Flutter waves may be concealed in the QRS or T wave; transient AV block can reveal atrial activity but adenosine does not terminate atrial flutter.
Treat instability with a synchronised 70-120 J shock, escalating stepwise if required, with sedation or anaesthesia for a conscious patient where feasible.
Stable management addresses ventricular rate, stroke risk, reversible drivers and a rhythm-control plan.
Assess thromboembolic risk and cardioversion anticoagulation using the AF framework; restoring sinus rhythm does not automatically remove long-term stroke risk.
Cavotricuspid-isthmus ablation is an effective definitive treatment for recurrent or symptomatic typical flutter, but later atrial fibrillation remains possible.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Atrial structural disease

Heart failure, valve disease, chronic lung disease and other causes of atrial enlargement or scar can create conduction barriers that support macro-re-entry. Hypertension and ageing commonly contribute to the broader atrial substrate shared with AF.

Surgery, ablation or congenital anatomy

Atriotomy scars, prior ablation lines and repaired congenital heart disease can form boundaries for atypical flutter circuits, which may not use the cavotricuspid isthmus.

Acute systemic triggers

Thyrotoxicosis, alcohol excess, infection, electrolyte disturbance and recent surgery can precipitate flutter in a susceptible atrium and should be sought alongside rhythm treatment.

Shared substrate with AF

Age, atrial enlargement and fibrosis predispose to both flutter and atrial fibrillation. Either rhythm may precede the other, including after apparently successful flutter ablation.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
A macro-re-entrant circuit forms
In typical flutter, a depolarisation wave rotates around the tricuspid annulus and traverses the cavotricuspid isthmus, using anatomical and functional barriers to sustain the circuit.
2
Rapid organised atrial activation
The circuit depolarises the atria at roughly 300 per minute, producing continuous flutter waves and little effective atrial contraction rather than the chaotic activation of AF.
3
The AV node limits transmission
The AV node commonly conducts every second impulse, giving a regular ventricular rate near 150 per minute. Changing block makes the ventricular rhythm irregular and may mimic AF.
4
Sustained rate impairs the ventricle
Persistent rapid conduction shortens diastolic filling and raises myocardial demand. Over time it can produce or worsen LV systolic dysfunction and clinical heart failure.
5
Thromboembolic risk must be assessed
Reduced atrial mechanical function, underlying atrial disease and frequent coexistent AF can promote left-atrial thrombus, so stroke prevention must be considered separately from symptom or circuit control.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Classic ECG pattern

Continuous atrial activity without an isoelectric baseline gives negative saw-tooth flutter waves in II, III and aVF in typical counter-clockwise flutter.

The 150/min clue

A regular narrow-complex tachycardia close to 150/min should prompt a deliberate search for flutter with 2:1 conduction.

Variable block

Changing AV conduction produces an irregular ventricular response and can be mistaken for atrial fibrillation; organised flutter waves distinguish it.

Symptoms

Palpitations, exertional limitation, dyspnoea, dizziness and fatigue are common; persistent rapid conduction can cause or worsen heart failure.

Adverse featuresRed flag

Shock, severe or ongoing hypotensive syncope, myocardial ischaemia, pulmonary oedema or a post-ROSC state mandate emergency treatment.

Common context

Look for hypertension, heart failure, ischaemic or valvular disease, lung disease, thyrotoxicosis, alcohol excess, recent surgery and acute illness.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
12-lead ECGFirst step
Why
Confirm flutter, AV conduction ratio, QRS width and ventricular rate.
Interpretation and limitations
Atrial activity near 300/min with a fixed or variable conduction ratio supports flutter; compare with prior ECGs for onset and recurrence.
02
Continuous ECG monitoring
Why
Detect changing conduction, pauses after conversion and associated atrial fibrillation.
Interpretation and limitations
Very rapid 1:1 conduction is dangerous and can be precipitated by some antiarrhythmics without AV nodal protection.
03
U&Es, magnesium, FBC and thyroid function
Why
Find reversible triggers and establish safety for rate/rhythm drugs.
Interpretation and limitations
Correct hypokalaemia or hypomagnesaemia and treat thyroid or systemic disease.
04
Transthoracic echocardiogram
Why
Assess atrial size, LV function and structural or valvular disease.
Interpretation and limitations
LV impairment may be tachycardia-mediated and influences drug choice and urgency.
05
TOE when indicated before cardioversion
Why
Exclude left atrial appendage thrombus when an early imaging-guided cardioversion strategy is chosen.
Interpretation and limitations
Thrombus precludes immediate elective cardioversion; anticoagulate and repeat assessment according to the specialist plan.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Sinus tachycardia

Sinus rate usually changes gradually with physiology and each QRS has a consistent preceding sinus P wave. A fixed narrow-complex rate near 150 should prompt a search for flutter.

AVNRT or AVRT

These AV-node-dependent regular tachycardias usually have no continuous saw-tooth atrial activity and may terminate with adenosine. In flutter, transient AV block may instead reveal continuing atrial activity without terminating the circuit.

Atrial fibrillation

AF has no organised repeating atrial waveform and is irregularly irregular. Flutter with variable block remains irregular but retains a consistent macro-re-entrant atrial pattern.

Focal or multifocal atrial tachycardia

Focal tachycardia has discrete abnormal P waves from one site; multifocal tachycardia has at least three P-wave morphologies. Both typically retain an isoelectric baseline, unlike continuous typical flutter.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01unstableEmergency flutterFirst stepFlutter is accompanied by a life-threatening adverse feature.

1Perform ABCDE assessment, attach pads and monitoring, obtain IV access and call for expert resuscitation/anaesthetic help.
2For a conscious patient, provide carefully titrated sedation or anaesthesia if this does not delay treatment or worsen haemodynamics.
3EscalationDeliver a synchronised biphasic shock at 70-120 J; confirm synchronisation is enabled and escalate energy stepwise if unsuccessful.
4If up to three shocks fail and instability persists, give RCUK procainamide 10-15 mg/kg IV over 20 minutes (maximum 1 g) or amiodarone 300 mg IV over 10-20 minutes, then repeat synchronised cardioversion.

02stableStable ventricular-rate controlNo life-threatening adverse feature is present.

1Confirm the rhythm and assess LVEF, blood pressure, comorbidity and reversible causes.
2Use a beta-blocker for rate control when appropriate; if LVEF is above 40%, verapamil, diltiazem or digoxin are conditional alternatives, while reduced LVEF narrows choices to a beta-blocker or digoxin.
3Assess CHA2DS2-VASc stroke risk and bleeding risk and offer anticoagulation when indicated; do not use aspirin as a substitute.
4Arrange cardiology/electrophysiology review for rhythm control, especially when symptoms persist or rate control is difficult.

03cardioversionPlanned restoration of sinus rhythmRhythm control is selected without emergency instability.

1Establish onset and duration and assess anticoagulation status and thrombus risk.
2If duration exceeds 48 hours or is uncertain, use at least 3 weeks of therapeutic anticoagulation before cardioversion, or a specialist TOE-guided strategy when earlier treatment is justified.
3Perform synchronised cardioversion with appropriate sedation/anaesthesia and monitoring.
4Continue post-cardioversion anticoagulation for the required period and decide long-term treatment from stroke risk, not simply the apparent rhythm.

04definitiveTypical-flutter ablationPreferredDefinitiveTypical flutter is recurrent, symptomatic, drug-intolerant or a durable rhythm strategy is preferred.

1Refer to electrophysiology and confirm that the circuit is cavotricuspid-isthmus dependent.
2Discuss radiofrequency ablation, procedural risks and the possibility of later AF.
3Maintain peri-procedural anticoagulation as directed by the rhythm and stroke-risk plan.
4After successful ablation, reassess symptoms and rhythm but do not stop anticoagulation solely because flutter is no longer visible.

Key medicines and prescribing safety2 treatments · regimens, roles and cautions

Ventricular-rate control in stable flutter when a beta-blocker is appropriate.

Bisoprolol

5 mg by mouth once daily is the cited SmPC starting dose for hypertension or angina; ventricular-rate control in atrial flutter is off-label for this product. Titrate to response, often using a lower initial dose in frail patients or heart failure.

Avoid or reduce in symptomatic bradycardia, hypotension, high-grade AV block without pacing or decompensated heart failure; do not stop abruptly.

One DOAC option when anticoagulation is indicated and there is no mechanical valve or moderate-to-severe rheumatic mitral stenosis.

Apixaban

5 mg by mouth twice daily is the licensed dose for eligible NVAF. When used for isolated flutter under the NICE AF/flutter stroke-risk framework, treatment is guideline-directed but outside the cited product's NVAF indication. Reduce to 2.5 mg twice daily when at least two apply: age 80 years or older, weight 60 kg or less, serum creatinine 133 micromol/L or more; for NVAF, also use 2.5 mg twice daily when Cockcroft-Gault creatinine clearance is 15-29 mL/min regardless of the two-of-three rule.

Check Cockcroft-Gault renal function, bleeding risk and interactions. Apixaban is not recommended by the cited SmPC when creatinine clearance is below 15 mL/min or during dialysis. Dose reduction is criteria- or severe-renal-impairment-based, not a general response to age alone.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Tachycardia-mediated cardiomyopathy

Persistent rapid ventricular activation can depress LV systolic function, causing breathlessness and congestion. Ventricular function may improve substantially after durable rate or rhythm control.

Stroke and systemic embolism

Atrial mechanical dysfunction and coexistent AF permit thrombus formation and embolisation. Successful circuit ablation does not itself prove that long-term thromboembolic risk has disappeared.

Hypotension, ischaemia or pulmonary oedema

Rapid conduction can critically reduce filling and raise oxygen demand, especially in structural heart disease, producing haemodynamic instability that requires urgent synchronised cardioversion.

Recurrent flutter or later AF

The underlying atrial substrate persists even after conversion. Atypical circuits can recur, and subsequent atrial fibrillation remains common enough to justify continued rhythm and stroke-risk review.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Track ventricular rate at rest and with activity, symptoms and evidence of heart failure.
Repeat ECG after rate or rhythm treatment to document conduction, QT/QRS effects and post-conversion bradycardia.
Monitor blood pressure and for bradycardia after AV-nodal blocking treatment.
For anticoagulation, review renal function, haemoglobin, bleeding, adherence and interactions at clinically appropriate intervals.
After ablation, remain alert for atrial fibrillation and reassess stroke and bleeding risk rather than assuming cure eliminates risk.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Adenosine is diagnostic, not curative

Transient AV block may unmask flutter waves, but the atrial circuit continues. Do not repeatedly escalate adenosine expecting flutter termination.

Regular does not mean SVT

Fixed 2:1 flutter can be strikingly regular. A ventricular rate near 150/min is the classic examination clue.

Shock energy differs by rhythm

Current RCUK guidance starts atrial flutter at 70-120 J, lower than VT with a pulse at 120-150 J and unlike AF, for which maximum defibrillator output is a reasonable initial strategy.

Ablation and anticoagulation answer different questions

Ablation treats the circuit; anticoagulation prevents thromboembolism. The latter depends on stroke risk and coexistent AF.

Look for tachycardia-mediated cardiomyopathy

LV dysfunction may improve after durable rate or rhythm control, so document baseline and follow-up ventricular function.

11Common pitfallsFrequent interpretation and management errors.

01
Calling a regular narrow tachycardia at 150/min sinus tachycardia without examining atrial activity.
02
Using adenosine repeatedly as though it will terminate flutter.
03
Delaying synchronised cardioversion in an unstable patient to complete non-essential tests.
04
Stopping anticoagulation after apparent ablation success without reassessing stroke risk and AF history.
05
Combining AV-nodal blocking drugs without monitoring for hypotension, bradycardia or heart block.