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Atrial Flutter, Multifocal Atrial Tachycardia & Premature Beats

Name: Atrial Flutter, Multifocal Atrial Tachycardia & Premature Beats
Creator: Veli Bakalov, MD

Sawtooth at 150, three P waves in sick lungs, and when extra beats matter

Cardiology·Arrhythmias & Conduction·5 min read·9 high-yield points·Reviewed by Veli Bakalov, MD @HemeOncBuddy

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Typical flutter = counterclockwise cavotricuspid-isthmus reentry at ~300 bpm with negative sawtooth F waves in II, III, aVF (positive in V1); 2:1 block gives a regular rate of ~150, 4:1 gives ~75.
A regular narrow-complex tachycardia at exactly 150 is flutter until proven otherwise: vagal maneuvers or adenosine unmask the F waves without terminating the rhythm.
Class IC drugs (flecainide, propafenone) can slow flutter enough for 1:1 conduction, so always pair them with an AV-nodal blocker.
Unstable flutter → synchronized cardioversion at low energy; rate control is difficult, so rhythm control is often preferred.
Anticoagulate flutter exactly like AF: CHA2DS2-VASc ≥2 in men or ≥3 in women; for ≥48 h or unknown duration, 3 weeks of anticoagulation or TEE before cardioversion and ≥4 weeks after.
Cavotricuspid isthmus ablation cures more than 90% of typical flutter and is first-line for recurrent episodes; AF often develops later.
MAT = irregular rhythm >100 bpm with ≥3 P-wave morphologies in acutely ill lung patients: treat hypoxemia and the cause, give magnesium, stop theophylline, use verapamil or diltiazem; cardioversion does not work and no anticoagulation is needed.
PACs and PVCs in a structurally normal heart are benign: check K, Mg, TSH, and an echo, remove stimulants, and use a β-blocker for symptoms; avoid class IC drugs after MI (CAST).
A PVC burden above ~10–15% can cause a reversible cardiomyopathy; catheter ablation of the focus (often the RV outflow tract) is most effective.

Atrial flutter: mechanism and recognition

One big loop. Typical atrial flutter is a macroreentrant circuit that spins counterclockwise around the tricuspid annulus in the right atrium, passing through the cavotricuspid isthmus. The atria fire at about 250–350 bpm (classically 300). Flutter occurs with structural heart disease, COPD, recent cardiac surgery, and preexisting atrial fibrillation.

ECG. Negative sawtooth F waves in II, III, and aVF (positive in V1), with no flat baseline between them. The AV node cannot conduct every impulse, so the ventricular rate depends on the block ratio:

~300atrial rate in typical flutter

~150ventricular rate with 2:1 block (most common)

~75ventricular rate with 4:1 block

A regular rate of 150 is flutter until proven otherwise. With 2:1 block, every other F wave hides inside the QRS or T wave, so the rhythm is easily mistaken for sinus tachycardia or another SVT. Vagal maneuvers (such as carotid sinus massage) or IV adenosine during continuous ECG recording briefly deepen AV block and unmask the sawtooth. This diagnoses flutter without ending it, because the circuit lies entirely in the atrium. Variable block makes the ventricular rhythm irregular.

Class IC drugs (flecainide, propafenone) can slow the flutter circuit to about 200 bpm, slow enough for the AV node to conduct 1:1. The result is a very fast, wide-complex rhythm, so a class IC drug is always paired with an AV-nodal blocker (β-blocker, diltiazem, or verapamil).

Managing atrial flutter

Unstable (hypotension, ischemia, shock, acute heart failure)Synchronized cardioversion. Flutter converts at low energy, often 50–100 J or less.
Stable: rate or rhythmRate control with β-blockers, diltiazem or verapamil, or digoxin is harder than in AF, because the rate jumps between fixed ratios (150 → 75) instead of slowing smoothly. Rhythm control (cardioversion, ibutilide, dofetilide, ablation) is often preferred.
Anticoagulate as for AFDecide by CHA₂DS₂-VASc and follow the pericardioversion rules.
Recurrent or symptomatic typical flutterCavotricuspid isthmus (CTI) ablation.

Stroke prevention. Stroke risk in flutter resembles AF, so the same rules apply. Using CHA₂DS₂-VASc (heart failure, hypertension, age ≥75 [2 points], diabetes, prior stroke or TIA [2 points], vascular disease, age 65–74, female sex), anticoagulate at a score of ≥2 in men or ≥3 in women and consider it at 1 in men or 2 in women. A DOAC is preferred over warfarin unless there is a mechanical valve or moderate-to-severe mitral stenosis.

Cardioversion. For flutter lasting 48 hours or more, or of unknown duration, either give 3 weeks of anticoagulation first or do a TEE to exclude atrial thrombus, then continue anticoagulation for at least 4 weeks afterward. Rapid atrial overdrive pacing, for example through epicardial wires after cardiac surgery, can also terminate typical flutter.

CTI ablation. A linear lesion across the cavotricuspid isthmus interrupts the circuit with more than 90% success. It is first-line for recurrent or symptomatic typical flutter and is often preferred over long-term antiarrhythmic drugs such as amiodarone. Many patients develop AF later, so stroke-risk assessment continues after ablation.

Multifocal atrial tachycardia

Definition. An irregularly irregular rhythm above 100 bpm with at least three distinct P-wave morphologies in one lead, varying PR and P–P intervals, and an isoelectric baseline between P waves. It mimics AF, but discrete P waves are visible. Below 100 bpm the same pattern is called wandering atrial pacemaker.

Who gets it. Older, acutely ill patients: COPD exacerbation, hypoxemia or hypercapnia, pneumonia, pulmonary embolism, heart failure, or sepsis. Theophylline toxicity, β-agonists, hypomagnesemia, and hypokalemia increase atrial automaticity; check the theophylline level in a patient who takes it.

Treat the lungs, not the rhythm. Correct hypoxemia and treat the exacerbation, stop theophylline, and give IV magnesium (helpful even when the level is normal) and potassium. If the rate stays fast, use verapamil or diltiazem, or a β₁-selective blocker if there is no bronchospasm; nonselective propranolol can worsen COPD. Cardioversion, antiarrhythmics, digoxin, and adenosine are ineffective, and MAT itself needs no anticoagulation.

Cardioversion fails in MAT because the rhythm comes from several automatic atrial foci, not a single reentrant circuit that a shock can reset.

Flutter, MAT, and atrial fibrillation

Feature	Typical flutter	MAT	Atrial fibrillation
Mechanism	Single right-atrial reentry loop	Multiple automatic atrial foci	Chaotic atrial activity
Atrial activity	Sawtooth F waves, ~300 bpm	≥3 distinct P waves, varying PR	No organized P waves; fibrillatory baseline
Ventricular rhythm	Regular (irregular if block varies)	Irregularly irregular	Irregularly irregular
Driver	Structural heart disease, surgery, COPD	Lung disease, hypoxemia, theophylline	Atrial remodeling: age, hypertension, valve disease
Cardioversion	Works at low energy	Ineffective	Works
Anticoagulation	By CHA₂DS₂-VASc	Not for MAT itself	By CHA₂DS₂-VASc

Premature atrial and ventricular beats

PACs vs PVCs

Feature	PAC	PVC
ECG	Early, differently shaped P wave; narrow QRS	Early wide QRS with no preceding P wave
Pause	Usually less than compensatory (resets the sinus node)	Usually a full compensatory pause
Clinical weight	Benign in a normal heart; may herald AF	Benign in a normal heart; high burden can weaken the LV

Triggers and workup. Caffeine, alcohol, nicotine, stimulants and decongestants, sleep loss, stress, low potassium or magnesium, and hyperthyroidism all provoke ectopy. Evaluate with an ECG, a Holter monitor to measure burden, potassium, magnesium, TSH, and an echocardiogram. In bigeminy, every other beat is a weak early beat, so the pulse may feel slow or "skipped" despite a normal electrical rate.

Structurally normal heart. Isolated PACs and PVCs are benign. Reassure, cut back caffeine, alcohol, and stimulants, and correct electrolytes. For bothersome palpitations use a β-blocker (or a non-dihydropyridine calcium channel blocker). Avoid class IC drugs after MI: they raised mortality in the CAST trial.

PVC-induced cardiomyopathy. Very frequent PVCs, above about 10–15% of all beats on Holter, can cause a reversible cardiomyopathy. Suspect it when the ejection fraction falls with no other cause after coronary disease, scar, and infiltration are excluded. Catheter ablation of the focus, often in the right ventricular outflow tract, is the most effective therapy, with β-blockers or amiodarone as alternatives, and the EF often normalizes. Flecainide is avoided when EF is reduced, and because the cardiomyopathy is reversible, it is not by itself an indication for an ICD.