Focal Atrial Tachycardia
Focal Atrial Tachycardia
A regular narrow-complex tachycardia driven by one ectopic atrial focus, with an abnormal P before every QRS and a flat baseline between them.
On the trace
Read the strip in this order.
- Rate and regularity.
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160 bpm, and the R-R interval barely moves: every beat lands within a millisecond or two of the last. - Find the P wave.
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There is one before every QRS, and in lead II it points downward. A sinus P points up in this lead. Inverted means the atria were driven from the bottom upward, so the focus sits low in the atrium. - Look at the line between the waves.
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It returns flat and stays flat, for about 75 ms between the P and the QRS it produces. This is the most useful thing on the strip: flutter has no flat segment anywhere, because a circuit sweeps the atrium continuously. - Measure the QRS.
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76 ms, well under 120. Below the atria nothing has changed. - Notice where the P sits.
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About 150 ms before the QRS it produces, and 250 ms after the one before it: closer to the beat it causes than to the beat that came before. That makes this a long RP tachycardia.
How to recognise it
| Feature | Value | Notes |
|---|---|---|
| Rate | 100–250 bpm | Occasionally up to 300. 160 here. |
| Rhythm | Regular | Irregularity suggests multifocal AT or fibrillation. |
| P wave | One abnormal P before every QRS | Its shape differs from sinus because the impulse does not start at the SA node. |
| P wave axis | Points back to the focus | Upright inferiorly means a high focus; inverted, as here, means a low one. Left versus right atrium needs leads I, aVL and V1. |
| Baseline | Isoelectric between P waves | The finding that rules out flutter. |
| PR interval | Normal, 120 ms or more | About 124 ms here. Short or absent PR points at a junctional rhythm. |
| QRS | Narrow, under 120 ms | Unless bundle branch block widens it, which does not change the mechanism. |
The strip
Mechanism
The impulse starts somewhere other than the sinus node, so it crosses the atria by a different route. That is the whole reason the P wave changes shape. Nothing below the atria is involved, so the impulse still descends normally and the QRS stays narrow.
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Background
Focal atrial tachycardia occurs in structurally normal hearts as readily as in diseased ones.
Why the focus wins
Whichever pacemaker fires fastest sets the rhythm, and the sinus node normally wins by being quickest at 60 to 100 beats per minute. A focus running at 160 reaches threshold first every time. It depolarises the atria before the sinus node can, and the sinus node stays silent for as long as the tachycardia lasts. Nothing is blocked and nothing is damaged: the sinus node is simply outpaced, and it resumes the moment the focus stops.
What the P shape reports
The P wave is the summed direction of atrial depolarisation, so its shape says where that depolarisation began. About two thirds of foci sit in the right atrium, most often along the crista terminalis or the tricuspid annulus, and about a third in the left, typically at a pulmonary vein or the mitral annulus. Finding that one point on a map of the atrium is exactly what makes ablation curative: there is a single spot to destroy rather than a circuit to interrupt.
What this strip does not show
The simulation runs at a steady 160 bpm. A real focal AT is usually automatic rather than re-entrant, so it tends to speed up over the first few beats and slow down before it stops, instead of switching on and off abruptly the way AVNRT does. That warm-up and cool-down is a genuine diagnostic clue and it is not reproduced here.
Adenosine
Focal AT often survives adenosine where AVNRT and AVRT terminate. Even when it does not stop the rhythm, the transient AV block it produces is useful: it strips the QRS complexes away and leaves the atrial activity exposed, which usually settles the diagnosis.
Clinical impact
Left ventricular function usually recovers once the rhythm is controlled. That is the argument for treating the arrhythmia definitively, rather than settling for rate control, in anyone whose tachycardia is close to continuous.
Management
Unstable: cardiovert now
Hypotension, ischaemic chest pain, acute heart failure or altered mental state mean synchronised cardioversion, without waiting for a firm rhythm diagnosis.
Stable: adenosine, as much to see as to treat
6 mg by rapid IV push, then 12 mg if needed. It may terminate the tachycardia; if it does not, the AV block it causes exposes the atrial activity.
Stable: rate and rhythm control
An IV beta-blocker, or diltiazem or verapamil. Drugs have limited efficacy in most patients with AT. Class Ic agents such as flecainide can work, but not where there is structural heart disease.
Definitive: catheter ablation
Ablation targeting the site of earliest activation is the preferred rhythm-control approach for symptomatic focal AT, and is advised for incessant AT with cardiomyopathy. Treat the reversible triggers alongside it: alcohol, catecholamine excess, digoxin toxicity.
Differential
Flutter has a continuous sawtooth baseline with no flat segment anywhere. Focal AT has discrete P waves separated by a flat line, which is what step 3 looks for.
The sinus P is upright in lead II, and the rate climbs and falls with demand rather than switching on at a fixed rate.
Both can show an inverted P close to the QRS. The PR interval decides it: normal in atrial tachycardia, short or absent in a junctional rhythm.
AVNRT buries its retrograde P inside the QRS, so no P is visible at all. Focal AT shows one before every complex.
References
- Management of patients with atrial tachycardia: a clinical consensus statement of the European Heart Rhythm Association (EHRA) of the ESC — EP Europace, 2025
- 2019 ESC Guidelines for the management of patients with supraventricular tachycardia — European Heart Journal, 2020
- 2015 ACC/AHA/HRS Guideline for the Management of Adult Patients With Supraventricular Tachycardia — Circulation, 2016