Focal Atrial Tachycardia
cautionFocal Atrial Tachycardia
Focal atrial tachycardia is a regular narrow-complex tachycardia driven by a single ectopic focus in the atria that fires faster than the sinus node and takes over from it. It occurs in structurally normal hearts as readily as in diseased ones, and most episodes are paroxysmal - symptomatic, but not dangerous in themselves.
Every QRS is preceded by an INVERTED P wave.
The atria are being driven from the bottom upward, so the wave of depolarisation travels away from the positive electrode of lead II and inscribes downward instead of up.
The baseline between P waves is flat.
A single focus fires discretely and the atrium falls silent between beats, leaving a true isoelectric segment. A re-entrant circuit would instead sweep the atrium continuously with nothing flat between.
Each P falls late in the cycle, nearer the QRS it produces than the one before it.
The focus fires on its own schedule and the AV node conducts promptly, so a short P-to-QRS delay is followed by a long gap - a long RP tachycardia.
- Rate100-250 bpmOccasionally up to 300.
- RhythmRegular
- P waveOne abnormal P before every QRSIts shape differs from sinus because the impulse does not start at the SA node.
- P wave axisPoints to the focusUpright inferiorly means a high atrial focus; inverted, as here, means a low one. Left versus right atrium needs leads I, aVL and V1 - a single lead cannot tell you.
- BaselineIsoelectric between P waves
- PR intervalNormal (120 ms or more)
- QRSNarrow (under 120 ms)Unless there is pre-existing or rate-related bundle branch block, which widens it without changing the mechanism.
Because the impulse starts somewhere other than the sinus node, it spreads across the atria along a different path - which is the whole reason the P wave changes shape. Everything below the atria is untouched, so the impulse still descends through the AV node and His-Purkinje system and the QRS stays narrow.
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Whichever pacemaker fires fastest sets the rhythm, and the sinus node normally wins simply by being quickest at 60-100 beats per minute. An atrial focus running at 160 reaches threshold first every time: it depolarises the atria before the sinus node can, and the sinus node is held silent for as long as the tachycardia lasts. Nothing is blocked and nothing is damaged - the sinus node is just outpaced, and it resumes the moment the focus stops.
The P wave is only the summed direction of atrial depolarisation, which is why its shape reports where that depolarisation began: start the wave somewhere else and it travels a different way across the atria, and every lead sees the change. 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 starting 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.
Left ventricular function usually recovers once the rhythm is controlled, which is the argument for definitive treatment rather than rate control alone in anyone whose tachycardia is near-continuous.
Unstable - cardiovert
Hypotension, ischaemic chest pain, acute heart failure or altered mental state: synchronised cardioversion now. Do not wait for a rhythm diagnosis.
Stable - adenosine
6 mg rapid IV push, then 12 mg if needed. It blocks the AV node and exposes the P waves, which usually settles the diagnosis.
Stable - rate and rhythm control
IV beta-blocker, or a non-dihydropyridine calcium-channel blocker (diltiazem or verapamil). If those fail: flecainide, sotalol or amiodarone - avoid class Ic agents where there is structural heart disease.
Definitive - catheter ablation
First-line curative therapy for symptomatic, sustained or incessant AT, with drug therapy downgraded in recent consensus. Treat the reversible triggers alongside it: alcohol, catecholamine excess, digoxin toxicity.
Flutter has a continuous sawtooth baseline with no isoelectric segment anywhere; focal AT has discrete P waves separated by a flat line.
The sinus P is upright in lead II, and the rate climbs and falls with physiological 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.