VT whose frontal axis flips with every beat, about 150 per minute, from digoxin toxicity: two fixed shapes in strict alternation at a regular rate.
On the trace
The tracing above is digoxin toxicity. Each recording is new, so your numbers will differ a little.
- Look at II, III and aVF in a run. One beat points down, the next up, the next down: the axis flips with every beat. In this run it swings between about −80° and +140°.
- Look at I and aVL. They flip too, the other way round from III and aVF.
- Look at V1. An R wave in both shapes, a right bundle branch block-like pattern; one of the two also has a deep S.
- Measure the QRS. About 140 ms: wide, but narrower than most VT. The beats start in the conduction system.
- Measure the R-R in a run. About 400 ms, regular: about 150 per minute. Two shapes, one rate.
- Look between the runs. A slow sinus rhythm (about 60 per minute) with a long, lengthening PR and dropped beats, or narrow junctional beats at about 80 per minute: digoxin acts on the nodes too.
How to recognise it
| Feature | Value | On this tracing |
|---|---|---|
| QRS shapes | Two, alternating every beat | Axis about −80° and +140° |
| Rhythm | Regular in the run | R-R about 400 ms |
| Rate | 140 to 180 per minute | About 150 per minute |
| QRS width | 120 to 150 ms | About 140 ms |
| V1 | Right bundle branch block-like | An R in both shapes; one with a deep S |
| QT on the sinus beats | Normal | QT 379 ms at 60 per minute |
| Between runs | Digoxin's other effects | Sinus about 60, Wenckebach, junctional beats at about 80 |
Mechanism
Digoxin blocks the sodium-potassium pump. Sodium builds up inside the cell, and the sodium-calcium exchanger, which normally removes calcium, brings it in instead. A little extra calcium strengthens contraction: that is digoxin's therapeutic effect. At a toxic level the cell's calcium store overloads and releases calcium during diastole. The release drives an inward current, a delayed afterdepolarisation (DAD), and if it reaches threshold the cell fires: a triggered beat.
Each fast triggered beat loads the store further, so the next DAD is likelier: the beats come in runs. In the left bundle's network of fascicles, two sites take turns. A beat from one site reaches the other just as its store is ready to fire, and that beat reaches the first in turn: a ping-pong (Baher and colleagues, 2011). A beat from near the posterior fascicle reaches the rest of the left ventricle through the anterior one late, and looks like right bundle branch block with left anterior fascicular block. A beat from near the anterior fascicle looks like right bundle branch block with left posterior fascicular block. So the axis flips with every beat.
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Digoxin on the nodes
Digoxin also increases vagal action on the sinus and AV nodes: a slow sinus rate, a long PR, Wenckebach. Its calcium loading speeds up the AV junction, giving an accelerated junctional rhythm. AV block with an accelerated junctional rhythm, or a regular slow rhythm in someone with AF, is digoxin toxicity until proven otherwise.
Who becomes toxic
Kidney failure (digoxin is cleared by the kidneys), old age, low potassium and magnesium (which make the pump more sensitive to digoxin), and interacting drugs (amiodarone, verapamil, macrolides) raise the level or its effect.
CPVT, the other cause
In catecholamine-sensitive polymorphic VT, an inherited defect makes the calcium store leak. With exercise or emotion, the same DADs give the same bidirectional VT, in a child or young adult with a normal resting ECG and no digoxin (Viskin and colleagues, 2021).
Clinical impact
Bidirectional VT in a patient on digoxin means a dangerous level, whatever the laboratory result.
Management
Give the antidote
Digoxin-specific antibody fragments (Fab) for a ventricular arrhythmia in digoxin toxicity. They act within minutes.
Stop digoxin, correct the electrolytes
Stop the drug. Correct potassium and magnesium; low levels make the toxicity worse.
Be careful with shocks
A shock can tip the digoxin-toxic heart into VF that will not convert. Use it if the patient is pulseless or unstable and the antidote is not at hand, at the lowest effective energy.
No digoxin: think CPVT
Bidirectional VT with exercise or stress, in a normal heart, is CPVT: sedation, beta-blockers and flecainide.
Differential
Changes shape every beat too, but at random, with no repeating pair, at an irregular rate. Bidirectional VT has exactly two shapes in strict alternation.
The other cause: the same alternation, with exercise or emotion, in a normal heart with no digoxin.
Regular too, but every complex is the same. Two clearly different shapes alternating every beat make it bidirectional.
Changes gradually, in a spindle, on a long QT. Bidirectional VT flips every beat, and the QT is normal.
References
- Polymorphic Ventricular Tachycardia: Terminology, Mechanism, Diagnosis, and Emergency Therapy — Circulation, 2021
- Bidirectional ventricular tachycardia: ping pong in the His-Purkinje system — Heart Rhythm, 2011
- 2022 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death — European Heart Journal, 2022