No P waves, no QRS complexes, no T waves: a chaotic undulation of changing size and shape, 4 to 8 per second, with no cardiac output. Defibrillate.
On the trace
The tracing above is acute ischaemia: sinus rhythm, a premature beat on the T, a few beats of polymorphic VT, then VF. It all happens about five seconds into the recording, so watch the first sweep; the finished sheet is all VF. Each recording is new, so your numbers will differ a little.
- Look at the sinus beats first. Sinus rhythm at 75 per minute with a normal QT (QTc about 380 ms).
- Find the trigger. A single wide premature beat lands on the T of a sinus beat, 280 ms after it: R on T.
- Follow what it starts. About a second of very fast polymorphic VT, about 330 per minute, its complexes all different.
- See it break up. The complexes can no longer be picked out: ventricular fibrillation.
- Look for any organised complex. There are no P waves, QRS complexes or T waves, and no repeating pattern, in any lead.
- Judge the size. The undulations are 3 to 8 mm in most leads, largest in V2 and V3: coarse VF. Count them: about 5 to 6 per second.
How to recognise it
| Feature | Value | On this tracing |
|---|---|---|
| P, QRS and T | Absent | None after the onset |
| Rhythm | None: no repeating pattern | Irregular undulations |
| Frequency | 4 to 8 per second | About 5.5 per second |
| Size | Coarse (3 mm or more) early; fine (under 3 mm) later | Coarse, 3 to 8 mm |
| Start | A premature beat on the T, or VT that breaks up | R on T at 280 ms, then polymorphic VT |
| Pulse | Absent |
A trace that looks like VF in a patient with a pulse is artefact: check the patient and the leads.
Mechanism
In VF there is no single wave crossing the ventricles. Many small wavelets turn at once, each round tissue it has just made refractory, colliding and breaking up into new ones. Each activates a small patch of muscle, so the ventricles quiver rather than contract, and output stops at once.
Each wavelet turns at about the recovery time of the tissue it runs in. The outer layer of the wall recovers fastest and the middle layer slowest, so their wavelets turn between about 5 and 8 times a second, and the ECG shows their sum: about 5.5 per second here. Drugs that lengthen recovery, such as sodium-channel blockers, slow VF.
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How it starts here
Minutes after a coronary artery closes, the cells in its territory recover more slowly and unevenly. After each beat there is a short window, near the peak of the T, in which some of the ventricles have recovered and some have not: the vulnerable window. A premature beat in that window conducts into the recovered muscle, blocks at the rest, and comes back round it: re-entry.
In early, mild ischaemia that re-entry turns very fast, faster than the healthy muscle around it can recover. The muscle cannot follow it beat for beat, the wave breaks up, and within a few beats the rhythm is VF. More severe ischaemia gives a slower re-entry that the muscle can follow: sustained polymorphic VT instead. VF clusters in the first minutes of an infarction.
Ischaemic VF on the ECG
Ischaemic VF starts when the ST elevation is at its highest, and its first beat has a very short coupling interval: 305 ± 53 ms (Viskin and colleagues, 2021), as short as in idiopathic VF. Torsades starts with a long one, over 450 to 500 ms.
What makes a ventricle fibrillate
- Acute ischaemia: the commonest. The first sign of coronary disease is often a cardiac arrest from ischaemic VF.
- Structural heart disease: scar, and hypertrophic or dilated cardiomyopathy.
- Torsades de pointes that does not stop, from a long QT.
- Channelopathies in a structurally normal heart: Brugada syndrome, the short QT syndrome, CPVT, and idiopathic VF, from a short-coupled Purkinje trigger.
- Pre-excited AF: an accessory pathway conducting AF at 250 to 300 per minute.
- A blow to the chest on the T wave (commotio cordis), or an electric shock.
Coarse and fine
As the minutes pass, the heart's energy runs down and the waves shrink: coarse becomes fine, and fine becomes asystole. Coarse VF is more likely to be shocked into a perfusing rhythm. Fine VF can look flat in one lead: check a second lead before calling it asystole.
The Hs and Ts
The reversible causes to look for while CPR and shocks continue: hypoxia, hypovolaemia, hydrogen ion (acidosis), hypo- or hyperkalaemia, hypothermia; tension pneumothorax, tamponade, thrombosis (coronary or pulmonary), and toxins.
Clinical impact
High-quality CPR and early defibrillation are the only treatments proven to improve survival to discharge. Survival is several times higher when a bystander starts CPR and an AED is used within minutes.
Management
Defibrillate immediately
VF is shockable. Shock as early as possible, without waiting for IV access, drugs or an airway, then resume CPR at once and reassess after 2 minutes.
High-quality CPR between shocks
100 to 120 compressions a minute, at least 5 cm deep, with full recoil and as few pauses as possible.
Refractory VF: adrenaline, then amiodarone or lidocaine
Adrenaline 1 mg IV every 3 to 5 minutes once shocks have failed. Amiodarone 300 mg IV (then 150 mg) or lidocaine. Do not stop CPR to give drugs.
Ischaemic VF: treat the cause
Urgent coronary angiography after the return of a pulse with ST elevation, or when VF keeps recurring. For recurrent ischaemic VF, guidelines endorse IV beta-blockers and deep sedation, and amiodarone and lidocaine should be considered.
Differential
If QRS complexes can still be picked out, however variable, it is polymorphic VT. Pulseless, the two are treated the same.
A fast torsades run can look like VF. The long QT before it, and the twisting spindle, point to torsades: magnesium after the shock, not amiodarone.
VF from high potassium follows a sine wave, not a premature beat. Give calcium as well as shocks.
Fine VF can look flat in one lead. Confirm in two: any fibrillatory activity in any lead is VF, which is shocked; asystole is not.
References
- Polymorphic Ventricular Tachycardia: Terminology, Mechanism, Diagnosis, and Emergency Therapy — Circulation, 2021
- Part 3: Adult Basic and Advanced Life Support: 2020 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care — Circulation, 2020
- 2022 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death — European Heart Journal, 2022
- Amplitude of ventricular fibrillation waveform and outcome after cardiac arrest — Annals of Internal Medicine, 1985