ecgsweep

Ventricular Fibrillation

critical
Lead II
25 mm/s10 mm/mV
HR—bpm
RR—
QT—

Chaotic, disorganised ventricular electrical activity with no identifiable complexes and no cardiac output: the most common immediate cause of sudden cardiac death.

Updated

On the trace

Read the strip in the order it happens, then act.

Try each step, then check it.
  1. Find the trigger.
    Show A few sinus beats, then an R-on-T PVC (the arrow): the usual start in acute ischaemia.
  2. See what replaces the rhythm.
    Show No P waves, no QRS complexes, no T waves: an irregular, chaotic undulation with no repeating pattern. Any organised complex means it is not VF.
  3. Judge the amplitude.
    Show Coarse VF has most waves 3 mm (0.3 mV) or taller. Leave the simulation running: over the next few minutes the waves shrink to fine VF, as the myocardium runs out of energy. Replay starts it coarse again.
  4. Check a second lead before calling a flat-looking trace asystole.
    Show Fine VF can look flat in one lead.

How to recognise it

FeatureValueNotes
RhythmNoneChaotic, with no repeating pattern.
RateNot measurableSeveral hundred irregular waves a minute, but no beats.
P, QRS and TAbsentNo identifiable complexes of any kind.
AmplitudeCoarse early, fine lateCoarse: most waves ≥ 3 mm (0.3 mV), recent onset, more likely to shock. Fine: < 3 mm, prolonged arrest.
PulseAbsentThe clinical definition. A VF-like trace with a pulse is artefact: check the patient.

The strip

Thirty seconds of lead II in which sinus rhythm degenerates into ventricular fibrillation, drawn by the simulator. Work through the steps above on it, in the order it happens.

Mechanism

Instead of one wavefront sweeping the ventricles, many unstable re-entrant wavelets form, collide and break up continuously, each activating a small patch of muscle. The ventricles quiver rather than contract, and output stops at once.

The usual trigger is an R-on-T PVC during acute ischaemia. Ischaemic tissue recovers unevenly, so a premature impulse finds re-entrant paths wherever it turns, and once enough wavelets exist the fibrillation sustains itself. As the minutes pass, energy stores run down and the waves get smaller: coarse becomes fine, and fine becomes asystole.

Go deeper

What makes a ventricle fibrillate

  • Acute ischaemia: the commonest substrate, which is why VF clusters at the onset of infarction.
  • Structural heart disease: scar, hypertrophic or dilated cardiomyopathy give fixed slow-conduction zones; VF can occur at rest without an obvious trigger.
  • Channelopathies: long and short QT, Brugada syndrome and CPVT cause VF in structurally normal hearts. A young survivor with no structural cause needs evaluating for all of them.

The Hs and Ts

The reversible causes to look for while CPR and shocks continue:

  • Hypoxia: secure the airway and oxygenate early.
  • Hypovolaemia: in trauma, stop the bleeding.
  • Hydrogen ion (acidosis): bicarbonate has a place in severe acidosis or hyperkalaemia.
  • Hypo- or hyperkalaemia: IV calcium for hyperkalaemia.
  • Hypothermia: VF may not convert until the core is rewarmed.
  • Tension pneumothorax: needle decompression.
  • Tamponade: pericardiocentesis.
  • Thrombosis, coronary: angiography after ROSC, or during refractory VF where ECPR is available.
  • Thrombosis, pulmonary: consider thrombolysis during CPR.
  • Toxins: digoxin, tricyclics, cocaine and others need specific treatment.

Time is survival

High-quality CPR and early defibrillation are the only interventions proven to improve survival to discharge. Survival falls by roughly 10% for every minute without a shock, and is several times higher when a bystander starts CPR and an AED is used within minutes, which is why public-access defibrillators exist.

Clinical impact

Many re-entrant wavelets replace organised ventricular activation
No coordinated contraction: cardiac output stops at once
Consciousness is lost within about 10–20 seconds; brain injury begins within minutes without CPRCardiac Arrest
Untreated, VF decays from coarse to fine, then to asystoleDeath

Management

1

Defibrillate immediately

VF is shockable. Shock as early as possible (120–200 J biphasic, or 360 J monophasic), without waiting for IV access, drugs or an airway, then resume CPR at once and reassess after 2 minutes.

2

High-quality CPR between shocks

100–120 compressions a minute, at least 5 cm deep, full recoil, minimal interruptions. Every pause in compressions lowers the chance of ROSC.

3

Refractory VF: adrenaline and amiodarone

Adrenaline 1 mg IV every 3–5 minutes once shocks have failed. Amiodarone 300 mg IV (then 150 mg) improves survival to admission, though not proven to improve neurologically intact survival. Do not stop CPR to give drugs.

4

After ROSC: find the cause

12-lead ECG at once (STEMI goes to the catheterisation laboratory), electrolytes, blood gas, troponin and echocardiography; temperature control if comatose. Survivors without a reversible cause need assessment for an ICD and channelopathy testing.

Differential

Torsades de Pointes

A fast torsades run can look like VF. The sinus beats before it show a long QT, and the full run shows a spindle. It matters because torsades needs magnesium and amiodarone makes it worse; when pulseless, both are shocked.

Polymorphic Ventricular Tachycardia

If discrete QRS complexes can be picked out, however variable, it is polymorphic VT rather than VF. Pulseless, the two are treated the same.

Asystole

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

  1. 2019 AHA Focused Update on Advanced Cardiovascular Life Support: Use of Advanced Airways, Vasopressors, and Extracorporeal Cardiopulmonary Resuscitation During Cardiac Arrest — Circulation, 2019
  2. 2022 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death — European Heart Journal, 2022
  3. Amplitude of ventricular fibrillation waveform and outcome after cardiac arrest — Annals of Internal Medicine, 1985