TextbookCardiologyVentricular Fibrillation

Ventricular Fibrillation

Chaotic, disorganised ventricular electrical activity producing no effective cardiac output. A shockable cardiac arrest rhythm requiring immediate defibrillation.

Key Facts

ECG: chaotic, irregular waveform with no identifiable QRS complexes, varying amplitude and frequency Clinical: cardiac arrest — no pulse, no cardiac output, loss of consciousness Treatment: immediate defibrillation (unsynchronised shock 150-200J biphasic) — single most important intervention Every minute delay in defibrillation reduces survival by ~7-10% Commonest initial arrest rhythm in out-of-hospital cardiac arrest (~25%); most common cause of SCD ALS algorithm: CPR → shock → CPR 2 min → shock; amiodarone 300mg IV after 3rd shock Most common cause: acute myocardial ischaemia/infarction Survival to discharge: ~8-10% for out-of-hospital VF arrest; better with bystander CPR + early defibrillation

Overview

Key Facts

Ventricular fibrillation (VF) is a chaotic cardiac rhythm originating from multiple re-entrant circuits within the ventricles, resulting in no coordinated ventricular contraction and therefore no cardiac output. It is invariably fatal without immediate defibrillation.

Epidemiology

  • ~60,000 out-of-hospital cardiac arrests (OHCA) per year in the UK
  • VF/pulseless VT is the initial rhythm in ~25% of OHCA (declining proportion)
  • Overall OHCA survival to discharge: ~8-10%
  • VF/pVT has the best prognosis of all arrest rhythms if defibrillated promptly
  • Bystander CPR doubles survival; immediate defibrillation can achieve >50% survival

Aetiology

  • Acute myocardial ischaemia/infarction: most common cause
  • VT degeneration: sustained VT → VF
  • Reversible causes (4Hs and 4Ts): hypoxia, hypovolaemia, hypo/hyperkalaemia, hypothermia, thrombosis (coronary/PE), tension pneumothorax, tamponade, toxins
  • Inherited conditions: long QT syndrome, Brugada, CPVT, HCM, ARVC
  • Electrolyte abnormalities: hypokalaemia, hypomagnesaemia
  • Drug toxicity: proarrhythmic drugs, cocaine, digoxin

Pathophysiology

  • Multiple re-entrant wavelets propagating chaotically through ventricular myocardium
  • No organised depolarisation → no coordinated contraction → no cardiac output
  • Brain damage begins within 3-5 minutes without perfusion
  • Degenerates from coarse VF → fine VF → asystole over time without treatment
  • Defibrillation simultaneously depolarises the entire myocardium, allowing the sinus node to resume control

Clinical Presentation

Presentation

  • Sudden loss of consciousness
  • No pulse (cardiac arrest)
  • No breathing or agonal gasps only
  • Rapidly progresses to death without intervention

Preceding Symptoms (if witnessed)

  • Chest pain (ischaemia)
  • Palpitations
  • Dizziness or syncope
  • Dyspnoea
  • May occur without any warning

Settings

  • Out-of-hospital: home, public places (community AEDs)
  • In-hospital: coronary care, cath lab, emergency department
  • Exercise-related: suspect HCM, ARVC, LQTS, anomalous coronary artery
  • Post-MI: highest risk in first 48 hours

Red Flags

  • Any cardiac arrest is a red flag requiring immediate action
  • Family history of sudden cardiac death in young (<40 years)
  • Prior syncopal episodes with exertion
  • Known structural heart disease or channelopathy

Differential Diagnosis

DiagnosisKey FeaturesInvestigation
Pulseless VTOrganised wide-complex rhythm on monitor, no pulseCardiac monitor/ECG
AsystoleFlat line (confirm in 2 leads)Cardiac monitor
PEAOrganised rhythm on monitor but no pulseCardiac monitor, echo
Fine VF vs asystoleVery low amplitude VF may mimic asystoleAdjust gain, check 2 leads
ArtefactMovement/loose lead mimicking VFClinical assessment

Diagnosis / Investigation

Bedside (during resuscitation)

  • Cardiac monitor/defibrillator: rhythm analysis — confirms VF
  • ABG: pH, K⁺, lactate, oxygenation
  • Point-of-care USS: cardiac activity, tamponade, PE, LV function
  • Capnography: ETCO₂ monitoring during CPR (confirms ETT placement, guides CPR quality, ROSC detection)

Bloods (post-ROSC)

  • Troponin: MI assessment
  • U&Es: K⁺, Mg²⁺ — correct abnormalities
  • FBC, glucose, lactate: metabolic status
  • Coagulation: DIC screen
  • Toxicology: if drug-related arrest suspected

Imaging (post-ROSC)

  • Coronary angiography: urgent if STEMI or suspected ACS
  • CT head: if neurological deficit
  • CTPA: if PE suspected
  • Echocardiography: LV function, structural abnormalities

Special Tests (post-ROSC)

  • Cardiac MRI: scar assessment, viability
  • EP study: inducibility testing
  • Genetic testing: if suspected channelopathy or familial condition

Management

Non-pharmacological

Immediate (ALS algorithm):

  1. Confirm cardiac arrest: unresponsive, no normal breathing
  2. Call for help, start CPR 30:2 (100-120 compressions/min, 5-6cm depth)
  3. Attach defibrillator → rhythm analysis
  4. VF confirmed: deliver unsynchronised shock (150-200J biphasic)
  5. Resume CPR immediately for 2 minutes (do not pause to check rhythm)
  6. Rhythm check at 2 minutes → shock if still VF
  7. Continue cycle: CPR 2 min → shock → CPR 2 min → shock

Pharmacological (during ALS)

  • After 3rd shock: amiodarone 300mg IV bolus (diluted in 5% dextrose)
  • After 5th shock: amiodarone 150mg IV bolus
  • Adrenaline 1mg IV every 3-5 minutes (after 3rd shock in VF/pVT; immediately in non-shockable rhythms)
  • Address reversible causes: 4Hs and 4Ts
  • Correct K⁺ >4.0 mmol/L, Mg²⁺ >1.0 mmol/L

Post-ROSC (return of spontaneous circulation):

  • Targeted temperature management: 32-36°C for ≥24 hours (TTM2 trial: 33°C vs 36°C — no difference)
  • Coronary angiography: if STEMI or suspected ACS — emergent PCI
  • ICU management: ventilation, haemodynamic support, seizure management
  • Neuroprognostication: at ≥72 hours post-ROSC (multimodal approach)

Surgical/Interventional

  • Emergency PCI: if acute coronary occlusion
  • ICD implantation: secondary prevention if survived VF arrest with treatable cause excluded
    • Wait ≥40 days post-MI; ≥3 months after revascularisation
  • VT ablation: if recurrent VT/VF with identifiable substrate
  • Wearable cardioverter-defibrillator (LifeVest): bridge to ICD decision

Referral Criteria

  • All cardiac arrest survivors: ICU, cardiology review
  • Consider referral to specialist inherited cardiac conditions service if young, structurally normal heart
  • Family screening if inherited condition suspected

Prognosis

  • Overall OHCA survival to discharge: ~8-10%
  • VF/pVT arrest: best prognosis of all arrest rhythms (~25-30% survival if promptly defibrillated)
  • Every minute delay in defibrillation reduces survival by 7-10%
  • Bystander CPR doubles survival
  • Neurological outcome: ~50% of survivors have good neurological recovery (CPC 1-2)
  • In-hospital VF arrest: survival ~40-50%
  • Post-MI VF (within 48h): does not independently worsen long-term prognosis if revascularised
  • Late VF (>48h post-MI or with structural disease): ICD indicated, high recurrence risk without

Other Relevant Information

ALS Shockable Rhythm Algorithm Summary

StepAction
1CPR 30:2 while defibrillator attached
2Rhythm check: VF/pVT confirmed
3Shock 1 (150-200J biphasic)
4CPR 2 minutes
5Shock 2
6CPR 2 minutes
7Shock 3 + Amiodarone 300mg IV + Adrenaline 1mg IV
8CPR 2 minutes, continue cycles
9Shock 5 + Amiodarone 150mg IV

Reversible Causes (4Hs and 4Ts)

4Hs4Ts
HypoxiaThrombosis (coronary)
HypovolaemiaThrombosis (PE)
Hypo/HyperkalaemiaTension pneumothorax
HypothermiaTamponade (cardiac)