ventricular fibrillation (VF)

see also:

• BLS and ALS for Mx of cardiac arrest
• ventricular tachycardia (VT)
• return of spontaneous circulation (ROSC) post-arrest

• VF is most likely to occur in the ischaemic heart with either electrolyte imbalance, local acidosis or sympathetic stimulation (hence the obsession with electrolytes, rest, stress reduction and early commencement of beta adrenergic blockers in the acute coronary syndrome patient)
• common causes include:
  • acute coronary thrombosis causing acute severe ischaemia or infarct
  • post-infarct acute inflammation
    • a peptide resistin-like molecule γ (Retnlg or RELMγ), an antimicrobial pore-forming peptide derived from recruited neutrophils, destabilizes heart rhythm by binding to and attacking stressed cardiomyocytes - once bound, the peptide punctures the cardiomyocyte membranes, creating pores that alter cellular ion flux, triggering delayed depolarization, cell death, and the formation of tissue abnormalities that promote arrhythmia ¹⁾
  • exertion in a patient with critical coronary stenosis (eg. Wellen's syndrome)
  • severe metabolic derangements
  • certain overdoses - particularly medications with sympathomimetic activity, including local anaethetic toxicity
• VF may arise in synchronised DC reversion if machine confuses R waves for T waves as may occur in patients with AF due to pre-excitation syndromes including WPW
• a rare cause is commotio cordis - a hard object such as a baseball or another player hitting the chest of an otherwise healthy person during a critical 15msec interval of the cardiac cycle (1% of the cycle), reliably results in VF. Presumably this was the cause of this young footballer's arrest after a bump to the chest during a game, and the French fitness model Rebecca Burgess when she was struck in the chest by an exploding nitrous oxide powered whipped cream canister.
• a patient may remain conscious in VF if they have a left ventricular assist device (LVAD) in situ to pump the blood mechanically and thus retain sufficient cardiac output for the brain

• attempt defibrillation ASAP
  • prepare for defibrillation:
    • open patient's clothing to expose chest
    • ensure skin site is clean and dry
    • check for physical and electrical hazards:
      • GTN patch or ointment - remove and clean skin to avoid explosions or burns
      • permanent pacemakers - place pad 2.5cm below the scar
      • ensure no intervening ECG electrodes or monitor leads in the way
      • oxygen cylinders should be at least 1m away
      • water spillages or body fluids may conduct electricity - remove and dry area
      • hairy chest may prevent effective contact of pads - may need to clip hair (avoid shaving as may result in burns)
    • apply one pad on right anterior chest wall just below right clavicle and the other on lower left lateral chest wall
    • ensure pads are adherent with no wrinkles or air bubbles
    • pacing pads can remain for up to 8 hours
    • gel pads for use with paddles need to be changed after 3 defibrillation shocks
    • if using paddles, ensure no direct contact with patient skin
    • once defibrillator joules has been set, press the charge button on the paddles and state clearly “Charging”.
    • call “Stand clear” loudly and distinctly before defibillation
    • When safe to do so press both shock buttons, keeping the paddles firmly on the patient’s chest until the shock is discharged.
  • single shock unless witnessed arrest, then give up to 3 stacked shocks
  • defibrillation:
    • monophasic 360J in adults
    • biphasic truncated devices - 200J is default for adults but some manufacturers (eg. Philips) advise 150J with their machines
    • rectilinear biphasic machines - 120 J for adults
    • paediatric initial defibrillation dose is 2 J/kg first dose and then 4 J/kg
• add good CPR for 5 cycles without checking for pulse, then re-check rhythm
• attempt defibrillation again - single shock
• give 1mg or 10mcg/kg in children adrenaline / epinephrine iv/io (followed by 20-30ml normal saline flush) or ETT, and repeat every 4 minutes of cardiac arrest until return of spontaneous circulation.
  • or vasopressin 40 U once IV or IO to replace first or second dose of adrenaline (has longer half life of 10-20 minutes)
• attempt defibrillation again - single shock
• give amiodarone iv (or lignocaine if amiodarone unavailable) if refractory VT or VF after 3rd DC shock
• magnesium in cardiac arrest has only been shown to be useful for either:
  • hypomagnesaemic states
  • digoxin toxicity
  • torsade de pointes VT

• induced hypothermia cooled to 32-34°C for 24 hours for unconscious adults with return of spontaneous circulation (ROSC) is no longer recommended.
  • NB. a 2013 study of 950 out-of-hospital cardiac arrests failed to show any additional benefit of cooling to 33°C vs 36°C ²⁾

Mr Bean - CPR at the bus stop