2006B07 Outline the drug and non-drug treatment of ventricular fibrillation in the adult.
Briefly describe their mechanisms of action and side effects.
Do not discuss basic life support, airway therapies or oxygen



·      Intro: definition, problem, cause, priorities, ALS shockable algorithm

·      Non-drug treatment

·      Drug treatment




·  Chaotic ventricular depolarisation and repolarization


·  No cardiac output

·  LOC in seconds

·  Eeath in minutes


·  Hypotension, hypoxia, hypothermia, electrolyte disturbance

·  AMI, PE, tamponade, tension pneumothorax, drug/toxin


·  Early unbroken CPR (↑survival)

·  Early defibrillation (↑survival)

·  Treat causes in order of ease and likelihood

ALS algorithm: shockable

·  CPR 2 mins -> rhythm check -> defibrillation (repeat)

·  Adrenaline 1mg: after 2nd loop, then every 2nd loop

·  Amiodarone 300mg: after 3 x defib


Non-drug treatment:

Praecordial thump

·  Heel of hand -> sternum

·  Only if witnessed, monitored VF arrest and no ready access to defib

·  Mechanism of action (MoA): mechanical energy -> electrical energy (2-5J) -> mild depolarisation -> silence -> sinus rhythm

·  Side effects (SEs): sternal or rib fracture, myocardial contusion


·  Electric shock of heart between two gel pads or paddles

·  Device: 5kV step up transformer + capacitors in charging circuit; inductor in discharging circuit; switch between

·  Shock has specific magnitude and duration

·  200J biphasic better than 360J monophasic

o ↔/↑ effectiveness

o ↓ energy -> ↓ electrical injury

·  MoA: depolarize whole myocardium -> silence -> sinus rhythm

·  SEs: skin burns, internal burns, electrocution of staff, fire/explosion

Non-drug measures

More helpful for non-shockable

·  IV fluid (restore blood volume, preload)

·  Pericardiocentesis for tamponade (restore preload)

·  Needle decompression of tension pneumothorax (restore preload)


Drug treatment:


·  Dose: 1mg

·  Catecholamine

·  At high dose α1 > β1 > β2 effect

·  MoA: peripheral vasoconstriction++ ->

o ↑coronary perfusion pressure -> ↑defib success

o ↑cerebral perfusion pressure -> ↑survival

·  SEs: (observed after ROSC)

o ↑↑HR

o ↑↑mAP

·  N.B. new evidence suggests adrenaline may not improve outcome


·  Dose: 300mg slow push

·  First line for refractory VF

·  MoA:

o Class 3 > 1,2,4 antiarrhythmic

o Mainly K+ channel block

o Complex MoA

o Stabilizes myocyte membrane -> terminate tachyarrhythmias

·  SEs (after ROSC)

o CVS: ↓HR, ↓mAP, ↑QTc -> ↑risk of TdP

o Displace highly plasma protein bound drugs -> ↑free [drug] (e.g. warfarin)

o Tissue toxicity: pulmonary fibrosis, cirrhosis, hypothyroidism


·  Dose: 1mg/kg

·  Second line for refractory VF

·  MoA: class 1b Na+ channel blockade

o Minimal ↓slope phase 0

o ↓Absolute refractory period

·  SE:

o Cardiac: AV block, ↓ inotropy, arrhythmias

o CNS: excitation (tinnitus, perioral tingling, seizure)


·  Dose: 40 IU once only

·  Alternative to adrenaline if already running

·  MoA: bind V1 -> peripheral vasoconstriction

o ↑Cororonary perfusion pressure -> facilitate successful defib

o ↑Cerebral perfusion pressure -> preserve neuronal integrity


·  Dose: 5mmol IV slow push

·  Use if VF follows torsades de pointes or in the setting of hypomagnesaemia

·  MoA: increases membrane stability, competes for calcium

·  SE: vasodilatation, sedation, muscle weakness, resp failure


·  Dose: 5mmol

·  Indication: hypokalaemia

·  MoA: restore resting potential


·  10mmol as CaCl2

·  Use if: ↑[K+], ↓[Ca2+]

·  MoA: MSA if ↑[K+], ↑inotropy

·  SE: excitotoxicity of brain and heart; vascular irritation (gluconate safe peripherally)


·  1mmol/kg

·  Use if: metabolic acidosis, prolonged arrest

·  MoA: buffer

·  SE: worsen ICF acidosis, ↑Na+, ↑osmolality


·  Thrombolytics

·  Glucose

·  Specific antidotes e.g. naloxone, flumazenil



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