Outline the causes, and principles of management of ventricular fibrillation
Ventricular fibrillation requires an initiating stimulus in a susceptible myocardium. VF can be induced in a previously normal myocardium as a result of electrical stimulation (electrocution, lightning) or by trauma (commotio cordis). The myocardium can be made more susceptible by the presence of hypoxaemia (e.g. respiratory arrest), electrolyte disturbances (low K and Mg), altered autonomic and vagal inputs, and mechanical stimuli (e.g. wire or catheter in RV). The myocardium may be abnormally susceptible due to congenital (e.g. conduction abnormalities) or acquired disorders (including ischaemia, hypertrophy, myocarditis, pro-arrhythmic drugs, etc).
Principle of management include early defibrillation, but in concert with correction of any correctible cause (e.g. wire, electrolytes, hypoxaemia etc), support of the cardio-respiratory state with adequate basic life support, and restoration of an appropriate metabolic milieu to support a normal rhythm. This latter approach may require performance of cardiopulmonary resuscitation, and administration of specific anti-arrhythmic drugs. Defibrillation is performed with either monophasic (200/200/360J) or biphasic (150/150/150J) defibrillator waveforms in a series of up to three sequential shocks. Subsequent monophasic shocks should be administered at maximal dose.
This question is identical to Question 6 from the first paper of 2006.