Outline the causes and principles of management of ventricular fibrillation.
Causes: 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).
Principles 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 vasoconstrictors and specific anti-arrhythmic drugs, especially in the setting of prolonged VF. According to the ALS guidelines in place when the question was set, defibrillation is performed with an appropriate energy level for either monophasic (eg.
200/200/360J) or biphasic (eg. 150/150/150J) defibrillator waveforms in a series of up to three sequential shocks. Subsequent monophasic shocks should be administered at maximal dose.
The longer-term management, including the use of implantable defibrillators should be considered according to published guidelines.
Candidates were not penalised if they did not discuss the new guidelines (including higher energy levels for monophasic, and a single shock approach).
This question is grounded in the ARC guidelines.
Causes of VF:
- Cardiac ischaemia
- Electrical myocardial injury
- Traumatic myocardial injury
- Irritating mechanical stimulus (eg. CVC guidewires, PA catheter)
Predisposition to VF:
- Low potassium
- Low magnesium
- Arrhythmogenic drugs eg. theophylline, sympathomimetics
- Congential and idopathic predisposition
- Prior cardiac surgery
- Cardiac chamber hypertrophy
- Severe hypothermia
Principles of management of VF:
- Cardiopulmonary resuscitation with an emphasis on uninterrupted chest compressions
- Early defibrillation - single shock
- When it is witnessed in a monitored environment and the defibrillator is readily available, three "stacked" shocks may be used.
- Correction of immediately responsible cause (eg. withdrawal of PA catheter, or immediate angiography for myocardial infarction)
- Correction of predisposing causes (eg. hypoxia, hypokalemia)
- Consideration for an automated implantable defibrilator (AICD).
Chen, Qiuyun, et al. "Genetic basis and molecular mechanism for idiopathic ventricular fibrillation." Nature 392.6673 (1998): 293-296.
Wiggers, Carl J. "The mechanism and nature of ventricular fibrillation." American Heart Journal 20.4 (1940): 399-412.
Beck, Claude S., Walter H. Pritchard, and Harold S. Feil. "Ventricular fibrillation of long duration abolished by electric shock." Journal of the American Medical Association 135.15 (1947): 985-986.