Ventricular Fibrillation

Description

Ventricular fibrillation (VF) describes disorganized and continuous electrical activity of the ventricular myocardium due to various inciting causes, resulting in cessation of cardiac output.
VF is often preceded by ventricular tachycardia.

Epidemiology

Sudden cardiac death carries an incidence of 0.1–0.2% per year and causes 400,000 deaths per year in US, the majority of which are due to VT/VF.
Unknown intraoperative incidence, although considered rare.

Cessation of cardiac output due to VF is fatal unless a perfusing rhythm is re-established.
Mortality is dependent on timely and appropriate intervention to treat the arrhythmia and underlying causes.
Operating room: 75% survival rate and 57% survival rate to discharge.
Non-OR interventional procedural areas: 64% survival rate and 41% survival rate to discharge.

Etiology/Risk Factors

Procedure-based risk:
- Intrathoracic/cardiac procedures
- ICD testing, interventional cardiac catheterization procedures
Patient comorbidities:
- Cardiomyopathy
- Ischemic heart disease
- Brugada syndrome
Metabolic derangements:
- Electrolyte disorders
- Acid–base disorders
- Hypothermia
- Hypoxia
Myocardial ischemia or acute coronary syndromes
Pathologic events:
- Hypovolemia
- Pulmonary embolus
- Tension pneumothorax
- Cardiac tamponade
Iatrogenic causes:
- Microshock/macroshock
- R on T phenomenon (asynchronous pacing, lithotripsy)
- Drug toxicity

Physiology/Pathophysiology

VF is defined by multiple re-entrant waves of electrical activity that conduct erratically through the myocardium. Dispersion of refractoriness and heterogeneity of conduction properties within the myocardium contribute to the perpetuation of disordered electrical and mechanical activity.
Mechanical activity is completely unsyncrhonized and uncoordinated (described as "quivering") and is insufficient to pump blood out of the heart. Cardiac arrest ensues and without emergency intervention, can be fatal within minutes.

Prevantative Measures

VF is a common end point for many critical pathologic processes. Avoid inciting events (ischemia, cardiac manipulation, micro/macroshock, electrolyte/acid–base derangements, surges in autonomic stimulation).
Anticipate the potential need for defibrillation in vulnerable patient populations. Consider pre-emptive placement of defibrillator pads on the patient, or having them in the room.
Patients predisposed to VT/VF may have implanted cardioverter defibrillators (ICDs). Device interrogation may yield pertinent information regarding arrhythmia burden.

Diagnosis ⬆ ⬇

Physical examination
- In conscious patients, palpitations may precede VF, with rapid loss of consciousness.
- Absent pulses.
- Absent heart sounds.
- Jugular venous distention (from the cardiac pump "backing up").
Monitors
- EKG with characteristic disorganization of electrical activity.
- Loss of ETCO₂; cessation of blood flow to the alveoli, with continued ventilation results in dead space ventilation. The PaCO₂ continues to increase, as it cannot be exhaled.
- Loss of plethysmography waveform/arterial line pulsatility.
- Hypotension.
- Disorganized contraction on TEE.
Labs
- Serum electrolyte panel (including calcium and magnesium).
- Arterial blood gas analysis to detect hypoxia.

Differential Diagnosis

Treatment ⬆ ⬇

In the operating room, VF is often witnessed, the airway is secured, IV access is present, and skilled personnel is available.
ACLS protocol with CPR and early/immediate defibrillation:
- Monophasic 360 J
- Biphasic 120–200 J
- Pediatric 2–4 J/kg, up to 10 J/kg
Vasopressor (epinephrine/vasopressin) therapy is considered after the first shock and CPR with the goal of improving myocardial perfusion via increased aortic root pressure.
- Epinephrine 1 mg IV q3–5 minutes
- Vasopressin 40 units IV may be substituted for the first and second dose of epinephrine
Consider amiodarone 300 mg IV bolus; a second dose of 150 mg may be given if no response.
Lidocaine 1–1.5 mg/kg up to 3 mg/kg may be considered if amiodarone is not available.
The underlying cause must be diagnosed and treated. VF may be refractory to defibrillation if causes of VF are not addressed (e.g., ischemia).

Follow-Up ⬆ ⬇

If hemodynamic stability and a stable cardiac rhythm are recovered promptly, continuing with the surgical procedure may be considered depending on the inciting event and feasibility of interrupting or delaying surgical procedure.
Must assess end-organ impact if a prolonged period of hypoperfusion occurred.
If diagnosis or treatment of the etiology is an ongoing process, a therapeutic strategy must be developed and care should be continued in an intensive care setting.
- Consider therapeutic hypothermia if neurologic insult is suspected.
- Identify and treat acute ischemia if present.
- Provide respiratory support.
- Provide hemodynamic support as needed to maintain end-organ perfusion.
- Assess prognosis and recovery potential.

References ⬆ ⬇

Mhyre JM , Ramachandran SK , Kheterpal S , et al. Delayed time to defibrillation after intraoperative and periprocedural cardiac arrest. Anesthesiology. 2010;113(4):782–793.
Mahajan A , Hoftman N. To beat or not to beat: is timing the only question? Survival after delayed defibrillation. Anesthesiology. 2010;113(4): 765–766.
Peberdy MA , Callaway CW , Neumar RW , et al. Part IX: post–cardiac arrest care: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation. 2010;122:S768–S786.