- Ventricular fibrillation (VF) is the the most important shockable cardiac arrest rhythm.
- The ventricles suddenly attempt to contract at rates of up to 500 bpm.
- This rapid and irregular electrical activity renders the ventricles unable to contract in a synchronised manner, resulting in immediate loss of cardiac output.
- The heart is no longer an effective pump and is reduced to a quivering mess.
- Unless advanced life support is rapidly instituted, this rhythm is invariably fatal.
- Prolonged ventricular fibrillation results in decreasing waveform amplitude, from initial coarse VF to fine VF and ultimately degenerating into asystole due to progressive depletion of myocardial energy stores.
- Chaotic irregular deflections of varying amplitude
- No identifiable P waves, QRS complexes, or T waves
- Rate 150 to 500 per minute
- Amplitude decreases with duration (coarse VF -> fine VF)
In the presence of ischemic heart disease VF may be preceded by:
The underlying mechanism of Ventricular Fibrillation is not fully understood, several mechanisms have been hypothesised:
- Multiple wavelet mechanism – In which multiple small wandering wavelets are formed. The fibrillation is maintained by re-entry circuits formed by some of the wavelets.
- Mother rotor mechanism – In which a stable re-entry circuit is formed, the ‘mother rotor’. The ‘mother rotor’ then gives rise to propagating unstable ‘daughter’ wavefronts, which results in the chaotic electrical activity seen on the ECG. Animal models suggest in any instance of VF there may be one or multiple ‘mother rotors’.
- Myocardial ischemia / infarction
- Electrolyte abnormalities
- Cardiomyopathy (dilated, hypertrophic, restrictive)
- Long QT (acquired / congenital) causing TdP –> VF
- Brugada syndrome
- Drugs (e.g. verapamil in patients with AF+WPW)
- Environmental – electrical shocks, drowning, hypothermia
- Pulmonary embolism
- Cardiac tamponade
- Blunt trauma (Commotio Cordis)
There is a nice list of causes here.
- Typical rhythm strip of ventricular fibrillation
- Appearance of fine VF
- VF should never be diagnosed from the 12-lead ECG!
- “R on T” phenomenon causing Torsades de Pointes, which subsequently degenerates to VF.
- Notice how in this case the rhythm strip was recorded after the standard 12 leads (unlike many other ECG machines which record them simultaneously).
- R on T leads to polymorphic VT, which then degenerates to VF.
- The inferior ST elevation in the first part of the ECG may represent either inferior STEMI or simply the effects of ventricular pacing. Note the small pacing spikes in front of each QRS complex.
- The magnitude of ST elevation (>5mm) suggests that this may be an inferior STEMI in a paced patient (see Sgarbossa’s criteria).
- Again, the rhythm strip is recorded after the standard 12 leads.
- This patient is shocked out of VF five times in ten minutes!
- The subsequent rhythm in each case appears to be an accelerated idioventricular rhythm (broad QRS with AV dissociation), possibly with some fusion complexes in the second and third rhythm strips.
- Australian Resuscitation Guidelines 2010.
- Chan TC, Brady WJ, Harrigan RA, Ornato JP, Rosen P. ECG in Emergency Medicine and Acute Care. Elsevier Mosby 2005.
- Ideker RE, Rogers JM. Human Ventricular Fibrillation : Wandering Wavelets, Mother Rotors, or Both? Circulation. 2006;114(6):530-2 [full text].
- Nash MP, Mourad A, Clayton RH, Sutton PM, Bradley CP,Hayward M, Paterson DJ, Taggart P, Evidence for Multiple Mechanisms in Human Ventricular Fibrillation. Circulation 2006, 114:536-542 [full text].
- Surawicz B, Knilans TK. Chou’s Electrocardiography in Clinical Practice. 6th Edition. Saunders Elsevier 2008.
- Tusscher KHWJ, Mourad A, Nash MP, Clayton RH, Bradley CP, Paterson DJ, Hren R, Hayward M, Panfilov AV, Taggart P. Organization of ventricular fibrillation in the human heart: experiments and models. Exp Physiol 2009 May;94(5):553-62 [full text].