Ventricular fibrillation, ventricular tachycardia and defibrillation

Several questions from the CICM fellowship exam ask what seems like a fairly straightforward question about the management of shockable rhythms. VF and VT are the main culprits here. The answer, of course, is electricity. The topic of cardioversion in the ICU, including its mechanism of action,  is discussed elsewhere. This chapter deals mainly with recognition and management of non-perfusing rhythms.

• Question 20 from the second paper of 2019 (polymorphic VT)
• Question 15.1 from the first paper of 2018 (polymorphic VT)
• Question 15.2 from the first paper of 2018 (monomorphic VT)
• Question 30.1 from the second paper of 2017 (Brugada criteria)
• Question 6 from the first paper of 2006 (VF: a repeat)
• Question 12  from the second paper of 2003 (VF)
• Question 7 from the second paper of 2000 (VT)

The main sources for the summary below are derived from the ARC 2016 Guidelines, so as to render the content locally relevant and repeatable in the CICM exam. If one has infinite spare time and wishes to delve deep into the physiological mechanisms underlying VF, one is invited to read the excellent review by Weiss et al (2000). The best single reference about the causes and predisposition to VT is a 2009 Lancet article by John et al.

Management of ventricular fibrillation

Causes of VF:

In a normal myocardium VF can be caused by the following insults:

• Cardiac ischaemia
• Electrical myocardial injury
• Traumatic myocardial injury (contusio cordis), which gives rise to traumatic VF (commotio cordis)
• Irritating mechanical stimulus (eg. CVC guidewires, PA catheter)
• Myocarditis
• Idiopathic (i.e. random VF in an otherwise healthy person)

Predisposition to VF:

• Low potassium
• Low magnesium
• Hypoxia
• Arrhythmogenic drugs eg. theophylline, sympathomimetics
• Congential and idopathic predisposition, eg. WPW syndrome
• Prior cardiac surgery
• Cardiac chamber hypertrophy
• Ischaemic heart disease
• Cardiomyopathy of ischaemic heart disease (particularly, with a low ejection fraction - a patient with an LVEF under 30%-35% should become the recipient of an AICD)

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).

Timing of defibrillation

The ARC/ANZCOR Guideline 11.4 is my resource for the following summarised recommendations:

• The ARC literature review did not identify any consistent evidence for an improved in-hospital mortality with either shock-first or CPR-first approaches
• The current guideline is that the shock should be given immediately as the defibrillator becomes available.
• However, Eftestøl et al (2004) have demonstrated that pre-defib CPR may actually improve the chances of successful defibrillation.
• The patients who benefit from CPR first are those in whom CPR is delayed for 4-5 minutes after the arrest. In this population, ROSC is more likely with a period of pre-defibrillation CPR

Circumstances in which the patient may be refractory to defibrillation

• Extreme hypothermia has been traditionally said to make one refractory to defibrillation, but numerous animal trials and human case studies have demonstrated that defibrillation is possible and may even be facilitated by profound hypothermia (eg. Boddicker et al, 2005).
• Intoxication with volatile solvents, eg. petrol-sniffing
• Prolonged resuscitation, or prolonged period of "hands-off down-time" (arrested but without CPR in progress)
• Chronic amiodarone therapy increases the energy requirement of AICD shocks by about 60% (Pelosi et al, 2000)
• Phenytoin therapy may theoretically increase the resistance of the myocardiom to all sorts of electrical stimulus, be it pacing or defibrillation

Ventricular tachycardia

Structural causes of VT

• Acute cardiac ischaemia: the leakage of potassium out of dead myocytes leads to increased extracellular potassium that depolarizes myocytes in the ischemic border zone and leads to electrical heterogeneity of conduction and refractoriness that provide a substrate for reentry, resulting in polymorphic VT and/or VF.
• Myocardial scarring or structural distortion:
  • An old infarct
  • Dilated cardiomyopathy
  • Hypertrophic cardiomyopathy
  • LV aneurysm
  • Infiltrative heart disease, eg. sarcoid
  • RV dysplasia
• Bundle branch reentry: the circulating wavefront travels antegrade down the right bundle branch and retrograde up the left bundle branch. This is usually monomorphic, and each time it happens the QRS morphology is exactly the same

Familial causes of VT

• Brugada syndrome
• Long QT
• Catecholaminergic polymorphic VT
• Arrhythmogenic right ventricular dysplasia (ARVD

Idiopathic VT

• By definition, VT which occurs in the absence of structural heart disease, genetic conditions such as long QT syndrome, or metabolic/electrolyte abnormalities.
• These tend to originate from a few locations, most commonly the RVOT.
• Mostly monomorphic and has an LBBB appearance

Polymorphic VT

This is defined as "ventricular tachycardia with varying QRS amplitude, axis and duration." In short, it differs from regular VT by having a different QRS morphology for every beat. It  is important to note that polymorphic VT is not torsades de pointes, but torsades des pointes is one form of polymorphic VT, specifically associated with QT prolongation. 

Causes specific for polymorphic VT:

A good article (Koplan & Stevenson, 2009) lists the following:

• Acute coronary ischaemia
• Long QT (congenital or acquired)
• Brugada syndrome
• Catecholaminergic polymorphic VT
• Arrhythmogenic right ventricular dysplasia (ARVD)
• Cardiomyopathy of any cause
• Hypokalemia
• Hypomagnesemia

Discriminating VT from SVT

Question 30.1 from the second paper of 2017 asked for ECG criteria which can help distinguish VT from SVT with aberrant conduction. The best resources for this are (as always) LITFL and ECGPedia. In short, there are multiple different criteria you can choose from, and none are massively superior to any other. It is possible to list these in a big table, so that one can see the sort of answers which would have been suitable for Question 30.1. Some of the criteria are somewhat duplicated because the features are listed according to the society guideline being quoted. It makes sense that most of the guideline-makers would agree on such obvious things as "wide QRS" and "regular", etc.

How to Tell VT from SVT with Aberrancy

Criterion	Findings associated with SVT	Findings associated with VT
ACC/AHA Guidelines (2003)
QRS duration	<120 msec	> 120 msec
Rhythm	Irregular	Regular
A-V relationship	Atrial rate faster than ventricular rate	Ventricular rate faster than atrial rate
Axis	Normal, right or left axis	Bizarre axis (+90 to -90)
QRS morphology in the precordial leads	Typical RBBB or LBBB	Concordance; no R/S pattern; onset of R to nadir is longer than 100 msec. In RBBB pattern:  - qR, Rs or Rr patter in V1 In LBBB pattern: - R in V1 longer than 30msec - R to nadir of S in V1 longer than 60 msec - qR or qS in V6
Brugada algorithm (1991)
RS complex in precordial leads	Present	Absent
R-S interval in one precordial lead	<100 msec	>100 msec
A-V relationship	Associated	Dissociated
QRS morphology criteria for VT	Not met	Met
Brugada QRS morphology criteria for LBBB pattern
Initial R period	<100 msec	>100 msec
S-wave  in V1 or V2	Normal downwards leg	Slurred or notched downwards leg
Q to nadir QS in V1 or V2	<100 msec	>100 msec
Q or QS in V6	Absent	Present
Brugada QRS morphology criteria for RBBB pattern
R or qR in V1	Normal	Monophasic
R to R' size	R shorter than R'	R taller than R'
R in V6	No Rs	Rs present in V6
Vereckei algorithm (2007)
A-V relationship	Associated	Dissociated
R in aVR	Absent	Present
QRS morphology	Like a RBBB or LBBB	Unlike RBBB or LBBB
Vi/Vt	Vi (initial QRS upstroke y-axis distance during the first 40 msec) is greater than Vt (terminal QRS downstroke y-axis distance during the last 40 msec of the QRS)	Vi is smaller than Vt

Management of ventricular tachycardias

Question 15.2 from the first paper of 2018 asked the candidates how they would assess and manage a regular broad complex tachycardia. The ARC has a pretty straightforward view of these sort of tachyarrhythmias. If it is haemodynamically unstable, you shock it. If it is haemodynamically stable, you can afford to think about drugs. If it is without pulse, the patient is dead and you should proceed according to the ALS algorithm for shockable rhythms (nowadays we don't do those three shocks anymore). Stability is defined by the absence of the following features:

• Systolic BP < 90 mmHg
• Heart rate > 150/min
• Chest pain
• Heart failure
• Drowsiness or confusion

Management of perfusing VT

• haemodynamically stable:
  • control arrhythmia with antiarrhytmic medications
  • Amiodarone is now the preferred agent (ARC guideline 11.9, 2009)
  • 300mg amiodarone over 20-60 minutes, followed by an infusion of 900mg over 24 hrs.
  • Class 1a agents like lignocaine are a reasonable alternative, particularly if the QT interval is prolonged.
  • Avoid calcium channel blockers
• Haemodynamically unstable:
  • Synchronised cardioversion
  • If this does not work, give 300mg amidoarone over 10-20min, and then attempt cardioversion again
  • Follow this with 900mg amiodarone over 24 hours.

Management of pulseless VT

• consider a praecordial thump
• commence CPR
• progress according to ILCOR ALS algorithm for shockable rhythms

Prevention of recurrence

• correct electrolyte disturbance
• rule out cardiac ischaemia as cause
• cease arrhythmogenic medications
• address mechanical causes of VT: for example, PA catheter or very low CVC tips
• Commence antiaarhythmic medications

Polymorphic VT (torsades de pointes)

Thomas and Behr (2015) have published a good article which describes the management strategies for torsades, which is helpful for people trying to answer part (b) of Question 30.1 from the second paper of 2017. In short:

• Preventative strategies
  • Stop the QT-prolonging drugs
  • Keep the serum K⁺ around 4.7 - 5.2 mmol/L
• Immediate treatment
  • IV magnesium sulphate
  • Isoprenaline (to increase heart rate to 100-110)
  • Overdrive pacing
  • Lignocaine
• Experimental treatments and last resort measures
  • Clonidine
  • Ranolazine

Third line therapies for the management of  refractory VT

So; the VT just won't go away. What other things could you try?
A certain ladder of escalation from most to least accepted therapies can be suggested. In the process of writing some notes about it, I fell into a deep rabbit hole, and found enough material to extend this into an entirely separate summary chapter on the management of super-refractory ventricular tachycardia.

• First-line: amiodarone.
• Second-line: lignocaine, mexelitine, etc
• Third-line: Cardioversion, overdrive pacing
• End of the line: 
  • Phenytoin
  • Sodium lactate 
  • Sodium bicarbonate
  • Beta-blockers
  • Thoracic epidural
  • Surgical sympathectomy
  • Selective sequential endocardial resection