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.
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.
In a normal myocardium VF can be caused by the following insults:
The ARC/ANZCOR Guideline 11.4 is my resource for the following summarised recommendations:
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.
A good article (Koplan & Stevenson, 2009) lists the following:
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.
|Criterion||Findings associated with SVT||Findings associated with VT|
|ACC/AHA Guidelines (2003)|
|QRS duration||<120 msec||> 120 msec|
|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|
|QRS morphology criteria for VT||Not met||Met|
|Brugada QRS morphology criteria for LBBB pattern|
|Initial R period||<100 msec||>100 msec|
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)|
|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|
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:
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:
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.
ARC Guideline 11.2: Protocols for Adult Advanced Life Support
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