Clinical presentation:As with all tachyarrythmias, symptoms depend upon the ventricular rate and pre-existing cardiovascular state.
These symptoms and signs may be mild (consisting of dizziness or light-headedness), moderate (eg. chest pain or shortness of breath), or severe (with cardiovascular collapse or profound shock).
Differential for Wide Complex Regular Tachycardias
Ventricular Tachycardia
SVT with aberrant conduction (eg. WPW)
Atrial flutter with 2:1 & aberrant conduction
Sinus Tachycardia with aberrant conduction
Ventricular Tachycardia
VT is the most common, and one of the most life threatening causes of a broad complex tachycardia. It is defined as: three or more ventricular extrasystoles
in succession at a rate of greater than 120 beats/min.
They most often occur in the context of structural heart disease which makes accessory pathways and re-entrant arrhythmias much more likely. It can easily degenerate into VF, and accounts for 80% of sudden cardiac deaths due to fatal arrhythmia.
VT can be defined according to duration, site of
origin (left or right ventricle), or morphology (monomorphic or
polymorphic):
- Ventricular tachycardia lasting for less than 30 seconds is defined as “non-sustained”
-
Right bundle branch block morphology - if the terminal portion of the
QRS complex in V1 is positive and suggests activation from the left
ventricle or septum
- Left bundle branch block morphology -
if the terminal portion of the QRS complex in V1 is negative and
suggests activation from the right ventricle
- An inferior axis (positive QRS in aVF, negative in V1) - suggests activation from the outflow tracts
- A superior axis (negative QRS in aVF, positive in V1) - suggests activation from the apex
- A relatively narrow QRS (100 to 120 ms) implies a septal focus
Wolff-Parkinson-White
If a patient with suspected Wolff-Parkinson-White syndrome develops a broad complex tachycardia, then you should avoid AV nodal blocking drugs. This is because these may increase ventricular activation over the accessory pathway and cause a dangerously fast heart rate. Instead, you should give an intravenous class IC drug such as flecainide, or a class III drug such as amiodarone.
Antidromic AVRT
The ventricles are
activated directly by an accessory pathway, and the atria are activated
retrogradely over the AV node. The management is similar to orthodromic AVRT, and you may be
able to use adenosine to terminate the arrhythmia. In patients with
atrial fibrillation and Wolff-Parkinson-White syndrome, rapid
ventricular conduction across the accessory pathway from the atrium to
the ventricle may result in ventricular fibrillation.
Outflow tract ventricular tachycardia
Outflow
tract ventricular tachycardia tends to be related to exertion and may
respond to adenosine and the Valsalva manoeuvre. It may be
haemodynamically well tolerated and less likely to cause sudden cardiac
death than other ventricular arrhythmias. You should aim to suppress
right ventricular outflow tract tachycardia with the use of beta
blockers and verapamil.
Idiopathic left ventricular tachycardia
This
ventricular tachycardia originates from the left bundle branches, most
commonly the posterior fascicle. It has a relatively narrow morphology.
Polymorphic VT
This is uncommon and rarely sustained. When polymorphic VT is encountered in the acute setting it is frequently the result of an acute cardiac insult and it rapidly deteriorates into ventricular fibrillation. The main features are:
1. QRS rate is rapid (200 – 250 beats/min)
2. Amplitude of the QRS complexes change in a sinusoidal fashion
3. Usually self limiting but may be recurrent
4. Between episodes the QT interval is prolonged (see Figure 5)
VT or SVT with aberrant conduction
Most rules are unreliable. If in doubt...treat as VT and shock the patient.
VT more likely than SVT:
- Absence of typical RBBB or LBBB morphology
- Extreme axis deviation (“northwest axis”) – QRS is positive in aVR and negative in I + aVF.
“if it’s up in aVR the axis is bizarre!”
-
Very broad complexes (>160ms)
- AV dissociation (P and QRS complexes at different rates)
-
Capture beats - occur when the sinoatrial node transiently ‘captures’ the ventricles, in the midst of AV dissociation, to produce a QRS complex of normal duration.
- Fusion beats - occur when a sinus and ventricular beat coincides to produce a hybrid complex.
- Concordance - all the QRS complexes in the chest leads are either positive or negative. The identification of positive or negative concordance suggests the origin of the VT lies in the posterior ventricular wall or anterior ventricular wall respectively.
- Brugada’s sign – The distance from the onset of the QRS complex to the nadir of the S-wave is > 100ms
- Josephson’s sign – Notching near the nadir of the S-wave
- RSR’ complexes with a taller left rabbit ear. This is the most specific finding in favour of VT. This is in contrast to RBBB, where the right rabbit ear is taller.
SVT+ Aberrancy more likely than VT
- Age <35
- Rate =150 beats/minute
- Rate >200 beats/minute and patient asymptomatic
- QRS Duration < 0.14 seconds
- Axis normal
- Absence of independent atrial activity or concordance
Management
Intravenous amiodarone is the first choice of drug.
In patients with torsades de pointes, correction of serum potassium
levels and infusion of intravenous magnesium is needed.
Temporary pacing might be indicated in those patients whose arrhythmia
is triggered by bradycardia. Beta blockers may then maintain sinus
rhythm and prevent further episodes of polymorphic ventricular
tachycardia.
Start with a synchronised DC cardioversion at 200 joules (monophasic) or
120-150 joules (biphasic). If unsuccessful repeat the cardioversion up
to a maximum of 3 attempts before giving amiodarone. Changing the paddle
position may be helpful in resistant cases.
In patients who are
tolerating their arrhythmia, intravenous amiodarone (in a dose of
5mgs/kg up to a maximum of 300mgs) administered over 30 minutes is the
treatment of choice. If unsuccessful, DC cardioversion should be
considered.
Correction of any underlying abnormalities that might
be precipitating the arrhythmia (eg. hypo/hyperkalaemia and
hypomagnesaemia) is also required. Consider Calcium gluconate premedication or post treatment if BP falls.
LinksEnlightenMe
http://www.enlightenme.org/knowledge-bank/cempaedia/broad-complex-tachycardias
GoogleFOAM
https://circ.ahajournals.org/content/106/25/e206.full
http://academiclifeinem.com/pv-card-brugada-criteria-svt-aberrancy-vs-vt/
http://bja.oxfordjournals.org/content/92/1/140.full
http://ekgumem.tumblr.com/post/59400445975/wide-complex-tachycardia-vt-vs-svt-with
http://ekgumem.tumblr.com/post/24960326577/wide-complex-tachycardia-episode-40-june-12
http://ekgumem.tumblr.com/post/23993343074/wide-complex-regular-tachycardia-deadly-av
http://hqmeded-ecg.blogspot.co.uk/2014/03/incessant-regular-wide-complex.html
http://lifeinthefastlane.com/ecg-library/basics/vt_vs_svt/
http://lifeinthefastlane.com/vt-versus-svt-with-aberrancy/
BMJ Learning
Tachycardia - not the best module
Difficult cardiology scenarios
Broad Complex Tachycardias
Doctors.net
http://www.doctors.net.uk/ecme/wfrmNewIntro.aspx?moduleid=1535
http://www.doctors.net.uk/ecme/wfrmNewIntro.aspx?moduleid=1582
