Ventricular

Tachyarrhythmias

Definition
Nonsustained VT
Sustained monomorphic VT
Polymorphic VT: often associated with
hemodynamic collapse or instability
VF: associated with disorganized
mechanical contraction, hemodynamic
collapse and sudden death

Etiology
VT associated with structural heart
disease
Ischemia
Nonischemia cardiomyopathy: progressive
dilation and fibrosis of the ventricular
myocardium
Infiltrative cardiomyopathy
Prior repair of congenital heart disease
Arrhythmogenic right ventricular dysplasia
or cardiomyopathy: LBBB morphology VT
Bundle branch reentry VT

 VT in the absence of structural heart

disease
Inherited ion channelopathies: Brugada
and long QT syndrome
Catecholaminergic polymorphic VT:
irregular calcium processing
Idiopathic VT: RVOT

Clinical Presentation
Assess vital signs and clinical
symptoms
If unstable ACLS management
If stable, several questions can be asked
for D/Dx
Structural heart disease?
Pacemaker / ICD / Baseline wide QRS?
Medications? Class I and III antiarrhythmics,
antibiotics, antipsychotics, digoxin

Differential Diagnosis

SVT with aberrant conduction

VT
Antidromic AVRT
Hyperkalemia-induced arrhythmia
Pacemaker-induced tachycardia

Diagnostic Testing
Lab: metabolic panel, Mg, CBC,
cardiac enzyme
ECG in VT
Absence of typical RBBB or LBBB
morphology
Extreme axis deviation (northwest
axis) QRS is positive in aVR and
negative in I + aVF.
Very broad complexes (>160ms)

 AV dissociation

 Capture beats: occur when the SA 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.

 Positive or
negativeconcordancethroughout the
chest leads, i.e. leads V1-6 show entirely
positive (R) or entirely negative (QS)
complexes, with no RS complexes seen.

 Brugadas sign: The distance from the

onset of the QRS complex to the nadir of
the S-wave is > 100ms

Josephsons sign Notching near the

nadir of the S-wave

 RSR complexes with ataller leftrabbit

ear. This is the most specific finding in
favor of VT. This is in contrast to RBBB,
where the right rabbit ear is taller.

 Brugada Algorithm

 Morphological Criteria for VT: Leads

V1-2 and V6.
If there is a dominant R wave in V1
RBBB-like morphology

If there is a dominant S wave in V1

LBBB-like morphology

 RBBB-like morphology in V1
Smooth monophasic R wave

Notched downslope to the R wave the

taller left rabbit ear (= Marriotts sign)

 A qR complex (small Q wave, tall R

wave) in V1

 Comparison: Typical RBBB

 RBBB-like morphology in V6
QS complex a completely negative
complex with no R wave (= strongly
suggestive of VT).

R/S ratio < 1 small R wave, deep S

wave (indicates VT only if LAD is also
present)

 LBBB-like morphology
in V1-2
Initial R wave > 30-40
ms duration.
Notching or slurring of
the S wave
(Josephsons sign).
RS interval (time from
R wave onset to S wave
nadir) > 60-70 ms.

 LBBB-like morphology in V6
QS waves in V6 (as with RBBB-like
patterns, this finding is very specific for
VT)

qR pattern = small Q wave, large R

wave.

 Comparison: LBBB in V6

Treatment
Pulseless VT and VF: immediate
unsynchronized DC cardioversion
Nonpharmacologic therapy
ICDs
Radiofrequency catheter ablation of VT:
idiopathic VT, BBRT, VT associated with
ischemic heart disease

 Medications:
First line
Amiodarone: IV 150mg over 10 min,
1mg/min*6hrs 0.5mg/min
Beta-blockers

Second line
Sotalol: class III agent; chronic treatment of
VT/VF, prevent recurrence
Lidocaine: class Ib; management of
sustained and recurrent VT/VFl
Mexiletine: used in combination with
amiodarone/sotalol
Phenytoin: digitalis-induced ventricular
arrhythmias

Special Considerations
TdP associated with long QT
syndrome
Immediate DC cardioversion
Bolus administration of MgSO4