Ventricular tachycardia (VT)

1. Pathophysiology
   1. usually re-entrant
      1. most common in the first 30 minutes following AMI
      2. may occur 3 days to several weeks after infarction
   2. increased automaticity’
      1. 12 hours after infarction
      2. damage to the epicardium produces denervation hypersensitivity to catecholamines in the area beyond the infarct
      3. endocardial lesions interrupt vagal fibres leaving the actions of sympathetic fibres unopposed
2. Types

Monomorphic

1. QRS morphology same for all complexes
2. more common in structural / ischaemic heart disease
3. usually originates in the LV close to the septum
4. right ventricular outflow tachycardia
   1. LBBB pattern
   2. right axis deviation
   3. responsive to beta blockers or calcium channel antagonists

Polymorphic

1. beat to beat variations in QRS complex morphology
2. torsades de pointes is a sub class based on prolongation of the QT interval
3. more common in the setting of poisoning

6. ECG
   1. Main reason for ECG is to differential SVT with Aberrancy vs VY
   2. There are several electrocardiographic features that increase the likelihood of VT:
      1. Positive or negative concordance throughout the chest leads, i.e. leads V1-6 show entirely positive (R) or entirely negative (QS) complexes, with no RS complexes seen

2. Absence of typical RBBB or LBBB morphology
3. Extreme axis deviation (“northwest axis”) — QRS is positive in aVR and negative in I + aVF.
4. Very broad complexes (>160ms)
5. AV dissociation (P and QRS complexes at different rates)
6. 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.

7. Fusion beats — occur when a sinus and ventricular beat coincides to produce a hybrid complex

(the first of the narrower complexes is a fusion beat (the next two are capture beats)

8. Brugada’s sign (red callipers) –  The distance from the onset of the QRS complex to the nadir of the S-wave is > 100ms

9. Josephson’s sign (blue arrow) – Notching near the nadir of the S-wave
10. 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

Brugada Criteria:: 

RS Complex	R to S interval >100 msec (2.5 small boxes)
AV dissociation	Morphology Criteria for VT in V1-2 and aVR
AV dissociation = Ventricular rate is same or faster than the atrial rate Occurs when P waves (represents atrial depolarization) are seen at different rates than the QRS complex.  This is present in only a small percentage of VT ECG tracings, but is diagnostic of VT. Frequently, this is difficult to see due to the fast rate of the QRS complex. Complete Heart Block = Atria are beating independent of ventricles with atrial rate being faster than ventricular rate

The likelihood of VT is increased with:

• Age > 35 (positive predictive value of 85%)
• Structural heart disease
• Ischaemic heart disease
• Previous MI
• Congestive heart failure
• Cardiomyopathy
• Family history of sudden cardiac death (suggesting conditions such as HOCM, congenital long QT syndrome, Brugada syndrome or arrhythmogenic right ventricular dysplasia that are associated with episodes of VT)

The likelihood of SVT with aberrancy is increased if:

• Previous ECGs show a bundle branch block pattern with identical morphology to the broad complex tachycardia.
• Previous ECGs show evidence of WPW (short PR < 120ms, broad QRS, delta wave).
• The patient has a history of paroxysmal tachycardias that have been successfully terminated with adenosine or vagal manoeuvres.

7. Management
   1. pulseless VT treated as ventricular fibrillation
   2. if in any doubt as to whether VT or SVT with aberrant conduction, treat as VT
      1. VT is much more common than SVT with aberrant conduction
      2. the consequences of missing the diagnosis of VT are more serious

3. Electrical cardioversion
   1. elective or emergent
      1. synchronised unless pulseless
   2. indications
      1. chest pain
      2. hypotension
      3. florid APO
   3. recommended synchronised energy settings in the compromised patient (biphasic)
      1. 100J in adults
      2. 0.5 J/Kg then 1J/Kg then 2J/Kg in children
   4. successful in approximately
      1. 90% when the rate is < 200/min.
      2. 70% when the rate is > 200/min.
   5. procedural sedation
      1. provision of sedation is usually limited when the patient is severely compromised
      2. defibrillation should not be delayed
      3. 1-2mg midazolam may be useful in providing amnesia
      4. sedation with ketamine/midazolam/propofol appropriate when haemodynamically stable
4. Overdrive pacing
   1. Pharmacological
      1. amiodarone
         1. Amiodarone 300mg + 250ml 5% glucose, over 30mins
         2. then 900mg + 500ml 5% glucose over 23Hrs (break it to 11.5hr infusions)
   2. lignocaine (lidocaine)
      1. if no amiadarone
      2. less effective than procainamide or sotalol
      3. more effective in ischaemic VT due to depression of automaticity
      4. effective in only 20% with initial bolus of 100 mg
      5. second bolus of 50 mg effective in another 10%
      6. even less effective in non ischaemic VT and best avoided
   3. procainamide
      1. probably the most effective agent
      2. negative inotropic actions limit utility
      3. 100 mg IV bolus, 50 mg/min IV until reversion or 500 mg used
   4. sotalol
      1. 1.5 mg/kg over 5 minutes
      2. only if not haemodynamically compromised and QTc normal
      3. reversion rate of approximately 65%

5. Treatment in special circumstances
   1. digitalis toxicity
      1. phenytoin
      2. ow considered to be of questionable value
   2. Na+ channel blocker toxicity (e.g. TCAD)
      1. HCO3-
   3. hypothermia
      1. rapid rewarming
      2. bretylium/magnesium
   4. hypokalaemia / hypomagnesaemia
      1. potassium / magnesium replacement