- The most common cause of VT is myocardial ischaemia or myocardial scarring following acute MI
- A broad-complex SVT with aberrancy from ventricular pre-excitation (WPW) is treated the same as VT ⇒ Regard al broad complex tachycardia as VT until, or unless, proved otherwise
- The identification of P waves dissociated from QRS complexes during broad complex tachycardia confirms VT
- Accelerated idioventricular rhythm (idioventricular rhythm with a heart rate of 50-110 beats/min) is not categorised at VT and commonly occurs after successful thrombolysis or PCI (see ACS)
Differential Diagnosis of Wide Complex Tachycardias
- Ventricular tachycardia
- A supraventricular tachycardia with aberrant conduction (eg, supraventricular tachycardia with underlying bundle-branch block); often rate-related, appearing only with fast heart rates
- AV reciprocating tachycardia (antidromic tachycardia) in a patient with preexcitation (eg, WPW)
- Paced rhythms
Management
- Unstable VT
- No recordable BP and no palpable pulse (pVT)
- Call for cardiac arrest trolley and proceed with ALS
- Prioritise early defibrillation
- VT with hypotension, angina, LVF or impaired mental status
- Call for senior help
- Apply high-flow oxygen by mask and gain IV access
- Attach ECG monitor/defibrillator to the patient and confirm rhythm
- Prepare procedural sedation such as propofol 200mg in 20mL IV and call an anaesthetist
- Once senior assistence is present proceed with DC cardioversion (start with 120-150 J biphasic and repeat up to three times, with stepwise increase in joules)
- No recordable BP and no palpable pulse (pVT)
- Stable VT
- Deterioration can be rapid, be prepared
- Call for cardiac arrest equipment and senior assistance
- Give the patient 100% by mask
- Attach an ECG monitor to the patient
- Make sure than IV line is in place
- Obtain a 12-lead ECG and review QRS complexes and determine if it is monomorphic or polymorphic
- Monomorphic: ECG shows a broad-complex QRS, regular rhythm, rate >100 beats/min with constant QRS
- LV function unknown or impaired:
- Give amiodarone 300 mg IV bolus over 20-60 minutes followed by infusion of 900 mg over 24 hours
- LV function known to be normal:
- Administer amiodarone as above
- Prepare for synchronised cardioversion if amiodarone is unsuccessful or the condition deteriorates
- Transfer to ICU/CCU for continuous ECG monitoring
- Look for precipitating cause of the VT such as myocardial ischaemia, eletrolyte abnormality (hypokalaemia, hypomagnesaemia, hypocalcaemia) or drug toxicity (antiarrhythmic and other sodium-channel blocking drugs especially TCAs)
- LV function unknown or impaired:
- Polymorphic: ECG shows a braod-complex QRS, regular rhythm, rate >100 beats/min but with a variable and changing axis
- Review the baseline 12-lead ECG
- Normal baseline QT interval
- Give amiodarone as for monomorphic VT
- Baseline QT interval is prolonged leading to ‘torsades de pointes’
- Causes include electrolyte abnormality (e.g. hypokalaemia, hypomagnesamia, tricyclic antidepressants) drug interactions or a congenital disorder
- Give magnesium sulfate 2g (8mmol or 4mL of 49.3% solution) IV over 1-2 min
- Correct any underlying metabolic disorder, particularly hypokalaemia
- DC cardioversion is essential for critical hypotension but the torsades de points rhythym often recurs and may require several shocks
- Avoid drugs that prolong QT interval (including amiodarone)
- Monomorphic: ECG shows a broad-complex QRS, regular rhythm, rate >100 beats/min with constant QRS