CardiologyTier 1Disease (DEADMAN)

Cardiac arrhythmias - ventricular tachycardia

Description

	Monomorphic	Polymorphic
Morphology	Single stable QRS	Varying QRS
Mechanism	Scar reentry	Ischaemia, or long QT (torsades)
Implication	Structural substrate	Acute trigger

Assume every wide-complex tachycardia is VT until proven otherwise
- With known structural heart disease, a WCT is VT ~95% of the time

Most VT occurs on structural heart disease - post-MI scar the largest single group
Idiopathic VT (RVOT, fascicular) occurs in structurally normal hearts - younger, good prognosis
VT degenerating to VF is the mechanism of most sudden cardiac death

Mechanism

Scar-related reentry - dominant mechanism
- Infarct or fibrosis -> zones of slow conduction + unidirectional block
- -> reentrant circuit -> monomorphic VT
Triggered activity - digoxin toxicity, long QT (early afterdepolarisations), CPVT (delayed)
Enhanced automaticity - ischaemia, electrolytes, catecholamines

Substrates

Ischaemic - prior MI (commonest), acute ischaemia
Non-ischaemic - DCM, HCM, ARVC, cardiac sarcoid, amyloid, myocarditis, Chagas
Channelopathies - long QT, Brugada, CPVT, short QT
Idiopathic - RVOT VT (LBBB morphology, inferior axis), fascicular VT (RBBB, left axis, verapamil-sensitive)
Reversible - hypokalaemia, hypomagnesaemia, QT-prolonging drugs, ischaemia, thyrotoxicosis

VT vs SVT with aberrancy

AV dissociation - the single most specific finding
- Capture beats, fusion beats
Concordance across V1-V6 - all dominantly positive or all dominantly negative
Very wide QRS, extreme (northwest) axis
*Haemodynamic stability does not distinguish them - stable VT is common*
Brugada and Vereckei algorithms exist; when in doubt, treat as VT

Workup

Acute - unstable

Acute - stable

12-lead ECG first, then:
IV amiodarone; lidocaine an option in ischaemic VT; sotalol
Correct K+ and Mg2+ in everyone
Adenosine only if the diagnosis is genuinely uncertain - diagnostic, not therapeutic
*Verapamil in an undiagnosed wide-complex tachycardia can precipitate collapse*

Polymorphic VT

Long QT (torsades): IV magnesium, stop offending drugs, correct K+, overdrive pacing or isoprenaline
Normal QT: assume acute ischaemia -> urgent angiography

Electrical storm

Long-term - with structural heart disease

ICD for secondary prevention (AVID)
Beta blocker in everyone
Add amiodarone or sotalol for frequent episodes or shocks
Catheter ablation for recurrent VT despite drugs, or for storm
Optimise heart failure therapy; revascularise where relevant
CAST and EMIAT: antiarrhythmic drugs do not improve survival post-MI, and class I agents are harmful

Long-term - structurally normal heart

Prognosis is that of the underlying substrate, not the arrhythmia
Sustained VT with structural disease -> high recurrence and high SCD risk without an ICD
NSVT: a risk marker in cardiomyopathy; benign in structurally normal hearts

Complications

Monitor

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