Ventricular tachycardia Flashcards
Name 5 different types of ventricular tachycardia.
VT = wide QRS complex tachycardia with rate of >100bpm.
Sustained VT - >100bpm lasting >30sec or requiring early termination due to haemodynamic instability
Non-sustained VT ->100bpm lasting >3 consecutive beats but terminating spontaneously in less than 30 seconds and not resulting in significant instability
Polymorphic VT - multiple different wide QRS complex morphologies
Monomorphic - organised, single-morphology QRS complec arising from one of the ventricles
Haemodynamically stable VT - normal BP and no symptoms
Haemodynamically unstable VT - hypotension, reduced cerebral perfusion, diminished coronary perfusion symptoms.
Idiopathic VT - absence of structural HD, known channelopathy, drug toxicity or electrolyte imbalance.
Torsades de pointes (TdP) - polymorphic VT with characteristic twisting morphology in setting of QT interval prolongation.
Catecholaminergic polymorphic VT - cellular abnormalities of Ca handlung, esp in sympathetic stimulation –> high intracellular Ca
Outflow tract VT - idiopathic VT which arises from RV outflow tract, due to cAMP-mediated triggered activity and so is very sensitive to adenosine treatmnet.
Fascicular VT - idiopathic VT from LV with re-entract circuit partially involving Purkinje fibres, characteristically sensitive to verapamil
What is a sustained ventricular tachycardia?
Ectopic ventricular rhythm >100bpm lasting >30seconds OR requiring termination earlier due to haemodynamic instability, with a QRS >120ms
What is a non-sustained ventricular tachycardia?
Ectopic ventricular rhythm >100bpm lasting >3 consecutive beats but terminating spontaneously in less than 30 seconds
Has a wide QRS complex >120ms or more
What is seen on ECG in VT?
Presence of a wide complex tachycardia (QRS ≥120 msec) at a rate ≥100 bpm.
Name a polymorphic VT which occurs with QT interval prolongation.
Torsades de pointes
has a characteristic twisting morphology occurring in the setting of QT interval prolongation.
TdP is initiated by an early after-depolarisation and perpetuated by re-entry.
What % of sudden deaths are cardiac in origin?
90% - most due to VT or VF
Who is more predisposed to torsades de pointes?
Women - they have longer QT intervals compared to men, whether drug-induced/congenital long QT syndromes, and so are more likely to show torsades de pointes
What is the aetiology of VT?
Structural heart disease
- ischaemia
- prior infarction
- cardiomyopathy
- valvular disease
- arrhythmogenic RV cardiomyopatthy
- LV non-compaction
- other disorders of the myocardium
Channelopathy
- potassium channels -long QT syndrome, short QT syndrome
- sodium channels - Brugada syndrome, congenital long QT syndrome
- calcium channels - catecholaminergic polymorphic VT
Drug toxicity
Electrolyte imbalance
What are the risk factors for VT?
- CAD/ MI
- LV systolic dysfunction
- HOCM
- long QT syndrome
- short QT syndrome
- Brugada syndrome
- ventricular pre-excitation
- arrhythmogenic RV cardiomyopathy
- electrolyte imbalance - esp low K and low Mg
- drug toxicity - long QT interval occurs with macrolides, chlorpromazine, haloperidol, and domperidone
- Chagas disease and other cardiomyopathies
- FH of sudden death
- mental or physical stress
What are the clinical features of VT?
VT and SVT symptoms overlap
- Tachycardia
- Palpitations
- Cannon A waves - sign of AV dissociation, diagnostic of VT
- Dyspnoea/chest discomfort
- Nausea/diaphoresis
- Syncope/presyncope
If sustained for long enough:
- Hypotension
- Weak pulse
- Airway compromise
What investigations would you do for VT?
ECG or Holter monitor - wide complex tachycardia with HR >100 and QRS >120ms for at least 3 beats; must differentiate SVT and VT as management will differ.
Electrolytes and cardiac enzymes - Mg, K, CK and troponin I
TTE echo - determines structural heart disease
Stress test/ cardiac catheterisation - establish presence of CAD, ischaemia.
MRI - if suspected RV cardiomyopathy evaluates for presence of fibro-fatty infiltration or RV and its dysfunction.
EP testing (electrophysiological ) - may distinguish VT from SVT where this cannot be done by ECG
Genetic screening - available for mutations assoc w/ long and short QT syndrome, Brugada syndrome, hypertrophic cardiomyopathy, and catecholaminergic polymorphic VT.
What abnormality is shown here?
QT prolongation (510ms)
Normal QT - 400-440ms. Women have a longer QT interval.
How do you distinguish SVT from VT on ECG?
1. Absence of RS complex in precordial leads = VT
2. If RS complex is present in 1, measure QRS onset to nadir of S wave. R-S of >100ms = VT
3. If R-S is <100ms then check for AV dissociation. If present = SVT
4. If no AV dissociation, check V1 and V6 for LBBB or RBBB.
- If none of these steps favour VT, diagnosis of SVT is made.*
- VT shown below.*
How is VT managed?
Haemodynamically unstable:
- Synchronised cardioversion - attempt before drug therapy in those with symptoms. Repeat until rhythm is controlled. Treat cause of VT, ABCDE protocol.
- Then anti- arrhythmic medication - e.g. amiodarone/lidocaine.
Haemodynamically stable:
- Anti-arrhythmic medications + treat cause - adenosine, procainamide or amiodarone
- If no response then as above for unstable.
Non-idiopathic VT with risk of VT/sustained VT/cardiac arrest without identifiable reversible cause:
-
Implantable cardioverter defibrillator (ICD) - provides continuous monitor for cardiac rhythm control and terminating VT. Reduces mortality by 30-40%
* AND anti arrhythmic medication - e.g. mexiletine, flecainide, propafenone, sotalol, amiodarone
Catheter ablation - for those with structural heart disease experiencing recurrent episodes of VT; with moderate to severe symptoms and idiopathic causes.
NB: non sustained VT which does not have an underlying cause to treat → reassure and self-monitor or BB (metoprolol/atenolol) or CCB (verapamil/diltiazem)
What are the complications of VT? What is the prognosis?
- ICD system malfunction
- VF
- Sudden cardiac death
- ICD-related infection
- Cardiomyopathy - from frequent VT
- Amiodarone-induced thyroid dysfunction
Prognosis:
- Idiopathic VT usually has favourable prognosis and is not progressive.
- Non-idiopathic VT which can cause VF has a high mortality rate. ICD is important to reduce mortality.
Describe this ECG.
Initiation of wide QRS rhythm is not preceded by a P-wave, suggesting non-sustained ventricular tachycardia
Describe this ECG.
Long-QT syndrome
Describe this ECG.
Brugada’s syndrome - showing terminal positive R-wave and ST-segment elevation in lead V1. J point elevation and downwards-sloping ST-segment elevation in the right pre-cordial leads
