Discuss the Features of Ventricular Tachycardia (VT) – Definition & Features
->Sustained vs Non-sustained VT
* Non-sustained VT: < 30 sec
VT
Causes
and
Risk factors
Brugada criteria
RS interval - calculated from start of R to nadir of S
Morphology criteria in Brugada
=>RBBB criteria:
i)Smooth monophasic R wavein V1
ii) Notched downslope of R wave- Lt rabbit ear taller than Rt in V1
iii) qR complex in V1
iv) Completely Negative complex- no R wave in V6
=>LBBB criteria:
i) Broad R wave- > 40msec in V1
ii) R-S interval >60msec
iii) Notching/ Slurrig of S wave in V1- josephson’s sign(in the downslope)
iv) q waves in V6
If in doubt, treat as VT
Differential Diagnosis of Wide-Complex Tachycardia
=>Several arrhythmias can present as a wide-complex tachycardia (QRS > 120 ms), including:
VT Storm (Electrical Storm)
Definition
=> Definition: ≥ 3 or more episodes of sustained VT / VF within 24 hours → requires cardioversion / defibrillation ± antiarrhythmics or, recurrent ICD firing.
-> Sustained VT = lasting > 30 sec or requiring termination due to haemodynamic compromise.
->Refractory VT
* Recurrent episodes of VT / VF → can be shocked out of VT easily but keep re-entering into arrhythmia.
OR
* Remain in VT, never go into sinus rhythm
Pathophysiology of
VT/VF storm due to ischaemia
Symptoms
> VT/VF causes ⬆️ intracellular Ca levels→ proarrhythmogenic
->Recurrent shocks and episodes of cardiac arrests→ myocardial injury + pain → ⬆️catecholamines →proarrhythmogenic
->VF/VT storm is not self-limiting unless treated, hence Need aggressive therapy
->Symptoms: palpitations, Dizziness→ syncope → cardiac arrest.
Mx of VT Storm
Initial evaluation & Management
1). Accurate diagnosis of underlying arrhythmia
* e.g. VT vs SVT with BBB / aberrancy
* If in doubt, Wide complex tachycardia should always be treated as VT (esp. if structural heart disease).
* (Treating VT as SVT may precipitate cardiac arrest).
2). Identify causative factors(FAST ICE)
* Acute ischaemia → urgent angio ± revascularisation
* Worsening CCF
* Electrolyte imbalance → correct (K⁺, Ca²⁺, Mg²⁺).
* Endocrine (thyrotoxicosis) → β-blockers, anti-thyroid drugs.
* Antiarrhythmic drugs → proarrhythmia (esp. catecholamines).
* Sepsis / fever → treat underlying sepsis.
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3). Rapid correction
* Of any quickly correctable causes.
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4). Analgesia & sedation
* Electrical storm may be very distressing.
* Anxiety → ↑ catecholamines → worsening of storm.
* Intubation Ventilation, sedation, analgesia to suppress sympathetic drive worsening VT storm unless a quickly correctable cause eg- electrolyte imbalance can be found
Mx cont..
Pharmacological Mx
1)Adrenergic blockade with beta blockers- rarely possible because of associated hypotension–> If BP maintained- Propranolol - DOC
2) Amiodarone
3) Lignocaine
4)Anaesthetic agents
ii. Amiodarone
->Most used antiarrhythmic therapy.
->Rapid IV administration →
- blocks fast Na⁺ channels(more blockade in faster HR)
- Also blocks K⁺ channels → prolongs AP duration & refractoriness.
- Blocks L-type Ca²⁺ channels
- Inhibits NE release
–>dose- 5mg/kg iv bolus foll. by 1mg/minx6hrs → 0.5mg/min→not to exceed 2.2gm in 24hrs
* **ARREST trial: Amiodarone vs placebo → improved survival to hospital admission in VF / pulseless VT.** * Effective when other agents have been ineffective.
Loading dose req. even in pts on chronic amiodarone therapy
iii. Lignocaine
Mechanism
&
Dose
pharmacological therapycont..
Anaesthetic agents and procedures
Adjunctive / Non-pharmacological Therapy
cont..
=> Non-pharmacological therapy
-> IABP / LVAD
* Malignant Arrhythmias are accepted indication for IABP / LVAD.
-⬆️es Coronary Perfusion Pressure, relieves ischemia
-In Nonischemic aetiology, → Reduces afterload & LV wall stress
-> ECMO
- If deemed necessary → should be done early to prevent end-organ damage.
-> Intracardiac mapping & Radiofrequency ablation.
Clinical Syndromes of Electrical Storm
Classified as:
->Determining cause of E-storm is essential → treatment must be directed towards underlying mechanism.
->Classified on basis of QRS / ECG morphology:
1. Monomorphic VT
2. Polymorphic VT
3. VF
Monomorphic VT
->Usually associated with structural heart disease.
->Mechanism = reentry around a fixed anatomic substrate (scar tissue after MI).
->Trigger: usually premature ventricular depolarisation.
* Does not require acute ischaemia as trigger.
* Uncommon in patients with acute MI.
->Degree of haemodynamic compromise depends on:
* Ventricular rate
* LV function
* Presence of IHD
* Loss of A–V synchrony
Therapy
=>Reverse ischaemia:
* Coronary revascularisation, thrombolytics, antiplatelets.
* Amiodarone / β-blockers → antiarrhythmics of choice.
* Lignocaine: less effective than Amiodarone, but can be used in ischaemic settings.
* Electrolyte correction: correct K⁺, Mg²⁺, Ca²⁺.
* Mg²⁺: unlikely to help in polymorphic VT unless QT is prolonged (torsades).
*** Torsades de pointes = pause-dependent polymorphic VT.** * Associated with long QT. * Often triggered by bradycardia.
⚠️ Do not use isoprenaline or other catecholamines in polymorphic VT → instead use Amiodarone / β-blockers.
Risk Factors for Torsades
*Female gender
* Bradycardia
* Heart block
* Hypokalaemia
* Hypomagnesaemia
* Hypocalcaemia
* Inherited long QT
* Proarrhythmic drugs (sotalol, amiodarone, erythromycin, haloperidol, methadone)
polymorphic VT
Definition
Causes
Mechanism
->VTwith varying QRS amplitude and Axis- appear to twist around the baseline
->Causes[HIM]
* Most often acute Ischaemic syndromes (often initial manifestation of ischaemia).
Acute Myocarditis
* HOCM
->Mechanism: ischaemia → Purkinje cell automaticity & spontaneous firing of fibres → degeneration to polymorphic VT / VF.HR>200/min
Ventricular Fibrillation (VF)
->Primary mechanism: ischaemia.
->Can be triggered by closely coupled PVCs in healthy heart or post-MI.
* RF ablation of these sites can cure further VF episodes.
Brugada Syndrome
->Inherited Na⁺ channelopathy.
->Characteristic ECG: RBBB + ST elevation in V1–V3.
->Can cause recurrent VF → sudden cardiac death.
->Predisposing factors: fever, increased vagal tone, bradycardia.
Class I antiarrhythmics (Na⁺ channel blockers) can unmask Brugada syndrome–>Contraindicated.
ICD required for prevention of sudden death.
Treatment algorithm for multiple ICD shocks
ICD & Electrical Storm
Important points
1->Transient ST-segment changes & mild troponin rise → common after multiple shocks.
2->Rapid SVT / AF may cause inappropriate shocks.
- Place a magnet over ICD to inhibit sensing of arrhythmias.
- If patient develops true arrhythmias, removing magnet re-enables delivery of therapy.
- Applying a magnet does not alter pacing ability of ICD.
3->Antiarrhythmic medications can reduce frequency of ICD shocks (Amiodarone & β-blocker).
4->Coordination with EP team essential.
5->CRT may ↓ incidence of electrical storm (progressive LV dysfunction = predictor of storm).
CRT- cardiac resynchronisation therapy