VT, VF Flashcards

(22 cards)

1
Q

Discuss the Features of Ventricular Tachycardia (VT) – Definition & Features

A
  • ≥ 3 consecutive beats
  • HR 100–250 bpm
  • Slow VT: 100–120 bpm
  • Ventricular flutter: > 250 bpm
  • Broad QRS complexes- Usually > 160 msec
  • Axis: North-west axis
  • ECG features: Capture beats, Fusion beats

->Sustained vs Non-sustained VT
* Non-sustained VT: < 30 sec

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2
Q

VT
Causes
and
Risk factors

A
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3
Q

Brugada criteria

A

RS interval - calculated from start of R to nadir of S

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4
Q

Morphology criteria in Brugada

A

=>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

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5
Q

Differential Diagnosis of Wide-Complex Tachycardia

A

=>Several arrhythmias can present as a wide-complex tachycardia (QRS > 120 ms), including:

  • Ventricular Tachycardia
  • SVT with aberrant conduction due to bundle branch block
  • SVT with aberrant conduction due to the pre-excitation syndromes
  • Pace-maker mediated tachycardia
  • Metabolic derangements e.g. hyperkalaemia
  • Poisoning with sodium-channel blocking agents (e.g. tricyclic antidepressants)
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6
Q

VT Storm (Electrical Storm)
Definition

A

=> 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

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6
Q

Pathophysiology of
VT/VF storm due to ischaemia
Symptoms

A

> 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.

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7
Q

Mx of VT Storm

A

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.

3). Rapid correction
* Of any quickly correctable causes.

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

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8
Q

Mx cont..
Pharmacological Mx

A

1)Adrenergic blockade with beta blockers- rarely possible because of associated hypotension–> If BP maintained- Propranolol - DOC
2) Amiodarone
3) Lignocaine
4)Anaesthetic agents

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9
Q

ii. Amiodarone

A

->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

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10
Q

iii. Lignocaine
Mechanism
&
Dose

A
  • Binds to fast Na⁺ channels.
  • Binding ↑ with acidosis & ↑ heart rate
  • Relatively weak antiarrhythmic properties, but useful in ischaemic VT.
    Dose: 1-1.5mg/kg bolus foll by 1mg/min as iv infusion.
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11
Q

pharmacological therapycont..
Anaesthetic agents and procedures

A
  • Anaesthetic agents:
    • Short-acting anaesthetics (e.g. propofol, midazolam) → conversion & suppression of VT.
  • Stellate Ganglion block
  • Thoracic Epidural block
    -directly target sympathetic nerves innervating myocardium.
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12
Q

Adjunctive / Non-pharmacological Therapy
cont..

A

=> 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.

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13
Q

Clinical Syndromes of Electrical Storm
Classified as:

A

->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

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14
Q

Monomorphic VT

A

->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

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15
Q

Therapy

A

=>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.

15
Q

Risk Factors for Torsades

A

*Female gender
* Bradycardia
* Heart block
* Hypokalaemia
* Hypomagnesaemia
* Hypocalcaemia
* Inherited long QT
* Proarrhythmic drugs (sotalol, amiodarone, erythromycin, haloperidol, methadone)

15
Q

polymorphic VT
Definition
Causes
Mechanism

A

->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

15
Q

Ventricular Fibrillation (VF)

A

->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.

16
Q

Brugada Syndrome

A

->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.

17
Q

Treatment algorithm for multiple ICD shocks

18
Q

ICD & Electrical Storm
Important points

A

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