1: Broad Complex Tachyarrythmias Flashcards
What does broad complex tachycardia indicate
Arrhythmia has arisen from the ventricles
What are the two types of ventricular tachycardia
Monomorphic + Polymorphic
What is the most common type of VT
Monomorphic
What causes monomorphic VT
MI
What is a subtype of polymorphic VT
Torsades de pointes
What causes torsades de pointes
Prolongation of the QT interval
What is sustained VT
VT lasting more than 30s leading to haemodynamic compromise
What is non sustained VT
3 or more consecutive ventricular complexes terminating spontaneously in 30s
What causes monomorphic VT
MI or previous MI scars
What causes polymorphic VT
Torsades de points (gradual prolongation of QT)
What are the congenital causes of prolonged QT interval
Jervell-Lange Nielsen
How does Jervell-Lange Nielsen present
With deafness
How does Romano Ward present
Without deafness
What drugs may prolong the QT interval
Macrolide antibiotics TCA Amiodarone Sotolol Class I anti-arrythmics (procainmide) Chloroquinine Terfenadine
What are other causes of prolong QT
- Hypocalcaemia
- Hypokalaemia
- Hypomagnesaemia
- MI
- Myocarditis
- Hypothermia
- Subarachnoid haemorrhage
How will non-sustained VT present
Asymptomatic
How will sustained VT present
Palpitations Chest Pain Hypotension Shock Syncope
What may sustained VT progress to
VF and death
What are the 3 pathophysiolgocial mechanisms of VT
- Re-entry
- Triggered activity
- Automaticity
What is the commonest mechanism underlying VT
Re-entry
What is re-entry
Requires two distinct conduction pathways with a block in one and slowing in another
What commonly causes re-entry
Scar from MI
What is triggered activity
Where there are either early or late depolarisations
What is abnormal automaticity
Region of ventricular cells causing abnormal conduction
What is first line Ix for VT
ECG
How will VT present on ECG
AV disassociation (no relationship between P wave and QRS)
How will monomorphic VT present
QRS complexes appear the same
How will polymorphic VT present
QRS complexes appear different
How is haemodynamically unstable VT assessed
Whether a pulse is present or not
How is haemodynamically unstable VT without pulse managed
Defibrillation
How is haemodynamically unstable VT with pulse managed
DC cardioversion
What is first-line for haemodynamically stable VT
Amiodarone
How should Amiodarone be administered
Via a central line
What is second line for Stable VT
Lidnocaine
When should lidnocaine be used with caution
Individuals with severe left ventricular impairment
What is 3rd line for VT
Procainmide
What is used for long-term management of VT
Implantable cardiac defibrillator (ICD)
How is torsades de pointes managed acutely
Magnesium sulphate
How is torsades de pointes managed in the long-term
B blocker
What is the main complication of VT
Can progress to VF and cause sudden cardiac death
What is VF
A life-threatening cardiac arrhythmia characterised by high frequency ventricular contractions resulting in diminished cardiac output
Explain the pathophysiology of VF
- when the ventricles are damaged there is tissue heterogeneity (cells have different electrical properties)
- if ventricular pacemaker cells fire at the wrong time but a group of adjacent cells also fire this can cause a premature ventricular contraction
- > 3 PVC (VT) can lead to VF
- If adjacent cells have different electrical properties it can lead to re-entry circuits
How will ECG present in VF
No discernible P waves or QRS
How is VF managed
Advanced Cardiac Life Support
What is the main complication of VF
Sudden cardiac death
