A short informative presentation about the ECG changes in ventricular arrhythmias.

1. Ventricular Arrhythmias
Ilkin Bakirli
Internal Cardiology Presentation
22.05.19

2. Content Layout
▪ Introduction
▪ PrematureVentricular Contractions
▪ VentricularTachycardia
▪ Torsades de Pointes
▪ Ventricular fibrillation
▪ Burgada syndrome
▪ Treatment of ventricular arrhythmias

3. Introduction
▪ Ventricular arrhythmias are arrhythmias that originate in the
ventricular myocardium or in the bundle of His
▪ They emerge from a focus in the myocardium or purkinje fibers
▪ Typically the QRS complex is wide, >0.12 seconds

4. Premature Ventricular Contractions (PVC)
▪ These are ectopic beats arising in the diastolic period of preceding
sinus beat
▪ They can be multifocal, unifocal or ventricular couplets
▪ Causes include ischaemia, electrolyte imbalances, drug intoxication
▪ Normal sinus beats are interspersed with broad QRS complexes
▪ Ectopic beats are followed by a full compensatory pause
▪ Ectopic QRS complexes are wider and have a different axis than the
sinus QRS complexes

5. Premature Ventricular Contraction (PVC)

6. Monomorphic Ventricular tachycardia
(MVT)
▪ Three or more consecutive ventricular ectopic beats at a rate of > 100 bpm
▪ Onset of the R wave is slurred
▪ Signs of atrioventricular dissociation (P wave dissociation)
▪ Wide QRS > 0.12 s
▪ Nonsustained > 30 s
▪ Mechanism is a re-entry pathway, automatic focus or a triggered activity
due to a previous MI, cardiomyopathy or CAD.The depolarisation does not
spread through the bundle of his, resulting in a slurred, broad and slow QRS
▪ VT is potentially life threatening and may result in cardiac arrest

7. Monomorphic Ventricular tachycardia
(MVT)

8. Polymorphic Ventricular Tachycardia
(PMVT)
▪ QRS complexes are broad and morphologically different than in sinus
rhythm
▪ QRS rate is > 100bpm and morphology changes beat to beat
▪ RR intervals vary
▪ Dissociated P waves present
▪ PMVT occurs when there is an abnormal focus of electrical activity in
the ventricular myocardium.The pattern of depolarisation varies
randomly.
▪ The common causes are acute ischemia, electrolyte disturbances or
hereditary conditions

9. Polymorphic Ventricular Tachycardia
(PMVT)

10. Torsades de Pointes (TDP)
▪ Regular broad QRS complexes
▪ Rapidly changing axis and QRS morphology
▪ ‘R’ on ‘T’ phenomenon at the onset of tachycardia
▪ TDP (twisting of the points) is a form of ventricular tachycardia with a
congenital or acquired long QT syndrome. The long QT segment
shows a long refractory and repolarisation time. If there is a
premature ventricular beat, it falls on theT wave of the normal sinus
beat.This is known as ‘R’ on ‘T’ phenomenon.
▪ Causes include quinidine or phenothiazine use, hypokalemia

11. Torsades de Pointes (TDP)

12. Ventricular fibrillation
▪ Completely chaotic ECG recordings
▪ As ventricular fibrillation continues the QRS complex gets smaller,
until eventually the ECG recording has the appearance of an asystole
▪ Completely disordered electrical activity in the ventricles causes
them to fibrillate. Neither ventricular filling nor ventricular systole
can occur, and cardiac arrest ensues
▪ Causes include cardiac ischemia, electrolyte imbalance, drugs,
pulmonary embolism and chest trauma

13. Ventricular fibrillation

14. Burgada syndrome
▪ BS is an autosomal dominant condition with variable expression.There is
an abnormality of cardiac sodium channels. Abnormal action potentials
are created in the cardiac myocytes
▪ Pseudo- RBBB appearance inV1 toV3
▪ ST elevation in leadsV1 toV3
▪ ECG changes may be present all the time, may be transient, or may occur
only when given provoking drugs
▪ The pattern of ST elevation depends on the type of the syndrome;
Type 1: coved ST elevation > 2mm,T wave inverted
Type 2: saddle shaped STelevation >2mm,T wave positive or biphasic
Type 3: saddle shaped ST elevation < 2mm,T wave positive

15. Burgada syndrome

16. Treatment options
ACUTE LONGTERM
Amiodarone Beta blockers
Procainamide Amiodarone
Sotalol ICD
Lidocaine
DC cardioversion