4. Ventricular arrhythmias- classification, etiology,ECG, clinical characteristics, treatment.

Conduction system
 SA node- primary pacemaker of heart, normal beat initiated by SA node, inherent rate 60-100BPM= P wave
 Internodal and inter-atrial pathways
 AV node- Located in septum of heart, inherent 40-60 BPM, represents PR segment of QRS complex
 Bundle of his- represents ventricles depolarizing, origin of all ventricular rhythms, inherent rate 20-40 BPM
 Perkinje fibers

Classification of RCD
1. Disorders in Automatism
2. Disorders in excitation
 Supraventricular
 Ventricular
3. conduction disorders
 SA block and inter-atrial block
 BBB( left and right)
4. Pre-excitation syndromes (conducting a pathological link)

Arrhythmias that originate in ventricular myocardium/ his purkinje system include

1. Premature ventricular contraction- are ectopic beats arising in the diastolic period of preceding sinus beat
 Unifocal
 Multifocal
 Ventricular couplets
 Caused by electrical Irritability- ischemia, electrolyte imbalances and drug intoxication
 Coupled PVCs occur in pairs
 Clinical significance when
 ≥3 PVC’s in a row (run of V-tach)
 Come close/ on top of preceding T-wave ( R-T)
 >30% of complexes and increasing in frequency
 PVC’s come from different foci (“multifocal”/ “ multiforme”)
 May preclude occurrence of Ventricular tachycardia/ Ventricular fibrillation

-Fusion beat(left red arrow)- p-wave infront of PVC and PVC is narrower than other PVCs- indicates the
beat is product of both sinus node and ectopic ventricular focus.
-Capture beat- complex is narrow enough to suggest normal ventricular conduction- indicates that atrial
impulse has made it through and conduction of ventricles is relatively normal.

2. Ventricular tachycardia- ≥ 3 consecutive ectopic beats at rate of > 100 bpm, originate in the ventricles
 Non-sustained <30secs
 Sustained >30secs
 Most patients have significant heart diseases – CAD, previous MI, Cardiomyopathy
 ECG
 Rates range from 100-250 BPM
 P waves often dissociated as seen (arrow)

 AV dissociation- when Atria and ventricles Act indecently, due additional Ventricular focus
 Mechanisms of VT
o Reentrant- Reentrant ventricular arrhythmias
 Premature ventricular complexes
 Idiopathic left ventricular tachycardia
 Bundle branch reentry
 Ventricular tachycardia and fibrillation when associated with chronic heart disease- due previous MI and
cardiomyopathy
o Automatic- Automatic Ventricular arrhythmias
 Premature ventricular complexes
  Ischemic ventricular tachycardia
 Ventricular tachycardia and fibrillation when associated with Acute medical conditions
 Acute MI or ischemia
 Electrolyte and Acid-base disturbances, hypoxemia
 Increased sympathetic tone and drugs
o Triggered- Triggered activity ventricular arrythmias
 Pause- dependent triggered activity
 Early after depolarization (phase 3)- due hypokalemia etc
 Polymorphic ventricular tachycardia
 Catechol- dependent triggered activity
 Late after depolarization (phase 4) – due local catecholamines, hypercalcemia, digitalis
intoxication
 Idiopathic right ventricular tachycardia
2b. Idioventricular tachycardia- enhanced idioventricular rhythm, manifests when rate = sinus rate, characterized by
 Bizarre QRS complexes/ fusion beats
 Rapid idioventricular rate (70-80BPM)
 AV dissociation and capture beats
 Absence of pacemaker protection-abolished by faster sinus
rhythm
ECG clues for Diagnosis of Ventricular tachycardia
 Av dissociation (capture beats, fusion beats)
 Concordance of QRS complex in all precordial leasa
 Front plane : LAD with QRS > 140 ms
 Precordial leads: RS pattern, onset of R to Nadir of S > 100ms
 RBBB pattern with
o V6: QS or dominant S
o V1: R> R’
o V1: Monophasic R or biphasic qR or R/S with initial deflection
different from sinus initiated QRS
 LBBB pattern with
o Right axis: negative deflection in V1> V6
o V6: qR or QS
o V1: R > 40ms
o
3. Ventricular flutter- very rapid and REGULAR ectopic ventricular discharge
 Mechanism- caused by re-entry with frequency of 300 BPM  ventricles depolarizing in a circular pattern 
minimal CO
 ECG shows
 Grossly abnormal intraventricular conduction- QRS and deflexions are very wide and bizarre, one merging
with another
 Difficult to define QRS complex, ST segment and T-wave
  continuous sine-like waveform
 Atrial frequency 60-100 bpm
 Ventricular frequency 150-300bpm
 Regularity regular
 Origin: ventricles
 P-wave AV dissociation

4b. Ventricular flutter “Torsades De pointes”- twisting of point
 Etiology- congenital long QT, Drugs- Quinidine, Phenothiazines, Hypokalemia/Hypomagnesaemia, 3 degree blocks
 ECG shows
 QRS bizarre and multiform
 OQRS have sharply pointed apices- which are directed upwards for a short
period and then direct downward for a short period
 QRS form and axis undulate
 Multiform ventricular flutter
 4. Ventricular Fibrillation- expression of chaotic, uncoordinated, ventricular depolarization. It is a terminal event
 Etiology- IHD esp acute MI, Quinidine and digitalis intoxication esp with hypokalemia and hypothermia <28 C
 Mechanism- Advanced physiological asymmetry of biventricular chamber such as in MI, or Premature/Rapid
stimulation of asymmetrical chambers e.g by PVCs, VT or V. flutter
 ECG shows
 Completely irregular, chaotic and deformed deflexion of varying height, width and shape
 P-waves, QRS complexes, ST segments and T waves cannot be identified

Difference B/W V. flutter and V.Fib

 V, Flutter- deflexion are Uniform, Constant, Regular and Relatively Large amplitude
 V. Fib- deflexion are Small, completely chaotic and Irregular

Brugada Syndrome
 RBB + persistent ST elevation in right precordial leads
 Sudden cardiac death
 3 patterns
 Type1 – J point elevation with ST segment elevation ≥ 2 mV followed by negative -Twave
 Type 2- saddle-back configuration of ST elevation > 0.2 mV – Downsloping ST elevation-
positive or biphasic T wave not touching baseline
 Type 3- St elevation < 0.1 mV with either of morphologies

Acute management of Sustained

Long
term
therapy