Profil

• Dr. Dian Zamroni, SpJP, FIHA

• Pendidikan :
• Dokter Umum
Fakultas Kedokteran Universitas Indonesia/RS Cipto
Mangunkusumo Jakarta 2001
• Dokter Spesialis Jantung
Fakultas Kedokteran Universitas Indonesia / Pusat
Jantung Nasional Harapan Kita Jakarta 2012
• Fellowship Intensive Cardiovascular Care 2014
• Fellowship Cardiovascular Intervention 2015

• Posisi
• Staf Pengajar Departemen Kardiologi dan Kedokteran
Vaskular FKUI
• Staf Divisi Critical Care dan Cardiovascular Emergency
Pusat Jantung Nasional Harapan Kita
1
 Ventricular Arrhytmia

Dian Zamroni, MD, FIHA

Departemen Kardiologi dan Kedokteran Vaskular FKUI/
Pusat Jantung Nasional Harapan Kita Jakarta
CONDUCTION SYSTEM
 Arrhythmias

Supraventricular Ventricular
Narrow Complex QRS Wide Complex QRS> 0,12 dt
(except: BBB, WPW,aberans)
 Ventricular arrhythmias

Premature ventricular Tachycardia Arrhythmias

contraction

Ventricular Tachycardia Ventricular fibrillation

N N
100-250 x/mnt > 350 x/mnt
Ventricular arrhythmias
 Commonly occur as a
result of ectopic
focus/foci distal to the
bundle of His

 Most common one is

the premature
ventricular
contraction (PVC)

 Most are benign but

can be lethal
Mechanisms of ventricular arrhythmias

 Impulse Formation Disorders

 Abnormal Automaticity
○ Discharge from a pathologic ectopic ventricular focus

 Triggered beats
○ Afterdepolarizations (AD): Abnormal depolarizations of myocytes that
interrupt phase 2, 3, or 4 of the AP

 Impulse Conduction Disorders

 Delayed conduction
○ Delayed SA/AV nodal impulse allows initiation of inherent ventricular
impulse

 Re-entry
○ Creation of a circuit that leads to 2 or more depolarizations in
surrounding tissue
 Afterdepolarization

Early afterdepolarization (EAD)

occurs with abnormalities during phase 2 (interrupted due to augmented opening of Ca
channels) or phase 3 (opening of Na channels)

Delayed afterdepolarization (DAD)

begin during phase 4 - after repolarization is completed, but before another action
potential would normally occur. Due to elevated cytosolic Ca concentrations (digoxin
toxicity)
medresidents.stanford.edu/TeachingMaterials/EKGs%20and%20Arrhythmias/Arrythmias%20and%20EKGs%203.ppt
Types
• Premature ventricular contraction (PVC)
• Bigeminy, trigeminy, couplets, interpolated, monomorphic,
multimorphic, fusion beat
• Ventricular tachycardia (VT)
• Torsades de pointes
• Ventricular fibrillation (VF)
• Idioventricular rhythm/ accelerated idioventricular
rhythm
 Premature Ventricular Contractions (PVCs)

 Epidemiology
 Very common; occur in healthy people & pts
with cardiac disease

 Etiology
 Cardiac: CAD, post-MI, MVP, CHF, rheumatic
heart disease, congenital arrhythmias
 Non-cardiac: acid-base disturbance, electrolyte
abnormalities, meds, caffeine, anxiety

 Symptoms
 Palpitations, “skipped beats”
 Chest or neck discomfort

 Physical exam findings

 Presence of premature beat
 Hypotension
 Decreased or absent peripheral pulses (radial)
ECG Characteristics of PVCs
• Ectopic beat originating from ventricles occurring before
next expected beat (premature)
• Usually not proceeded by P wave
• Wide QRS: at least > 0.12 sec, usually 0.16-0.2 with
bizarre morphology
• Large T wave in the opposite direction of the major QRS
deflection
 VES VES

SR SR
SR SR SR SR

Sinus rhythm with multifocal VES

PVC Morphology
• Monomorphic • Polymorphic
• PVCs originate from a • PVCs origniate from
single ventricular multiple ventricular
ectopic focus ectopic foci
• Single wave • ≥ 2 morphologies
morphology
Sinus rhythm with VES, R on T
ECG Characteristics of PVCs
 R on T phenomenon
 PVC begins during mid/late T wave
 Associated with vulnerable ventricles often predisposing to
polymorphic VT or VF, especially in acute ischemia
PVC Patterns
 Bigeminy
 PVC every other beat
 “Rule of bigeminy”:
often becomes self-
perpetuating

 Trigeminy
 PVC every 3rd beat

 Couplets
 Two successive PVCs

 Triplets
 Tree successive PVCs
 Rate <100bpm
 Ventricular Tachycardia (VT)
 Life threatening arrhythmia
 May lead to VF and sudden death
 Etiologies
 Heart disease (prior MI, CAD, CM, valvular)
 ECG findings
 ≥3 consecutive PVCs with a rate of 100-250 bpm
 No P waves
 QRS axis -30° to -180°
 AV dissociation
 Fusion beats and captured beats
 Duration
○ Non-sustained: <30sec
○ Sustained: >30 sec or requiring termination because of hemodynamic
collapse
Ventricular Tachycardia

Monomorphic VT

Polymorphic VT
Torsades de Pointes

 “twisting of points” : changing axis of polymorphic QRS VT

 Associated with congenital or acquired long QT, severe bradycardia, hypoK, hypoMg, meds
(TCAs, procainimide, quinidine)
 ECG findings
 Wide QRS complexes of changing amplitudes
 Ventricular rate 200-250 bpm
 Usually initiated by a long RR interval (like post PVC compensatory pause) followed by a short RR cycle (
e.g. R on T)
 Treatment
 Acquired: IV Magnesium + ventricular or atrial pacing
 Congenital: B-blockers
 Anti-arrhythmia drugs prolong the QT interval and worsen the arrhythmia
Ventricular fibrillation
Ventricular Fibrillation

 Disordered ventricular impulses with no coordinated ventricular contraction

 No cardiac output occurs & pt immediately loses consciousness
 Can occur with any type of cardiac disease, electrolyte imbalance, hypoxemia,
acidosis, shock, drugs (epi, cocaine)
 ECG findings
 Chaotic, irregular complexes; no discrete QRS waveforms
 Rate: 350-450 bpm
 Can occur spontaneously or preceded by PVCs or VT
 Treatment
 Immediate defibrillation followed by anti-arrhythmic drugs to suppress further ventricular ectopy
 Idioventricular (Escape) rhythm
• Escape rhythm due to failure of
SA/AVN ventricular activation or
complete conduction block
• Inherent 20-40bpm takes over
since it is no longer suppressed
• Regular wide QRS
• Etiologies
• Post-MI, CM, digoxin toxicity
Accelerated Idioventricular Rhythm (AIVR)

Sinus bradycardia
AIVR

 May result from accelerated ventricular focus that is faster than the
prevailing sinus rate
rd
and takes over or can occur as escape rhythm (
generally with 3 degree AVN block)
 Usually 60-100 bpm (differentiates from VT)
 Regular wide QRS
 Associated with post-MI (especially inferior wall MI), reperfusion tx, digoxin
toxicity, or after a PVC
 Usually self limited, rarely see progression to VT/VF
Take home points
 PVCs are very common arrhythmias that can occur in healthy or
diseased hearts with multiple features on ECG

 VT and VF are dangerous arrhythmias that can lead to sudden

cardiac death
THANK YOU