Ventricular Tachycardia - Budi Baktijasa, MD, FIHA PDF

VENTRICULAR
TACHYCARDIA
Budi Baktijasa Dharmadjati
Oryza Sativa
CARDIOVASCULAR EMERGENCIES COURSE

Bumi Surabaya Hotel, November 7-8th, 2015
DEFINITION
broad complex tachycardia originating in the ventricles
Characterized by three or more consecutive, abnormally

shaped PVCs with rate > 100 bpm (usually 150-200 bpm)
with wide QRS complexes (QRS > 0.12 s)
The focus originated from ventricle (left or right) or as a

result of reentry process in some part of the bundle
branch (bundle branch reentry VT)
Olgin J, Zipes DP. 2012 CARDIOVASCULAR EMERGENCIES COURSE

CLASSIFICATION OF
VENTRICULAR TACHYCARDIA

QRS COMPLEXES
MORPHOLOGY
Monomorphic VT Polymorphic VT
Most common Beat to beat changes of
QRS complexes
Uniform complexes appears twist around the
baseline
Priori SG, Blomstorm-Lundqvist C, Amzzanti A. 2015;

Olgin J, Zipes DP, 2012;
Katrisis DG, Zareba W, Camm AJ, 2012
TORSADES DE POINTES

ETIOLOGY
Idiopathic
Right ventricular outflow tract (RVOT) VT
Left ventricular outflow tract (LVOT) VT
Idiopathic left ventricular tachycardia (ILVT)
Cathecolaminergic Polymorphic VT (CPVT)
VT in cardiomyopathy (non-ischemic)
Bundle Branch Reentrant VT
Arrhythmogenic Right Ventricular Cardiomyopathy
(ARVC)
Ischemic VT

CLINICAL MANIFESTATION
Stable VT Unstable VT
Hemodynamically stable Hemodynamically
compromised
Usually dont require
specific intervention Hypotension, chest pain,
heart failure, decrease
LOC

Zipes DP, Camm AJ, Borggrefe M. 2006; Olgin J, Zipes DP. 2012 CARDIOVASCULAR EMERGENCIES COURSE
DURATION
Sustained VT Non-sustained VT
Duration > 30 seconds Duration < 30 seconds
Leads to hemodynamic Self terminating
compromise
Usually without
Requires further hemodynamic instability
intervention to terminate
the episode

Katrisis DG, Zareba W, Camm AJ. 2012
EPIDEMIOLOGY
Most common cause of VT is coronary artery disease
VT/VF is the most frequent complication caused by ACS that
leads to sudden cardiac death
CAD will cause scar tissue which, when accompanied by an

increased activity of reentrant circuit will trigger VT
Panchon M, Almendral J. 2011; Goldberger JJ, Basu A, Boineau R. 2011;
Priori SG, Blomstorm-Lundqvist C, Amzzanti A. 2015; Zipes DP, Camm AJ, Borggrefe M. 2006
Non structural heart disease px associated with more

benign form of VT
Prystowsky EN, Padanilam BJ, Joshi S. 2012; Katrisis DG, Zareba W, Camm AJ. 2012;
Koplan BA, Stevenson WG. 2009
Predisposing factors includes:
Tissue ischemia
Hypoxemia
Autonomic system (sympathetic activity that would
increased HR)
Metabolic abnormality (lactic acidosis)
Haemodynamic disturbance (decreased coronary
perfusion)
Drugs (digitalis)
Electrolyte imbalance (hypokalemia due to forced
diuresis)
Acute reperfusion due to trombolytic agents
Olgin J, Zipes DP. 2012; Prystowsky EN, Padanilam BJ, Joshi S. 2012;
Katrisis DG, Zareba W, Camm AJ. 2012
PATHOPHYSIOLOGY
Most common mechanism
of VT: reentry
Caused by scarred
myocardium or
cardiomyopathy
Scarred myocardium or
ischemic tissue interspersed
between normal viable
myocardium may provided
substrate for reentry
mechanism
Triggered activity is more
common in the non
ischemic or normal heart
Olgin J, Zipes DP. 2012; Gaztanaga L, Marchlinski FE, Betensky BP. 2012;
Chen P, Antzelevitch E. 2011
REENTRY
Scar tissue isolated viable

bundles of conducting
myocardium with slow
conduction from the normal
conducting myocard in the
remainder of ventricle
When a stimulus reaching the

area surrounded by scar, it will
travel with such delay that the
wavefront arrives at distal
terminus of the bundle to
encounter fully repolarized
myocardium allowing
reentrant circuit
Gaztanaga L, Marchlinski FE, Betensky BP. 2012;
Chen P, Antzelevitch E.2011
TRIGGERED ACTIVITY
Impulse initiation caused
afterdepolarizations (membrane
potential oscillations that occur
during or immediately following a
preceding AP)
Afterdepolarizations occur only

in the presence of a previous AP
(the trigger), and when they
reach the threshold potential, a
new AP is generated
This may be the source of a new

triggered response, leading to
self-sustaining VT.
Myocardial damage
oscillations transmembrane
potential after depolarization
treshold potential VT
EAD DAD
Arise during the plateau Arise during the resting
phase or the repolarization phase of the last beat and
phase of the last beat and maybe the cause of
may be the cause of digitalis-induced
torsades de pointes arrhythmia

Triggered activity is not a self genertaing rhythm
Occurs as a response to a preceeding impulse

(the trigger)
Automatic rhythms can arrive de novo in the

absence of prior electrical activity

CLINICAL EXAMINATION
VT frequently precede significant haemodynamic

collapse
Asymptomatic individuals with or without

electrocardiographic abnormalities
Persons with symptoms potentially attributable to

VT
Palpitations
Dyspnea
Chest pain
Syncope and presyncope
Zipes DP, Camm AJ, Borggrefe M. 2006 CARDIOVASCULAR EMERGENCIES COURSE
Risk factors for developing VT : MI, SHD, or family
history of SCD
Every px aged < 40 yo with family history of SCD

should be evaluated for genetic arrhythmias
syndrome (LQTS, Brugada syndrome, RV
arrhythmogenic dysplasia, hypertrophic
cardiomyopathy)
Goldberger JJ, Basu A, Boineau R. 2011; Priori SG, Blomstorm-Lundqvist C,

Amzzanti A. 2015;
Zipes DP, Camm AJ, Borggrefe M. 2006Prystowsky EN, Padanilam BJ, Joshi S.
2012; Katrisis DG, Zareba W, Camm AJ. 2012;
From physical examination :
Tachycardia (related to hypotension and
tachypnea)
Lack of tissue perfussion leads to decreased LOC,
diaphoresis and shock
Variated 1st heart sound (AV dissociation)
Murmur or S3 gallop (related to underlaying heart
disease)

WORK UP
Detect underlying heart disease (including inherited
and acquired cardiomyopathy)
Resting 12 lead electrocardiography evaluate the
presence of myocardial scar (Q-waves or fractionated
QRS complexes), the QT interval, ventricular
hypertrophy
Echocardiography RV and LV structure and function,
valvular abnormalities, and pulmonary artery systolic
pressure
Recommended for px symptomatic PVCs, a high
frequency of PVCs (.10% burden), or when the presence
of SHD is suspected.

ECG DIAGNOSTIC CRITERIA
1. Three or more consecutive Fusion beat, when impulses

PVCs originated from SA Node
conducted to ventricle by and
2. Heart rate 100-250 bpm merging with impulses originated
3. AV dissociation from ventricle
Independent P wave, not
related with QRS
complexes, with different
rate

Captured beat, impulses 5. Positive or negative
originated from atrium concordance
depolarize ventricle through
normal conduction pathway
early and narrow QRS complexes
6. Brugadas sign, the distance
from the onset of the QRS
complexes to the nadir of the S-
wave is > 100 ms
4. Extreme axis deviation

(northwest axis) : positive QRS
complexes in aVR, negative in
lead I and aVF

Positive concordance of VT

7. Josephsons sign, notching
near the nadir of the S-wave.
8. RSR complexes with higher

left rabbit ear

Zipes DP, Camm AJ, Borggrefe M. 2006; Olgin J, Zipes DP, 2012;
Prystowsky EN, Padanilam BJ, Joshi S. 2012; Alzand BS, Crijins HJ.. 2011
VT vs SVT with abberancy
Brugada Algorithm
Absence of on R2 complex in
VT
all precordial leads
Yes
No
R to S interval > 100ms in
one precordial lead? VT
Yes
No
AV dissociation ? VT
No Yes
Morphology criteria for VT

present in both in precordial VT
leads V1-2 and V6 ? Yes
No
SVT

Morphology Criteria of VT

LONG TERM MANAGEMENT
Beta blocker Amiodarone Procainamide
Counters the Class III Class 1A
arrhythmogenic effects Repolarizing K+ Sodium blockers,
of excess currents, markedly prolongs repolarization
cathecolamine prolongs repolarization times
stimulations times Inotropic -
countering the the First choice in VT with Stable sustained VT
proarrhythmic effects hemodynamic
of increased cAMP and instability in the setting
Ca-dependent of CHD
triggered arrhytmias
Prevents monomorphic
If channel effects; VT reccurency
indirect Ca channels
Manages refractory VT
blocker
in CHD or with
All px with VT, decreased ventricular
precluded by functions
hypotension,
bradycardia, and other
clinical factor

LONG TERM MANAGEMENT
ICD
(implantable cardiac device) CATHETER ABLATION
VT in cardiomyopathy and Refractory monomorphic VT
ischemic VT unresponsive to medicine
Decreased LVEF (< 35%) Mostly used for idiopathic VT

lower mortality rate than Failed procedure structural
OMT problem
Selection criteria Mortality during procedure
Primary : no history of uncontrollable life threatening
cardiac arrest or sustained VT
VT
Secondary : survived Complication : tamponade
cardiac arrest, life alongside perforation and
threatening VT or syncope coronary occlusion in
episode related to VT pericardial or aortic root

PROGNOSIS
VT associated with cardiac arrest in many cases

LV function projected by EF and functional capacity (NYHA
class, maximum oxygen uptake, duration of activity) is a
major determinant of mortality and SCD risk
Cardiac arrest or SCD more frequent in px with same history
of VT
Stable recurrent VT have lower risk of SCD
Idiopathic VT have better prognosis than ischemic VT and/or
VT in cardiomyopathy (non ischemic), which have higher risk
of cardiac arrest (syncope and decreased LV function
related to worse prognosis)

SUMMARY
VT diagnosed by three or more consecutive PVC, with regular and

wide QRS complexes.
The electrical mechanism are reentry (in ischemic heart disease
and cardiomyopathy) and triggered activity in (non-ischemic heart
disease or with normal heart)
The presence of structural heart disease affects pathophysiology,
treatment and worsen the prognosis of VT episodes
After acute management based on ACLS guideline, it is
recommended to prevent reccurency of VT episodes with OMT or
device therapy
ICD is the choice for VT in cardiomyopathy and ischemic VT
Catheter ablation is the better choice for refractory monomorphic
VT unresponsive to OMT or VT episode in SHD

Thank you
CASE


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VENTRICULAR

CARDIOVASCULAR EMERGENCIES COURSE

broad complex tachycardia originating in the ventricles

Characterized by three or more consecutive, abnormally

The focus originated from ventricle (left or right) or as a

Olgin J, Zipes DP. 2012 CARDIOVASCULAR EMERGENCIES COURSE

CARDIOVASCULAR EMERGENCIES COURSE

Priori SG, Blomstorm-Lundqvist C, Amzzanti A. 2015;

CARDIOVASCULAR EMERGENCIES COURSE

CARDIOVASCULAR EMERGENCIES COURSE

Priori SG, Blomstorm-Lundqvist C, Amzzanti A. 2015;

Priori SG, Blomstorm-Lundqvist C, Amzzanti A. 2015;

CAD will cause scar tissue which, when accompanied by an

Non structural heart disease px associated with more

Scar tissue isolated viable

When a stimulus reaching the

Afterdepolarizations occur only

This may be the source of a new

Gaztanaga L, Marchlinski FE, Betensky BP. 2012;

Occurs as a response to a preceeding impulse

Automatic rhythms can arrive de novo in the

Gaztanaga L, Marchlinski FE, Betensky BP. 2012;

VT frequently precede significant haemodynamic

Asymptomatic individuals with or without

Persons with symptoms potentially attributable to

Every px aged < 40 yo with family history of SCD

Goldberger JJ, Basu A, Boineau R. 2011; Priori SG, Blomstorm-Lundqvist C,

Priori SG, Blomstorm-Lundqvist C, Amzzanti A. 2015;

Priori SG, Blomstorm-Lundqvist C, Amzzanti A. 2015;

1. Three or more consecutive Fusion beat, when impulses

CARDIOVASCULAR EMERGENCIES COURSE

4. Extreme axis deviation

CARDIOVASCULAR EMERGENCIES COURSE

CARDIOVASCULAR EMERGENCIES COURSE

8. RSR complexes with higher

Priori SG, Blomstorm-Lundqvist C, Amzzanti A. 2015;

Morphology criteria for VT

CARDIOVASCULAR EMERGENCIES COURSE

CARDIOVASCULAR EMERGENCIES COURSE

CARDIOVASCULAR EMERGENCIES COURSE

Decreased LVEF (< 35%) Mostly used for idiopathic VT

CARDIOVASCULAR EMERGENCIES COURSE

VT associated with cardiac arrest in many cases

CARDIOVASCULAR EMERGENCIES COURSE

VT diagnosed by three or more consecutive PVC, with regular and

CARDIOVASCULAR EMERGENCIES COURSE

CARDIOVASCULAR EMERGENCIES COURSE

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