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
CLASSIFICATION OF
VENTRICULAR TACHYCARDIA
QRS COMPLEXES
MORPHOLOGY
Monomorphic VT
Most common
Uniform complexes
Priori SG, Blomstorm-Lundqvist C, Amzzanti A. 2015;

Olgin J, Zipes DP, 2012;
Katrisis DG, Zareba W, Camm AJ, 2012
Polymorphic VT
Beat to beat changes of
QRS complexes
appears twist around the
baseline
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
Hemodynamically stable
Usually dont require
specific intervention

Zipes DP, Camm AJ, Borggrefe M. 2006; Olgin J, Zipes DP. 2012
Unstable VT
Hemodynamically
compromised
Hypotension, chest pain,

heart failure, decrease
LOC
DURATION
Sustained VT
Non-sustained VT
Duration > 30 seconds
Duration < 30 seconds
Leads to hemodynamic
Self terminating
compromise
Requires further
intervention to terminate
the episode

Katrisis DG, Zareba W, Camm AJ. 2012
Usually without
hemodynamic instability
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
Arise during the plateau
phase or the repolarization

phase of the last beat and
may be the cause of
torsades de pointes

DAD
Arise during the resting
phase of the last beat and

maybe the cause of
digitalis-induced
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
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
PVCs
2. Heart rate 100-250 bpm

3. AV dissociation
Independent P wave, not
Fusion beat, when impulses
originated from SA Node

conducted to ventricle by and
merging with impulses originated
from ventricle
related with QRS

complexes, with different
rate
Captured beat, impulses
originated from atrium

depolarize ventricle through
normal conduction pathway
early and narrow QRS complexes
5. Positive or negative
concordance
6. Brugadas sign, the distance

from the onset of the QRS
complexes to the nadir of the Swave 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
all precordial leads
VT
Yes
No
R to S interval > 100ms in
one precordial lead?
VT
Yes
No
AV dissociation ?
No
Morphology criteria for VT
present in both in precordial
leads V1-2 and V6 ?
VT
Yes
VT
Yes
No
SVT
Morphology Criteria of VT
LONG TERM MANAGEMENT

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

ICD
(implantable cardiac device)
CATHETER ABLATION
VT in cardiomyopathy and
Refractory monomorphic VT
Decreased LVEF (< 35%)
Mostly used for idiopathic VT
ischemic VT
lower mortality rate than

OMT
Selection criteria
Primary : no history of
cardiac arrest or sustained

VT
Secondary : survived
cardiac arrest, life
threatening VT or syncope
episode related to VT
unresponsive to medicine
Failed procedure structural

problem
Mortality during procedure
uncontrollable life threatening

VT
Complication : tamponade
alongside perforation and
coronary occlusion in
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

Bumi Surabaya Hotel, November 7-8th, 2015

Characterized by three or more consecutive, abnormally

CARDIOVASCULAR EMERGENCIES COURSE

Bumi Surabaya Hotel, November 7-8th, 2015

CARDIOVASCULAR EMERGENCIES COURSE

Bumi Surabaya Hotel, November 7-8th, 2015

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

CARDIOVASCULAR EMERGENCIES COURSE

Bumi Surabaya Hotel, November 7-8th, 2015

CARDIOVASCULAR EMERGENCIES COURSE

Bumi Surabaya Hotel, November 7-8th, 2015

Bumi Surabaya Hotel, November 7-8th, 2015

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

Hypotension, chest pain,

CARDIOVASCULAR EMERGENCIES COURSE

Bumi Surabaya Hotel, November 7-8th, 2015

Duration > 30 seconds

Duration < 30 seconds

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

CARDIOVASCULAR EMERGENCIES COURSE

Bumi Surabaya Hotel, November 7-8th, 2015

CAD will cause scar tissue which, when accompanied by an

Panchon M, Almendral J. 2011; Goldberger JJ, Basu A, Boineau R. 2011;

Non structural heart disease px associated with more

CARDIOVASCULAR EMERGENCIES COURSE

Bumi Surabaya Hotel, November 7-8th, 2015

Predisposing factors includes:

CARDIOVASCULAR EMERGENCIES COURSE

Bumi Surabaya Hotel, November 7-8th, 2015

ischemic tissue interspersed

Triggered activity is more

CARDIOVASCULAR EMERGENCIES COURSE

Bumi Surabaya Hotel, November 7-8th, 2015

CARDIOVASCULAR EMERGENCIES COURSE

Bumi Surabaya Hotel, November 7-8th, 2015

Impulse initiation caused

Afterdepolarizations occur only

This may be the source of a new

Gaztanaga L, Marchlinski FE, Betensky BP. 2012;

CARDIOVASCULAR EMERGENCIES COURSE

Bumi Surabaya Hotel, November 7-8th, 2015

phase or the repolarization

Gaztanaga L, Marchlinski FE, Betensky BP. 2012;

phase of the last beat and

CARDIOVASCULAR EMERGENCIES COURSE

Bumi Surabaya Hotel, November 7-8th, 2015

Triggered activity is not a self genertaing rhythm

Occurs as a response to a preceeding impulse

Automatic rhythms can arrive de novo in the

Gaztanaga L, Marchlinski FE, Betensky BP. 2012;

CARDIOVASCULAR EMERGENCIES COURSE

Bumi Surabaya Hotel, November 7-8th, 2015

Asymptomatic individuals with or without

Persons with symptoms potentially attributable to

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

CARDIOVASCULAR EMERGENCIES COURSE

Bumi Surabaya Hotel, November 7-8th, 2015

Risk factors for developing VT : MI, SHD, or family

Every px aged < 40 yo with family history of SCD

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