Transcript Ventricular Tachyarrhythmia

IN THE NAME OF GOD
Ventricular
Tachyarrhythmia
Dr Amirhossein Azhari
Electrophysiologist
VENTRICULAR
TACHYARRHYTHMIAS
VENTRICULAR TACHYCARDIA
VENTRICULAR FIBRILLATION
Underlying Arrhythmia of Sudden
Death
Primary
VF
8% Torsades
de Pointes
13%
VT
62%
Bradycardia
17%
Adapted from Bayés de Luna A. Am Heart J. 1989;117:151-159.
DEFINITION
 Occurrence of a series of three or more
consecutive abnormaly shaped premature
ventricular complexes,
 WHOSE DURATION EXCEEDS 120 ms,
 With the ST-T vector pointing opposite the
major QRS deflection
Symptoms occurring during VT depend on
The ventricular rate,
Duration of tachycardia,
Presence and extent of the underlying
heart disease and peripheral vascular
disease.
VT can occur in several forms:
Short, asymptomatic, Nonsustained
episodes;
Sustained,
Hemodynamically stable events, generally
occurring at slower rates or in otherwise
normal hearts;
Unstable runs, often degenerating into VF
VENTRICULAR TACHYCARDIA
VT
NONSUSTAINED
SUSTAINED
NONSUSTAINED VT
Three or more consecutive ventricular
premature depolarizations,
up to a maximum duration of 30 seconds
before spontaeous termination
Importance of NSVT
 Most tachyarrhythmias come to our attention
because of the symptoms they produce
 In contrast,most instances of NSVT do not
cause symptoms
 Rather it derives its importance from the
prognostic significance it carries in some patient
populations
SUSTAINED VT
MONOMORPHIC
POLYMORPHIC
UNIFORM
MULTIFORM ,PLEOMORPHIC
SUSTAINED VT
IN PATIENTS WITH
NORMAL HEARTS
IN PATIENTS WITH
ORGANIC HEART DISEASE
VT in normal hearts
 1-Idiopathic VT
 2-long Q-T syndrome
 3-Brugada syndrome
 4-Catecholaminergic polymorphic VT
 5-Short Q-T syndrome
IDIOPATHIC VT
ADENOSINE
-SENSITIVE VT
TRIGGERED ACTIVITY
VERAPAMIL
-SENSITIVE VT
INTRAFASCICULAR
REENTRY
PROPRANOLOL
-SENSITIVE VT
AUTOMATICITY
IDIOPATHIC VT
ADENOSINE-SENSITIVE VT
CLINICAL CHARACTERISTICS
 THE MOST COMMON FORM OF
IDIOPATHIC VT(75-90%)
 ORIGINATES FROM RIGHT
VENTRICULAR OUTFLOW TRACT
RVOT VT
USUALLY EXHIBITS ONE OF TWO
PHENOTYPES
 NONSUSTAINED REPETITIVE
MONOMORPHIC VT(RMVT)
 PAROXYSMAL EXERCISE INDUCED
SUSTAINED VT
THERE IS A CONSIDERABLE OVERLAP BETWEEN THESE
TWO PHENOTYPES OF ADENOSINE-SENSITIVE RVOT VT
RF ABLATION
Long QT
Acquired
Congenital
The acquired form has a long-QT interval
caused by various drugs, such as
Quinidine, procainamide, sotalol,
amiodarone, disopyramide,
phenothiazines, tricyclic antidepressants,
erythromycin, pentamidine, antimalarials,
cisapride, and probucols
Electrolyte abnormalities, such as
Hypokalemia and hypomagnesemia;
The effects of a liquid protein diet and
starvation;
Central nervous system lesions; significant
bradyarrhythmias.
GENETIC BASIS OF LONG QT
SYNDROME
DESIGNATIO
N
GENE
GENE
PRODUCT
ION
CHANNEL
LQT1
11p15.5
LQT2
KvLQT Iksα-subunit Iks
1
HERG Ikr α-subunit Ikr
LQT3
SCN5A Na+ channel
INa
3q21-24
-
4q25-27
LQT4
ANKB
unit
Ankyrin-B
LQT5
Mink
Iks β-subunit Iks
LQT6
LQT7
MiRP1 Ikr β-subunit Ikr
KCNJ2 IKl
IKl
CHROMOSOM
E LOCUS
7q35-36
21q22.1-2
21q22.1
17q23
CLINICAL MANIFESTATIONS
 The principal symptoms are syncope and
SCD,from TDP
 Most often,TDP is self-terminating and cause a
syncopal episode from which the patient quickly
recovers
 Cardiac arrest occurs if the TDP is more
persistent,and SCD results if the rhythm does
not return to normal spontaneously
QT Duration
 A widely accepted method for correcting QT
interval for rate is Bazett’s formula
 Lead II is generally the best single lead for
measuring QT interval.
 Traditionally, QTc >440 msec were considered
prolonged; however, values up to 460 msec may
still be normal among females
 Affected gene carriers can have a QTc of 410
msec or less and no normal person has a QTc of
470 or more (men) or 480 or more (women)
ECG MANIFESTATIONS
 A QTC of 0.47 sec in men and 0.48 sec
in women is 100% sensitive for LQTS
 A QTC less than 0.40 sec in men and
0.42 sec in women is 100% specific for
excluding LQTS
Treatment
Intravenous magnesium is the initial
treatment of choice for torsades de pointes
from an acquired cause, followed by
temporary ventricular or atrial pacing.
In all patients with torsades de pointes,
administration of class IA, possibly some
class IC, and class III antiarrhythmic
agents ( amiodarone, dofetilide, sotalol)
can increase the abnormal QT interval and
worsen the arrhythmia.
For patients who have idiopathic long-QT
syndrome but
Not syncope,
Complex ventricular arrhythmias,
A family history of sudden cardiac death,
QTc no longer than 500 milliseconds
No therapy or treatment with a beta
blocker is generally recommended
In patients with :
Syncope caused by ventricular
arrhythmias or aborted sudden death,
An ICD is warranted
Brugada Syndrome
Brugada syndrome is a distinct form of
idiopathic VF in which patients have right
bundle branch block and ST-segment
elevation in the anterior precordial leads,
without evidence of structural heart
disease
Mutations in genes responsible for the
sodium channel (SCN5A) and calcium
channel have been identified in many
families with Brugada syndrome
Brugada Syndrome
Brugada Syndrome
Currently, no pharmacologic treatment
reliably prevents VF in these patients.
ICDs are the only effective treatment to
prevent sudden death
Ischemic Cardiomyopathy
Patients with previous myocardial
infarction are at risk for development of
VT. In the setting of a remote myocardial
infarction, the mechanism of VT is reentry,
involving the infarct scar and in particular
the border zone or other areas of the scar
with deranged conduction. As a result, the
VT in this setting is typically monomorphic
VT based on reentry
VT
1 sec
In general, ICDs are indicated to prevent
sudden cardiac death from VT in this
group of patients, especially in those with
depressed LV function
VT IN DCM
 BUNDLE BRANCH REENTRY MAY BE SEEN IN
THIS POPULATION AND CAN BE TREATED BY
ABLATING THE RBB
VT IN HCM
RISK FACTORS FOR SCD IN HCM
 CARDIAC ARREST(VF)
 SUSTAINED VT
 SYNCOPE PARTICULARLY IF RECURRENT AND EXERTIONAL
 FAMILIAL SUDDEN HCM- RELATED DEATH IN
FIRST DEGREE RELATIVES
 NSVT ON HOLTER
FREQUENT,REPETITIVE AND
PROLONGED
 ABNORMAL BP RESPONSE IN EXERCISE >20
mm HG
 EXTREME LV HYPERTROPHY >30 mm
Acute Management of Sustained
Ventricular Tachycardia
VT that does not cause hemodynamic
decompensation can be treated medically
to achieve acute termination by the
intravenous administration of amiodarone,
lidocaine, or procainamide, followed by an
infusion of the successful drug
In general, amiodarone
loading dose of 15 mg/min is given during
a 10-minute period.
This dose is followed by an infusion of
1 mg/min for 6 hours and then
a maintenance dose of 0.5 mg/min for the
remaining 18 hours and for the next
several days, as necessary
If the arrhythmia does not respond to
medical therapy
Hypotension,Shock
Angina,
Congestive heart failure
Symptoms of cerebral hypoperfusion
should be treated promptly with DC
cardioversion.
Very low energies can terminate VT,
beginning with a synchronized shock of 10
to 50 J.
The goal of long-term therapy is to prevent
sudden cardiac death and recurrence of
symptomatic VT.
Asymptomatic nonsustained ventricular
arrhythmias in low-risk populations
(preserved LV function) often need not be
treated.
In patients with symptomatic nonsustained
tachycardia, beta blockers are frequently
effective in preventing recurrences.
In patients refractory to beta blockers,
class IC agents, sotalol, or amiodarone
can be effective.
However, class IC agents should be
avoided in patients with structural heart
disease, especially those with coronary
artery disease because of the increased
mortality associated with these drugs
caused by proarrhythmia.
Sotalol should be used cautiously because
of its potential for prolonging the QT
interval and producing torsades de
pointes.
Patients with nonsustained VT after
myocardial infarction and poor LV function
are at significant risk for sudden death
In patients who have survived a cardiac
arrest or who have sustained VT resulting
in hemodynamic compromise and poor LV
function, an ICD is the treatment of choice.
In patients who refuse an ICD, empiric
amiodarone may be the next best therapy
Amiodarone
Toxicity
– Pulmonary fibrosis
– Hypo- or hyper-thyroidism
– Liver failure
– Bone marrow suppression
– Renal failure
– Photosensitivity
– Corneal deposits
Side effects
– Myalgias
– Gait disturbance
– Insomnia
– Prolongation of coagulation time (PT)
(need to reduce coumadin dosage)
– Digoxin toxicity (need to reduce digoxin
dosage)
Although RF ablation of certain types of
idiopathic VT is very effective, ablation for
postinfarction VT or that associated with
dilated cardiomyopathy is somewhat less
effective
VF
These arrhythmias represent severe
derangements of the heartbeat that
usually terminate fatally within 3 to 5
minutes unless corrective measures are
undertaken promptly.
VF is recognized by the presence of
irregular undulations of varying contour
and amplitude . Distinct QRS complexes,
ST segments, and T waves are absent.
Fine-amplitude fibrillatory waves (0.2 mV)
are present with prolonged VF. These fine
waves identify patients with worse survival
rates and are sometimes confused with
asystole.
VF occurs in various clinical situations but
most commonly in association with
coronary artery disease and as a terminal
event
Ventricular flutter or VF results in
faintness, followed by loss of
consciousness, seizures, apnea, and
eventually, if the rhythm continues
untreated, death
In patients resuscitated from out-ofhospital cardiac arrest,
75% have VF.
Bradycardia or asystole, which can occur
in 15% to 25% of these patients, is
associated with a worse prognosis than
VF and is usually associated with more
advanced LV dysfunction
Management should follow
basic life support and
advanced cardiac life support guidelines.
Immediate nonsynchronized DC electrical
shock using 200 to 400 J is mandatory
therapy for VF and for ventricular flutter
that has caused loss of consciousness.
Thanks for your
attention