Ventricular Arrhythmia - VT

Braghmandaru A.B
Introduction
 Most common cause of wide complex tachycardia.(80%)
 Major cause of morbidity and mortality in patients with structural
heart disease.
 Major cause of sudden cardiac death –60 % cases on holter
monitoring.
 Relatively organised tachyarryhthmias with discrete QRS
complexes.
 Diagnosis still a challenge ….on presentation.
 Reentry is the most common mechanism.
 Recurrence is more common in less than one year of onset.
 ICD implantation is a the absolute indication in presence of
LVEF <30%.
Classification of Ventricular Arrhythmia
by Clinical Presentation
•Hemodynamically stable
♥ Asymptomatic
♥ Minimal symptoms, e.g., palpitations
•Hemodynamically unstable
♥ Presyncope
♥ Syncope
♥ Sudden cardiac death
♥ Sudden cardiac arrest
Classification of Ventricular Arrhythmia
by Electrocardiography
•Nonsustained ventricular tachycardia (VT)
♥ Monomorphic
♥ Polymorphic
•Sustained VT
♥ Monomorphic
♥ Polymorphic
•Bundle-branch re-entrant tachycardia
•Bidirectional VT
•Torsades de pointes
•Ventricular flutter
•Ventricular fibrillation
 Classification of Ventricular Arrhythmia
by Morphology

Difference of MVT,PVT
MONO MORPHIC VT POLYMORPHIC VT

1. Stable tachycardia Unstable,dynamic

2. Reproducible, recurrent Less reproducible

phenomenon
3. Initiated by pacing ,programmed Not reliably initiated
ventricular stimulation
4. Normal hearts./structural heart Acute ischemia ,myocarditis,drugs
disease
5. Reentry circuit Pause dependent VT,TRIGERRING

6. Hemodynamically stable Not so

7. MVT—PVT—VF/VFL PVT—VF/VFL

8. Catheter ablation,pacing,AAD Bbs ,pacing…/ablation?

 Classification According to Tachycardia
Morphology
Torsades de pointes is a polymorphic VT associated with a long QT
interval, and electrocardiographically characterized by twisting of the
peaks of the QRS complexes around the isoelectric line during the
arrhythmia.

Bidirectional VT is associated with a beat to beat alternans in the QRS

frontal plane axis, often associated with digitalis toxicity
Torsades de Pointes

• French term literally means twisting of points

 Classification According to Tachycardia
Morphology
Ventricular flutter is a regular (cycle length [CL] variability less than 30
milliseconds), rapid (approximately 300 beats/min) ventricular arrhythmia
with a monomorphic appearance but no isoelectric interval between
successive QRS complexes.

Ventricular fibrillation (VF) is a rapid, usually more than 300 beats/min,

grossly irregular ventricular rhythm with marked variability in QRS CL,
morphology, and amplitude.
 Ventricular Flutter
Spontaneous conversion to NSR (12-lead ECG)
VF with Defibrillation (12-lead ECG)
 Classification According to Tachycardia
Duration
Sustained VT lasts for more than 30 seconds or requires termination in
less than 30 seconds because of hemodynamic compromise.

Nonsustained VT is VT lasting for three or more complexes at more than

100 beats/min but for less than 30 seconds.

However, during electrophysiological (EP) testing, nonsustained VT is

defined as more than five or six complexes of non–bundle branch
reentrant (BBR) VT, regardless of morphology.
 Epidemiology of VA & SCD
Classification of Ventricular Arrhythmia
by Disease Entity
•Chronic coronary heart disease
•Heart failure
•Congenital heart disease
•Neurological disorders
•Structurally normal hearts
•Sudden infant death syndrome
•Cardiomyopathies
♥ Dilated cardiomyopathy
♥ Hypertrophic cardiomyopathy
♥ Arrhythmogenic right ventricular (RV)
cardiomyopathy
Mechanism of occurrence of VT

 REENTRY
 ENHANCED AUTOMATICITY
 TRIGGERED ACTIVITY
 Reentry circuit
 Two potentially conduction pathways or more.
 Unidirectional block must occur in one
pathway
 An activation front that passes around the
zone of unidirectional block over the alternate
pathway.
 Activation of the myocardium distal to block
with delay.
 The activation wavefront to activate the block
by retrogradely and reexcite the tissue where
the actviation wavefront originated.
 For reentry to occur the wavefront should
find the tissue to be excitable in the
direction of its propagation.
Automaticity
 Abnormal automaticity
 Occurs in the setting of acute ischemia
 It is due to the physiologiccal ion channel
changes rather than morphological.
 Transient…
 Takes up the role of pacemaker and
discharges the impulses.
Triggered activity
 Is due to the depolarization phase changes
 Occur in bursts…
 But may turn up into VF /VFL
 Two syndromes
 Pause dependent
 Catecholaminergic dependent
 Phase3 –depends upon QT interval
 Phase 4 --- depends upon the sympathetic tone.
 Pause dependent VT
 It is due to the afterdepolarizations that occur during the phase 3 of the
action potential early after depolarization.
 When they reach the threshold potential of the cardiac cell –cause another
action potential.
 Related to long QT syndrome
 Hypokalemia
 Class 1 a antiarryhthmic drugs use.
 Prolonged repolarization.
 The longer the QT interval the more abberation is the TU wave.
 Long coupling interval.
VT Cousins

VT Cousins
 Narrow QRS Wide QRS - BBB
(Aberrant conduction)
AVN

A HB B
RB LB

Wide QRS - Preexcitation Wide QRS - VT

(Conduction via AP)

C D
 DIAGNOSTIC CRITERIA OF VT
 AV dissosciation(capture,fusion beats)
 QRS duration>140 ms for RBBB type V1morphology:
 QRS duration>160 ms for LBBB type V1 morphology.
 FRONTAL PLANE AXIS ---90 to 180
 Delayed activation during initial phase of QRS complex:
 LBBB pattern –R wave in V1,V2 >40 ms
 RBBB pattern –onset of R wave to nadir of S wave > 100 ms
 Bizzare QRS pattern that does not mimic typical RBBB or LBBB type
QRS complex
 concordance of QRS complex in all precordial leads.
 RS or dominant S in V6for RBBB vt
 Qwave in V6 with LBBB pattern
 Monophasic R or biphasic qR or R/S in V1 with RBBB PATTERN
 concordance=Polarity
 Negative: All QRS in V1-6 -VE
 Positive: All QRS in V1-6 +VE

 Negative: All QRS in V1-6 -VE

 Positive: All QRS in V1-6 +VE
 Capture beat/ Dessler Beat
 When there is interference dissociation between sinus rhythm
and faster subsidiary rhythm,the interference occurs in the AV
node.

 Both the impulses cannot be conducted due to the refractoriness

of the AV node as a result of the wave from each focus.

 At a particular time the slow sinus waves passes through the AV

node when it is no longer refractory and hence conducts down
the ventricles..ventricular capture beat, momentary activation of
the ventricles by sinus impulse in AV dissosciation.
 Fusion beat
 It is due to the combination of the sinus impulse and the ectopic
impulse leading to a QRS c0mplex that varies in the morphology with
the change in the occurrence of fusion from the AVnode.
 Summation complex or fusion complex or combination beat
 It may be like that of sinus impulseQRS ,or ectopic one,or
intermediate..location can be known by morphology.
 Algorithms for the ECG
Diagnosis of Wide
Complex Tachycardia

Algorithm 1. The most commonly used

algorithm is the so-called Brugada
algorithm or Brugada criteria
 Vereckei Algorithms for
the ECG Diagnosis of
Wide Complex
Tachycardia

Algorithm 2. This algorithm had

superior overall total accuracy than
that of the Brugada algorithm (90.3%
versus 84.8%
Arrhythmogenic RV Dysplasia/
Cardiomyopathy
• ARVD occurs in young adults (80% are younger than
40 years) and is more common in men. The mean age
at diagnosis of familial ARVD is approximately 31 years.
The disease is almost never diagnosed in infancy and
rarely before the age of 10.

• The prevalence of the disease in the general population

is estimated at 0.02% to 0.1% but is dependent on
geographic circumstances. In certain regions of Italy
(Padua, Venice) and Greece (island of Naxos), an
increased prevalence of 0.4% to 0.8% for ARVD has
been reported.
• Approximately 50% of patients with ARVD present with symptomatic
ventricular arrhythmias, most commonly sustained and non-
sustained VT with LBBB configuration, although right bundle branch
block (RBBB) configuration also can be observed, manifested by
palpitations, dizziness, and/or syncope.

• The frequency of ventricular arrhythmias in ARVD varies with the

severity of the disease, ranging from 23-100% in patients with
severe disease.

• Ventricular arrhythmias characteristically occur during exercise.

Sudden cardiac death occurs in patients with ARVD and can be the
first presentation of the disease. ARVD is an important cause of
sudden cardiac death in young adults in northern Italy, accounting
for approximately 11% of cases overall and 22% in athletes.
The diagnosis of arrhythmogenic right ventricular dysplasia-cardiomyopathy
(ARVD) has been used to describe the right ventricular (RV) myopathy
associated with multiple left bundle branch block (LBBB)- type VT.

ARVD is characterized by progressive replacement of the right ventricular

myocardium by fibrofatty tissue.

This disorder usually involves the RV, but the left ventricle (LV) and septum
also can be affected. Fibrofatty replacement of myocardium produces
“islands” of scar region that can lead to reentrant VTs, and these patients
have an increased risk of sudden cardiac death, mostly secondary to VT.

Dysplasia in this region usually leads to dilatations or aneurysms having

paradoxical systolic motion.
Two patterns of inheritance have been described in ARVD:
autosomal dominant disease and Naxos disease. ARVD has
been associated with an autosomal dominant inheritance
pattern, with 30% to 50% of family members of index patients
having manifestations of the disease.

A variant form of ARVD with autosomal recessive inheritance

is familial palmoplantar keratosis, also called Naxos disease
and mal de Meleda disease.

This disorder is characterized by typical features of ARVD

accompanied by non epidermolytic palmoplantar keratosis, a
disorder of the epidermis causing hyperkeratosis of the palms
and soles and woolly hair.
• The patchy replacement of the RV myocardium by fatty
and fibrous tissue provides a substrate for reentrant
ventricular arrhythmias.

• The most striking morphological feature of the disease

is the diffuse or segmental loss of RV myocytes, with
replacement by fibrofatty tissue and thinning of the RV
wall.

• Fibrofatty replacement usually begins in the

subepicardium or midmural layers and progresses to
the subendocardium. Only the endocardium and
myocardium of the trabeculae may be spared.
• Anatomical malformations of the RV consist of mild to severe
global RV dilation, RV aneurysms and segmental RV hypokinesia.

• The sites of involvement are found in the so-called triangle of

dysplasia—namely, the RV outflow tract, apex, and inferolateral
wall near the tricuspid valve.

• However, the fibrofatty pattern of ARVD is limited not only to the

RV; the disease also can migrate to the interventricular septum and
the LV free wall, with a predilection for the posteroseptal and
posterolateral areas. LV involvement may even be the first
manifestation of the disease
Patients with ARVD at increased risk for sudden death include the
following:

(1)younger patients (age< 33 y)

(2)patients who present with or have recurrent syncope,
(3)Patients with a previous history of cardiac arrest or a history of VT
with hemodynamic compromise;
(4)Patients with LV involvement;
(5)Patients with ARVD2, who can develop polymorphic VT and
juvenile sudden death associated with sympathetic stimulation;
(6) patients with an increase in QRS dispersion (maximum measured
QRS duration minus minimum measured QRS duration ≥ 40
milliseconds);
(7) patients with S wave upstroke ≥0 milliseconds on the 12- lead
ECG; and
(8) patients with Naxos disease.
Pharmacological Therapy

Therapy with beta blockers, sotalol, or amiodarone can be

effective in suppressing ventricular arrhythmias and possibly in
preventing sudden cardiac death. Among asymptomatic
patients and those with mild disease, beta blockers are a
reasonable recommendation to reduce the possibility of
adrenergically induced arrhythmia.

Patients with well tolerated and non–life-threatening ventricular

arrhythmias are at relatively low risk for sudden death and can
be treated with antiarrhythmic drugs, guided either
noninvasively with ambulatory monitoring or with EP testing.
Pharmacological Therapy

Among patients who have VT, those who are treated

with antiarrhythmic drugs generally have a low risk of
arrhythmic death, with an overall mortality rate of 0.08%
per year.

Thus, initial therapy with sotalol is a reasonable option

for many patients for primary prevention. For those that
do not respond to sotalol, response to other drugs is
unlikely, and consideration should be given to
nonpharmacological therapy. Sotalol can also be given
to reduce the frequency of implantable cardioverter-
defibrillator (ICD) discharges.
Avoidance exercise

Because of the association between exercise and the induction of

ventricular tachyarrhythmias, a diagnosis of ARVD is considered
incompatible with competitive sports and/or moderate- to high-
intensity level recreational activities. Furthermore, any activity,
competitive or not, that causes symptoms of palpitations,
presyncope, or syncope should be avoided

Cardioverter-Defibrillator Implantation
Patients who are considered to be at high risk for sudden cardiac
death should receive an ICD.
Catheter Ablation

Catheter ablation of VT may be indicated for some ARVD

patients, either as a primary therapy or as an adjunct to
ICD implantation in patients with numerous VT episodes
or those who are intolerant of antiarrhythmic drugs, to
reduce the number of ICD therapies and improve quality
of life. However, given the high long-term recurrence rate,
this technique is far from curative
Bundle branch reentrant tachycardia

BBR-VT
 Macro reentry circuit
 Antegrade direction down the right branch
 Retrograde up the left posterior or anterior fascicles/LBB
 Mimic RV pacing with LBBB pattern,leftward superior axis.
 Opposite occurrence then RBBB
 Readily amenable to catheter ablation therapy.
 Coupled with ICD due to risk of SCD.
 Occurs in nonischemic cardiomyopathy or valvular
cardiomyopathy.
Idiopathic VT

- Wulan Anggrahini -
 structurally normal hearts.
 Young patients
 Benign course
 Focal
 Monomorphic
 No scar
 12-lead ECG extremely useful
 Treatment :reassurance, medical therapy, and
catheter ablation.
 Prevalence estimates accounted for
7%-38% of all patients referred for VT
 Realistic estimation is closer to 10%.
Idiopathic VTs are of two types :

 The more common one is the focal VT caused by cyclic

adenosine monophosphate (cAMP)–mediated triggered
activity. This VT is sensitive to adenosine, beta blockers,
and calcium channel blockers. (Outflow tract VT)

 The less common variety is a verapamil-sensitive reentrant

left fascicular VT, which commonly originates from close to
the left posterior fascicle of the left bundle branch and less
commonly from the left anterior fascicle.
  RVOT Tachycardia
 LVOT/Aortic Cusp Tachycardia
 Epicardial Outflow Tract VT

Mechanism

Triggered activity due to catecholamine-mediated delayed after-depolarizations.

This triggered activity results from a catecholamine-mediated increase in cyclic
adenosine monophosphate, with subsequent increase in intracellular calcium from
the sarcoplasmic reticulum, resulting in delayed after-depolarizations and
triggered activity. This underlying mechanism leads to tachycardia initiation with
catecholamines and termination with adenosine, -blockers, or calcium channel
blockers.
 most common IPVT-70%
 LBBB/Inf axis
 Female 2x than male
 Triggered by exercise or stress, and may also occur
during hormonal cycles in women
 Third to fifth decade of life
 C/F: palpitations/chest pain, fatigue, and presyncope or
syncope/isolated PVCs/nonsustained VT/sustained VT.
 10%-15% of IPVT, Male >Female
 Anatomy
Noncoronary cusp does not directly contact ventricular
myocardium, ventricular arrhythmias are rare.
The base of the left and right coronary cusps lies in direct
contact to the ventricular myocardium, and LV muscle
fibers may extend into the aortic root,serving as a source of
these PVCs. These extensions may be a remnant from
embryonic development, and these myocardial fibers
persist providing an arrhythmogenic substrate. When
mapping more inferiorly in the aortic root, successful
ablation may be related to necrosis of ventricular myocytes
arising from the most superior portion of the ostium of the
LV.
 LBBB /inferior axis/ precordial transition earlier than their
RVOT-VT . The precordial R-wave transition typically occurs at
or before lead V3. VT originating from the left.coronary cusp
has an earlier R-wave transition (typically by V1/2) than the
right coronary cusp (V2/3). A broader R-wave duration (_0.5
ms) and a taller R/S-wave Amplitude in V1 and V2 favor aortic
cusp location. When the precordial transition occurs at lead
V3, a precordial transition earlier than sinus rhythm transition
is suggestive of LVOT-VT.
VERAPAMIL-SENSITIVE IDIOPATHIC
FASCICULAR VENTRICULAR TACHYCARDIA

 Idiopathic left fascicular VT= fascicular VT=LBB-ANT/POST

 ECG classify to left posterior fascicular VT, left anterior
fascicular VT, and left upper septal VT.
 LPFVT- most common then LAFVT & septal is rare
 young male(60%)- 15 and 40 years, younger female.
 paroxysmal
 Symptoms – palpitations/syncope /tachycardia-mediated
cardiomyopathy .
Verapamil-sensitive VT

 RBBB/LAD/ VT induced by atria pacing.

 Verapamil sensitive tachycardia originates from the Purkinje
network of the mechanism of verapamil-sensitive left VT is
reentry/induced, entrained, and terminated by ventricular or
atrial stimulation. The proposed reentrant circuit consists of an
area of slow conduction that forms the orthodromic limb in the
LV septum from base to apex, with the retrograde limb using
the Purkinje network false tendons is arrythmogenic.
 RBBB/left superior axis pattern/narrow/confused for SVT
 LPFT - RBBB and left axis deviation(LAFB)
 LAFT-RBBB/RAD(LFBB)
 septal VT demonstrates an incomplete RBBB and normal axis.
 Excellent prognosis
 Medical Therapy
Intravenous verapamil is effective for acute
termination. Chronic oral verapamil therapy is
often an effective regimen for patients with
symptoms who do not wish to pursue catheter
ablation.-adrenergic blockers have also been used
with some success.
 Catheter Ablation: successful-90%,
 2008, Doppalapudi et al. first to report idiopathic VT from posterior PM
 Posterior papillary muscle origin is more common.
Papillary muscle VT is usually exercise induced and is catecholamine
sensitive, requiring isoproterenol or epinephrine for induction
 Mechanism is typically focal in nature and not reentrant. This VT cannot be
entrained, and has a lack of late potentials at the site of ablation.
 Papillary muscle VT often exhibits multiple QRS morphologies, with
subtle changes seen spontaneously or during ablation. These subtle
morphologic changes are thought to be from preferential conduction to
different exit sites or multiple regions of origins within the complex
structure of the papillary muscles.
 RFA-quite usuful.
 majority from anterior mitral annulus
 ECG in MAVT:RBBB pattern/ monophasic R or Rs in leads
V2-V6.
 Catheter ablation is highly successful with ablation delivered at
the site of earliest ventricular activation or sites with a 12/12
pace-map match by mostly endocardial approach or coronary
venous system
 8% of IPVT
 5% of right-sided VT
 Septal sites > free-wall sites
 septal locations-anteroseptal or para-Hisian.
 ECG: A positive component (any r or R) was recorded in lead aVL
in 95% of patients
 QRS duration and Q-wave amplitude V1-V3 were greater in
VT/PVCs arising from the free wall of the tricuspid annulus
compared with the septum. Notching of the QRS complex was
seen more often in free-wall sites, as well as later precordial
transition. A Q-wave in lead V1 was observed more often in septal
tricuspid annular VTs.
 RF catheter ablation successful for the free wall (90%) compared
with the septal (57%) group. Low success rate in the septal
tricuspid annular group was thought to be due to the likelihood of
impairing AV nodal conduction with RF ablation.
 Van Herendael reported 278 IPVT from
10% -lower RV body.
48% -Within 2 cm of the tricuspid annulus
28% -Basal RV
24% -the apical RV.
 VT/PVC from the RV free wall had a longer QRS duration and
deeper S-wave in lead V2/V3.
 Apical VT/PVC more often had precordial R-wave transition
V6, smaller R-waves in lead II, and an S-wave in aVR.
 RF catheter ablation was acutely successful in 96% of
patients.
 Doppalapudi described 4/340 patients referred for IPVT
 Epicardial , junction of the middle cardiac vein and the coronary sinus
 Sustained / syncope or presyncope
 Induced/stimulation or burst pacing from the RV, and often required
Isoproterenol
 ECG demonstrates a leftward superior axis QRS morphology with an
early precordial transition and delayed intrinsicoid deflection.
 EP study: The earliest activation was present in the middle cardiac vein.
Coronary angiography demonstrated the site of earliest activation within
5-10 mm of the proximal posterior descending artery or proximal coronary
sinus
 Ablation from the coronary sinus or middle cardiac vein was attempted in
all, but was successful in only one.Percutaneous epicardial ablation was
attempted in two of the remaining three, and successfully abolished VT in
both.
 POLYMORPHIC VENTRICULAR
TACHYCARDIA AND VENTRICULAR
FIBRILLATION IN THE ABSENCE OF
STRUCTURAL HEART DISEASE
Long QT Syndrome
 Long QT Syndrome (LQTS) is a cardiac channelopathy, in
which the heart muscle cells take longer than normal to
recover electrically after each beat, primarily due to
alterations in the sodium or potassium channels.
 There have been multiple genes and proteins identified
with varied mutations responsible for altering repolarizing
currents in the myocardium – leading to the description of
some 14 sub-types of LQTS to date.
 LQT1, LQT2, & LQT3 are the most common, accounting
for about 80-90% of known genotyped patients.
QT DURATION
Jarvelle and Lange-Nielsen Syndrome is an autosomal recessive form of LQTS with
associated congenital deafness. In untreated inviduals with JLNS, about 50 percent
die by the age of 15 years due to ventricular arrhythmias.

Romano-Ward Syndrome is an autosomal dominant form of LQTS that is not

associated with deafness .

Clinical Presentation
The symptom of LQTS is sudden, temporary loss of consciousness
(syncope).
 The major arrhythmic events in LQTS usually occur without warning.
They often occur during or just following physical exertion or
emotional excitement, however they may also occur during sleep or
at rest, albeit less frequently.
 People with LQTS are at risk of developing an abnormally rapid
heart rhythm (arrhythmia) called “Torsades de Pointes.”
• LQT1 have an increased risk of cardiac events during vigorous
activities such as exercise and competitive sports
• LQT2 patients have an increased risk of cardiac events triggered by
auditory stimulation, especially during sleep.
• LQT3 patients usually have arrhythmias during sleep or at rest when
they are relatively bradycardic.
• Beta-blocker therapy is less effective in LQT3 patients as compared to
LQT1 and LQT2 patients
Management of LQTs
 Medical therapy with beta-blockers is first line prophylactic therapy.
Beta-blockers should be administered to all intermediate or high-risk
affected individuals and considered on an individual basis in low-risk
patients.

 Beta-blocker therapy is associated with a significant reduction in the risk

of life-threatening cardiac events in high-risk LQTS patients.

 However, despite these beneficial effects, cardiac events have been

reported in patients receiving beta blocker therapy. Therefore, patients
who remain symptomatic despite treatment with beta-blockers should be
considered for other, more invasive therapies.

 Implantable cardioverter defibrillators (ICD):

Implanted defibrillators in combination with beta-blockers are indicated for
secondary prevention in LQTS patients and for primary prevention in high-
risk patients who remain symptomatic despite beta-blocker therapy.
 Surgical left cervicothoracic sympathetic denervation (LCSD ):
LCSD should be considered in patients who are symptomatic
(recurrent syncope despite beta-blocker therapy) and in patients
who experience arrhythmia storms or shocks with an ICD

 Lifestyle restriction:
Avoidance of triggers such as competitive sports, swimming
(especially in LQT1 patients), alarm clocks, and QT-prolonging
drugs is usually recommended for LQTS patients.

 Genotype specific treatment:

Knowledge of the LQTS genotype may be used to tailor the
treatment plan. For instance, LQT3 patients benefit less from
beta-blockers, so a lower threshold should be used for ICD
placement in LQT3 patients
BRUGADA SYNDROME
 Brugada Syndome was described asa clinical entity in 1992.

 The condition is genetically transmitted as an autosomal

dominant syndrome with incomplete penetrance.

 BS is reported to be responsible for 4% of all sudden deaths

and 20% of sudden deaths in those without structural heart
disease and is a leading cause of death in subjects under the
age of 40 years.

 Familiy history is present in about 20 to 30% of patients.

 Sudden unexpected death syndrome (SUDS) in East Asia and

Southeast Asia is a major cause of death in young men without
known underlying cardiac diseases.

 Roughly 80% of the clinically affected patients are male, and

the sudden death typically occurs at night.
 Three subtypes have been recognised, based on different
ECG features:

 Type 1: Cove-shaped ST elevation in right precordial leads

with J wave or ST elevation of 2mm (mV) at its peak followed
by a negative T wave with little or no isoelectric interval in
more than one right precordial leads V1-V3.

 Type 2: The ST segments also have a high take-off but the J

amplitude of 2mV gives rise to a gradually descending ST
elevation remaining 1mV above the baseline followed by a
positive or biphasic T wave that results in a saddle back
configuration.

 Type 3: Right precordial ST elevation of <1mm of saddle-back

type or coved type
Drug Challenge

• Intravenous administration of Na+ channel blocking drugs like

ajmaline, flecainide, pilscanide and, to a variable extent,
procainamide, are useful in bringing out Type 1 Brugada pattern on
the ECG when ECG changes are not diagnostic.

• Ajmaline is an ideal drug for this purpose because of its short

duration of action and higher sensitivity than flecainide

• A test using procainamide (and other antiarrhytmic drugs like

ajmaline or flecainide) infusion is used in patients with type 2 or
type 3 ECG to decide if they are or not affected by the syndrome.

• In most of the affected patients during infusion of one of the drugs

the ECG will convert into a type 1.
Management
Management
 CATECHOLAMINERGIC
POLYMORPHIC
VENTRICULAR TACHYCARDIA
 Catecholaminergic polymorphic VT (CPVT) is a highly
malignant form of arrhythmogenic disorder characterized by
exercise- or emotion-induce polymorphic VT in patients with
structurally normal hearts.
 CPVT is associated with mutations of cardiac ryanodine
receptor (RyR2) and cardiac calsequestrin (CASQ2), inherited
as autosomal dominant and recessive patterns, respectively.
 The resting ECG is often unremarkable, although sinus
bradycardia and prominent U waves can be observed in some
patients. Typically, initially frequent monomoprhic or
polymorphic PVCs are noted during exercise stress test or
Holter monitoring (during exercise).
 With continued exercise, bidirectional VT and polymorphic VT
as well as supraventricular
Bidirectional VT
 The bidirectional VT is characterized by alternating QRS axis with a
rotation of 180 degrees on a beat-to-beat basis in the frontal plane
 Different sites in the His-Purkinje system had different heart rate
thresholds for delayed after depolarization– induced bigeminy.
 When the heart rate exceeded the threshold for bigeminy at the first
site in the His-Purkinje system, ventricular bigeminy developed,
causing the heart rate to accelerate and exceed the threshold for
bigeminy at the second site. Thus the triggered beat from the first
site induced a triggered beat from the second site.
 The triggered beat from the second site next reciprocated by
inducing a triggered beat from the first site, and so forth. Bigeminy
from two sites produced bidirectional VT and that from three or
more sites produced polymorphic VT.
 Bidirectional VT occurs in only 35% of patients, and the
remaining patients have polymorphic VT or VF.
 When the exercise stops, arrhythmias gradually disappear.
 The presence of a prominent U wave is a frequent finding,
although it cannot be considered to be a diagnostic indicator
of CPVT. U wave alternans (beat-to-beat variability) in the
recovery phase of exercise can be seen when VT is induced.