Transcript Ventricular Arrhythmia

Ventricular
Arrhythmia
Dr Mostafa Hekmat
Cardiologist
Electrophysiologist
VENTRICULAR TACHYCARDIA

VT Arises Distal To
The Bifurcation Of
The HB

In The Specialized
Conduction System

In The Ventricular
Muscle

Or In Combination Of
Both Tissues
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Note
Any
wide QRS complex
tachycardia should be
treated as ventricular
tachycardia until
definitive evidence is
found to establish another
diagnosis
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Types of Ventricular Arrhythmia

Premature Ventricular Complexes

Ventricular Tachycardia
 Monomorphic
 Polymorphic
 Torsade
de point
 Normal
QT

Ventricular Flutter

Ventricular Fibrillation
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Ventricular Arrhythmias
Definitions
 Premature
Ventricular beats
 Single
beats
 Ventricular Bigeminy, the appearance of
one PVC after each sinus beat
 Couplets, two consecutive premature
beats
 Triplets, three consecutive premature
beats
 Salvos, runs of 3-10 premature beats
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Ventricular Arrhythmias
Definitions
Accelerated Idioventricular Rhythm
(Slow VT), rate 60-100 bpm
 Ventricular Tachycardia (VT), rate over
100 bpm
 Ventricular Flutter, regular large
oscillations at a rate of 150-300 bpm
 Ventricular Fibrillation (VF), irregular
undulations of varying contour and
amplitude

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PVC
•
•
•
•
•
Rate?
Regularity?
P waves?
PR interval?
QRS duration?
60 bpm
Occasionally irreg.
None for 7th QRS
0.14 s
0.08 s (7th wide)
Interpretation? Sinus Rhythm with
7 1 PVC
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VT
•
•
•
•
•
Rate?
Regularity?
P waves?
PR interval?
QRS duration?
160 bpm
Regular
None
None
Wide (> 0.12 sec)
Interpretation? Ventricular Tachycardia
8
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VF
•
•
•
•
•
Rate?
Regularity?
P waves?
PR interval?
QRS duration?
None
Irregularly irreg.
None
None
Wide, if recognizable
Interpretation? Ventricular Fibrillation
9
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Premature Ventricular Complexes


Premature occurrence of a QRS complex that
is abnormal in shape
Duration usually exceeding the dominant
QRS complex




Generally longer than 120 milliseconds
The T wave is usually large and opposite in
direction to the major deflection of the QRS
A fully compensatory pause usually follows a
PVC
The PVC may not produce any pause and
may therefore be interpolated
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Ventricular fusion beat
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PVC and ventricular echo
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An interpolated PVC
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Ventricular Premature Complexes
Compensatory Pause
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Interpolated VPC
15
Premature Ventricular Complexes

Bigeminy
 Pairs
of complexes and indicates a normal
and premature complex

Trigeminy
 Premature
complex that follows two
normal beats

Quadrigeminy
 Premature
complex that follows three
normal beats is called
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Multiform
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Salvos
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CLINICAL FEATURES

The prevalence of premature complexes
increases with age

Male gender

Hypokalemia

PVCs are more frequent in the morning in
patients after MI

This circadian variation is absent in patients
with severe left ventricular (LV) dysfunction.
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CLINICAL FEATURES

Activity that increases the heart rate
can decrease
 The
patient’s awareness of the premature
systoles
 Reduce

their number.
Sleep
 Usually
associated with a decrease in the
frequency of ventricular arrhythmias
 But
some patients can experience an
increase.
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The importance of PVCs

Depends on the clinical setting

In the absence of underlying heart
disease, the presence of PVCs usually
has no impact on longevity or
limitation of activity
 Antiarrhythmic
drugs are not indicated
 Patients
should be reassured if they
are symptomatic
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PVC and MI

Those occurring close to the preceding T wave

More than five or six per minute

Bigeminal or multiform complexes

Those occurring in salvoes of two or three or more

Do not occur in about 50% of patients in
whom VF develops

And VF does not develop in about 50% of
patients who have these PVCs

Thus, these PVCs are not particularly helpful
prognostically
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Idioventricular Rhythm
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Accelerated idioventricular rhythm
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ECG Distinction of VT from SVT with
Aberrancy
Favors VT
Favors SVT
with Aberrancy
Morphology Precordial concordance
If LBBB:
If RBBB:
V1 duration > 30 ms
S wave > 70 ms
S wave notched or slurred
V6:
qR or QR
V1:
V6:
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monophasic R wave
qR
If triphasic, R > R1
R<S
R wave monophasic
R < R1
28
VENTRICULAR FLUTTER &
VENTRICULAR FIBRILLATION
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A-V Dissociation, Fusion, and
Capture Beats in VT
V1
E
F
C
CAPTURE
ECTOPY
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FUSION
30
Accelerated Idioventricular Rhythm

The arrhythmia occurs as a rule in patients who
have heart disease, such as those with acute
myocardial infarction or with digitalis toxicity.

Reperfusion of a previously occluded coronary
artery

During resuscitation

It is transient and intermittent

Episodes lasting a few seconds to a minute

Does not appear to seriously affect the patient’s
clinical course or the prognosis
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Therapy
when

Considered when AV dissociation results in loss of
sequential AV contraction

An accelerated idioventricular rhythm occurs together
with a more rapid VT

An accelerated idioventricular rhythm begins with a
PVC discharging in the vulnerable period of the
preceding T wave

The ventricular rate is too rapid and produces
symptoms

VF develops as a result of the accelerated
idioventricular rhythm.
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Therapy
Increasing
the sinus rate
with Atropine or atrial
pacing suppresses the
accelerated
idioventricular rhythm
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Clinical Impact of VT/VF

PVCs and even runs of nonsustained VT may be
frequently seen in people with normal and abnormal
hearts
Sustained
VT and VF
usually develop in
patients with advanced
structural heart disease
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Clinical Impact of VT/VF
 CAD
is the most frequent cause of
SCD and clinically documented VT
and VF
80%
 There
is no reason to neglect the
device even if the stable VT has
been successfully ablated
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VT + RBBB

(1) the QRS complex is monophasic or
biphasic in V1, with an initial
deflection different from that of the
sinus-initiated QRS complex

(2) the amplitude of the R wave in V1
exceeds the R′

(3) a small R and large S wave or a QS
pattern in V6 may be present.
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VT + LBBB
 (1)
the axis can be rightward,
with negative deflections deeper
in V1 than in V6,
 (2)
a broad prolonged (more than
40 milliseconds) R wave in V1
 (3)
a small Q–large R wave or QS
pattern in V6 can exist
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VT

QRS duration exceeding 140 milliseconds

In precordial leads with an RS pattern, the
duration of the onset of the R to the nadir of the
S exceeding 100

Fusion beat

Capture beat

AV dissociation has long been considered a
hallmark of VT

Retrograde VA conduction to the atria from
ventricular beats occurs in at least 25% of
patients
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Supraventricular arrhythmia
with aberrancy

(1) consistent onset of the tachycardia with a
premature P wave

(2) very short RP interval (0.1 sec)

(3) QRS configuration the same as that occurring from
known supraventricular conduction at similar rates

(4) P wave and QRS rate and rhythm linked to suggest
that ventricular activation depends on atrial
discharge (an AV Wenckebach block)

(5) slowing or termination of the tachycardia by vagal
maneuvers
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
A QRS complex in V1 - V6,  either all
negative or all positive  favors a VT

The presence of a 2 : 1 VA block  VT

Positive QRS complex in V1 - V6 can also
occur from conduction over a left-sided
accessory pathway.

Supraventricular beats with aberration

Triphasic pattern in V1

An initial vector of the abnormal complex similar
to that of the normally conducted beats

Wide QRS complex with long-short cycle sequence
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Sustained Monomorphic VT
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Increased risk in VT

Reduced LV function

Spontaneous ventricular arrhythmias

Late potentials on signal-averaged ECG

QT interval dispersion

T wave alternans

Prolonged QRS duration

Heart rate turbulence

Inducible sustained VTs
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Treatment
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Treatment
Frequent
PVCs, even in
the setting of an acute
MI, need not be treated
unless they directly
contribute to
hemodynamic
compromise
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Treatment

Beta blockers are often the first line of
therapy.

If they are ineffective, class IC drugs seem
particularly successful in suppressing PVCs

Flecainide and Moricizine have been shown
to increase mortality in patients treated
after MI


Should be reserved for patients without coronary
artery disease or LV dysfunction
Amiodarone

Should be reserved for highly symptomatic
patients and those with structural heart disease.
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Treatment

VT that precipitates

Hypotension

Shock

Angina

Congestive heart failure

Symptoms of cerebral hypoperfusion
 Should
be treated promptly with DC
cardioversion

Very low energies can terminate VT  a synchronized
shock of 10 to 50 J.

Digitalis-induced VT is best treated pharmacologically.
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Thump Version

Can terminate VT by mechanically
inducing a PVC that presumably
interrupts the reentrant pathway
necessary to support it.

Chest stimulation at the time of the
vulnerable period
 Can
accelerate the VT or
 Possibly

provoke VF.
Intermittent VT  best treated
pharmacologically
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Treatment


In patients in whom procainamide

Ineffective

Procainamide may be problematic

Severe heart failure

Renal failure
Intravenous Amiodarone is often
effective

Loading dose of 15 mg/min is given during a
10-minute period

Infusion of 1 mg/min for 6 hours

Maintenance dose of 0.5 mg/min for the
remaining 18 hours and for the next several
days
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Reversible conditions

VT related to ischemia  antianginal

Hypotension  vasopressors

Hypokalemia  potassium

Correction of HF  reduce the frequency of
ventricular arrhythmias

Sinus bradycardia or AV block  PVCs and
ventricular tachyarrhythmias, which can be
corrected by administration

Atropine

Temporary isoproterenol administration

Pacing
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Long-Term Therapy

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
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CLASSIFICATION OF IDIOPATHIC
MONOMORPHIC VT
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RMVT
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Both Forms Are Characterized By
Adenosine Sensitivity
And Are Thought To Be Caused By
Cyclic Amp Mediated Triggered
Activity
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VT Can Be Terminated With Adenosine,
Verapamil, The Valsalva Maneuver or CSP
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VERAPAMIL-SENSITIVE VT
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VERAPAMIL-SENSITIVE VT
 90-95%
HAS RBBB AND LEFT
SUPERIOR-AXIS MORPHOLOGY
 THE
REMAINDER OF PATIENTS HAVE
VT WITH RBBB AND RIGHT INFERIORAXIS MORPHOLOGY
 RS INTERVAL IS USUALLY 60-80 ms (in
VTs associated with structural heart disease
RS is longer than 100 ms )
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CPVT

Inherited VT

Children and adolescents

Without any overt structural heart disease.

Patients typically present with syncope or aborted
sudden death

Highly reproducible, stress-induced VT

Bidirectional

Mutations of the ryanodine receptor gene result in an
autosomal dominant

Mutations in the calsequestrin gene result in an
autosomal recessive
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CPVT
 The
treatment of choice is
beta blockers and an ICD
 Sympathectomy
 Avoid
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vigorous exercise
62
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Long QT
Syndrome
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Congenital LQTS
 The
congenital LQTS is a rare
disorder (incidence 1:10,000 to
1:15,000) characterized by
Prolongation
of the Q–T interval
on the surface ECG
Recurrent syncope
Sudden death
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Congenital LQTS

Romano-Ward syndrome
 Autosomal
 Only

dominant inheritance
Cardiac Arrhythmias
Jervell and Lange-Nielson syndrome
 Autosomal
recessive inheritance Cardiac
Arrhythmias
 Congenital

deafness.
Andersen-Tawil syndrome
 Ventricular
Arrhythmias
 Periodic
paralysis & Facial/Skeletal
dysmorphism
68
The acquired form of long-QT

Quinidine

Cisapride

Procainamide

Probucol

N-acetylprocainamide

Hypokalemia

Sotalol

Hypomagnesemia

Amiodarone

liquid protein diet

Disopyramide

Starvation

Phenothiazines


Tricyclic antidepressants
central nervous system
lesions

Erythromycin

Bradyarrhythmias

Pentamidine

cardiac ganglionitis

mitral valve prolapse
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K or Na
 The
principal abnormality in LQTS is
prolongation of action potential
duration caused by a reduction in
outward potassium current (LQT1
and LQT2)
 or,
less commonly, a persistent
inward sodium current during the
plateau phase (LQT3).
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
Action potential prolongation 
development of early after depolarizations
 triggered action potential  premature
beat  can initiate a polymorphic VT
known as torsades de pointes,

Which underlies the clinical symptoms of
palpitations, syncope, or sudden death
due to VF.
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Triggers of cardiac event 1
 The
classic description of
events in LQTS involves
exercise- or emotion-induced
clinical events.
 Symptoms often begin in
adolescence, though they may
begin earlier in LQT1.
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Triggers of cardiac event 2
 Adrenergic
Stimuli in LQTS
with Loss of function of K (iKsLQTS1 , iKr-LQTS2) TDP
 Adrenergic Stimuli 
Transmural disturbances 
 Β Blocker are useful in LQTS1
& LQTS2
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LQTS1

Rhythm disturbances mainly occur during sports especially
swimming
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LQTS 2

Rhythm disturbances mainly triggered by Auditory stimuli
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LQTS 3

Malfunction of iNaL , Symptom mostly occur at rest or
during night

No adrenergic triggers

B Blockers Contraindicated
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 In
10% of patient SCD is the first &
tragic symptom.
 LQTS1
and LQTS2 are more cardiac
events
 Benign
cardiac symptoms such as
palpitation and syncope degenerate
more easily to SCD in LQTS3
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LQTS
 The
hallmark of this condition is
prolongation of the QTc greater
than 460 ms,
 QTc may be normal in up to 1/3
of genotype-positive patients.
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LQTS
 Causes
of considerable temporal
variation in QTc
 Repolarization
is affected by factors
such as
 Sympathetic
 Electrolyte
outflow
balance
 Pharmacologic
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LQTS

The mean QTc does not differ between the LQT1, LQT2, and
LQT3 types

But is significantly longer in Jervell and Lange-Neilson
syndrome.

Other electrocardiographic abnormalities that may be found
in LQTS include

ST–T wave changes

U waves, T wave alternans

Increased QT dispersion

Sinus bradycardia
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MANAGEMENT

For patients who have idiopathic longQT syndrome but not
 Syncope
 Complex
 Family
 QTc

ventricular arrhythmias,
history of sudden cardiac death
longer than 500 milliseconds,
No therapy or treatment with a beta
blocker is generally recommended.
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MANAGEMENT

In asymptomatic patients with

Complex ventricular arrhythmias,

Family history of early sudden cardiac death

QTc longer than 500 milliseconds

Beta adrenoceptor blockers at maximally
tolerated doses are recommended.

PPM to prevent the bradycardia or pauses
that may predispose to the development of
TDP may be indicated
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MANAGEMENT
 In
patients with syncope caused
by ventricular arrhythmias or
aborted sudden death, an ICD is
warranted.
 Concomitant
beta blockers
 Overdrive
atrial pacing (via the
ICD) to minimize the frequency
of ICD discharges
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MANAGEMENT

Most competitive sports are
contraindicated for patients with the
congenital long-QT syndrome

For patients with the acquired form
and TDP, intravenous Mg and atrial or
ventricular pacing are initial choices.
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Survival is dramatically improved by
 Aggressive
treatment with βBlocker drugs
 Cardiac pacing
 Left cervical sympathectomy
 Implantable cardioverter
defibrillator (ICD).
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Short QT
Syndrome
Definition
QT
of less than 350
milliseconds at
rates of less than
100 beats/min
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 Short-QT
interval has recently
been identified to carry an
increased risk of sudden death
due to VF
 One of the syndromes
responsible for “idiopathic
VF”
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Causes
 Hyperkalemia
 Hypercalcemia
 Hyperthermia
 Acidosis
 Digitalis
 Genetic
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abnormalities
97
Treatment
 ICDs
are considered the
treatment of choice in
symptomatic patients to prevent
sudden cardiac death.
 Quinidine
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