2. Module Objectives –
Ventricular Tachyarrhythmias
After completion of this module,
the participant should be able to:
• Differentiate types of ventricular
tachycardias using ECG
3. Module Outline –
Ventricular Tachyarrhythmias
I.
Description
II.
Characteristics
A.
Mechanisms
B.
Sustained vs. nonsustained
C.
Premature ventricular contractions
4. Module Outline –
Ventricular Tachyarrhythmias
III. Classification
A.
Monomorphic
1.
Idiopathic
a.
b.
ECG recognition
c.
2.
Description
Treatment – ablation
Bundle branch
a.
Description
b.
ECG recognition
c.
Treatment –ablation
5. Module Outline –
Ventricular Tachyarrhythmias
III. Classifications - continued
1.
Ventricular flutter
a.
4.
Ventricular fibrillation
a.
B.
ECG recognition
ECG recognition
Polymorphic
1.
Torsades de pointes
a.
b.
Description
ECG recognition
6. Ventricular Tachycardia (VT)
• Originates in the ventricles
• Can be life threatening
• Most patients have significant heart disease
–
Coronary artery disease
–
A previous myocardial infarction
–
Cardiomyopathy
7. Mechanisms of VT
• Reentrant
–
Reentry circuit (fast and slow pathway) is confined to
the ventricles and/or bundle branches
• Automatic
–
Automatic focus occurs within the ventricles
• Triggered activity
–
Early afterdepolarizations (phase 3)
–
Delayed afterdepolarizations (phase 4)
8. Reentrant
• Reentrant ventricular arrhythmias
–
Premature ventricular complexes
–
Idiopathic left ventricular tachycardia
–
Bundle branch reentry
–
Ventricular tachycardia and fibrillation when
associated with chronic heart disease:
•
Previous myocardial infarction
•
Cardiomyopathy
9. Automatic
• Automatic ventricular arrhythmias
–
Premature ventricular complexes
–
Ischemic ventricular tachycardia
–
Ventricular tachycardia and fibrillation when
associated with acute medical conditions:
•
Acute myocardial infarction or ischemia
•
Electrolyte and acid-base disturbances, hypoxemia
•
Increased sympathetic tone
12. Sustained vs. Nonsustained
• Sustained VT
–
Episodes last at least 30 seconds
–
Commonly seen in adults with prior:
•
Myocardial infarction
•
Chronic coronary artery disease
•
Dilated cardiomyopathy
• Non-sustained VT
–
Episodes last at least 6 beats but < 30 seconds
13. Premature Ventricular
Contraction
• PVC
–
Ectopic beat in the ventricle that can occur singly
or in clusters
–
Caused by electrical irritability
• Factors influencing electrical irritability
–
Ischemia
–
Electrolyte imbalances
–
Drug intoxication
18. Distinguishing wide complex SVT
from ventricular tachycardia
In VENTRICULAR TACHYCARDIA
• H/O coronary disease or infarction
• QRS width >0.14 sec
• AV dissociation showing capture or fusion beats
• Extreme right axis deviation
• Q wave in V6
19. The Brugada Criteria
Table I.
Diagnosis Of Wide QRS Complex Tachycardia With A Regular Rhythm
Step 1. Is there absence of an RS complex in all precordial leads V1 – V6?
If yes, then the rhythm is VT.
•
Sens 0.21 Spec 1.0
Step 2. Is the interval from the onset of the R wave to the nadir of the S
wave greater than 100 msec in any precordial leads?
If yes, then the rhythm is VT.
•
Sens 0.66 Spec 0.98
Step 3. Is there AV dissociation?
If yes, then the rhythm is VT.
•
Sens 0.82 Spec 0.98
Step 4. Are morphology criteria for VT present? See Table II.
If yes, then the rhythm is VT.
•
Sens 0.99 Spec 0.97
20. Morphology Criteria for VT
Table II.
Morphology Criteria for VT
Right bundle type requires waveform from both V1 and V6.
V1
V6
Monophasic R wave
QR
or
QS
RS
or
QR
R/S <1
Left bundle type requires any of the below morphologies.
V1or V2
V6
R wave > 30 msec
QR
or
QS
Notched downstroke
S wave.
Greater than 60msec
nadir S wave.
Adapted from Brugada et al. A new approach to the differential diagnosis of regular tachycardia with a wide QRS complex.
Circulation 1991; 83:1649-59.
21. Idiopathic Right
Ventricular Tachycardia
• Right ventricular idiopathic VT
–
Focus originates within the right ventricular
outflow tract
–
Ventricular function is usually normal
–
Usually LBBB, inferior axis
• Treatment options:
–
Pharmacologic therapy (beta blockers, verapamil)
–
RF ablation
23. Case History: Idiopathic VT
39 y.o. female with no prior cardiac history
• First episode
–
9 hours of palpitations
–
In ER, found to be in wide-complex tachycardia of
LBBB, inferior axis, at 205 bpm
–
Converted with IV lidocaine; placed on tenormin
• Second episode
–
While on tenormin, patient had onset of palpitations
at airport
–
In ER, converted with IV lidocaine
• Patient underwent EP study
24. Case History: Idiopathic VT
• At EP study, tachycardia focus was mapped
and localized to right ventricular outflow tract
• The focus was successfully ablated
using radiofrequency energy, with no
subsequent inducible or clinical VT
27. Bundle Branch Reentry
• Reentry circuit is confined to the left and right
bundle branches
• Usually LBBB, during sinus rhythm
• Presents with:
–
Syncope
–
Palpitations
–
Sudden cardiac death
• Treatment: RF ablation of right bundle
36. Mechanism
• Events leading to TdP are:
–
Hypokalemia
–
Prolongation of the action potential duration
–
Early afterdepolarizations
–
Critically slow conduction that contributes to reentry
37. ECG Recognition
• QRS morphology continuously changes
• Complexes alternates from positive to negative
38. A 67 year old male with history of previous infarct and
reduced LV function presents with palpitations and dizziness.
His blood pressure is 80/40. The appropriate next step is ?
• A. Synchronized cardioversion for VT
• B. I.V. Procainamide for Atrial Fibrillation with
WPW syndrome
• C. Synchronized cardioversion for unstable SVT
with aberrancy.
• D. I.V. Amiodarone for SVT with aberrancy in a
patient with reduced LV function.
39.
40. Answer A.
• This patient has ventricular tachycardia. An RS
interval of greater than 100 msec is clearly visible.
In addition, by history this patient is
overwhelmingly likely to present with VT with a
wide complex rhythm. Also this patient is not
stable with relative hypotension requiring
immediate cardioversion as opposed to
pharmacologic therapy.
41. A 46 year old female is admitted with dizziness. She is
an alcoholic, on methadone, with schizophrenia. She
began feeling dizzy after starting a fluoroquinalone for a
UTI. Which of the following should be your next step?
• A. Administer I.V . Procainamide
• B. Consult E.P. for placement of a defibrillator
• C. Discontinue antibiotic, treat with I.V. magnesium, discontinue
antipsychotic, and consider temporary pacing
• D. Administer I.V. amiodarone because it is unlikely
Torsades de Pointes.
cause
42.
43. Answer C.
• This patient has Torsades de Pointes with classic
polymorphic VT and prolonged QT demonstrated
in the bottom strip. Antipsychotics,
hypomagnesemia, quinolones all may predispose
to this arrhythmia. Procainamide or amiodarone
would worsen this rhythm. ICD is not indicated .
Welcome to VENTRICULAR TACHYARRHYTHMIAS – AN ELECTROPHYSIOLOGIC OVERVIEW. This module contains a discussion of the various characteristics and classifications of ventricular tachycardia (VT). ECG recognition and treatment of the various tachycardias will be explored. Focus is given to the use of RF ablation as a treatment for certain VTs.
Participant objectives, for this module, are as listed.
This module will start by discussing the characteristics of VT.
VTs are generally classified as being either monomorphic or polymorphic. Detailed discussions of monomorphic VTs, (idiopathic, bundle branch, ventricular flutter,and ventricular fibrillation) will include a description of the rhythm, ECG characteristics, and treatment options.
The presentation will conclude with a discussion of Torsades de pointes.
Sudden death affects approximately 250,000 or more Americans annually according to the AHA. Most causes of sudden death can be attributed to VT or ventricular fibrillation (VF).
As the name implies, ventricular tachycardia, originates in the ventricles. Rates can range from 110 – 250 bpm.
Ventricular tachyarrhythmias are often, life threatening and require immediate intervention. Occasionally, slower VTs may be relatively well tolerated.
While most ventricular arrhythmias occur in patients with a history of heart disease, they have also been seen in patients with healthy hearts.
Ventricular tachycardia can be attributed to one of three mechanisms.
Reentry is a common cause of ventricular tachyarrhythmias. It is the mechanism that is responsible for the arrhythmias listed on this slide.
Left idiopathic ventricular tachycardia is rare.
Automaticity enables the cell to spontaneously produce an electrical impulse without an external stimulus. It is the mechanism for arrhythmias listed on this slide.
Of note, hypoxemia is deficient oxygenation of the blood.
This graphic illustrates the cause of automaticity: abnormal acceleration of phase 4 of the action potential in a cardiac cell. This reduces the time of repolarization, and allows the cell to depolarize again.
Automaticity enables some cardiac cells (ectopic cells) to act as backup pacemakers when the SA node malfunctions. Ectopic sites may generate impulses in addition to the impulses generated by the SA node, or the ectopic sites may generate impulses out of sync with the normal heart rhythm. Enhanced automaticity occurs when the SA node or ectopic sites generate electrical impulses too quickly, which may affect heart rhythm or rate. Ectopic sites may be located in the atria, AV node, or in the ventricles and can produce tachycardias reflective of the site of origination.
Figure A illustrates the early afterdepolarizations in phase 3 of the action potential, responsible for pause-dependent triggered activity.
Figure B illustrates late afterdepolarizations seen in late phase 3 or phase 4 of the action potential, responsible for catechol-dependent triggered activity.
Another characteristic, used to describe VT, is whether it is sustained or non-sustained.
PVC’s can lead to ventricular tachycardia or fibrillation in individuals with ischemic or damaged hearts.
PVCs can occur in many combinations (e.g., bigeminal, trigeminal, couplets) or from many ectopic foci, (e.g., multifocal PVCs).
Ventricular tachycardia can be classified as being either monomorphic or polymorphic. The following slides present a discussion for each rhythm listed, along with EGC identification and treatment options.
Ventricular flutter is rarely seen, and may be seen just prior to the onset of ventricular fibrillation.
Torsades de pointes is associated with a long QT interval.
Monomorphic VT is regular, with uniform beat-to-beat morphology. It can be sustained, nonsustained, idiopathic or caused by bundle branch reentry.
ECG characteristics that help define VTs are:
The QRS complexes are rapid, wide, and distorted.
The T waves are large with deflections opposite the QRS complexes.
The ventricular rhythm is usually regular.
P waves are usually not visible.
The PR interval is not measurable.
A-V dissociation may be present.
V-A conduction may or may not be present.
It may be difficult to distinguish VT from SVT with aberrancy from a surface ECG. Many texts offer tips for distinguishing these rhythms. The presence of capture and fusion beats generally occur in VT.
This tachycardia may terminate with adenosine. It is catecholamine sensitive and usually inducible with isoproterenol.
This slide is a recording of RVOT VT.
The following slides discuss the case of a 39 year old white female, who presented with idiopathic VT.
Idiopathic left ventricular tachycardia has been seen in younger patients with normal hearts.
This ECG is left ventricular tachycardia.
Bundle branch reentry tachycardia is another VT that is treatable with RF ablation. With this type of tachycardia, the HV interval is increased.
Ablation of the right bundle does cure this form of reentry. However, given the underlying LBBB, ablation of the RBBB results in either very impaired His/Purkinje function or in complete heart block. A pacer is usually required.
The most helpful criteria to consider when diagnosing VT due to bundle branch reentry is the comparison of this LBBB morphology to the LBBB seen in sinus. The morphology does not have to be exactly the same (if there is some conduction down the left bundle) but it should be really similar.
Rarely seen, ventricular flutter may occur just prior to the onset of ventricular fibrillation. It degenerates into ventricular fibrillation in a matter of seconds.
Ventricular fibrillation (VF) will convert to fine VF and then no electrical activity will be seen. Patients resuscitated from VF are deemed sudden cardiac death survivors.
The following ECG findings help electrophysiologists to diagnose VF:
P waves and QRS complexes are not present.
Heart rhythm is highly irregular.
The heart rate is not defined (without QRS complexes).
A second classification of VT is polymorphic VT.
TdP is a rapid and distinct VT with a twisting configuration of the QRS morphology, associated with prolonged repolarization. It may be acquired or congenital. It is a very deadly form of VT.
The early afterdepolarizations initiate the tachycardia; reentry sustains it.
Torsades de pointes (twists of points) is a unique VT in which the QRS complexes change from positive to negative and appear to twist around the isoelectric line.
