VENTRICULAR
TACHYCARDIA
TOPIC DISCUSSION
VENTRICULAR TACHYCARDIA
DEFINITION
3 or More ORS Complexes of Ventricular
Origin
Rate exceeding 100 bpm
VENTRICULAR TACHYCARDIA
INTRODUCTION
VT & VF are Major Causes of SCD
Ambulatory ECG Recordings at SCD Have
Shown 50%-60% of Sustained Monomorphic
VT as The Initial Event
VENTRICULAR TACHYCARDIA
KEY FEATURES
SUSTAINED MONOMORPHIC VT:
Most Common Mechanism Could be Re-Entry
in Scarred Myocardium in Patients with
Structural Heart Disease
POLYMORPHIC VT:
Caused by Abnormalities in Repolarization by
Both Intrinsic or Transient Factors
VENTRICULAR TACHYCARDIA
CLASSIFICATION
ECG MORPHOLOGY
Monomorphic VS Polymorphic, BBB Pattern,
Axis
DURATION
Sustained VS Nonsustained
MECHANISM
ETIOLOGY
VENTRICULAR TACHYCARDIA
CLINICAL PRESENTATION
Quite varied (Asymptomatic, Syncope, Sudden
Death)
Duration, HR, Underlying Heart Disease, Other
medical Conditions
VENTRICULAR TACHYCARDIA
CLINICAL SIGNIFICANCE
Decreased CO
1. Rapid HR with Poor Ventricular Filling
HR <150 bpm, well tolerated in short term; CHF occur
in poor ventricular function patients
HR >150 bpm, <200 bpm, tolerated with variability
HR >200 bpm, virtually symptomatic in all patients
VENTRICULAR TACHYCARDIA
CLINICAL SIGNIFICANCE
Decreased CO
2. Asynchrony between AV Conduction
3. Abnormal Sequence of Ventricular Activation
4. Loss of Atrial Contribution
VENTRICULAR TACHYCARDIA
CLINICAL SIGNIFICANCE
Degenerative to VF
SCD
VENTRICULAR TACHYCARDIA
DIFFERENTIAL DIAGNOSIS
1. SVT with Aberrant Intraventricular
Conduction
2. BBB
3. Morphological Changes of QRS Secondary to
Metabolic Derangement
4. Pacing
VENTRICULAR TACHYCARDIA
BRUGADA CRITERIA
(D/D VT VS SVT with Aberrant Intraventricular
Conduction)
1. Most Helpful with 99% Sensitivity and 96.5%
Specificity Without Pre-Existing BBB
2. Stepwise Approach
VENTRICULAR TACHYCARDIA
1ST ALGORITHM
From Harrisons
Internal
Medicine, 15th
Edi.
VENTRICULAR TACHYCARDIA
2ND ALGORITHM (D/D VT VS Antidromic
Tachycardia over An Accessory Pathway)
VENTRICULAR TACHYCARDIA
PATHOPHYSIOLOGY
1. Studies in experimental animals and intraoperative
mapping in humans as well as pacings during VT
2. In post MI patients, VT was caused by a re-entrant
mechanism
3. Areas of slow conduction have been identified as the
substrate for re-entry.
4. In experimental MI, continuous electrical activity
regularly and predictably bridged the entire diastolic
interval could be demonstrated at the onset of VT by
the use of electrodes
VENTRICULAR TACHYCARDIA
PATHOPHYSIOLOGY
5. These findings are corroborated by the anatomic
characteristics of MI, which may show islands of
relatively viable muscle alternating with areas of
necrosis and later fibrosis
6. Such tissue may result in fragmentation of the
propagating electromotive forces
7. Gardner et al. showed that induced slow conduction
alone did not cause fragmented activity
8. Highly fractionated electrograms occurred only in
preparations from chronic infarcts with interstitial
fibrosis forming insulating boundaries between muscle
bundles
VENTRICULAR TACHYCARDIA
PATHOPHYSIOLOGY
9. Another possibility is that there is a marked reduction
in conduction velocity caused by a diminished
intercellular coupling, which would be expected to
cause high resistance to current flow between cells
10. The size of region necessary for occurrence of re-entry
has not yet been fully established
11. Finally, a close correlation between the presence of
continuous fractionated electrical activity and
perpetuation of VT was demonstrated by Garan et al.
VENTRICULAR TACHYCARDIA
THERAPY
Medical Treatment
(No Hemodynamic Compromise)
DCC
(Unstable, Symptomatic)
New Guidelines for VT in 2000
VENTRICULAR TACHYCARDIA
THERAPY
Medical Treatment
1. IV Procainamide, Xylocaine or Amiodarone
2. Reversible Cause Correction (eg.. Ischemia,
Electrolyte Imbalance, Bradycardia)
3. Hypotension Treatment
4. Offending Agents Removal, and Antidotes if
Necessary
VENTRICULAR TACHYCARDIA
THERAPY
DCC
1. At Least 100 J DCC Initially in Stable Patient
2. 200 J DCC Synchronized in Unstable,
Symptomatic VT
3. 200 J DCC Unsynchronized in Pulseless VT
VENTRICULAR TACHYCARDIA
PREVENTION & PROPHYLAXIS
MEDICAL THERAPY
Shift of Class I to Class III Maintenance
Therapy in CAST Trial
CURATIVE CATHETER-BASED
THERAPIES
SURGICAL PROCEDURES
ICD -- Greatest Impact on Survival in SCD
VENTRICULAR TACHYCARDIA
PREVENTION & PROPHYLAXIS
MEDICAL THERAPY
ESVEM Trial
It was Disappointing with Sotalol to be The
Most Effective Drug
EMIAT & CAMIAT Trial (Amiodarone post AMI)
It Revealed A Decrease in Arrhythmia Deaths
with No Survival Benefit
VENTRICULAR TACHYCARDIA
PREVENTION & PROPHYLAXIS
MEDICAL THERAPY
COMBINATION THERAPY With ICD in High
Risk Patients in New Era
VENTRICULAR TACHYCARDIA
PREVENTION & PROPHYLAXIS
MEDICAL THERAPY
Calcium Channel Blocker is Effective in
Some Idiopathic Monomorphic VTs:
1. VT from RVOT with LBBB
2. VT from LV Apex with RBBB
3. VT from Digoxin Toxicity
VENTRICULAR TACHYCARDIA
PREVENTION & PROPHYLAXIS
CURATIVE CATHETER-BASED
THERAPIES
Radiofrequency Ablation is Used to Eliminate
The Slow Conduction Pathway in A Re-entrant
Circuit
50%-70% Successful Rate
Progressively Developing
Electrophysiologic study
in ventricular
tachycardia. (Re-entry
type from previous MI)
(a) A single
extrastimulus (S2) after
an 8-beat drive at 550ms
cycle length (S1–S1)
initiates sustained
monomorphic
ventricular tachycardia
(VT). Note the presence
of atrioventricular
dissociation and the
absence of a His
potential before the QRS.
(b) A burst of rapid
ventricular pacing (RVP)
is used to restore normal
sinus rhythm (NSR). A,
atrium; HRA, high right
atrium; HBE, bundle of
His; RVA, right
Catheters are typically positioned in RA, Bundle of His region, ventricular apex; V,
and the RV apex. The standard stimulation protocol may use
ventricle.
up to 3 ventricular extrastimuli delivered at 2 basic cycle
lengths from 2 RV sites.
VENTRICULAR TACHYCARDIA
PREVENTION & PROPHYLAXIS
ICD
MADIT & AVID Trial
(High Risk in EF <35% or Inducible Sustained
VT at EPS)
A Decided Advantage in ICD was Noted in Both
Trials With 30%-50% Reductions in Mortality
VENTRICULAR TACHYCARDIA
CLINICAL PRESENTATION AND
COURSE OF VT
ISCHEMIC
NON-ISCHEMIC
TORSADES DE POINTS
VENTRICULAR TACHYCARDIA
CLINICAL PRESENTATION AND
COURSE OF VT
ISCHEMIC
Altered Cellular Level Function
Anatomic Scar Tissue Formation
A Re-entrant Circuit With 2 Pathways
Normal QT Interval
VENTRICULAR TACHYCARDIA
CLINICAL PRESENTATION AND
COURSE OF VT
ISCHEMIC
Predictors: Larger Infarcts With Greater
Resultant Impairment of LV Systolic Function
LV Systolic Function is The Single Most
Important Predictor of SCD due to
Arrhythmia
Revascularization Seemed to Decrease The Risk
VENTRICULAR TACHYCARDIA
CLINICAL PRESENTATION AND
COURSE OF VT
ISCHEMIC
AIVR
It is Seen Almost Exclusively in Ischemic Heart
Disease, esp. During AMI or Reperfusion of An
Occluded Territory (Enhanced Automaticity)
It May be Seen in Digoxin Toxicity
It is Rarely of Clinical Significance
VENTRICULAR TACHYCARDIA
CLINICAL PRESENTATION AND
COURSE OF VT
ISCHEMIC
AIVR
VENTRICULAR TACHYCARDIA
CLINICAL PRESENTATION AND
COURSE OF VT
ISCHEMIC
AIVR
Therapy is Rarely Necessary Unless
1. Loss of AV Synchrony with Hemodynamic
Change
2. R on T
3. Rapid Ventricular Rate or VF
VENTRICULAR TACHYCARDIA
CLINICAL PRESENTATION AND
COURSE OF VT
NON-ISCHEMIC
1. BB Re-entry, WPW Syndrome
2. Idiopathic VT
3. Congenital Long QT Syndrome
4. Genetically Associated VT
5. Idiopathic Polymorphic VT
6. Infection, Inflammation or Drug VT
7. Arrhythmogenic RV Dysplasia
VENTRICULAR TACHYCARDIA
CLINICAL PRESENTATION AND
COURSE OF VT
NON-ISCHEMIC
BB Re-entry
Common in DCM, Usually >= 200 BPM
Typically LBBB, with less RBBB
Most commonly With
Right Bundle Antegrade Conduction
Left Bundle Retrograde Conduction
Confirmed by EPS
Electrophysiologic findings in bundle branch re-entry. The tracings shown are
surface ECG leads 1, aVF and V1, and intracardiac recordings from the high right
atrium (HRA), the bundle of His (HBE) and the right ventricular apex (RVA). The
surface leads show the typical pattern of left bundle branch block. The
intracardiac recordings show atrioventricular dissociation and a His potential
preceding each ventricular depolarization. A, atrium; His, His potential; RVA,
right ventricular apex.
VENTRICULAR TACHYCARDIA
CLINICAL PRESENTATION AND
COURSE OF VT
NON-ISCHEMIC
Idiopathic VT (VT From RVOT, VT From LV Apex)
Otherwise Structurally Normal Hearts
No Significant CAD
No Family History of Arrhythmia or Sudden
Death
Normal Surface ECG
Usually Responsive to Calcium Channel Blocker
VENTRICULAR TACHYCARDIA
CLINICAL PRESENTATION AND
COURSE OF VT
NON-ISCHEMIC
Congenital Long QT Syndrome
From Manual of Cardiovascular Medicine. By Steven P. Marso, Brian P. Griffin, Eric J. Topol
From Manual of Cardiovascular Medicine. By Steven P. Marso, Brian P. Griffin, Eric J. Topol
VENTRICULAR TACHYCARDIA
CLINICAL PRESENTATION AND
COURSE OF VT
NON-ISCHEMIC
Congenital Associated VT
Muscular Dystrophies
Duchenne’s Muscular Dystrophy
Myotonic Dystrophy
VENTRICULAR TACHYCARDIA
CLINICAL PRESENTATION AND
COURSE OF VT
NON-ISCHEMIC
Congenital Associated VT
Muscular Dystrophies
Frequent Defects in Conduction System
Heart Block, BBB, and SCD due to VT
VENTRICULAR TACHYCARDIA
CLINICAL PRESENTATION AND
COURSE OF VT
NON-ISCHEMIC
Idiopathic Polymorphic VT
Structurally Normal Hearts
Normal QT Interval
VENTRICULAR TACHYCARDIA
CLINICAL PRESENTATION AND
COURSE OF VT
NON-ISCHEMIC
Idiopathic Polymorphic VT
1. Persistent ST Elevation
2. Exercise Reproducible Arrhythmias with
Exercise and Responsive to β-Blocker
3. Polymorphic VT Triggered by VPCs with High
SCD Incidence not Prevented by β-Blocker
VENTRICULAR TACHYCARDIA
CLINICAL PRESENTATION AND
COURSE OF VT
NON-ISCHEMIC
Drug-Induced VT
Both Polymorphic & Monomorphic
Particularly True in Ischemic or Infarcted
Hearts
VENTRICULAR TACHYCARDIA
CLINICAL PRESENTATION AND
COURSE OF VT
NON-ISCHEMIC
Drug-Induced VT
Phenothiazines, TCA, Digoxin, Epinephrine,
Cocaine, Nicotine, Alcohol, and Glue Are
Implicated With Monomorphic VT
NSVT & Depressed LV Function Remained
Risk Factors for SCD
VENTRICULAR TACHYCARDIA
CLINICAL PRESENTATION AND
COURSE OF VT
NON-ISCHEMIC
Drug-Induced VT
Torsades De Points Due to QT Prolongation
Digoxin Can Propagate DAD to VT
VENTRICULAR TACHYCARDIA
CLINICAL PRESENTATION AND
COURSE OF VT
NON-ISCHEMIC
DCM & HCM
Increased Risk of VT to SCD
VENTRICULAR TACHYCARDIA
CLINICAL PRESENTATION AND
COURSE OF VT
NON-ISCHEMIC
DCM
Difficult to Predict
Asymptomatic VT Are Common
ICD in Life-Threatening Arrhythmia
Ablation if BB Re-entry is The Mechanism
VENTRICULAR TACHYCARDIA
CLINICAL PRESENTATION AND
COURSE OF VT
NON-ISCHEMIC
HCM HIGH RISK: Syncope, Family SCD History of First Degree,
NSVT on Ambulatory ECG
SVT, AF, and Ischemia Are Poorly Tolerated And
May Lead to VT
EPS May be Helpful in Stratifying Risk
Amiodarone May be Beneficial
Dual Chamber Pacing: Decrease Outflow Gradient
VENTRICULAR TACHYCARDIA
CLINICAL PRESENTATION AND
COURSE OF VT
NON-ISCHEMIC
Structural Abnormalities
Repaired TOF
Often Originates in RVOT
Cured by Ablation or Surgical Resection
MVP (Quite Good Prognosis)
Uncommonly Linked to SCD
VENTRICULAR TACHYCARDIA
CLINICAL PRESENTATION AND
COURSE OF VT
NON-ISCHEMIC
Arrhythmogenic RV Dysplasia
Cardiomyopathy Begins in RV and Often
Progress to LV
RV Dilatation with Resultant Poor Contractile
Function
RV Muscle Becomes Replaced by Adipose and
Fibrous Tissue
VENTRICULAR TACHYCARDIA
CLINICAL PRESENTATION AND
COURSE OF VT
NON-ISCHEMIC
Arrhythmogenic RV Dysplasia
Re-entrant Type (Scarring & Late Potentials)
With LBBB Morphology
Often Inversion T Over Right Chest Leads
Slurred Terminal Portion of QRS Complex
(Epsilon Wave)
A ventricular tachycardia with a left bundle pattern and superior axis from the same
patient. LAO, left anterior oblique.
VENTRICULAR TACHYCARDIA
CLINICAL PRESENTATION AND
COURSE OF VT
NON-ISCHEMIC
Arrhythmogenic
RV Dysplasia
VENTRICULAR TACHYCARDIA
CLINICAL PRESENTATION AND
COURSE OF VT
NON-ISCHEMIC
Arrhythmogenic RV Dysplasia
The Risk of VT Correlate With The Extent of
Myocardial Involvement
Therapy With Sotalol & Amiodarone May be
Successful
The Effect of Catheter Ablation is Temporizing
ICD is The Only Reliable Therapy in SCD
VENTRICULAR TACHYCARDIA
CLINICAL PRESENTATION AND
COURSE OF VT
NON-ISCHEMIC
Inflammatory or Infectious Conditions
Sarcoidosis
Heart Block, VT or VF
Amiodarone or Sotalol Are Most Efficacious
ICD May be Necessary
VENTRICULAR TACHYCARDIA
CLINICAL PRESENTATION AND
COURSE OF VT
NON-ISCHEMIC
Inflammatory or Infectious Conditions
Acute Myocarditis
Monomorphic & Polymorphic VT
Anti-arrhythmic & Anti-inflammatory
Therapy Are Generally Combined
VENTRICULAR TACHYCARDIA
CLINICAL PRESENTATION AND
COURSE OF VT
NON-ISCHEMIC
Inflammatory or Infectious Conditions
Chagas’ Disease (Trypanosoma Cruzi)
Cardiomyopathy in South & Central USA
VT & Other Arrhythmias Due to Conduction
System Involvement (Pacemaker or ICD)
Antiparasitic, CHF, Anti-arrhythmic
Treatment
VENTRICULAR TACHYCARDIA
CLINICAL PRESENTATION AND
COURSE OF VT
TORSADES DE POINTES
Delayed Myocardial Repolarization, Most Often
Prolonged QT Interval
The Duration is Typically Brief (< 20 sec), But
Also May Degenerate to VF
Irregular Ventricular Rate in Excess of 200 bpm
Polymorphic Structure With An Undulating
Twist (QRS) Around An Isoelectrical Axis
VENTRICULAR TACHYCARDIA
CLINICAL PRESENTATION AND
COURSE OF VT
TORSADES DE POINTES
VENTRICULAR TACHYCARDIA
CLINICAL PRESENTATION AND
COURSE OF VT
TORSADES DE POINTES
Congenital
Acquired
VENTRICULAR TACHYCARDIA
CLINICAL PRESENTATION AND
COURSE OF VT
TORSADES DE POINTES
Congenital
VENTRICULAR TACHYCARDIA
CLINICAL PRESENTATION AND
COURSE OF VT
TORSADES DE POINTES
Acquired
Drug Induced (Most Often)
Electrolyte Abnormalities
Hypothyroidism
Cerebrovascular Events
MI or Ischemia
VENTRICULAR TACHYCARDIA
CLINICAL PRESENTATION AND
COURSE OF VT
TORSADES DE POINTES
Acquired
Starvation Diets
Organophosphate Poisoning
Myocarditis
Severe CHF
MVP
VENTRICULAR TACHYCARDIA
CLINICAL PRESENTATION AND
COURSE OF VT
TORSADES DE POINTES
Drug Induced (Most Often)
Class IA Drugs (Most Often)
Class III Drugs (Less Often) & Ibutilide
Phenothiazines, Haloperidol, TCA
Antibiotics (Macrolides & Antihistamines Combination,
TMP/SMX)
Antihistamines Combination With Azoles
VENTRICULAR TACHYCARDIA
CLINICAL PRESENTATION AND
COURSE OF VT
TORSADES DE POINTES
Bradycardia
In Patients With Prolonged QT
Ionic Contrast Media
Promotility Agents
Cisapride
VENTRICULAR TACHYCARDIA
CLINICAL PRESENTATION AND
COURSE OF VT
TORSADES DE POINTES
Electrolyte Abnormalities
Hypokalemia (Most Reliably Linked)
Hypomagnesemia
Hypocalemia (Rare)
VENTRICULAR TACHYCARDIA
CLINICAL PRESENTATION AND
COURSE OF VT
TORSADES DE POINTES
Cerebrovascular Events
SAH (Most Notably)
ICH (Transient for Weeks)
VENTRICULAR TACHYCARDIA
CLINICAL PRESENTATION AND
COURSE OF VT
TORSADES DE POINTES
Treatment
Prompt DCC in Sustained, Hemodynamic Compromise
Situation (50J - 100J, up to 360J)
Correction of Electrolytes (K>4; Mg>2; Ca)
MgSO4: 1-2 gm Bolus With All 2-4 gm in 10-15 Minutes
Isoproterenol IVD or TVP in Bradycardia; Occasionally
ß-Blocker, Lydocaine