Sir William Osler

It is much more important to know what sort of a

patient has a disease than what sort of a disease a patient has. Medicine is a science of uncertainty and an art of probability. The young physician starts life with 20 drugs for each disease, and the old physician ends life with one drug for 20 diseases

Louis Gallavardin

La Tension artrielle en Clinique, the standard text on the measurement of blood pressure. Realised the importance of electrocardiography, and published on arrhythmias, particularly ventricular tachycardia. described a type of aortic stenosis which was not rheumatic in origin, and described effort syncope in the condition.

Dr.Pedro Brugada

The Brugada syndrome is a genetic disease and an increased risk of

sudden cardiac death. named by the Spanish cardiologists Pedro Brugada and Josep Brugada. It is the major cause of Sudden Unexpected Death Syndrome (SUDS), and is the most common cause of sudden death in young men without known underlying cardiac disease in Thailand and Laos.

Bazetts Formula
QTcB=QTRR

Fridericia Formula
QTcF=QT3RR

Normal QTc interval is 0.46 sec Females>males Increases with age.

Hodges formula
With increasing heart rate and younger age the Bazett and

Hodges formulae overcorrect the QTc whereas the Fridericia and Framingham formulae undercorrect. The Hodges formula correlated best with the RR interval. Hodges formula: QT + 0.00175 (HR 60)

Torsades de Pointes

French term literally means twisting of points

Conduction System of the Heart

SA node ----internodal pathways ---AV node ----AV bundle (bundle of

HIS )----LBB,RBB----purkinjeefibres---cardiac muscle fibres.

0.03sec---0.09sec---0.04 sec ---total 0.16 sec..

SINO ATRIAL node action potential

Resting membrane potential -55 to -60 mV Cellular fibres are permeable to sodium and calcium ions Fast Na channels are inactive Absent of plateau phase as inactivation of slow Na and Ca current take place.

Ventricular muscle action potential

Resting membrane action potential is -85 to -90 mV

Fast Na channels are responsible for depolarisation Plateau phase present. No hyperpolarization

Capture 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..ventricularcaptur e 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.

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.

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.

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.

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.

Burst pacing
Also called as overdrive pacing Here we pace the ectopic focus (suppress it )by a external

device pacemaker Usually pacing done by transvenous placement of an electrode in the right ventricle..

 Introduction Definition Etiology Classification Clinical symptoms Algorithm of approach Diagnosis Differential diagnosis Treatment Conclusion Take home message Future

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%.

Questions
1 Do all cases of VT lead to hemodynamic collapse? 2.what is capture beat ?what does it signify? 3.bidirectional VT is due to ? 4.what is the drug of choice in case of idiopathic bundle branch

tachycardia? 5.which VT does not revert on usual catheter ablation? 6.which VT cannot be produced on programmed stimulation? 7.what is the etiology when PVT dose not occur along with QT prolongation? 8.drugs causing QT prolongation? 9.which is better formula for QTc interval estimation? 10.LV <30 % is ICD indicated?

Definition
The occurrence of three or more VPC complexes with a rate of >

120 bpm in succession is called as VT.

Non sustained is termination of VT by self less than 30 sec.
Sustained VT is presence of VT for > 30 sec.or hemodynamically

unstable but terminated in less than 30 sec.

Slow VT HR >100 < 120 bpm. Pulseless VT VT with hemodynamic collapse that requires DC

cardioversion.
Refractory VT that does not revert to sinus rhythm on

medication use or use of three shocks.

VT storm --- repeated VT episodes requiring the DC shocks/ICD

shocks .
Rate is 100300 bpm

Rate >220 bpm VF

Etiology
Acute MI After chronic infarction Ischaemic heart disease Dilated cardiomyopathy Hypertrophic cardiomyopathy Post CABG Post TOF surgery Electrolyte abnormalities Idiopathic Specific etiology-- genetic

Etiology
Usually as a complication of severe heart disease,can occur

in structurally normal hearts. In healthy individuals---RVOT,L V posterior/anterior fasciclecatheter ablation. Major complication of IHD,acutely following MI, chronically after a large infarction.. Early hours VT---VF epicardial injury.. Fleicainide ---convert non sustained VT to sustained VT. Sotalol- prolong QT interval--TDP

Mechanism of occurrence of VT
REENTRY ENHANCED AUTOMATICITY TRIGGERED ACTIVITY

Classification of VT
Sustained /non sustained VT Monomorphic VT/polymorphic VT Pulseless VT/hemodynamic stable VT Structural heart disease/idiopathic Unique VT syndromes

Difference of MVT,PVT
MONO MORPHIC VT POLYMORPHIC VT

1.
2. 3. 4. 5. 6. 7. 8.

Stable tachycardia
Reproducible, recurrent phenomenon Initiated by pacing ,programmed ventricular stimulation Normal hearts./structural heart disease

Unstable,dynamic
Less reproducible Not reliably initiated Acute ischemia ,myocarditis,drugs Pause dependent VT,TRIGERRING

Reentry circuit
Hemodynamically stable

Not so PVTVF/VFL Bbs ,pacing/ablation?

MVTPVTVF/VFL Catheter ablation,pacing,AAD

 Monomorphic VT with RBBB morphology,hr 180bpm,north west axis.

The morphology of the qrs complex is not uniform

Clinical features
Asymptomatic May have palpitations transient,sustained. Chest pain angina Syncope Presyncope Dizziness Cannon a waves Absent pulse Hypotension Variable s 1

Diagnosis
Algorithm based ECG 12 Lead with long rhythm strip of lead II. The focus can be known. 24 hr holter monitoring in case of transient episode 2d echo for the etiology. Routine investigations Serum electrolytes,calcium,magnesium ABG

S.No

SUPRAVENTRICULAR TACHYCARDIA Abberant QRS pattern that matches exactly that of the wide complex rhythm. Presence of p wave before QRS complex Preexcited QRS pattern on SR ECG indicates atrial arryhthmia.AFL,focal AT,antidromic macroreentrant tachycardia. Responds to vagal Manuevre,valsalva,adenosine Verapamil effective

VENTRICULAR TACHYCARDIA not in morphology of LBBB,RBBB,wide complexes present P waves and QRS complexes are dissosciated. Bizzare QRS complex

1.

2. 3.

4. 5.

Not so Worsens the LV dysfunction

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

Approach to broad complex tachycardia

Morphological criteria

RBBB morphology

Brugada algortihm

Vereckei algorithm

More likely to be VT

Brugada sign Josephsons sign

 Initiation of VT BY VPCs

 Torsades de pointes due to hypokalemia

Reversible causes of VT

Hypoxia Hyperthyroidism catecholamines Hypokalemia Metabolic acidosis Hypomagenesemia Hypocalcemia Drugs Alcohol Starvation www.torsades.org,www.qtdrugs.org,

Differential diagnosis
SVT with aberration due to BBB

WPW syndrome with AF/AFL

AIVR

Management
NON SUSTAINED VT : No treatment in absence of heart disease. Look for reversible factors. In termination of episodes IV BBs can be used. For preventing recurrences oral BBs /CCB s.

MONOMORPHIC VT with hemodynamic compromise

Severity of underlying structural heart disease Ventricular rate Origin of arryhthmia LVD Hypotension,pulmonary edema,MI.

Synchronised R wave shock is given. With appropriate

sedation.100j200-300-360 j After SR rhythm lidocaine 2-4 mg/min iv infusion.

ACC/AHA/ESC guidelines 2006 for ventricular arrythmias/STEMI

Sustained monomorphic VT ,stable

DC cardioversion effective in termination IV antiarryhthmic drugs can also be used.no response

cardioversion. presence /abscence LVD 1.with preserved LVF:only one drug to be used. IV PROCAINAMIDE---class II a recommendation More effective than amiodarone in termination. <50 mg/min---1-4 mg/min Preferred over other drugs. Rapid infusion causes hypotension.
ACC/AHA/ESC guidelines for Ventricular arryhthmias/STEMI

Sustained monomorphic VT ,stable

IV AMIODARONE :can be given in presence of LVDalso. Drug of choice according to 2004 guidelines,not so in 2006. When VT is refractory to electrical cardioversion,if VT is

unstable or recurrent inpsite of IV procainamide.

150mg IV given as bolus with in 10 min repeat after 10-15 min.

Infusion of 1 mg/min*6 hrs,0.5mg/min*18 hrs.

Max dose is 2.2 gms in 24 hrs. IV LIDOCAINE :due to acute myocardial ischemia --class II b IV bolus at 1mg/min0.5-0.75mg/min---1-4mg/min Refractory cases to cardioversion---temporary pacing class II a

ACC/AHA/ESC guidelines 2006 for Ventricular arryhthmias/STEMI

Sustained monomorphic VT ,stable

2.in presence of LVD LVD EF <40%-- amiodarone/lignocaine Dose is same .

SUSTAINED POLYMORPHIC VT
Usually hemodynamically unstable if sustained. Should be given asynchronous defibrillation. Minimal is 200 j monophasic /100 j biphasic. Asynchronous to avoid delay related to sensing of QRS complex. If persists repeat shocks with -200j300j-360j Pharmacological therapy depending upon QT interval

normal/prolonged Normal QT interval :myocardial ischemia Reversible ischemia---coroanry angio,IABP BBs in case of recurrent . IV amiodarone class I recommendationif recurrent IV lidocaine class II b recommendation in case of MI

SUSTAINED POLYMORPHIC VT
Torsades de pointes: IV BBs to be used as congenital QTc prolongation is adrenergic

mediated.baseline therapy. Correct electrolyte abn. Antiarrhythmic agents:class IA and class III are avoided. Magnesium class II b ,1-2gm of mgso4 diluted in 5% D loading doserapidly10-20 gm in 24 hrs. Lidocainedoes not prolong QT interval Isoproterenol ---bridge befor temporary pacemaker Pause dependent VT,bradycardia 2-10 mcg/min Phenytoin250mg in NS iv100 mg every 5 minmax dose of 500 mg ,no dextrose.not to be given in continous infusion. Temporary pacemakerpause dependent.

 PREVENTION OF VT --- ICD + antiarryhthmic drug to be used. sotalol /amiodarone monomorphic VT/polymorphic VT Evaluate the patient in case of nonsustained VT in presence of

structural heart disease.

Sotalol--20-120 mg (0.5-1.5 mg/kg) given by inj over 10 min,

may repeat every 6 hr if needed.

Catheter ablation
Cure rate > 90 % in absence of structural heart disease Use both endocardial and epicardial pacing. Recurrent VT For prevention of ICD shocks

VT storm
>2 episodes in 24 hrs ,repeated VT episodes requiring

external cardioversion,defibrillation.,repeat edICD shcok therapy. Recurrent polymorphic VT ,no QT prolongation IV amiodarone/IV lignocaine QT prolonged VT removal of offending drug. Brugada syndrome IV quinidine ,IV isoproterenol Acute ischemia IABP Vpc s ablation Monomorphic VT ---empirical treatment Catheter ablation

prognosis
Risk of SCD can be decreased by ICD implantation in

structurally heart disease patients. Normal hearts ,malignant VT,risk of SCD prolonged QTc,BRUGADA,ARVDICD Most common cause of death in acute MI

ICDs

ACC/AHA/ESC guidelines 2006 for management of

arryhthmias

Idiopathic outflow tract VT

No structural heart disease. RV 80%,LV 20% More in women.(hormonal triggers) Not associated with SCD. Symptoms on exercise,stress, caffeine ingestion. Vagal manuevres ,adenosine,BBs terminate the VTs . Calcium dependent triggered activity. Large monophasic R waves in inferior leads. LBBB pattern in V1 RVOT RBBB pattern in V1 ---LVOT

Treatment
Hemodynamically stable and nonsustained.. IV bb s useful in termination BBs and CCBs --chronic therapy Class Ia,Ic,sotalol Catheter ablation in resistant cases.site by 12 lead ECG Efficacy of therapy by treadmill testing and ECG

monitoring. EPS only when the diagnosis is in question or to perform catheter ablation.

Idiopathic LV septal /fascicular VT

Second most common. Macroreentry involving calcium dependent slow

response fibres/automaticity. Narrow RBBB+ LAD ---posterior fascicles Narrow RBBB+RAD anterior fascicles Unique nature suppression by verapamil Catheter ablation therapy effective.

VT assosciated with LV DCM

Monomorphic/polymorhic can occur. Mitral and aortic areas involved. Drug therapy ineffective After ICD implantation sotalol/amiodarone Less amenable to catheter ablation VT origin is from epicardium. EF <30% --prophylactic ICD

Bundle branch reentrant tachycardia

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.

VT assosciated with HOCM

ICD is usually indicated in presence of HOCM,h/o

sustained VT/VF,nexplained syncope,a strong family history of SCD,LV septal thickness >30 mm risk of SCD.

High frequency of VT/VF in

sarciodosis,chagas,amyloidosis,kearne sayre syndrome. AV conduction disturbances exist ICD implantation

Arrythmogenic RV dysplasia
Genetically determined dysplastic process or after a

suspected viral myocarditis. Sporadic nonfamilial nondysplastic is more common.

OTHERS
VT after operation of fallot repair

Fascicular tachycardia caused by digoxin toxicity.

Genetically determined are : Long QT syndrome Acquired LQTS Short QT syndrome Brugada syndrome Catecholaminergic polymorphic VT

Bidirectional VT

The QRS complexes are varying in their morphology and

axis cannot be determined

The ladder diagram

A-atria AV av node V ventricle Circle focus of

impulse
Perpendicular

line ---block.

 The ladder diagram for ventricular arryhthmias

The VPC is seen ---later R on T phenomenon----VT unsustained ---fusion beat

Nonsustained VT preceded by VPC with short coupling interval and R

on T phenomenon.

 Occurs in the setting of digoxin use..the signature VT of digoxin toxicity.

triggered activitycalcium overload,inhibiton of na,k pump Originates from LBBanterior and posterior fascicles alternating change in axis Iv infusion of digoxin specific Fab fragments

 Preceded by long pause and then short cycles..

 The QRS complexes are changing in their morphology..

Axis could not be determined.

Positive concordance in VT

Negative concordance of VT

See the pointed ones they are predominantly downward.

 Brugada sign,rabbit ear sign

Trials
1.Biventricular Tachycardias Outcome Trial (BITAC) 2. Cardiac Denervation Surgery for Prevention of Ventricular

Tachycardia (PREVENT VT) 3. The Efficacy and Safety of CARTO 3D Mapping System Versus Conventional Method in AF and VT (CARTOAF&VT) 4. RIGHT: Rhythm ID Going Head-to-Head Trial 5.Ventricular Tachycardia (VT) Ablation Versus Enhanced Drug Therapy (VANISH) 6.Optimal Anti-tachycardia Therapy in Implantable Cardioverterdefibrillator (ICD) Patients Without Pacing Indications (OPTION) 7.AVID trial 8.CASH trial Lot more Log onto www.clinicaltrials.gov

Questions
1 Do all cases of VT lead to hemodynamic collapse? 2.Are there cases of VT with narrow complex configuration? 3.what is capture beat ?what does it signify? 4.what is the drug of choice in case of idiopathic bundlebranch

tachycardia? 5.which VT does not revert on usual catheter ablation? 6.which VT cannot be produced on programmed stimulation? 7.what is the etiology when PVT dose not occur along with QT prolongation? 8.drugs causing Qt prolongation? 9.which is better formula for QTc interval estimation? 10.LV <30 % is ICD indicated?

answers
1.no. 2.fascicular VT,bidirectional VT 3.capture beat signifies the presence of AV dissosciation. 4. no drug catheter ablation is effective. 5.VT assosciated with DCM 6.idiopathic outflow tract VT 7.ACUTE MI 8.class Ia,class III drugs. 9.hodges formula. 10.class I recommendation

Take home message

VT is a broad complex tachycardia. TREAT any broad complex tachycardia as VT in case of doubt. Abnormal RBBB/LBBB pattern with structural heart disease is

VT most likely.
DC shock is most appropriate in case of hypotension

ICD implantation in case of LVD <30 %

Specific VT syndromes should be identified for effective therapy.

60 % causes of SCD.

QT prolonging drugs are avoided in PVT .

IV amiodarone in case of emipirical treatment

References

HARRISONS Principles of Internal Medicine ,17th ed Basic and Bedside electrocardiography,Romulo.F.Baltazar

Introduction to Electrocardiography Schamroth.

www.emedicine.com Cardiovascular Medicines pdf files www.ecglibrary.com Oxford handbook of Clinical Medicine,8th ed Oxford book of Principles of Critical Care by Farokh.k.Udwadia www.ecgblog.com www.clinicaltrials.gov Post Graduate Medicine,2008

Medicine Update,2005
Marriots Practical Electrocardiography---Galen.S.Wagner NEJM,JACC,CARDIOLOGY,HEART VARIOUS OTHER SITES ON NET..

Do you know?
VT is frequently referenced in the 1970s television series

Emergency! In the 2006 film Casino Royale, the protagonist, James Bond, suffers ventricular tachycardia from intoxication of digitalis and goes into cardiac arrest. "V-Tach" is what "The Satin Slayer" from the American soap opera All My Children used to kill his victims