VENTRICULAR TACHYCARDIA

Dr.Praveen Nagula

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 artérielle 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.

Bazett’s Formula

QTcB=QT⁄√RR

HENRY CUTHBERT BAZETT

Fridericia Formula

QTcF=QT⁄3√

RR

Normal QTc

interval is 0.46

sec

Females>males

Increases with

age.

Hodge’s formulaWith 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..ventricularcapture 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 syndromeHypokalemiaClass 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 changesOccur in bursts…But may turn up into VF /VFLTwo syndromesPause dependentCatecholaminergic dependentPhase3 –depends upon QT intervalPhase 4 --- depends upon the sympathetic tone.

AutomaticityAbnormal automaticityOccurs in the setting of acute ischemiaIt is due to the physiologiccal ion channel

changes rather than morphological.Transient…Takes up the role of pacemaker and

discharges the impulses.

Burst pacingAlso called as overdrive pacingHere we pace the ectopic focus (suppress it )by a

external device –pacemakerUsually pacing done by transvenous placement

of an electrode in the right ventricle..

VENTRICULAR TACHYCARDIA

IntroductionDefinitionEtiologyClassificationClinical symptomsAlgorithm of approachDiagnosisDifferential diagnosisTreatmentConclusionTake home messageFuture

IntroductionMost 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%.

Questions1 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?

DefinitionThe 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 100—300 bpm Rate >220 bpm –VF

EtiologyAcute MI After chronic infarction Ischaemic heart diseaseDilated cardiomyopathyHypertrophic cardiomyopathyPost CABGPost TOF surgeryElectrolyte abnormalitiesIdiopathicSpecific 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 fascicle—catheter 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 REENTRYENHANCED AUTOMATICITYTRIGGERED ACTIVITY

Classification of VT Sustained /non sustained VT Monomorphic VT/polymorphic VTPulseless VT/hemodynamic stable VTStructural heart disease/idiopathicUnique VT syndromes

Difference of MVT,PVTMONO MORPHIC VT POLYMORPHIC VT

1. Stable tachycardia Unstable,dynamic

2. Reproducible, recurrent phenomenon

Less reproducible

3. Initiated by pacing ,programmed ventricular stimulation

Not reliably initiated

4. Normal hearts./structural heart disease

Acute ischemia ,myocarditis,drugs

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?

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

The morphology of the qrs complex is not uniform…

Clinical featuresAsymptomaticMay have palpitations –transient,sustained.Chest pain –anginaSyncopePresyncopeDizzinessCannon a wavesAbsent pulse HypotensionVariable s 1

DiagnosisAlgorithm basedECG –12 Lead with long rhythm strip of lead II.The focus can be known.24 hr holter monitoring in case of transient

episode2d echo for the etiology.Routine investigationsSerum electrolytes,calcium,magnesiumABG

S.No SUPRAVENTRICULAR TACHYCARDIA

VENTRICULAR TACHYCARDIA

1. Abberant QRS pattern that matches exactly that of the wide complex rhythm.

not in morphology of LBBB,RBBB,wide complexes present

2. Presence of p wave before QRS complex

P waves and QRS complexes are dissosciated.

3. Preexcited QRS pattern on SR ECG indicates atrial arryhthmia.—AFL,focal AT,antidromic macroreentrant tachycardia.

Bizzare QRS complex

4. Responds to vagal Manuevre,valsalva,adenosine

Not so

5. Verapamil effective 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 signJosephson’s sign

Initiation of VT BY VPCs

Torsades de pointes due to hypokalemia

Reversible causes of VT HypoxiaHyperthyroidismcatecholaminesHypokalemiaMetabolic acidosisHypomagenesemiaHypocalcemiaDrugsAlcoholStarvationwww.torsades.org,www.qtdrugs.org,

Differential diagnosisSVT with aberration due to BBBWPW syndrome with AF/AFLAIVR

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 diseaseVentricular rate Origin of arryhthmiaLVD Hypotension,pulmonary edema,MI.Synchronised R wave shock is given. With

appropriate sedation.100j—200-300-360 jAfter 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 LVD1.with preserved LVF:only one drug to be used. IV PROCAINAMIDE---class II a recommendationMore effective than amiodarone in termination.<50 mg/min---1-4 mg/minPreferred 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/min—0.5-0.75mg/min---1-4mg/minRefractory 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/lignocaineDose 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 -200j—300j-360jPharmacological therapy depending upon QT interval

normal/prolongedNormal QT interval :myocardial ischemiaReversible ischemia---coroanry angio,IABPBBs 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 dose—rapidly—10-20 gm in 24 hrs.Lidocaine—does not prolong QT interval Isoproterenol ---bridge befor temporary pacemakerPause dependent VT,bradycardia 2-10 mcg/minPhenytoin—250mg in NS iv—100 mg every 5 min—max dose

of 500 mg ,no dextrose.not to be given in continous infusion.Temporary pacemaker—pause 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

diseaseUse 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 isoproterenolAcute ischemia –IABPVpc s –ablationMonomorphic VT ---empirical treatmentCatheter ablation

prognosisRisk of SCD can be decreased by ICD

implantation in structurally heart disease patients.

Normal hearts ,malignant VT,risk of SCD –prolonged QTc,BRUGADA,ARVD—ICD

Most common cause of death in acute MI

ICDs

ACC/AHA/ESC guidelines 2006 for management of arryhthmias

UNIQUE VT SYNDROMES

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 –RVOTRBBB pattern in V1 ---LVOT

TreatmentHemodynamically stable and nonsustained..IV bb s useful in terminationBBs and CCBs --chronic therapyClass Ia,Ic,sotalolCatheter ablation in resistant cases.site by 12

lead ECGEfficacy 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 fasciclesNarrow RBBB+RAD – anterior fasciclesUnique nature –suppression by verapamilCatheter ablation therapy effective.

VT assosciated with LV DCM Monomorphic/polymorhic can occur.Mitral and aortic areas involved.Drug therapy ineffective After ICD implantation –sotalol/amiodaroneLess amenable to catheter ablationVT origin is from epicardium.EF <30% --prophylactic ICD

Bundle branch reentrant tachycardiaMacro reentry circuitAntegrade direction down the right branchRetrograde up the left posterior or anterior

fascicles/LBBMimic 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 HOCMICD 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 existICD implantation

Arrythmogenic RV dysplasiaGenetically determined dysplastic process or

after a suspected viral myocarditis.Sporadic nonfamilial nondysplastic is more

common.

OTHERSVT after operation of fallot repairFascicular tachycardia caused by digoxin

toxicity.Genetically determined are :Long QT syndromeAcquired LQTSShort QT syndromeBrugada syndromeCatecholaminergic polymorphic VT

Bidirectional VT

The QRS complexes are varying in their morphology and axis cannot be determined

Lets have a look at the ECGs

The ladder diagram A-atria AV – av node V –ventricle Circle –focus

of impulse Perpendicula

r 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 activity—calcium 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 Cardioverter-

defibrillator (ICD) Patients Without Pacing Indications (OPTION) 7.AVID trial 8.CASH trial Lot more Log onto www.clinicaltrials.gov

Questions1 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?

answers1.no.2.fascicular VT,bidirectional VT3.capture beat signifies the presence of AV

dissosciation.4. no drug –catheter ablation is effective.5.VT assosciated with DCM6.idiopathic outflow tract VT7.ACUTE MI8.class Ia,class III drugs.9.hodges formula.10.class I recommendation

Take home messageVT 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 HARRISON’S 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 Marriot’s 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

Thank you

Sagittarian