Ventricular tachycardia can occur due to various causes like acute myocardial infarction, chronic infarction, dilated cardiomyopathy, etc. It is classified as sustained, non-sustained, monomorphic, polymorphic, etc. based on characteristics. Diagnosis involves ECG, echocardiogram, and monitoring. Treatment depends on hemodynamic stability and includes electrical cardioversion, antiarrhythmic drugs like amiodarone, lidocaine, ablation, and ICD implantation in selected cases. Recurrence risk is high in structurally abnormal hearts and prevention involves controlling triggers, antiarrhythmics, and ICDs.

1. Ventricular tachycardiaDr.Praveen Nagula

2. 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.

3. Medicine is a science of uncertainty and an art of probability.

4. The young physician starts life with 20 drugs for each disease, and the old physician ends life with one drug for 20 diseasesLouis GallavardinLa 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.

5. Dr.PedroBrugadaThe Brugada syndrome is a genetic disease and an increased risk of sudden cardiac death. named by the Spanish cardiologists Pedro Brugada and JosepBrugada. 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.

6. Bazett’s FormulaQTcB=QT⁄√RRHenry cuthbertbazett

7. Fridericia FormulaQTcF=QT⁄3√RRNormal QTc interval is 0.46 secFemales>malesIncreases with age.

8. 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)

9. Torsades de PointesFrench term literally means twisting of points

10. Conduction System of the HeartSA 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..

11. SINO ATRIAL node action potentialResting membrane potential -55 to -60 mVCellular fibres are permeable to sodium and calcium ions …Fast Na channels are inactiveAbsent of plateau phase as inactivation of slow Na and Ca current take place.

12. Ventricular muscle action potential Resting membrane action potential is -85 to -90 mVFast Na channels are responsible for depolarisationPlateau phase present.No hyperpolarization

13. Capture beatWhen 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.

14. Fusion beatIt 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 beatIt may be like that of sinus impulseQRS ,or ectopic one,or intermediate..location can be known by morphology.

15. Pause dependent VT It is due to the afterdepolarizationsthat 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.

16. Reentry circuitTwo potentially conduction pathways or more.Unidirectional block must occur in one pathwayAn 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 actviationwavefront originated.For reentry to occur the wavefront should find the tissue to be excitable in the direction of its propagation.

17. Triggered activityIs 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.

18. 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.

19. 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..

20. Ventricular tachycardia

21. IntroductionDefinitionEtiologyClassificationClinical symptomsAlgorithm of approachDiagnosisDifferential diagnosisTreatmentConclusionTake home messageFuture

22. 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 organisedtachyarryhthmias 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%.

23. 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?

24. 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.orhemodynamically 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 bpmRate >220 bpm –VF

25. EtiologyAcute MI After chronic infarction Ischaemic heart diseaseDilated cardiomyopathyHypertrophic cardiomyopathyPost CABGPost TOF surgeryElectrolyte abnormalitiesIdiopathicSpecific etiology-- genetic

26. 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

27. Mechanism of occurrence of VT REENTRYENHANCED AUTOMATICITYTRIGGERED ACTIVITY

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

29. Difference of MVT,PVT

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

31. The morphology of the qrs complex is not uniform…

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

33. 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

35. 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 msRBBB 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 vtQwave in V6 with LBBB patternMonophasic R or biphasic qR or R/S in V1 with RBBB PATTERN

37. Approach to broad complex tachycardia

39. Morphological criteria

40. RBBB morphology

41. Brugadaalgortihm

42. Vereckei algorithm

43. More likely to be VT Brugada signJosephson’s sign

44. Initiation of VT BY VPCs

45. Torsades de pointes due to hypokalemia

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

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

49. 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.

50. MONOMORPHIC VT with hemodynamic compromise Severity of underlying structural heart diseaseVentricular rate Origin of arryhthmiaLVD Hypotension,pulmonaryedema,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

51. Sustained monomorphic VT ,stableDC cardioversion –effective in terminationIV 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

52. Sustained monomorphic VT ,stableIV 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 aACC/AHA/ESC guidelines 2006 for Ventricular arryhthmias/STEMI

53. Sustained monomorphic VT ,stable2.in presence of LVD –LVD EF <40%-- amiodarone/lignocaineDose is same .

54. 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---coroanryangio,IABPBBs in case of recurrent .IV amiodarone class I recommendationif recurrentIV lidocaine class II b recommendation in case of MI

55. SUSTAINED POLYMORPHIC VT Torsades de pointes:IV BBs to be used as congenital QTc prolongation is adrenergic mediated.baseline therapy.Correct electrolyte abn.Antiarrhythmicagents: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 intervalIsoproterenol ---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.

56. PREVENTION OF VT --- ICD + antiarryhthmic drug to be used.sotalol /amiodarone –monomorphic VT/polymorphic VTEvaluate 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.

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

58. VT storm >2 episodes in 24 hrs ,repeated VT episodes requiring external cardioversion,defibrillation.,repeatedICDshcok therapy.Recurrent polymorphic VT ,no QT prolongation IV amiodarone/IV lignocaineQT prolonged VT –removal of offending drug.Brugada syndrome –IV quinidine ,IV isoproterenolAcute ischemia –IABPVpc s –ablationMonomorphic VT ---empirical treatmentCatheter ablation

62. 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—ICDMost common cause of death in acute MI

63. ICDsACC/AHA/ESC guidelines 2006 for management of arryhthmias

64. Unique VT syndromes

65. 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.Vagalmanuevres ,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

66. 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.

67. 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.

68. 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

69. 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 nonischemiccardiomyopathy or valvularcardiomyopathy.

70. VT assosciated with HOCMICD is usually indicated in presence of HOCM,h/o sustained VT/VF,nexplainedsyncope,a strong family history of SCD,LV septal thickness >30 mm –risk of SCD.High frequency of VT/VF in sarciodosis,chagas,amyloidosis,kearnesayre syndrome.AV conduction disturbances existICD implantation

71. Arrythmogenic RV dysplasiaGenetically determined dysplastic process or after a suspected viral myocarditis.Sporadic nonfamilialnondysplastic is more common.

72. OTHERSVT after operation of fallot repairFascicular tachycardia caused by digoxin toxicity.Genetically determined are :Long QT syndromeAcquired LQTSShort QT syndromeBrugada syndromeCatecholaminergic polymorphic VT

73. Bidirectional VT The QRS complexes are varying in their morphology and axis cannot be determined

74. Lets have a look at the ECGs

75. The ladder diagramA-atriaAV – av nodeV –ventricleCircle –focus of impulsePerpendicular line ---block.

76. The ladder diagram for ventricular arryhthmias

77. 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.

78. 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 axisIv infusion of digoxin specific Fab fragments

79. Preceded by long pause and then short cycles..

80. The QRS complexes are changing in their morphology..Axis could not be determined.

82. Positive concordance in VT

83. Negative concordance of VTSee the pointed ones they are predominantly downward.

84. Brugadasign,rabbit ear sign

85. Trials1.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 Trial5.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 trial8.CASH trialLot moreLog onto www.clinicaltrials.gov

86. 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?

87. 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

88. 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 hypotensionICD 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

89. ReferencesHARRISON’S Principles of Internal Medicine ,17thedBasic and Bedside electrocardiography,Romulo.F.BaltazarIntroduction to Electrocardiography –Schamroth.www.emedicine.comCardiovascular Medicines pdf fileswww.ecglibrary.comOxford handbook of Clinical Medicine,8thedOxford book of Principles of Critical Care by Farokh.k.Udwadiawww.ecgblog.comwww.clinicaltrials.govPost Graduate Medicine,2008Medicine Update,2005Marriot’s Practical Electrocardiography---Galen.S.WagnerNEJM,JACC,CARDIOLOGY,HEART VARIOUS OTHER SITES ON NET…..

90. 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