Ventricular tachycardia


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Ventricular tachycardia

  1. 1. Ventricular tachycardia<br />Dr.Praveen Nagula<br />
  2. 2. Sir William Osler <br /><ul><li>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. 3. Medicine is a science of uncertainty and an art of probability.
  4. 4. The young physician starts life with 20 drugs for each disease, and the old physician ends life with one drug for 20 diseases</li></li></ul><li>Louis Gallavardin<br />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. <br />
  5. 5. Dr.PedroBrugada<br />The 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.<br />
  6. 6. Bazett’s Formula<br />QTcB=QT⁄√RR<br />Henry cuthbertbazett<br />
  7. 7. Fridericia Formula<br />QTcF=QT⁄3√RR<br />Normal QTc interval is 0.46 sec<br />Females>males<br />Increases with age.<br />
  8. 8. Hodge’s formula<br />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.<br />Hodges formula: QT + 0.00175 (HR – 60) <br />
  9. 9. Torsades de Pointes<br />French term literally means twisting of points<br />
  10. 10. Conduction System of the Heart<br />SA node ----internodal pathways ---AV node ----AV bundle (bundle of HIS )----LBB,RBB----purkinjeefibres---cardiac muscle fibres.<br />0.03sec---0.09sec---0.04 sec ---total 0.16 sec..<br />
  11. 11. SINO ATRIAL node action potential<br />Resting membrane potential -55 to -60 mV<br />Cellular fibres are permeable to sodium and calcium ions …<br />Fast Na channels are inactive<br />Absent of plateau phase as inactivation of slow Na and Ca current take place.<br />
  12. 12. Ventricular muscle action potential <br />Resting membrane action potential is -85 to -90 mV<br />Fast Na channels are responsible for depolarisation<br />Plateau phase present.<br />No hyperpolarization<br />
  13. 13. Capture beat<br />When there is interference dissociation between sinus rhythm and faster subsidiary rhythm,the interference occurs in the AV node.<br />Both the impulses cannot be conducted due to the refractoriness of the AV node as a result of the wave from each focus.<br />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.<br />
  14. 14. Fusion beat<br />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.<br />Summation complex or fusion complex or combination beat<br />It may be like that of sinus impulseQRS ,or ectopic one,or intermediate..location can be known by morphology.<br />
  15. 15. Pause dependent VT <br />It is due to the afterdepolarizationsthat occur during the phase 3 of the action potential early after depolarization.<br />When they reach the threshold potential of the cardiac cell –cause another action potential.<br />Related to long QT syndrome<br />Hypokalemia<br />Class 1 a antiarryhthmic drugs use.<br />Prolonged repolarization.<br />The longer the QT interval the more abberation is the TU wave.<br />Long coupling interval. <br />
  16. 16. Reentry circuit<br />Two potentially conduction pathways or more.<br />Unidirectional block must occur in one pathway<br />An activation front that passes around the zone of unidirectional block over the alternate pathway.<br />Activation of the myocardium distal to block with delay.<br />The activation wavefront to activate the block by retrogradely and reexcite the tissue where the actviationwavefront originated.<br />For reentry to occur the wavefront should find the tissue to be excitable in the direction of its propagation.<br />
  17. 17. Triggered activity<br />Is due to the depolarization phase changes<br />Occur in bursts…<br />But may turn up into VF /VFL<br />Two syndromes<br />Pause dependent<br />Catecholaminergic dependent<br />Phase3 –depends upon QT interval<br />Phase 4 --- depends upon the sympathetic tone. <br />
  18. 18. Automaticity<br />Abnormal automaticity<br />Occurs in the setting of acute ischemia<br />It is due to the physiologiccal ion channel changes rather than morphological.<br />Transient…<br />Takes up the role of pacemaker and discharges the impulses.<br />
  19. 19. Burst pacing<br />Also called as overdrive pacing<br />Here we pace the ectopic focus (suppress it )by a external device –pacemaker<br />Usually pacing done by transvenous placement of an electrode in the right ventricle..<br />
  20. 20. Ventricular tachycardia<br />
  21. 21. Introduction<br />Definition<br />Etiology<br />Classification<br />Clinical symptoms<br />Algorithm of approach<br />Diagnosis<br />Differential diagnosis<br />Treatment<br />Conclusion<br />Take home message<br />Future<br />
  22. 22. Introduction<br />Most common cause of wide complex tachycardia.(80%)<br />Major cause of morbidity and mortality in patients with structural heart disease.<br />Major cause of sudden cardiac death –60 % cases on holter monitoring.<br />Relatively organisedtachyarryhthmias with discrete QRS complexes.<br />Diagnosis still a challenge ….on presentation.<br />Reentry is the most common mechanism.<br />Recurrence is more common in less than one year of onset.<br />ICD implantation is a the absolute indication in presence of LVEF <30%. <br />
  23. 23. Questions<br />1 Do all cases of VT lead to hemodynamic collapse?<br />2.what is capture beat ?what does it signify?<br />3.bidirectional VT is due to ?<br />4.what is the drug of choice in case of idiopathic bundle branch tachycardia?<br />5.which VT does not revert on usual catheter ablation?<br />6.which VT cannot be produced on programmed stimulation?<br />7.what is the etiology when PVT dose not occur along with QT prolongation?<br />8.drugs causing QT prolongation?<br />9.which is better formula for QTc interval estimation?<br />10.LV <30 % is ICD indicated?<br />
  24. 24. Definition<br />The occurrence of three or more VPC complexes with a rate of > 120 bpm in succession is called as VT. <br />Non sustained is termination of VT by self less than 30 sec.<br />Sustained VT is presence of VT for > 30 sec.orhemodynamically unstable but terminated in less than 30 sec.<br />Slow VT –HR >100 < 120 bpm.<br />Pulseless VT – VT with hemodynamic collapse that requires DC cardioversion.<br />Refractory VT –that does not revert to sinus rhythm on medication use or use of three shocks.<br />VT storm --- repeated VT episodes requiring the DC shocks/ICD shocks .<br />Rate is 100—300 bpm<br />Rate >220 bpm –VF <br />
  25. 25. Etiology<br />Acute MI <br />After chronic infarction <br />Ischaemic heart disease<br />Dilated cardiomyopathy<br />Hypertrophic cardiomyopathy<br />Post CABG<br />Post TOF surgery<br />Electrolyte abnormalities<br />Idiopathic<br />Specific etiology-- genetic <br />
  26. 26. Etiology <br />Usually as a complication of severe heart disease,can occur in structurally normal hearts.<br />In healthy individuals---RVOT,L V posterior/anterior fascicle—catheter ablation.<br />Major complication of IHD,acutely following MI, chronically after a large infarction..<br />Early hours VT---VF epicardial injury..<br />Fleicainide ---convert non sustained VT to sustained VT.<br />Sotalol- prolong QT interval--TDP<br />
  27. 27. Mechanism of occurrence of VT <br />REENTRY<br />ENHANCED AUTOMATICITY<br />TRIGGERED ACTIVITY<br />
  28. 28. Classification of VT <br />Sustained /non sustained VT <br />Monomorphic VT/polymorphic VT<br />Pulseless VT/hemodynamic stable VT<br />Structural heart disease/idiopathic<br />Unique VT syndromes<br />
  29. 29. Difference of MVT,PVT<br />
  30. 30. Monomorphic VT with RBBB morphology,hr 180bpm,north west axis.<br />
  31. 31. The morphology of the qrs complex is not uniform…<br />
  32. 32. Clinical features<br />Asymptomatic<br />May have palpitations –transient,sustained.<br />Chest pain –angina<br />Syncope<br />Presyncope<br />Dizziness<br />Cannon a waves<br />Absent pulse <br />Hypotension<br />Variable s 1<br />
  33. 33. Diagnosis<br />Algorithm based<br />ECG –12 Lead with long rhythm strip of lead II.<br />The focus can be known.<br />24 hr holter monitoring in case of transient episode<br />2d echo for the etiology.<br />Routine investigations<br />Serum electrolytes,calcium,magnesium<br />ABG <br />
  34. 34.
  35. 35. DIAGNOSTIC CRITERIA OF VT <br />AV dissosciation(capture,fusion beats)<br />QRS duration>140 ms for RBBB type V1morphology:<br />QRS duration>160 ms for LBBB type V1 morphology.<br />FRONTAL PLANE AXIS ---90 to 180 <br />Delayed activation during initial phase of QRS complex:<br />LBBB pattern –R wave in V1,V2 >40 ms<br />RBBB pattern –onset of R wave to nadir of S wave > 100 ms <br />Bizzare QRS pattern that does not mimic typical RBBB or LBBB type QRS complex<br /> concordance of QRS complex in all precordial leads.<br />RS or dominant S in V6for RBBB vt<br />Qwave in V6 with LBBB pattern<br />Monophasic R or biphasic qR or R/S in V1 with RBBB PATTERN<br />
  36. 36.
  37. 37. Approach to broad complex tachycardia<br />
  38. 38.
  39. 39. Morphological criteria<br />
  40. 40. RBBB morphology<br />
  41. 41. Brugadaalgortihm<br />
  42. 42. Vereckei algorithm <br />
  43. 43. More likely to be VT <br />Brugada sign<br />Josephson’s sign<br />
  44. 44. Initiation of VT BY VPCs<br />
  45. 45. Torsades de pointes due to hypokalemia<br />
  46. 46.
  47. 47. Reversible causes of VT <br />Hypoxia<br />Hyperthyroidism<br />catecholamines<br />Hypokalemia<br />Metabolic acidosis<br />Hypomagenesemia<br />Hypocalcemia<br />Drugs<br />Alcohol<br />Starvation<br />,,<br />
  48. 48. Differential diagnosis<br />SVT with aberration due to BBB<br />WPW syndrome with AF/AFL<br />AIVR<br />
  49. 49. Management <br />NON SUSTAINED VT :<br />No treatment in absence of heart disease.<br />Look for reversible factors.<br />In termination of episodes –IV BBs can be used.<br />For preventing recurrences –oral BBs /CCB s.<br />
  50. 50. MONOMORPHIC VT with hemodynamic compromise <br />Severity of underlying structural heart disease<br />Ventricular rate <br />Origin of arryhthmia<br />LVD <br />Hypotension,pulmonaryedema,MI.<br />Synchronised R wave shock is given. With appropriate sedation.100j—200-300-360 j<br />After SR rhythm lidocaine 2-4 mg/min iv infusion.<br />ACC/AHA/ESC guidelines 2006 for ventricular arrythmias/STEMI<br />
  51. 51. Sustained monomorphic VT ,stable<br />DC cardioversion –effective in termination<br />IV antiarryhthmic drugs can also be used.—no response—cardioversion.<br /> presence /abscence LVD<br />1.with preserved LVF:only one drug to be used.<br />IV PROCAINAMIDE---class II a recommendation<br />More effective than amiodarone in termination.<br /><50 mg/min---1-4 mg/min<br />Preferred over other drugs.<br />Rapid infusion causes hypotension.<br />ACC/AHA/ESC guidelines for Ventricular arryhthmias/STEMI <br />
  52. 52. Sustained monomorphic VT ,stable<br />IV AMIODARONE :can be given in presence of LVDalso.<br />Drug of choice according to 2004 guidelines,not so in 2006.<br />When VT is refractory to electrical cardioversion,if VT is unstable or recurrent inpsite of IV procainamide.<br />150mg IV given as bolus with in 10 min –repeat after 10-15 min.<br />Infusion of 1 mg/min*6 hrs,0.5mg/min*18 hrs.<br />Max dose is 2.2 gms in 24 hrs.<br />IV LIDOCAINE :due to acute myocardial ischemia --class II b <br />IV bolus at 1mg/min—0.5-0.75mg/min---1-4mg/min<br />Refractory cases to cardioversion---temporary pacing class II a<br />ACC/AHA/ESC guidelines 2006 for Ventricular arryhthmias/STEMI <br />
  53. 53. Sustained monomorphic VT ,stable<br /> presence of LVD –<br />LVD EF <40%-- amiodarone/lignocaine<br />Dose is same .<br />
  54. 54. SUSTAINED POLYMORPHIC VT <br />Usually hemodynamically unstable if sustained.<br />Should be given asynchronous defibrillation.<br />Minimal is 200 j monophasic /100 j biphasic.<br />Asynchronous to avoid delay related to sensing of QRS complex.<br />If persists repeat shocks with -200j—300j-360j<br />Pharmacological therapy depending upon QT interval normal/prolonged<br />Normal QT interval :myocardial ischemia<br />Reversible ischemia---coroanryangio,IABP<br />BBs in case of recurrent .<br />IV amiodarone class I recommendationif recurrent<br />IV lidocaine class II b recommendation in case of MI <br />
  55. 55. SUSTAINED POLYMORPHIC VT <br />Torsades de pointes:<br />IV BBs to be used as congenital QTc prolongation is adrenergic mediated.baseline therapy.<br />Correct electrolyte abn.<br />Antiarrhythmicagents:class IA and class III are avoided.<br />Magnesium –class II b ,1-2gm of mgso4 diluted in 5% D loading dose—rapidly—10-20 gm in 24 hrs.<br />Lidocaine—does not prolong QT interval<br />Isoproterenol ---bridge befor temporary pacemaker<br />Pause dependent VT,bradycardia 2-10 mcg/min<br />Phenytoin—250mg in NS iv—100 mg every 5 min—max dose of 500 mg ,no dextrose.not to be given in continous infusion.<br />Temporary pacemaker—pause dependent.<br />
  56. 56. PREVENTION OF VT --- ICD + antiarryhthmic drug to be used.<br />sotalol /amiodarone –monomorphic VT/polymorphic VT<br />Evaluate the patient in case of nonsustained VT in presence of structural heart disease. <br />Sotalol--20-120 mg (0.5-1.5 mg/kg) given by inj over 10 min, may repeat every 6 hr if needed. <br />
  57. 57. Catheter ablation <br />Cure rate > 90 % in absence of structural heart disease<br />Use both endocardial and epicardial pacing.<br />Recurrent VT <br />For prevention of ICD shocks<br />
  58. 58. VT storm <br />>2 episodes in 24 hrs ,repeated VT episodes requiring external cardioversion,defibrillation.,repeatedICDshcok therapy.<br />Recurrent polymorphic VT ,no QT prolongation IV amiodarone/IV lignocaine<br />QT prolonged VT –removal of offending drug.<br />Brugada syndrome –IV quinidine ,IV isoproterenol<br />Acute ischemia –IABP<br />Vpc s –ablation<br />Monomorphic VT ---empirical treatment<br />Catheter ablation<br />
  59. 59.
  60. 60.
  61. 61.
  62. 62. prognosis<br />Risk of SCD can be decreased by ICD implantation in structurally heart disease patients.<br />Normal hearts ,malignant VT,risk of SCD –prolonged QTc,BRUGADA,ARVD—ICD<br />Most common cause of death in acute MI <br />
  63. 63. ICDs<br />ACC/AHA/ESC guidelines 2006 for management of arryhthmias<br />
  64. 64. Unique VT syndromes<br />
  65. 65. Idiopathic outflow tract VT <br />No structural heart disease.<br />RV 80%,LV 20%<br />More in women.(hormonal triggers)<br />Not associated with SCD.<br />Symptoms on exercise,stress, caffeine ingestion.<br />Vagalmanuevres ,adenosine,BBs terminate the VTs .<br />Calcium dependent triggered activity.<br />Large monophasic R waves in inferior leads.<br />LBBB pattern in V1 –RVOT<br />RBBB pattern in V1 ---LVOT<br />
  66. 66. Treatment<br />Hemodynamically stable and nonsustained..<br />IV bb s useful in termination<br />BBs and CCBs --chronic therapy<br />Class Ia,Ic,sotalol<br />Catheter ablation in resistant by 12 lead ECG<br />Efficacy of therapy by treadmill testing and ECG monitoring.<br />EPS only when the diagnosis is in question or to perform catheter ablation.<br />
  67. 67. Idiopathic LV septal /fascicular VT <br />Second most common.<br />Macroreentry involving calcium dependent slow response fibres/automaticity.<br />Narrow RBBB+ LAD ---posterior fascicles<br />Narrow RBBB+RAD – anterior fascicles<br />Unique nature –suppression by verapamil<br />Catheter ablation therapy effective.<br />
  68. 68. VT assosciated with LV DCM <br />Monomorphic/polymorhic can occur.<br />Mitral and aortic areas involved.<br />Drug therapy ineffective <br />After ICD implantation –sotalol/amiodarone<br />Less amenable to catheter ablation<br />VT origin is from epicardium.<br />EF <30% --prophylactic ICD<br />
  69. 69. Bundle branch reentrant tachycardia<br />Macro reentry circuit<br />Antegrade direction down the right branch<br />Retrograde up the left posterior or anterior fascicles/LBB<br />Mimic RV pacing with LBBB pattern,leftward superior axis.<br />Opposite occurrence then RBBB <br />Readily amenable to catheter ablation therapy.<br />Coupled with ICD due to risk of SCD.<br />Occurs in nonischemiccardiomyopathy or valvularcardiomyopathy. <br />
  70. 70. VT assosciated with HOCM<br />ICD 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.<br />High frequency of VT/VF in sarciodosis,chagas,amyloidosis,kearnesayre syndrome.<br />AV conduction disturbances exist<br />ICD implantation <br />
  71. 71. Arrythmogenic RV dysplasia<br />Genetically determined dysplastic process or after a suspected viral myocarditis.<br />Sporadic nonfamilialnondysplastic is more common.<br />
  72. 72. OTHERS<br />VT after operation of fallot repair<br />Fascicular tachycardia caused by digoxin toxicity.<br />Genetically determined are :<br />Long QT syndrome<br />Acquired LQTS<br />Short QT syndrome<br />Brugada syndrome<br />Catecholaminergic polymorphic VT<br />
  73. 73. Bidirectional VT <br />The QRS complexes are varying in their morphology and axis cannot be determined <br />
  74. 74. Lets have a look at the ECGs<br />
  75. 75. The ladder diagram<br />A-atria<br />AV – av node<br />V –ventricle<br />Circle –focus of impulse<br />Perpendicular line ---block. <br />
  76. 76. The ladder diagram for ventricular arryhthmias<br />
  77. 77. The VPC is seen ---later R on T phenomenon----VT unsustained ---fusion beat <br />Nonsustained VT preceded by VPC with short coupling interval and R on T phenomenon.<br />
  78. 78. Occurs in the setting of digoxin use..the signature VT of digoxin toxicity.—triggered activity—calcium overload,inhibiton of na,k pump <br />Originates from LBBanterior and posterior fascicles –alternating change in axis<br />Iv infusion of digoxin specific Fab fragments <br />
  79. 79. Preceded by long pause and then short cycles..<br />
  80. 80. The QRS complexes are changing in their morphology..<br />Axis could not be determined.<br />
  81. 81.
  82. 82. Positive concordance in VT <br />
  83. 83. Negative concordance of VT<br />See the pointed ones they are predominantly downward.<br />
  84. 84. Brugadasign,rabbit ear sign <br />
  85. 85. Trials<br />1.Biventricular Tachycardias Outcome Trial (BITAC)<br />2. Cardiac Denervation Surgery for Prevention of Ventricular Tachycardia (PREVENT VT)<br />3. The Efficacy and Safety of CARTO 3D Mapping System Versus Conventional Method in AF and VT (CARTOAF&VT)<br />4. RIGHT: Rhythm ID Going Head-to-Head Trial<br />5.Ventricular Tachycardia (VT) Ablation Versus Enhanced Drug Therapy (VANISH)<br />6.Optimal Anti-tachycardia Therapy in Implantable Cardioverter-defibrillator (ICD) Patients Without Pacing Indications (OPTION)<br />7.AVID trial<br />8.CASH trial<br />Lot more<br />Log onto<br />
  86. 86. Questions<br />1 Do all cases of VT lead to hemodynamic collapse?<br />2.Are there cases of VT with narrow complex configuration?<br />3.what is capture beat ?what does it signify?<br />4.what is the drug of choice in case of idiopathic bundlebranch tachycardia?<br />5.which VT does not revert on usual catheter ablation?<br />6.which VT cannot be produced on programmed stimulation?<br />7.what is the etiology when PVT dose not occur along with QT prolongation?<br />8.drugs causing Qt prolongation?<br />9.which is better formula for QTc interval estimation?<br />10.LV <30 % is ICD indicated?<br />
  87. 87. answers<br /><br />2.fascicular VT,bidirectional VT<br />3.capture beat signifies the presence of AV dissosciation.<br />4. no drug –catheter ablation is effective.<br />5.VT assosciated with DCM<br />6.idiopathic outflow tract VT<br />7.ACUTE MI<br />8.class Ia,class III drugs.<br />9.hodges formula.<br />10.class I recommendation<br />
  88. 88. Take home message<br />VT is a broad complex tachycardia.<br />TREAT any broad complex tachycardia as VT in case of doubt.<br />Abnormal RBBB/LBBB pattern with structural heart disease is VT most likely.<br />DC shock is most appropriate in case of hypotension<br />ICD implantation in case of LVD <30 %<br />Specific VT syndromes should be identified for effective therapy.<br />60 % causes of SCD.<br />QT prolonging drugs are avoided in PVT .<br />IV amiodarone in case of emipirical treatment<br />
  89. 89. References<br />HARRISON’S Principles of Internal Medicine ,17thed<br />Basic and Bedside electrocardiography,Romulo.F.Baltazar<br />Introduction to Electrocardiography –Schamroth.<br /><br />Cardiovascular Medicines pdf files<br /><br />Oxford handbook of Clinical Medicine,8thed<br />Oxford book of Principles of Critical Care by Farokh.k.Udwadia<br /><br /><br />Post Graduate Medicine,2008<br />Medicine Update,2005<br />Marriot’s Practical Electrocardiography---Galen.S.Wagner<br />NEJM,JACC,CARDIOLOGY,HEART <br />VARIOUS OTHER SITES ON NET…..<br />
  90. 90. Do you know?<br />VT is frequently referenced in the 1970s television series Emergency!<br />In the 2006 film Casino Royale, the protagonist, James Bond, suffers ventricular tachycardia from intoxication of digitalis and goes into cardiac arrest.<br />"V-Tach" is what "The Satin Slayer" from the American soap opera All My Children used to kill his victims<br />
  91. 91. Thank you<br />Sagittarian<br />