tachyarrythmias d

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tachyarrythmias d

  1. 1. TACHYARRYTHMIAS Dr RAVI KANTH
  2. 2. DEFINITION ANATOMY OF CONDUCTION ELECTROPHYSIOLOGY DIAGNOSTIC APPROACH TREATMENT MODALITIES DESCRIPTION ABOUT INDIVIDUAL ARRYTHMIAS 2
  3. 3. DEFINITION  Any disturbance of the heart's rhythm, regular or irregular, resulting by convention in a rate over 100 beats/min . 3
  4. 4. CONDUCTION SYSTEM OF THE HEART AND ELECTROCARDIOGRAPHY
  5. 5. Conduction System of the Heart • SA node: sinoatrial node. The pacemaker. – Specialized cardiac muscle cells. – Generate spontaneous action potentials (autorhythmic tissue). – Action potentials pass to atrial muscle cells and to the AV node • AV node: atrioventricular node. – Action potentials conducted more slowly here than in any other part of system. – Ensures ventricles receive signal to contract after atria have contracted • AV bundle: passes through hole in cardiac skeleton to reach interventricular septum • Right and left bundle branches: extend beneath endocardium to apices of right and left ventricles • Purkinje fibers: – Large diameter cardiac muscle cells with few myofibrils. – Many gap junctions. – Conduct action potential to ventricular muscle cells (myocardium) 5
  6. 6. Conducting System of Heart 6
  7. 7. IMPULSE CONDUCTION THROUGH THE HEART 7
  8. 8. ACTION POTENTIAL  Duration – 200- 400 msec  Regulated by activity of time & voltage dependent ionic currents  Ionic currents maintained by  Ionic channels –passively conduct ions along electrochemical gradient  Pumps, transporters – transport ions against gradients  Exchangers- electrgenically exchange species  AP are regionally distinct 8
  9. 9. Electrical Properties of Myocardial Fibers 1. Rising phase of action potential • Due to opening of fast Na+ channels 2. Plateau phase • Closure of sodium channels • Opening of calcium channels • Slight increase in K+ permeability • Prevents summation and thus tetanus of cardiac muscle 3. Repolarization phase • Calcium channels closed • Increased K+ permeability 9
  10. 10. 10
  11. 11. 11
  12. 12. 12
  13. 13. Heart Physiology: Intrinsic Conduction System • Autorhythmic cells: – Initiate action potentials – Have unstable resting potentials called pacemaker potentials – Use calcium influx (rather than sodium) for rising phase of the action potential 13
  14. 14. DEPOLARIZATION OF SA NODE  SA node - no stable resting membrane potential  Pacemaker potential  gradual depolarization from -60 mV, slow influx of Na+  Action potential  occurs at threshold of -40 mV  depolarizing phase to 0 mV  fast Ca2+ channels open, (Ca2+ in)  repolarizing phase  K+ channels open, (K+ out)  at -60 mV K+ channels close, pacemaker potential starts over  Each depolarization creates one heartbeat  SA node at rest fires at 0.8 sec, about 75 bpm 14
  15. 15. Pacemaker and Action Potentials of the Heart 15
  16. 16. DEPOLARIZATION AND IMPULSE CONDUCTION  Depolarization in SA node precedes depolarization in atria, AV node, ventricles 16
  17. 17. ELECTROCARDIOGRAM  P wave  Depolarization of atria  Followed by contraction  QRS complex  3 waves (Q, R, & S)  Depolarization of ventricles  Followed by contraction  T wave  Repolarization of ventricles 17
  18. 18. ELECTROCARDIOGRAM  P-Q interval  Time atria depolarize & remain depolarized  Q-T interval  Time ventricles depolarize & remain depolarized 18
  19. 19. ELECTROCARDIOGRAM  Intervals show timing of cardiac cycle  P-P = one cardiac cycle  P-Q = time for atrial depolarization  Q-T = time for ventricular depolarization  T-P = time for relaxation 19
  20. 20. MECHANISMS OF ARRYTHMOGENESIS  Some tacyarythmias start by one mechanism & gets perpetuated by another mechanism  Some caused by one mechanism can precipitate another episode caused by different mechanism  Mechanisms are  Disorders of impulse formation  Disorders of impulse conduction  both 20
  21. 21.  DISORDERS OF IMPULSE FORMATION  Characterised by  Inappropriate discharge rate of normal pacemaker  Inappropriate discharge of ectopic pacemaker 21
  22. 22. Abnormal automaticity  Arise from cells that have reduced maximum diastolic potentials  Don’t need prior stimulation Triggered activity  Initiated by after depolarisations  Induced by one or more preceding action potentials 22
  23. 23. After depolarisations are of two types  Early after depolarisation- occurs during phase 2 & phase 3  Delayed after depolarisation- occurs during phase 4  All depolariations doesn’t reach threshold potential but if they reach they trigger another after depolarisation & thus perpetuate 23
  24. 24. 24
  25. 25. DAD’S  Result from activation of calcium sensitive inward current due to increase in intra cellular ca concentrations  Acquired or inherited abnormalities in  Sarcoplasmic reticulum properties  CA release channels  SR calcium binding proteins 25
  26. 26. 26
  27. 27. EAD’S  AP prolongation may increase ca influx through l-type ca channels during cardiac cycle , causing excessive ca accumulation in SR & spontaneous SR ca release  Increased intracellular ca cause depolarisation by activation of ca dependent cl currents ,NA +/CA + exchanger provoking EAD,S 27
  28. 28. Re-entry  Two types  Anatomical re-entry  Functional reentry ANATOMICAL REENTRY Characters -2 or more pathways with different electropohysiological properties -impulse blocked in one pathway -impulse conducts slowly in alternate pathway &returns in pathway initially blocked in reversed direction to re exite tissue proximal to site of block 28
  29. 29. 29
  30. 30.  For re entry to occur anatomical length of circuit should be greater than reentrant wave length  Conditions that depress conduction velocity & refractory period promote development of re entry[λ = c.v x rp]  Sustained reentry occurs due to excitable gap between activating head & recovery tail. 30
  31. 31. Fuctional reentry  Occur in fibres that exhibit functionally different EP properties caused by local differences in transmembrane AP  functional heterogenities can be fixed or change dynamically 31
  32. 32.  Mechanisms of termination are  When conduction & recovery characters of circuit change  When activating head of wave collides with tail 32
  33. 33. 33
  34. 34. DETERMINANTS OF AMPLITUDES OF AFTER DEPOLARISATIONS intervention Effect on amplitude of EAD’S Effect on amplitude of DAD’S Long cycles ↑ ↓ Long AP duration ↑ ↑ Reduced membrane potential ↑ ↓ Na channel blockers No effect ↓ Ca channel blockers ↓ ↓ catecholamines ↑ ↑ 34
  35. 35. APPROACH TO TACHYARRYTHMIAS HISTORY •Mode of onset •Mode of termination •Drug history •Dietary history •H/o systemic illness •Family history PHYSICAL EXAMINATION •Symptoms •Signs NON INVASIVE INVESTIGATIONS • 12 lead ECG • Holter monitor • Patient activated event monitor • Implanted loop ECG monitor • HUT • Exercise ECG • 2D ECHO INVASIVE INVESTIGATIONS •Electrophysio logical studies 35
  36. 36. HISTORY  MODE OF ONSET  Occuring in the setting of exercise and stress – caused by catecholamine sensitive automatic or triggered activity  At rest – may be caused by vagal initiation (AF)  Lightheadedness, syncope in setting of tightly fitting collar, turning head- suggests carotid hypersensitivity • MODE OF TERMINATION •If terminated by vagal manevoure – suggests AV node as integral part of tachyarrythmias May help determine diagnosis or further guide to diagnostic tests • DRUG HISTORY •nasal decongestants •Beta blockers •Drugs prolonging QT interval. 36
  37. 37.  DIETARY HISTORY  Alcoholic intake  Food containing Ephedrine  H/O SYSTEMIC ILLNESS  COPD  Thyrotoxicosis  Pericarditis  Congestive heart failure  FAMILY HISTORY  HOCM  Long QT syndromes  Myotonic dystrophies 37
  38. 38. PHYSICAL EXAMINATION MORE HELPFUL IF DONE DURING SYMPTOMATIC PERIOD  HR  >100  Regularly irregular  Irregularly irregular  JVP  Increased JVP  Cannon waves  Heart sounds  Variable heart sounds  murmurs  BP -- Variable  Physical manoeveurs– Can have diagnostic and therapeutic value. Valsalva/Carotid sinus massage - terminate or slow tachyarrythmias that depend on AV node. 38
  39. 39. 12 LEAD ECG  Primary tool in arrhythmia analysis  3 steps in diagnosing tachyarrythmia.  Step 1 – determine if QRS complex is narrow or wide.  Step 2 – determine if QRS complex is regular or irregular.  Step 3 -- look for p waves and relation to QRS complex.  Major branch point in DD is QRS duration.  QRS < .12 – always almost SVT  QRS >.12 – often VT 39
  40. 40.  24 hr Holter monitoring - for patients with daily symptoms  Patient activated event monitor – for patients with intermittent symptoms  Implanted loop ECG monitor – for patients with infrequent severe symptoms  Exercise ECG - to determine myocardial ischemia -For analysis of morphology of QT interval.  HUT – used in patients with recurrent syncope Syncope with injuries in absence of heart disease  2D ECHO – for cardiac chamber size and function. To rule out valvular diseases. 40
  41. 41. ELECTROPHYSIOLOGICAL STUDIES  For diagnostic purposes  For therapeutic purposes  COMPONENTS OF TEST  Measuement of conduction under resting , stress conditions and maneuvers 41
  42. 42. SITE OF ORIGIN  Atrial  SA node  Atrial muscle  Junctional  AV node  His bundle  Kent bundle  Bundle branches  Purkinje fibres  Ventricular muscle SUPRAVENTRICULAR VENTRICULAR 42
  43. 43.  Atrial Fibrillation  Paroxysmal supraventriculartachycardias (PSVT) -AV nodal reentry tachycardia (AVNRT) -AV junctional tachycardia -AV reentry tachycardia (AVRT) -WPW -AV reentry over concealed bypass tract –Atrial Tachycardia  VPC’S  VT  Ventricular flutter  Ventricular fibrillation  Brugada syndrome Supraventricular arryhthmias Ventricular arryhthmias
  44. 44. 44
  45. 45. 45
  46. 46. 46
  47. 47. 47
  48. 48. WIDE QRS TACHY CARDIA  Ventricular tachycardia  SVT with BBB  Antidromic AV re – entry tachycardia  Torsades de – pointes  LBBB with AF or Atrial flutter with variable block  WPW with AF or AFL with variable block WITH REGULAR RHYTHM WITH IRREGULAR RHYTHM 48
  49. 49. DIFFERENTIAL DIAGNOSIS OF WIDE QRS TACHYCARDIA  Initiation with premature P wave  Changes in P-P interval precedes R – R interval changes  Slowing or termination by vagal maneuvers  Initiation with premature QRS complex  Changes in R – R interval precedes P – P interval  AV – dissociation  Fusion ,capture beats  QRS duration- RBBB type V1 morphology - >140 ms LBBB type V1 - > 160 ms  Delayed activation – LBBB - R- wave > 40 ms RBBB- onset of R- wave to nadir of S – wave > 100 ms  Concordance of QRS complexes in all precordial leads SVT VT 49
  50. 50. ANTIARRYHTHMIC DRUGS Class IA.  This includes drugs that reduce V.max (rate of rise of action potential upstroke [phase 0]) and prolong action potential duration Eg-quinidine, procainamide, disopyramide. Class IB.  This class of drugs does not reduce V.max and shortens action potential duration— Eg-mexiletine, phenytoin, and lidocaine. Class IC.  This class of drugs can reduce V.max, primarily slow conduction, and prolong refractoriness minimall Eg-flecainide, propafenone, and moricizine. 50
  51. 51. Class II.  These drugs block beta-adrenergic receptors. Eg- propranolol, timolol, and metoprolol. Class III.  This class of drugs predominantly blocks potassium channels (such as IKr) and prolongs repolarization. Eg-sotalol, amiodarone, and bretylium. Class IV.  This class of drugs predominantly blocks the slow calcium channel (ICa.L)— Eg-verapamil, diltiazem, nifedipine, 51
  52. 52. 52
  53. 53. 53
  54. 54. 54 SINUS TACHYCARDIA  PHYSIOLOGICAL  fever  anxiety  anemia  sepsis  hyperthyroidism  congetive heart failure  hypoxemia  INAPPROPRIATE  viral – post viral dysautonomia
  55. 55. TREATMENT  Treat underlying cause  Beta blockers  Increase hydration  Beta blockers  Catheter ablation/pacing PHYSIOLOGICAL INAPPROPRIATE 55
  56. 56. 56 APC’S –  Incidence increases with age ECG –  Premature & abnormal P wave  Short PR interval  Precedes normal QRS complex  Compensatory pause is incomplete TREATMENT –  No treatment needed  If severely symptomatic –  Β-blocker, Catheter ablation .
  57. 57. 57
  58. 58. FOCAL ATRIAL TACHYCARDIAS  Can not be initaiated by programmed atrial stimulation  First P wave same as othr P waves  Response to adenosine –AV block seen -- slow or terminate  Initiated by programmed stimulation  First P wave different from others  Response to adenosine -AV block seen -cant slow or terminate Automatic AT Focal reenterant AT 58
  59. 59. ECG –  P wave distinct from sinus P wave  PR interval shorter than RP interval TREATMENT  Rate control  Rhytm control  Anticoagulation if LA diameter > 5cm  Catheter ablative theraphy  DC version 59
  60. 60. MULTIFOCAL ATRIAL TACHYCARDIA –  Mostly seen in patients of pulmonary disease ECG –  Atrial & ventricular rate – 100 – 150 bts / min  > 3 distinct P wave morphology  > 3 distinct PR interval TREATMENT –  Treat underlying pulmonary disease  CCB’s , amiodarone 60
  61. 61. ATRIAL FIBRILLATION  Most common sustained arrhythmia  Disorganised , rapid and irregular atrial activation and ventricular responses  Atrial rate – 400- 600 bpm  Ventricular rate – 120-150 bpm  CLASSIFICATION  Recurrent  Paroxysmal  Persistent  Permanent 61
  62. 62.  CAUSES  RHD  Ischaemic heart disease  Hypertension  Constrictive pericarditis  Hyperthyroidism  Acute alcoholism  Vascular,abdominal and thoracic surgery  Anemia  Acute vagotonic episode  Lone atrial fibrillation ( no structural heart disease) 62
  63. 63.  ECG  Atrial deflections are irregular and chaotic – ragged baseline  Ventricular rate is irregular  In longstanding cases, baseline almost straight with minimal undulation . 63
  64. 64. TREATMENT  Control ventricular rate  Betablockers  Ca channel blockers  Digoxin  Anticoagulation  When AF >12hrs and risk factors for stroke present.  Maintain INR – 2 to 3  Warfarin  DC cardioversion – 200 J  Pharmacological  To terminate - Amiodarone , Procainamide iv  To maintain restored sinus rhytm – beta blockers ,class Ic drugs.  Emergency If AF >24 - 48hrs  TEE done to r/o atrial thrombus  Heparin given with warfarin until INR > 1.8  Anticoagulate for 1 month after restoration of sinus rythm  Elective  Anticoagulate for atleast 3 weeks before cardioversion. RATE CONTROL TERMINATION OF AF ACUTE 64
  65. 65. CHRONIC  Beta blockers  Ca channel blockers  Digoxin  His bundle / AV junction ablation with implantation of activity sensor pacemaker  Anti coagulation  Surgical ablation of left atrial appendage  Catheter ablation – of atrial muscle sleeves entering pulmonary veins  Surgical ablation – COX – MAZE procedure RATE CONTROL TERMINATION OF AF SURVIVAL OUTCOME Restoration of sinus rhytm not superior to rate control with anticogulation as evidenced by AFFIRM and RACE trials 65
  66. 66. ATRIAL FLUTTER  atrial rate = 250-350 cycles/min  Ventricle rate is closer to 150, 100 or 75 beats/min  2:1, 3:1 and 4:1  F waves  “sawtooth” shape
  67. 67. ATRIAL FLUTTER  Reentrant type arrhythmia
  68. 68. ATRIAL FLUTTER  Treatment  DC – version 50 – 100 j  Anticoagulation  If asymptomatic – - rate control -rhythm control - catheter ablation
  69. 69. AV NOAL RE ENTERANT TACHYCARDIA –  Most common  Mostly in women  Repetitive activation down slow pathway & up fast pathway results in tachycardia ECG –  Rate – 120 – 150  P waves negative  Narrow QRS complexes  P wave not visible or distorts QRS complex 69
  70. 70. 70
  71. 71.  TREATMENT –  ACUTE  Vagal maneuvers  Adenosine – 6 – 12 mg iv  B – blockers ,CCB’s  DC - version -100- 200 j  PREVENTION  B-blockers , CCB’s  Catheter ablation – slow pathway 71
  72. 72. AV JUNCTIONAL RHYTHM  Rate – 40 – 50  Accelerated AVJR – 50 – 100 TREATMENT  Stop digoxin  B – blockers  Catheter ablation 72
  73. 73. WPW SYNDROME ECG  Short PR interval.  Short or long RP interval.  Delta waves  Narrow QRS complex. SITES OF BYPASS TRACTS  Left lateral  Right lateral  Posteroseptal  Anteroseptal 73
  74. 74. 74
  75. 75. A comment on PSVT in patient with WPW:
  76. 76. 76
  77. 77. MAIN SITES OF BYPASS 77
  78. 78. 78
  79. 79. 79
  80. 80. 80
  81. 81. 81
  82. 82. 82
  83. 83. COMPLICATIONS  Reciprocating tachycardia Orthodromic – AV reentry – conduction to ventricle via AV node and reentry via AP. Antidromic - conduction to ventricle via AP and reentry via His purkinje system – mimics VT  Atrial fibrillation 50% predisposed -fast ventricular rate results in hemodynamic compromise. 83
  84. 84. TREATMENT ACUTE  Orthodromic tachycardia Vagal stimulation Adenosine CCB s Betablockers  AF DC cardioversion Procainamide Ibutelide Digoxin avoided CHRONIC  Beta blockers  CCB s  Class Ia or Ic drugs CATHETER ABLATION  Indications -- recurrent symptomatic SVTs HR >200 84
  85. 85. 85
  86. 86. AIVR  >3 or more consecutive VPCs  VR >40 and <120  Benign rhytm  CAUSES  Idiopathic  Acute MI  Acute myocarditis  Digoxin intoxication  Postoperative cardiac surgery  Cocaine intoxication 86
  87. 87. 87
  88. 88.  TREATMENT  If hemodynamic compromise occurs  atropine  Atrial pacing 88
  89. 89. PREMATURE VENTRICULAR COMLEXES  Broad QRS > 120ms  T wave is large ,opposite in direction to QRS  No preceding p waves  Compensatory or noncompensatory pause  Fixed or variable coupling interval.
  90. 90. TYPES  BIGEMINY  TRIGEMINY  QUADRIGEMINY  COUPLET  TRIPLET  MONOMORPHIC  POLYMORPHIC
  91. 91.  Incidence >60% of healthy males during 24hr Holter  >80% post MI  Benign ectopics disappear on exercise  Pts –normal life span.
  92. 92. CLINICAL SIGNIFICANCE  LOWNs grading system of VPCs  Determines prognostic significance after MI  As grade advances, there is increased risk of SCD 92 GRADES VPCs 0 none 1 <30/hr 2 >30/hr 3 multiform 4A 2 consecutive 4B >3 consecutive 5 R on T phenomenon
  93. 93. MANAGEMENT In Normal heart  Asym- No treatment  Sym - betablockers Structural heart disease  betablockers  Class IA, III drugs
  94. 94. VENTRICULAR TACHYCARDIA  VT consists of at least three or more consecutive VPCs at a rate of 100bpm.  Types- -Nonsustained <30s -sustained > 30s  Rhythm- Regular / slightly irregular  Rate 70 to 250 / min
  95. 95. ECG DIAGNOSIS  QRS duration  RBBB > 140 ms  LBBB > 160 ms  Wellens et al  QRS >140ms good indicator of VT  QRS 120- 140 ms only 50% have VT
  96. 96. 102
  97. 97. 103
  98. 98. VT with RBBB (Wellens & Gulamhusein)
  99. 99. FUSION & CAPTURE BEATS  33 % cases of VT  Diagnosis of VT is certain  Seen in VT of lower rates(< 160)  Capture beat- sinus beat  Fusion beat- hybrid beat due to both atrial & ventricular activation.
  100. 100. BROARD QRS TACHYCARDIA AV DISSOCIATION FUSION & CAPTURE BEATS QRS DURATION QRS MORPHOLOGY QRS CONCORDANCE QRS AXIS
  101. 101. VT IN PATIENTS WITH CORONARY ARTERY DISEASE  Non-sustained VT (NSVT) -67%  Sustained VT 3.5% VF – 4.1%  VT + VF – 2.7 % Mortality  VT - 18.6%  VT + VF – 44%  1 yr mortality 7%  Without VT is 3 %
  102. 102. CLINICAL PRESENTATION  Symptoms are variable  Depend upon rate of VT & degree of LV dysfunction  Syncope / presyncope / dizziness  Palpitations  Sudden death
  103. 103. TREATMENT OF VT HEMODYNAMIC COMPROMISE --  DC – version asynchronously 200j , repeat with ↑energy if no response  IV lidocaine, amiodarone  DC –version synchronously with R wave  IV lidocaine , procainamide , amiodarone Polymorphic VT Monomorphic VT 111
  104. 104. NO HEMODYNAMIC COMPROMISE  Correction of k+ & mg  Removal of offending drug  B – blocker iv  Treat acute ischemia  Pacing  Catheter ablation  Quinidine,procainami de for BRUGADA syndrome  Lidocaine , procainamide , amiodarone  Catheter ablation Polymorphic VT Monomorphic VT 113
  105. 105. •B-BLOCKERSFocal out flow tract VT •VERAPAMILSeptal VT •ICD’S VT with structural heart disease 114
  106. 106. SPECIFIC TYPES OF VT ARRHYTHMOGENIC RT VENTRICULAR DYSPLASIA(0.4%)  LBBB contour with right axis deviation during VT  ICRBBB ,T waves inverted over the right precordial leads  Type of Cardiomyopathy, possibly familial, with hypokinetic thin walled RV  Abnormality in Chr 1 & Chr 10 -apoptosis
  107. 107.  Imp cause of VT in children & young adults with normal hearts  Rt heart failure or asymptomatic rt ventricular enlargement can be present with normal pulmonary vasculature  Males predominate  Pathology- Fatty & fibrofatty infiltration OR myocardial atrophy
  108. 108.  Preferentially affects rt ventricular inflow & outflow tracts & the apex  ECG- T wave inversion in V1 to V3, Terminal notch in QRS called “epsilon” wave can be present due to slowed intra ventricular conduction  ICDs are preferable to pharmacological  Radio frequency catheter ablation is often not successful
  109. 109. LEFT SEPTAL VT  Arises in the left posterior septum, often preceded by a fascicular potential.  It is sometimes called Fascicular tachycardia  Cause – Re-entry  Mgm – Verapamil or Diltiazem  Oral verapamil is less effective than iv verapamil
  110. 110. LEFT SEPTAL VT(FASCICULAR VT)  Seen in normal heart.  70% males ,15-40 yrs  Resting ECG normal  VT – RBBB pattern with left superior axis  QRS < 140 ms
  111. 111. Left septal ventricular tachycardia. This tachycardia is characterized by a right bundle branch block contour. the axis is rightward.
  112. 112.  C/F – palpitations, syncope  Not associated with sudden death  Treatment-  Verapamil .  RF ablation 85-100%  Prognosis – good
  113. 113. CATECHOLAMINERGIC POLYMORPHIC VT  Uncommon form of inherited VT  Occurs in children & adolescents without any overt structural heart disease  Adenosine sensitive  Pts present with syncope or aborted sudden death with highly reproducible stress induced VT that is often bidirectional  QT interval – Normal  Family history present in 30%
  114. 114.  During exercise typical responses, initial sinus tachycardia & ventricular extrasystoles followed by monomorphic or bidirectional VT, which eventually leads to polymorphic VT as exercise continues  Mgm – Beta blockers & ICDs  Lt cervicothoraic sympathetic ganglionectomy
  115. 115. BRUGADA SYNDROME  30-40% of idiopathic VF  AD, M:F 8:1  2-4th decade  Distinct form of idiopathic VT,V fib  RBBB & ST segment elevation in anterior precordial leads  No evidence of structural heart disease  Mutation in gene responsible for sodium channel
  116. 116.  Acceleration of Na channel recovery or nonfunctional channels  Common in apparently healthy south east Asians – 40-60%  Precise mechanism is not known  Can be reproduced by sodium channel blockers  ICDs are the only effective treatment to prevent sudden deaths
  117. 117. LONG QT SYNDROMES  Normal QT males - 440 ms females – 470ms  Congenital  Jervell Lange-Neilsen syndrome- AR with deafness  Ramano-Ward syndrome - AD with normal hearing  Defect in Na, K channels.
  118. 118. LQTS ECG PATTERNS
  119. 119. Acquired Drugs  Antiarrhythmic  Phenothiazines  Antihistaminics  Antimalarials,pentamidine  Tricyclic antidepressants  Ketoconazoles  Erythromycin  cisapride  Hypokalemia  Hypomagnesemia
  120. 120. C/F  Syncope, dizziness,sudden death Treatment  Underlying condition  Betablockers  ICD
  121. 121. CARDIOMYOPATHIES DILATED CARDIOMYOPATHY  Focus basal septum  Mutiple macrorentry  ICDs -life threatening ventricular arrhythmias  Comparing amiodarone v/s ICD, improved survival was found with ICD  In case bundle branch re-entry is the basis, ablate the RBB
  122. 122. HYPERTROPHIC CARDIOMYOPATHY  Risk of sudden death is increased by presence of syncope, family h/o, sudden death in 1st degree relative, septal thickness >3cms or presence of non sustained VT in 24 hr recordings  Infrequent episodes of non sustained VT have low mortality  Amiodarone – Useful symptomatic non sustained VT but not in improving survival
  123. 123. MITRAL VALVE PROLAPSE  VT in MVP has good prognosis although sudden death can occur  Treated with betablockers.
  124. 124. CHD  Can occur in pts some years after repair  Sustained VT can be caused by re entry at the site of surgery  Mgm- resection or catheter ablation of the area
  125. 125. VENTRICULAR FLUTTER  Severe derangement of heart beat  Macro-reentrant  Sine wave appearance, with large regular oscillations (150-300 Bpm)  Distinct QRS ,ST T are absent  Difficult to distinguish between rapid VT & V.flutter
  126. 126. VENTRICULAR FIBRILLATION  Grossly irregular ,undulation of varying amplitudes, contours with rates >300 /min  Starts with VT  Distinct QRS ,ST T are absent  Multiple wavelets of reentry  75% of sudden death after MI have VF.
  127. 127. MANAGEMENT
  128. 128. TORSADES DE POINTES VT characterized by  QRS complexes of changing amplitude that appear to twist around the isoelectric line & occur at rates of 200 to 250 /min  Prolonged ventricular repolarization with QT intervals generally exceeding 500 msec  U wave can also become prominent& merge with T wave
  129. 129.  Torsades de Pointes can terminate with progressive prolongation in cycle length with distinctly formed QRS complexes & culminate into basal rhythm, ventricular standstill, or VFib
  130. 130. Common causes  Potassium depletion  Congenital LQTS  Antiarrhythmic drugs IA,IC,III c/f  Palpitations, syncope, death  Women are at a greater risk
  131. 131. Management  IV magnesium  Temporary ventricular or atrial pacing+ ICD  Lidocaine, mexiletine or phenytoin can be tried  K channel activating drugs pinacidil, cromakalim  Cause of long QT should be treated
  132. 132. REFERENCES  BRAUNWALD ‘S HEART DISEASE 8 th ed  HARRISONS INTERNAL MEDICINE 17 th ed  HURST ‘S HEART DISEASES  SHAMMROTH ECG  MARRIOTS ECG  MEDICINE UPDATE 150

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