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tachyarrythmias d

This document provides an overview of tachyarrhythmias, including: - Definitions of tachyarrhythmias as disturbances in heart rhythm over 100 beats per minute. - Anatomy and electrophysiology of the heart's conduction system. - Mechanisms of arrhythmogenesis including disorders of impulse formation and conduction. - Diagnostic approach involving history, physical exam, ECGs, monitoring, and invasive studies. - Treatment modalities including antiarrhythmic drugs and ablation procedures for various specific arrhythmias like atrial fibrillation, supraventricular tachycardias, and ventricular arrhythmias.

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TACHYARRYTHMIAS Dr RAVI KANTH
DEFINITION ANATOMY OF CONDUCTION ELECTROPHYSIOLOGY DIAGNOSTIC APPROACH TREATMENT MODALITIES DESCRIPTION ABOUT INDIVIDUAL ARRYTHMIAS 2
DEFINITION  Any disturbance of the heart's rhythm, regular or irregular, resulting by convention in a rate over 100 beats/min . 3
CONDUCTION SYSTEM OF THE HEART AND ELECTROCARDIOGRAPHY
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
Conducting System of Heart 6
IMPULSE CONDUCTION THROUGH THE HEART 7
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
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
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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
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
Pacemaker and Action Potentials of the Heart 15
DEPOLARIZATION AND IMPULSE CONDUCTION  Depolarization in SA node precedes depolarization in atria, AV node, ventricles 16
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
ELECTROCARDIOGRAM  P-Q interval  Time atria depolarize & remain depolarized  Q-T interval  Time ventricles depolarize & remain depolarized 18
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
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
 DISORDERS OF IMPULSE FORMATION  Characterised by  Inappropriate discharge rate of normal pacemaker  Inappropriate discharge of ectopic pacemaker 21
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
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
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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
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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
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
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 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
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
 Mechanisms of termination are  When conduction & recovery characters of circuit change  When activating head of wave collides with tail 32
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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
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
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
 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
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
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
 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
ELECTROPHYSIOLOGICAL STUDIES  For diagnostic purposes  For therapeutic purposes  COMPONENTS OF TEST  Measuement of conduction under resting , stress conditions and maneuvers 41
SITE OF ORIGIN  Atrial  SA node  Atrial muscle  Junctional  AV node  His bundle  Kent bundle  Bundle branches  Purkinje fibres  Ventricular muscle SUPRAVENTRICULAR VENTRICULAR 42
 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
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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
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
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
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
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54 SINUS TACHYCARDIA  PHYSIOLOGICAL  fever  anxiety  anemia  sepsis  hyperthyroidism  congetive heart failure  hypoxemia  INAPPROPRIATE  viral – post viral dysautonomia
TREATMENT  Treat underlying cause  Beta blockers  Increase hydration  Beta blockers  Catheter ablation/pacing PHYSIOLOGICAL INAPPROPRIATE 55
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 .
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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
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
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
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
 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
 ECG  Atrial deflections are irregular and chaotic – ragged baseline  Ventricular rate is irregular  In longstanding cases, baseline almost straight with minimal undulation . 63
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
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
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
ATRIAL FLUTTER  Reentrant type arrhythmia
ATRIAL FLUTTER  Treatment  DC – version 50 – 100 j  Anticoagulation  If asymptomatic – - rate control -rhythm control - catheter ablation
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
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 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
AV JUNCTIONAL RHYTHM  Rate – 40 – 50  Accelerated AVJR – 50 – 100 TREATMENT  Stop digoxin  B – blockers  Catheter ablation 72
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
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A comment on PSVT in patient with WPW:
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MAIN SITES OF BYPASS 77
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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
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
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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
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 TREATMENT  If hemodynamic compromise occurs  atropine  Atrial pacing 88
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.
TYPES  BIGEMINY  TRIGEMINY  QUADRIGEMINY  COUPLET  TRIPLET  MONOMORPHIC  POLYMORPHIC
 Incidence >60% of healthy males during 24hr Holter  >80% post MI  Benign ectopics disappear on exercise  Pts –normal life span.
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
MANAGEMENT In Normal heart  Asym- No treatment  Sym - betablockers Structural heart disease  betablockers  Class IA, III drugs
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
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
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VT with RBBB (Wellens & Gulamhusein)
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.
BROARD QRS TACHYCARDIA AV DISSOCIATION FUSION & CAPTURE BEATS QRS DURATION QRS MORPHOLOGY QRS CONCORDANCE QRS AXIS
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 %
CLINICAL PRESENTATION  Symptoms are variable  Depend upon rate of VT & degree of LV dysfunction  Syncope / presyncope / dizziness  Palpitations  Sudden death
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
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
•B-BLOCKERSFocal out flow tract VT •VERAPAMILSeptal VT •ICD’S VT with structural heart disease 114
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
 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
 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
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
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
Left septal ventricular tachycardia. This tachycardia is characterized by a right bundle branch block contour. the axis is rightward.
 C/F – palpitations, syncope  Not associated with sudden death  Treatment-  Verapamil .  RF ablation 85-100%  Prognosis – good
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%
 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
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
 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
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.
LQTS ECG PATTERNS
Acquired Drugs  Antiarrhythmic  Phenothiazines  Antihistaminics  Antimalarials,pentamidine  Tricyclic antidepressants  Ketoconazoles  Erythromycin  cisapride  Hypokalemia  Hypomagnesemia
C/F  Syncope, dizziness,sudden death Treatment  Underlying condition  Betablockers  ICD
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
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
MITRAL VALVE PROLAPSE  VT in MVP has good prognosis although sudden death can occur  Treated with betablockers.
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
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
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.
MANAGEMENT
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
 Torsades de Pointes can terminate with progressive prolongation in cycle length with distinctly formed QRS complexes & culminate into basal rhythm, ventricular standstill, or VFib
Common causes  Potassium depletion  Congenital LQTS  Antiarrhythmic drugs IA,IC,III c/f  Palpitations, syncope, death  Women are at a greater risk
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
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
tachyarrythmias d

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tachyarrythmias d

  • 1.
  • 2.
    DEFINITION ANATOMY OF CONDUCTION ELECTROPHYSIOLOGY DIAGNOSTICAPPROACH TREATMENT MODALITIES DESCRIPTION ABOUT INDIVIDUAL ARRYTHMIAS 2
  • 3.
    DEFINITION  Any disturbanceof the heart's rhythm, regular or irregular, resulting by convention in a rate over 100 beats/min . 3
  • 4.
    CONDUCTION SYSTEM OFTHE HEART AND ELECTROCARDIOGRAPHY
  • 5.
    Conduction System ofthe 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.
  • 7.
  • 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.
    Electrical Properties ofMyocardial 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.
  • 11.
  • 12.
  • 13.
    Heart Physiology: Intrinsic ConductionSystem • 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.
    DEPOLARIZATION OF SANODE  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.
  • 16.
    DEPOLARIZATION AND IMPULSE CONDUCTION Depolarization in SA node precedes depolarization in atria, AV node, ventricles 16
  • 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.
    ELECTROCARDIOGRAM  P-Q interval Time atria depolarize & remain depolarized  Q-T interval  Time ventricles depolarize & remain depolarized 18
  • 19.
    ELECTROCARDIOGRAM  Intervals showtiming 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.
    MECHANISMS OF ARRYTHMOGENESIS  Sometacyarythmias 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.
     DISORDERS OFIMPULSE FORMATION  Characterised by  Inappropriate discharge rate of normal pacemaker  Inappropriate discharge of ectopic pacemaker 21
  • 22.
    Abnormal automaticity  Arisefrom 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.
    After depolarisations areof 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.
  • 25.
    DAD’S  Result fromactivation 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.
  • 27.
    EAD’S  AP prolongationmay 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.
    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.
  • 30.
     For reentry 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.
    Fuctional reentry  Occurin fibres that exhibit functionally different EP properties caused by local differences in transmembrane AP  functional heterogenities can be fixed or change dynamically 31
  • 32.
     Mechanisms oftermination are  When conduction & recovery characters of circuit change  When activating head of wave collides with tail 32
  • 33.
  • 34.
    DETERMINANTS OF AMPLITUDESOF 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.
    APPROACH TO TACHYARRYTHMIAS HISTORY •Modeof 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.
    HISTORY  MODE OFONSET  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.
     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.
    PHYSICAL EXAMINATION MORE HELPFULIF 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.
    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.
     24 hrHolter 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.
    ELECTROPHYSIOLOGICAL STUDIES  Fordiagnostic purposes  For therapeutic purposes  COMPONENTS OF TEST  Measuement of conduction under resting , stress conditions and maneuvers 41
  • 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.
     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.
  • 45.
  • 46.
  • 47.
  • 48.
    WIDE QRS TACHYCARDIA  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.
    DIFFERENTIAL DIAGNOSIS OFWIDE 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.
    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.
    Class II.  Thesedrugs 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.
  • 53.
  • 54.
    54 SINUS TACHYCARDIA  PHYSIOLOGICAL fever  anxiety  anemia  sepsis  hyperthyroidism  congetive heart failure  hypoxemia  INAPPROPRIATE  viral – post viral dysautonomia
  • 55.
    TREATMENT  Treat underlying cause Beta blockers  Increase hydration  Beta blockers  Catheter ablation/pacing PHYSIOLOGICAL INAPPROPRIATE 55
  • 56.
    56 APC’S –  Incidenceincreases 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.
  • 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.
    ECG –  Pwave 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.
    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.
    ATRIAL FIBRILLATION  Mostcommon 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.
     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.
     ECG  Atrialdeflections are irregular and chaotic – ragged baseline  Ventricular rate is irregular  In longstanding cases, baseline almost straight with minimal undulation . 63
  • 64.
    TREATMENT  Control ventricularrate  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.
    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.
    ATRIAL FLUTTER  atrialrate = 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.
  • 68.
    ATRIAL FLUTTER  Treatment DC – version 50 – 100 j  Anticoagulation  If asymptomatic – - rate control -rhythm control - catheter ablation
  • 69.
    AV NOAL REENTERANT 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.
  • 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.
    AV JUNCTIONAL RHYTHM Rate – 40 – 50  Accelerated AVJR – 50 – 100 TREATMENT  Stop digoxin  B – blockers  Catheter ablation 72
  • 73.
    WPW SYNDROME ECG  ShortPR interval.  Short or long RP interval.  Delta waves  Narrow QRS complex. SITES OF BYPASS TRACTS  Left lateral  Right lateral  Posteroseptal  Anteroseptal 73
  • 74.
  • 75.
    A comment onPSVT in patient with WPW:
  • 76.
  • 77.
    MAIN SITES OFBYPASS 77
  • 78.
  • 79.
  • 80.
  • 81.
  • 82.
  • 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.
    TREATMENT ACUTE  Orthodromic tachycardia Vagal stimulation Adenosine CCBs 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.
  • 86.
    AIVR  >3 ormore consecutive VPCs  VR >40 and <120  Benign rhytm  CAUSES  Idiopathic  Acute MI  Acute myocarditis  Digoxin intoxication  Postoperative cardiac surgery  Cocaine intoxication 86
  • 87.
  • 88.
     TREATMENT  Ifhemodynamic compromise occurs  atropine  Atrial pacing 88
  • 89.
    PREMATURE VENTRICULAR COMLEXES  BroadQRS > 120ms  T wave is large ,opposite in direction to QRS  No preceding p waves  Compensatory or noncompensatory pause  Fixed or variable coupling interval.
  • 90.
    TYPES  BIGEMINY  TRIGEMINY QUADRIGEMINY  COUPLET  TRIPLET  MONOMORPHIC  POLYMORPHIC
  • 91.
     Incidence >60%of healthy males during 24hr Holter  >80% post MI  Benign ectopics disappear on exercise  Pts –normal life span.
  • 92.
    CLINICAL SIGNIFICANCE  LOWNsgrading 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
  • 95.
    MANAGEMENT In Normal heart Asym- No treatment  Sym - betablockers Structural heart disease  betablockers  Class IA, III drugs
  • 100.
    VENTRICULAR TACHYCARDIA  VTconsists 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
  • 101.
    ECG DIAGNOSIS  QRSduration  RBBB > 140 ms  LBBB > 160 ms  Wellens et al  QRS >140ms good indicator of VT  QRS 120- 140 ms only 50% have VT
  • 102.
  • 103.
  • 106.
    VT with RBBB(Wellens & Gulamhusein)
  • 107.
    FUSION & CAPTUREBEATS  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.
  • 108.
    BROARD QRS TACHYCARDIA AVDISSOCIATION FUSION & CAPTURE BEATS QRS DURATION QRS MORPHOLOGY QRS CONCORDANCE QRS AXIS
  • 109.
    VT IN PATIENTSWITH 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 %
  • 110.
    CLINICAL PRESENTATION  Symptomsare variable  Depend upon rate of VT & degree of LV dysfunction  Syncope / presyncope / dizziness  Palpitations  Sudden death
  • 111.
    TREATMENT OF VT HEMODYNAMICCOMPROMISE --  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
  • 113.
    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
  • 114.
    •B-BLOCKERSFocal out flow tractVT •VERAPAMILSeptal VT •ICD’S VT with structural heart disease 114
  • 115.
    SPECIFIC TYPES OFVT 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
  • 116.
     Imp causeof 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
  • 117.
     Preferentially affectsrt 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
  • 119.
    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
  • 120.
    LEFT SEPTAL VT(FASCICULARVT)  Seen in normal heart.  70% males ,15-40 yrs  Resting ECG normal  VT – RBBB pattern with left superior axis  QRS < 140 ms
  • 121.
    Left septal ventriculartachycardia. This tachycardia is characterized by a right bundle branch block contour. the axis is rightward.
  • 122.
     C/F –palpitations, syncope  Not associated with sudden death  Treatment-  Verapamil .  RF ablation 85-100%  Prognosis – good
  • 123.
    CATECHOLAMINERGIC POLYMORPHIC VT  Uncommonform 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%
  • 124.
     During exercisetypical 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
  • 126.
    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
  • 127.
     Acceleration ofNa 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
  • 129.
    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.
  • 131.
  • 134.
    Acquired Drugs  Antiarrhythmic  Phenothiazines Antihistaminics  Antimalarials,pentamidine  Tricyclic antidepressants  Ketoconazoles  Erythromycin  cisapride  Hypokalemia  Hypomagnesemia
  • 135.
    C/F  Syncope, dizziness,suddendeath Treatment  Underlying condition  Betablockers  ICD
  • 136.
    CARDIOMYOPATHIES DILATED CARDIOMYOPATHY  Focusbasal 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
  • 137.
    HYPERTROPHIC CARDIOMYOPATHY  Riskof 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
  • 138.
    MITRAL VALVE PROLAPSE VT in MVP has good prognosis although sudden death can occur  Treated with betablockers.
  • 139.
    CHD  Can occurin 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
  • 140.
    VENTRICULAR FLUTTER  Severederangement 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
  • 142.
    VENTRICULAR FIBRILLATION  Grosslyirregular ,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.
  • 144.
  • 145.
    TORSADES DE POINTES VTcharacterized 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
  • 147.
     Torsades dePointes can terminate with progressive prolongation in cycle length with distinctly formed QRS complexes & culminate into basal rhythm, ventricular standstill, or VFib
  • 148.
    Common causes  Potassiumdepletion  Congenital LQTS  Antiarrhythmic drugs IA,IC,III c/f  Palpitations, syncope, death  Women are at a greater risk
  • 149.
    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
  • 150.
    REFERENCES  BRAUNWALD ‘SHEART DISEASE 8 th ed  HARRISONS INTERNAL MEDICINE 17 th ed  HURST ‘S HEART DISEASES  SHAMMROTH ECG  MARRIOTS ECG  MEDICINE UPDATE 150