ventricular tachycardia203.69.179.10/taitam/car_int/documents/vt.pdf · ventricular tachycardia....

TOPIC DISCUSSIONTOPIC DISCUSSION

VVENTRICULAR ENTRICULAR

TTACHYCARDIAACHYCARDIA

VENTRICULAR TACHYCARDIAVENTRICULAR TACHYCARDIA

DEFINITIONDEFINITION

3 or More ORS Complexes of Ventricular 3 or More ORS Complexes of Ventricular OriginOrigin

Rate exceeding 100 bpmRate exceeding 100 bpm


INTRODUCTIONINTRODUCTION

VT & VF are Major Causes of SCDVT & VF are Major Causes of SCD

Ambulatory ECG Recordings at SCD Have Ambulatory ECG Recordings at SCD Have Shown Shown 50%50%--60%60% of Sustained Monomorphic of Sustained Monomorphic VT as The Initial EventVT as The Initial Event


KEY FEATURESKEY FEATURES

SUSTAINED MONOMORPHIC VT:SUSTAINED MONOMORPHIC VT:Most Common Mechanism Could be ReMost Common Mechanism Could be Re--Entry Entry in Scarred Myocardium in Patients with in Scarred Myocardium in Patients with Structural Heart DiseaseStructural Heart Disease

POLYMORPHIC VT:POLYMORPHIC VT:Caused by Abnormalities in Repolarization by Caused by Abnormalities in Repolarization by Both Intrinsic or Transient FactorsBoth Intrinsic or Transient Factors


CLASSIFICATIONCLASSIFICATION

ECG MORPHOLOGYECG MORPHOLOGYMonomorphic VS Polymorphic, BBB Pattern, Monomorphic VS Polymorphic, BBB Pattern, AxisAxis

DURATIONDURATION

Sustained VS NonsustainedSustained VS Nonsustained

MECHANISMMECHANISMETIOLOGYETIOLOGY


CLINICAL PRESENTATIONCLINICAL PRESENTATION

Quite variedQuite varied (Asymptomatic, Syncope, Sudden (Asymptomatic, Syncope, Sudden Death)Death)

Duration, HR, Underlying Heart Disease, Other Duration, HR, Underlying Heart Disease, Other medical Conditionsmedical Conditions


CLINICAL SIGNIFICANCECLINICAL SIGNIFICANCE

Decreased CODecreased CO1. Rapid HR with Poor Ventricular Filling1. Rapid HR with Poor Ventricular FillingHR <150 bpm, well tolerated in short term; CHF occur HR <150 bpm, well tolerated in short term; CHF occur in poor ventricular function patientsin poor ventricular function patientsHR >150 bpm, <200 bpm, tolerated with variability HR >150 bpm, <200 bpm, tolerated with variability HR >200 bpm, virtually symptomatic in all patientsHR >200 bpm, virtually symptomatic in all patients



Decreased CODecreased CO2. Asynchrony between AV Conduction2. Asynchrony between AV Conduction

3. Abnormal Sequence of Ventricular Activation3. Abnormal Sequence of Ventricular Activation

4. Loss of Atrial Contribution4. Loss of Atrial Contribution



Degenerative to VFDegenerative to VF

SCDSCD


DIFFERENTIAL DIAGNOSISDIFFERENTIAL DIAGNOSIS

1. SVT with Aberrant Intraventricular 1. SVT with Aberrant Intraventricular ConductionConduction

2. BBB2. BBB3. Morphological Changes of QRS Secondary to 3. Morphological Changes of QRS Secondary to

Metabolic DerangementMetabolic Derangement4. Pacing4. Pacing


BRUGADA CRITERIA BRUGADA CRITERIA

(D/D(D/D VT VT VSVS SVT with Aberrant Intraventricular SVT with Aberrant Intraventricular Conduction)Conduction)

1. Most Helpful with 99% Sensitivity and 96.5% 1. Most Helpful with 99% Sensitivity and 96.5% Specificity Without PreSpecificity Without Pre--Existing BBBExisting BBB

2. Stepwise Approach2. Stepwise Approach


11STST ALGORITHMALGORITHM

客人

From Harrisons Internal Medicine, 15th Edi.


22NDND ALGORITHM ALGORITHM (D/D(D/D VT VT VSVS Antidromic Antidromic Tachycardia over An Accessory Pathway)Tachycardia over An Accessory Pathway)


PATHOPHYSIOLOGYPATHOPHYSIOLOGY1. Studies in experimental animals and intraoperative 1. Studies in experimental animals and intraoperative

mapping in humans as well as pacings during VTmapping in humans as well as pacings during VT2. In post MI patients, VT was caused by a re2. In post MI patients, VT was caused by a re--entrant entrant

mechanismmechanism3. Areas of slow conduction have been identified as the 3. Areas of slow conduction have been identified as the

substrate for resubstrate for re--entry.entry.4. In experimental MI, continuous electrical activity 4. In experimental MI, continuous electrical activity

regularly and predictably bridged the entire diastolic regularly and predictably bridged the entire diastolic interval could be demonstrated at the onset of VT by interval could be demonstrated at the onset of VT by the use of electrodesthe use of electrodes


PATHOPHYSIOLOGYPATHOPHYSIOLOGY5. These findings are corroborated by the anatomic 5. These findings are corroborated by the anatomic

characteristics of MI, which may show islands of characteristics of MI, which may show islands of relatively viable muscle alternating with areas of relatively viable muscle alternating with areas of necrosis and later fibrosisnecrosis and later fibrosis

6. Such tissue may result in fragmentation of the 6. Such tissue may result in fragmentation of the propagating electromotive forcespropagating electromotive forces

7. Gardner et al. showed that induced slow conduction 7. Gardner et al. showed that induced slow conduction alone did not cause fragmented activityalone did not cause fragmented activity

8. Highly fractionated electrograms occurred only in 8. Highly fractionated electrograms occurred only in preparations from chronic infarcts with interstitial preparations from chronic infarcts with interstitial fibrosis forming insulating boundaries between muscle fibrosis forming insulating boundaries between muscle bundles bundles


PATHOPHYSIOLOGYPATHOPHYSIOLOGY9. Another possibility is that there is a marked reduction 9. Another possibility is that there is a marked reduction

in conduction velocity caused by a diminished in conduction velocity caused by a diminished intercellular coupling, which would be expected to intercellular coupling, which would be expected to cause high resistance to current flow between cells cause high resistance to current flow between cells

10. The size of region necessary for occurrence of re10. The size of region necessary for occurrence of re--entry entry has not yet been fully establishedhas not yet been fully established

11. Finally, a close correlation between the presence of 11. Finally, a close correlation between the presence of continuous fractionated electrical activity and continuous fractionated electrical activity and perpetuation of VT was demonstrated by perpetuation of VT was demonstrated by Garan Garan et al.et al.


THERAPYTHERAPY

Medical TreatmentMedical Treatment(No Hemodynamic Compromise)(No Hemodynamic Compromise)

DCCDCC(Unstable, Symptomatic)(Unstable, Symptomatic)

New Guidelines for VT in 2000New Guidelines for VT in 2000


THERAPYTHERAPY

Medical TreatmentMedical Treatment1. IV Procainamide, Xylocaine or Amiodarone1. IV Procainamide, Xylocaine or Amiodarone2. Reversible Cause Correction (eg.. Ischemia, 2. Reversible Cause Correction (eg.. Ischemia,

Electrolyte Imbalance, Bradycardia)Electrolyte Imbalance, Bradycardia)3. 3. Hypotension TreatmentHypotension Treatment4. Offending Agents Removal, and Antidotes if 4. Offending Agents Removal, and Antidotes if

NecessaryNecessary


THERAPYTHERAPY

DCCDCC1. 1. At Least 100 J DCC Initially in Stable PatientAt Least 100 J DCC Initially in Stable Patient2. 200 J DCC Synchronized in Unstable, 2. 200 J DCC Synchronized in Unstable,

Symptomatic VT Symptomatic VT 3. 200 J DCC Unsynchronized in Pulseless VT3. 200 J DCC Unsynchronized in Pulseless VT


PREVENTION & PROPHYLAXISPREVENTION & PROPHYLAXIS

MEDICAL THERAPYMEDICAL THERAPYShift of Class I to Class III Maintenance Shift of Class I to Class III Maintenance Therapy in Therapy in CAST TrialCAST Trial

CURATIVE CATHETERCURATIVE CATHETER--BASED BASED THERAPIESTHERAPIES

SURGICAL PROCEDURESSURGICAL PROCEDURESICD ICD ---- Greatest Impact on Survival in SCDGreatest Impact on Survival in SCD



MEDICAL THERAPYMEDICAL THERAPYESVEM TrialESVEM TrialIt was Disappointing with Sotalol to be The It was Disappointing with Sotalol to be The Most Effective DrugMost Effective Drug

EMIAT & CAMIAT Trial EMIAT & CAMIAT Trial (Amiodarone post AMI)(Amiodarone post AMI)

It Revealed A Decrease in Arrhythmia Deaths It Revealed A Decrease in Arrhythmia Deaths with No Survival Benefitwith No Survival Benefit



MEDICAL THERAPYMEDICAL THERAPY

COMBINATION THERAPY COMBINATION THERAPY With ICD in High With ICD in High Risk Patients in New EraRisk Patients in New Era



MEDICAL THERAPYMEDICAL THERAPYCalcium Channel Blocker is Effective inCalcium Channel Blocker is Effective inSome Idiopathic Monomorphic VTs:Some Idiopathic Monomorphic VTs:1. VT from RVOT with LBBB1. VT from RVOT with LBBB2. VT from LV Apex with RBBB2. VT from LV Apex with RBBB3. VT from Digoxin Toxicity3. VT from Digoxin Toxicity



CURATIVE CATHETERCURATIVE CATHETER--BASED BASED THERAPIESTHERAPIES

Radiofrequency Ablation is Used to Eliminate Radiofrequency Ablation is Used to Eliminate The Slow Conduction Pathway in A ReThe Slow Conduction Pathway in A Re--entrant entrant CircuitCircuit

50%50%--70% Successful Rate70% Successful RateProgressively DevelopingProgressively Developing

Electrophysiologic study Electrophysiologic study in ventricular in ventricular tachycardia. tachycardia. (Re(Re--entry entry type from previous MI)type from previous MI)

(a) (a) A single A single extrastimulus (S2) extrastimulus (S2) after after an 8an 8--beat drive at 550ms beat drive at 550ms cycle length (S1cycle length (S1––S1)S1)initiates sustained initiates sustained monomorphic monomorphic ventricular tachycardia ventricular tachycardia (VT)(VT). Note the presence . Note the presence of of atrioventricular atrioventricular dissociationdissociation and and the the absence of a His absence of a His potential before the QRS.potential before the QRS.(b) A burst of (b) A burst of rapid rapid ventricular pacing (RVP)ventricular pacing (RVP)is used to restore normal is used to restore normal sinus rhythm (NSR). A, sinus rhythm (NSR). A, atrium; HRA, high right atrium; HRA, high right atrium; HBE, bundle of atrium; HBE, bundle of His; RVA, right His; RVA, right ventricular apex; V, ventricular apex; V, ventricle.ventricle.

Catheters are typically positioned in RA, Bundle of His region, Catheters are typically positioned in RA, Bundle of His region, and the RV apexand the RV apex. The standard stimulation protocol may use . The standard stimulation protocol may use up to 3 ventricular extrastimuli delivered at 2 basic cycle up to 3 ventricular extrastimuli delivered at 2 basic cycle lengths from 2 RV sites. lengths from 2 RV sites.



ICDICDMADIT & AVID Trial MADIT & AVID Trial (High Risk in EF <35% or Inducible Sustained (High Risk in EF <35% or Inducible Sustained

VT at EPS)VT at EPS)

A Decided Advantage in ICD was Noted in Both A Decided Advantage in ICD was Noted in Both Trials With 30%Trials With 30%--50% Reductions in Mortality50% Reductions in Mortality


CLINICAL PRESENTATION AND CLINICAL PRESENTATION AND COURSE OF VTCOURSE OF VT

ISCHEMICISCHEMIC

NONNON--ISCHEMICISCHEMIC

TORSADES DE POINTSTORSADES DE POINTS



ISCHEMICISCHEMICAltered Cellular Level FunctionAltered Cellular Level FunctionAnatomic Scar Tissue FormationAnatomic Scar Tissue FormationA ReA Re--entrant Circuit With 2 Pathwaysentrant Circuit With 2 PathwaysNormal QT IntervalNormal QT Interval



ISCHEMICISCHEMICPredictors: Larger Infarcts With Greater Predictors: Larger Infarcts With Greater Resultant Impairment of LV Systolic FunctionResultant Impairment of LV Systolic Function

LV Systolic Function is The Single Most LV Systolic Function is The Single Most Important Predictor of SCD due to Important Predictor of SCD due to ArrhythmiaArrhythmia

Revascularization Seemed to Decrease The Risk Revascularization Seemed to Decrease The Risk



ISCHEMICISCHEMICAIVR AIVR It is Seen Almost Exclusively in Ischemic Heart It is Seen Almost Exclusively in Ischemic Heart Disease, esp. Disease, esp. During AMIDuring AMI or or Reperfusion of An Reperfusion of An Occluded Territory Occluded Territory (Enhanced Automaticity)(Enhanced Automaticity)

It May be Seen in Digoxin ToxicityIt May be Seen in Digoxin ToxicityIt is Rarely of Clinical SignificanceIt is Rarely of Clinical Significance



ISCHEMICISCHEMICAIVRAIVR



ISCHEMICISCHEMICAIVRAIVRTherapy is Rarely Necessary UnlessTherapy is Rarely Necessary Unless1. 1. Loss of AV Synchrony with Hemodynamic Loss of AV Synchrony with Hemodynamic ChangeChange

2. R on T2. R on T3. Rapid Ventricular Rate or VF3. Rapid Ventricular Rate or VF



NONNON--ISCHEMICISCHEMIC1. BB Re1. BB Re--entry, WPW Syndromeentry, WPW Syndrome2. Idiopathic VT2. Idiopathic VT3. Congenital Long QT Syndrome3. Congenital Long QT Syndrome4. Genetically Associated VT4. Genetically Associated VT5. Idiopathic Polymorphic VT5. Idiopathic Polymorphic VT6. 6. Infection, Inflammation or Drug VTInfection, Inflammation or Drug VT7. 7. Arrhythmogenic RV DysplasiaArrhythmogenic RV Dysplasia



NONNON--ISCHEMICISCHEMICBB ReBB Re--entryentryCommon in Common in DCMDCM, Usually >= 200 BPM, Usually >= 200 BPMTypically LBBB, with less RBBBTypically LBBB, with less RBBBMost commonly With Most commonly With Right Bundle Antegrade ConductionRight Bundle Antegrade ConductionLeft Bundle Retrograde ConductionLeft Bundle Retrograde Conduction

Confirmed by EPSConfirmed by EPS

Electrophysiologic findings in bundle branch reElectrophysiologic findings in bundle branch re--entry. The tracings shown are entry. The tracings shown are surface ECG leads 1, aVF and V1, and intracardiac recordings frosurface ECG leads 1, aVF and V1, and intracardiac recordings from the high right m the high right atrium (HRA), the bundle of His (HBE) and the right ventricular atrium (HRA), the bundle of His (HBE) and the right ventricular apex (RVA). The apex (RVA). The surface leads show the typical pattern of left bundle branch blosurface leads show the typical pattern of left bundle branch block. The ck. The intracardiac recordings show intracardiac recordings show atrioventricular dissociationatrioventricular dissociation and a and a His potential His potential preceding each ventricular depolarizationpreceding each ventricular depolarization. A, atrium; His, His potential; RVA, . A, atrium; His, His potential; RVA, right ventricular apex.right ventricular apex.



NONNON--ISCHEMICISCHEMICIdiopathic VTIdiopathic VT (VT From RVOT, VT From LV Apex)(VT From RVOT, VT From LV Apex)

Otherwise Structurally Normal HeartsOtherwise Structurally Normal HeartsNo Significant CADNo Significant CADNo Family History of Arrhythmia or Sudden No Family History of Arrhythmia or Sudden DeathDeath

Normal Surface ECGNormal Surface ECGUsually Responsive to Calcium Channel BlockerUsually Responsive to Calcium Channel Blocker



NONNON--ISCHEMICISCHEMICCongenital Long QT SyndromeCongenital Long QT Syndrome

客人

From Manual of Cardiovascular Medicine. By Steven P. Marso, Brian P. Griffin, Eric J. Topol



NONNON--ISCHEMICISCHEMICCongenital Associated VTCongenital Associated VTMuscular DystrophiesMuscular DystrophiesDuchenneDuchenne’’s Muscular Dystrophys Muscular Dystrophy

Myotonic DystrophyMyotonic Dystrophy



NONNON--ISCHEMICISCHEMICCongenital Associated VTCongenital Associated VTMuscular DystrophiesMuscular DystrophiesFrequent Defects in Conduction SystemFrequent Defects in Conduction System

Heart Block, BBB, and SCD due to VTHeart Block, BBB, and SCD due to VT



NONNON--ISCHEMICISCHEMICIdiopathic Polymorphic VTIdiopathic Polymorphic VT

Structurally Normal HeartsStructurally Normal Hearts

Normal QT IntervalNormal QT Interval



NONNON--ISCHEMICISCHEMICIdiopathic Polymorphic VTIdiopathic Polymorphic VT1. Persistent ST Elevation 1. Persistent ST Elevation 2. Exercise Reproducible Arrhythmias with 2. Exercise Reproducible Arrhythmias with

Exercise and Responsive to Exercise and Responsive to ββ--BlockerBlocker3. Polymorphic VT Triggered by VPCs with High 3. Polymorphic VT Triggered by VPCs with High

SCD Incidence not Prevented by SCD Incidence not Prevented by ββ--BlockerBlocker



NONNON--ISCHEMICISCHEMICDrugDrug--Induced VTInduced VTBoth Polymorphic & MonomorphicBoth Polymorphic & MonomorphicParticularly True in Ischemic or Infarcted Particularly True in Ischemic or Infarcted HeartsHearts



NONNON--ISCHEMICISCHEMICDrugDrug--Induced VTInduced VTPhenothiazines, TCA, Digoxin, Epinephrine, Phenothiazines, TCA, Digoxin, Epinephrine, Cocaine, Nicotine, Alcohol, and Glue Are Cocaine, Nicotine, Alcohol, and Glue Are Implicated With Monomorphic VTImplicated With Monomorphic VT

NSVT & Depressed LV Function Remained NSVT & Depressed LV Function Remained Risk Factors for SCDRisk Factors for SCD



NONNON--ISCHEMICISCHEMICDrugDrug--Induced VTInduced VT

Torsades De Points Due to QT ProlongationTorsades De Points Due to QT Prolongation

Digoxin Can Propagate DAD to VTDigoxin Can Propagate DAD to VT



NONNON--ISCHEMICISCHEMICDCM & HCMDCM & HCM

Increased Risk of VT to SCDIncreased Risk of VT to SCD



NONNON--ISCHEMICISCHEMICDCMDCM

Difficult to PredictDifficult to PredictAsymptomatic VT Are CommonAsymptomatic VT Are CommonICD in LifeICD in Life--Threatening ArrhythmiaThreatening ArrhythmiaAblation if BB ReAblation if BB Re--entry is The Mechanismentry is The Mechanism



NONNON--ISCHEMICISCHEMICHCM HCM HIGH RISK: Syncope, Family SCD History of First Degree, HIGH RISK: Syncope, Family SCD History of First Degree,

NSVT on Ambulatory ECGNSVT on Ambulatory ECG

SVT, AF, and Ischemia Are Poorly Tolerated And SVT, AF, and Ischemia Are Poorly Tolerated And May Lead to VTMay Lead to VT

EPS May be Helpful in Stratifying RiskEPS May be Helpful in Stratifying RiskAmiodarone Amiodarone May be BeneficialMay be BeneficialDual Chamber PacingDual Chamber Pacing: Decrease Outflow Gradient: Decrease Outflow Gradient



NONNON--ISCHEMICISCHEMICStructural AbnormalitiesStructural AbnormalitiesRepaired TOFRepaired TOFOften Originates in RVOTOften Originates in RVOTCured by Ablation or Surgical ResectionCured by Ablation or Surgical Resection

MVP MVP (Quite Good Prognosis)(Quite Good Prognosis)Uncommonly Linked to SCDUncommonly Linked to SCD



NONNON--ISCHEMICISCHEMICArrhythmogenic RV DysplasiaArrhythmogenic RV DysplasiaCardiomyopathy Begins in RV and Often Cardiomyopathy Begins in RV and Often Progress to LVProgress to LV

RV Dilatation with Resultant Poor Contractile RV Dilatation with Resultant Poor Contractile FunctionFunction

RV Muscle Becomes Replaced by Adipose and RV Muscle Becomes Replaced by Adipose and Fibrous TissueFibrous Tissue



NONNON--ISCHEMICISCHEMICArrhythmogenic RV DysplasiaArrhythmogenic RV DysplasiaReRe--entrant Type entrant Type (Scarring & Late Potentials)(Scarring & Late Potentials)With LBBB MorphologyWith LBBB Morphology

Often Inversion T Over Right Chest LeadsOften Inversion T Over Right Chest LeadsSlurred Terminal Portion of QRS Complex Slurred Terminal Portion of QRS Complex (Epsilon Wave)(Epsilon Wave)

A ventricular tachycardia with a left bundle pattern and superioA ventricular tachycardia with a left bundle pattern and superior axis from the same r axis from the same patient. LAO, left anterior oblique.patient. LAO, left anterior oblique.



NONNON--ISCHEMICISCHEMICArrhythmogenic Arrhythmogenic RV DysplasiaRV Dysplasia



NONNON--ISCHEMICISCHEMICArrhythmogenic RV DysplasiaArrhythmogenic RV DysplasiaThe Risk of VT Correlate With The Extent of The Risk of VT Correlate With The Extent of Myocardial InvolvementMyocardial Involvement

Therapy With Sotalol & Amiodarone May be Therapy With Sotalol & Amiodarone May be SuccessfulSuccessful

The Effect of Catheter Ablation is TemporizingThe Effect of Catheter Ablation is TemporizingICD is The Only Reliable Therapy in SCDICD is The Only Reliable Therapy in SCD



NONNON--ISCHEMICISCHEMICInflammatory or Infectious ConditionsInflammatory or Infectious ConditionsSarcoidosisSarcoidosisHeart Block, VT or VFHeart Block, VT or VFAmiodarone or Sotalol Are Most EfficaciousAmiodarone or Sotalol Are Most EfficaciousICD May be NecessaryICD May be Necessary



NONNON--ISCHEMICISCHEMICInflammatory or Infectious ConditionsInflammatory or Infectious ConditionsAcute MyocarditisAcute MyocarditisMonomorphic & Polymorphic VTMonomorphic & Polymorphic VTAntiAnti--arrhythmic & Antiarrhythmic & Anti--inflammatory inflammatory Therapy Are Generally CombinedTherapy Are Generally Combined



NONNON--ISCHEMICISCHEMICInflammatory or Infectious ConditionsInflammatory or Infectious ConditionsChagasChagas’’ Disease (Trypanosoma Cruzi)Disease (Trypanosoma Cruzi)Cardiomyopathy in South & Central USACardiomyopathy in South & Central USAVT & Other Arrhythmias Due to Conduction VT & Other Arrhythmias Due to Conduction System Involvement System Involvement (Pacemaker or ICD)(Pacemaker or ICD)Antiparasitic, CHF, AntiAntiparasitic, CHF, Anti--arrhythmic arrhythmic TreatmentTreatment



TORSADES DE POINTESTORSADES DE POINTESDelayed Myocardial Repolarization, Most Often Delayed Myocardial Repolarization, Most Often Prolonged QT IntervalProlonged QT Interval

The Duration is Typically Brief (< 20 sec), But The Duration is Typically Brief (< 20 sec), But Also May Degenerate to VFAlso May Degenerate to VF

Irregular Ventricular Rate in Excess of 200 bpmIrregular Ventricular Rate in Excess of 200 bpmPolymorphic Structure With An Undulating Polymorphic Structure With An Undulating Twist (QRS) Around An IsoelectricalTwist (QRS) Around An Isoelectrical AxisAxis



TORSADES DE POINTESTORSADES DE POINTES



TORSADES DE POINTESTORSADES DE POINTESCongenitalCongenital

AcquiredAcquired



TORSADES DE POINTESTORSADES DE POINTESCongenitalCongenital



TORSADES DE POINTESTORSADES DE POINTESAcquiredAcquiredDrug Induced (Most Often)Drug Induced (Most Often)Electrolyte AbnormalitiesElectrolyte AbnormalitiesHypothyroidismHypothyroidismCerebrovascular EventsCerebrovascular EventsMI or IschemiaMI or Ischemia



TORSADES DE POINTESTORSADES DE POINTESAcquiredAcquiredStarvation DietsStarvation DietsOrganophosphate PoisoningOrganophosphate Poisoning

MyocarditisMyocarditisSevere CHFSevere CHFMVPMVP



TORSADES DE POINTESTORSADES DE POINTESDrug Induced (Most Often)Drug Induced (Most Often)

Class IA Drugs (Most Often)Class IA Drugs (Most Often)Class III Drugs (Less Often) & IbutilideClass III Drugs (Less Often) & IbutilidePhenothiazines, Haloperidol, TCAPhenothiazines, Haloperidol, TCAAntibiotics Antibiotics (Macrolides(Macrolides & Antihistamines Combination, & Antihistamines Combination, TMP/SMX)TMP/SMX)Antihistamines Combination With AzolesAntihistamines Combination With Azoles



TORSADES DE POINTESTORSADES DE POINTESBradycardiaBradycardia

In Patients With Prolonged QTIn Patients With Prolonged QT

Ionic Contrast MediaIonic Contrast MediaPromotility AgentsPromotility Agents

CisaprideCisapride



TORSADES DE POINTESTORSADES DE POINTESElectrolyte AbnormalitiesElectrolyte AbnormalitiesHypokalemia (Most Reliably Linked)Hypokalemia (Most Reliably Linked)HypomagnesemiaHypomagnesemiaHypocalemia (Rare)Hypocalemia (Rare)



TORSADES DE POINTESTORSADES DE POINTESCerebrovascular EventsCerebrovascular EventsSAH (Most Notably)SAH (Most Notably)ICH (Transient for Weeks)ICH (Transient for Weeks)



TORSADES DE POINTESTORSADES DE POINTESTreatmentTreatmentPrompt DCC in Sustained, Hemodynamic Compromise Prompt DCC in Sustained, Hemodynamic Compromise

Situation (50J Situation (50J -- 100J, up to 360J)100J, up to 360J)Correction of Electrolytes (K>4; Mg>2; Ca)Correction of Electrolytes (K>4; Mg>2; Ca)MgSO4: 1MgSO4: 1--2 gm Bolus With All 22 gm Bolus With All 2--4 gm in 104 gm in 10--15 Minutes15 MinutesIsoproterenol IVD or TVP in Bradycardia; Occasionally Isoproterenol IVD or TVP in Bradycardia; Occasionally

ßß--Blocker, LydocaineBlocker, Lydocaine

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