抗心律失常药物的离子流机制和临床应用进展Case1(病例1)QuestionforCase1(病例1)QuestionBasicElectrophysiologyNa+IRelationshipbetweenVolatge-dependentIonChannelStatusesandActionPotentialINa-mediatedactionpotentials(钠通道介导的动作电位,restingmembranepotential<-70mV):fastphase0upstrokeandconductionvelocitythatissuppressedbyINablockers.Atria,His-Purkinjeconductiontissues,ventricles,accessorypathways;ICa,L-mediatedactionpotentials(钙通道介导的动作电位,restingmembranepotential>-60mV):slowphase0upstrokeandconductionvelocitythatissuppressedbyICa,Lblockers.SinusandAVnodes.HeartElectricalSystemandActionPotentialFeaturesIonicCurrentsandDiseasesGenesisofCardiacArrhythmiasThewavelength=conductionvelocityxrefractoryperiodTricuspidormitralvalvesarealsotheelectricalobstacles.Canareentry(circusmovement)arrhythmiaoccuralongthetricuspidormitralvalves?AntiarrhythmicEffectsonReentryArrhythmiascanbepotentiallyArchivedviatheFollowingMechanismsCase2(病例2)QuestionforCase2(病例2)VaughanWilliamsClassificationofAntiarrhythmicDrugsEffectsOfAntiarrhythmicDrugClassesOnTheECGClinicalApplicationsofClassIAntiarrhythmicDrugsASpecificSideEffectAssociatedwiththeSodiumChannelBlockersCase3(病例3)ECG1ofCase3(病例3)SBPwasabout80mmHg,shewasalert;Intravenousamiodaronewasgiven.ECG2ofCase3(病例3)CardiacArrhythmiaSuppressionTrial(CAST)Case4(病例4)ECG2ofCase4(病例4)atERECGTracing3ofCase4(病例4)10minutesafterInitiationofIntravenousDiltiazemQuestionofCase4(病例4)QuestionCellularMechanismsResponsibleforSTSegmentElevationEffectofQuinidineintheJWaveSyndromeTheRolesofIto-mediatedEpicardialAPSpikeandDomeinSTSegmentElevationandVFduringAcuteMyocardialInfarctionBeta-adrenergicBlockersClassIIIAntiarrhythmicDrugsQuestion2ofCase2(病例2)Amiodarone–PartIAmiodarone–PartIIASpecificSideEffectAssociatedwithIKrBlockadeTdPAssociatedwithQTProlongingAgentsAllTdPswereinitiatedbyanR-on-Tectopicbeat.Thereisnoexception!EarlyAfterdepolarization(EAD)+EnhancedTransmuralDispersionRepolarization(TDR)ClassIVAntiarrhythmicdrugs(Non-dihydropyridineCalciumChannelBlockers)“Ideal”AntiarrhythmicDrugs