治疗心律失常的药物

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1、Anti-arrhythmicdrugsDrIslaMackenzieClinicalLecturerClinicalPharmacologySeminarContentPhysiologyofnormalcardiacrhythmDefinitionandmechanismsofarrhythmiasClassificationofdrugstotreatarrhythmiasImportantanti-arrhythmicdrugs(mechanismandpharmacologicalcharacteristics

2、)ArrhythmiasinclinicalpracticePhysiologyofcardiacrateandrhythmCardiacmyocytesareelectricallyexcitableRestingintracellularvoltageofmyocardialcellsisnegative-90mV(SAnodeis-40mV)Restingstate-K+insideandNa+outsidecell(Na+/K+pump)ActionpotentialoccurswhenNa+entersthec

3、ellandsetsupadepolarisingcurrentStimulationofasinglemusclefibrecauseselectricalactivitytospreadacrossthemyocardiumPhasesofactionpotentialofcardiaccellsPhase0rapiddepolarisation(inflowofNa+)Phase1partialrepolarisation(inwardNa+currentdeactivated,outflowofK+)Phase2

4、plateau(slowinwardcalciumcurrent)Phase3repolarisation(calciumcurrentinactivates,K+outflow)Phase4pacemakerpotential(SlowNa+inflow,slowingofK+outflow)‘autorhythmicity’Refractoryperiod(phases1-3)Phase4Phase0Phase1Phase2Phase30mV-80mVIIIIIIIVSinusrhythmSinoatrialnode

5、iscardiacpacemakerNormalsinusrhythm60-100beats/minDepolarisationtriggersdepolarisationofatrialmyocardium(‘forestfire’)ConductsmoreslowlythroughAVnodeConductsrapidlythroughHisbundlesandPurkinjefibresSinusrhythmSinoatrialratecontrolledbyautonomicnervoussystemParasy

6、mpatheticsystempredominates(M2muscarinicreceptors)Sympatheticsystem(ß1receptors)Increasedheartrate(positivechronotropiceffect)IncreasedautomaticityFacilitationofconductionofAVnodeECGRecordingofelectricalactivityoftheheartNetsumofdepolarisationandrepolarisationpot

7、entialsofallmyocardialcellsP-QRS-TpatternP-atrialdepolarisationQRS-ventriculardepolarisationT-ventricularrepolarisationDefinitionofarrhythmiaCardiacarrhythmiaisanabnormalityoftheheartrhythmBradycardia–heartrateslow(<60beats/min)Tachycardia–heartratefast(>100beats

8、/min)ClinicalclassificationofarrhythmiasHeartrate(increased/decreased)Heartrhythm(regular/irregular)Siteoforigin(supraventricular/ventricular)ComplexesonECG(na