高血压危象(英文版)-课件

高血压危象（英文版）PPT高血压危象（英文版）PPT1SCOPEofthePROBLEMHypertensionisanincreasinglyimportantmedicalandpublichealthissue.Theprevalenceofhypertensionincreaseswithadvancingagetothepointwheremorethanhalfofpeopleaged60to69yearsoldandapproximatelythree-fourthsofthoseaged70yearsandolderareaffectedDatafromobservationalstudiesinvolvingmorethan1millionindividualshaveindicatedthatdeathfrombothischemicheartdiseaseandstrokeincreasesprogressivelyandlinearlyfromBPlevelsSCOPEofthePROBLEMHypertensi2高血压危象(英文版)-课件3Definitionsandclassificationofbloodpressurelevels(mmHg)Definitionsandclassification4FactorsinfluencingprognosisFactorsinfluencingprognosis5FactorsinfluencingprognosisFactorsinfluencingprognosis6大家学习辛苦了，还是要坚持继续保持安静大家学习辛苦了，还是要坚持继续保持安静7高血压危象(英文版)-课件8High/VeryhighrisksubjectsHigh/Veryhighrisksubjects9BloodpressuremeasurementBloodpressuremeasurement10Positionstatement:AmbulatoryandhomeBPmeasurementPositionstatement:Ambulatory11JNC–VIIGuidelines

JNC–VIIGuidelines

12高血压危象(英文版)-课件13PatientcharacteristicsassociatedwithresistanthypertensionPatientcharacteristicsassoci14SecondarycausesofresistanthypertensionSecondarycausesofresistant15MedicationthatcaninterferewithbloodpressurecontrolMedicationthatcaninterfere16ConditionsfavouringuseofsomeantihypertensivedrugsversusothersConditionsfavouringuseofso17CompellingandpossiblecontraindicationstouseofantihypertensivedrugsCompellingandpossiblecontra18HypertensiveCrisisDefinitions-IsThis:ACrisis?AnEmergency?

AnUrgency?…ClinicalPresentationsTreatmentsHypertensiveCrisisDefinitions19OtherTerminologySeverelyelevatedBP(JNCVII)DefinedasBP>180/120“acceleratedHPT”termusedtodescribeindividualswithchronichypertensionwithassociatedgroup3Keith-Wagener-Bakerretinopathy“malignantHPT”describethoseindividualswithgroup4KWBretinopathychanges+papilledemaOtherTerminologySeverelyelev20Definitions

HypertensiveCrisisHypertensiveEmergency………1-2hoursRapid/progressiveendorgandamageHypertensiveUrgency………….24-48hrsInc.BPwithoutevidenceofendorgandamageUncontrolledHypertension……..1weekDonotrequireacuteinterventionShaynePH-AnnEmergMed-01-APR-2003;41(4):513-29Definitions

HypertensiveCrisi21HypertensiveEmergency

HypertensiveencephalopathyIntracerebralbleedAcuteMIAcuteCHFwithpulmedemaUnstableanginaAorticdissectionEclampsiaTx:parenteralagentBP>180/120withevidenceoftargetorgandysfunctionHypertensiveEmergency

Hyperte22CerebrovascularHypertensiveEmergenciesCerebralInfarctIntracerebralHemorrhageCerebralEdemaHypertensiveEncephalopathyCerebrovascularHypertensiveE23CerebralPerfusionPressureCerebralbloodflowafunctionofCPPAutoreg.Failsat25%ofMAPICP CPPVulnerableto MAPCBF=bloodflow;CPP=cerebralperfusionpressure;ICP=intracranialpressure;MAP=meanarterialpressure;TCA=totalcirculatoryarrest.CerebralPerfusionPressureCer24HypertensiveEncephalopathyPathophysiology:-LossofCerebralAutoregulationofbloodflowresultinginhyperperfusionofthebrain,lossofintegrityofthebloodbrainbarrier,andvascularnecrosis.LossofAutoregulationoccursataconstantcerebralbloodflowofaboveMAP150to160mmHg.AcuteOnsetReversibleHypertensiveEncephalopathyPat25HypertensiveEncephalopathySymptoms:Headache,Nausea/Vomiting,Lethargy,Confusion,Lateralizingneurologicalsymptomsthatarenotofteninananatomicaldistribution.Signs:Papilledema,RetinalHemorrhagesDecreasedlevelofconsciousness,ComaFocalneurologicalfindingsHypertensiveEncephalopathySym26HypertensiveencephalopathyClinicalmanifestationofcerebraledemaandmicrohemorrhagesseenwithdysfunctionofcerebralautoregulationDefinedasanacuteorganicbrainsyndromeordeliriuminthesettingofseverehypertensionHypertensiveencephalopathyCli27HPTEncephalopathyNotadequatelytreated–cerebralheamorrhage,comaanddeath.BUTwithpropertreatment–completely

reversibleClinicaldiagnoses(exclusion)HPTEncephalopathyNotadequate28ManagementofHypertensiveEncephalopathyReduceMeanArterialPressure(MAP)by20to25%(T.397)anddonotexceedthiswithinfirst30to60min.Rosenrecommendsreductionof30to40%(R.1759)MAP=1/3(SBP-DBP)+DBPTreatmentReducesvasospasmthatoccursatthesehighpressuresAvoidexcessiveBPreductiontopreventhypoperfusionofthebrainandfurthercerebralischemiaManagementofHypertensiveEnc29HypertensiveEncephalopathyCerebraloverperfusionMAPoverwhelmsautoregulationVasodilationandInc.Perm.CerebralEdemaHemorrhage,Coma,DeathTx:Nipride,Fenoldopam, Labatalol,NicardipineHypertensiveEncephalopathyCer30HemorrhagicCVA

causesHypertensiveVascularDiseaseArteriovenousAnomalies(AVM)ArterialAneurysmsTumorsTraumaHemorrhagicCVA

causesHyperten31HemorrhagicCVAManagementHemorrhagicCVA’scommonlyresultsinaprofoundreactiveriseinbloodpressureManagementisCONTROVERSIAL.SubarachnoidHemorrhage:oralnimodipine(nimotop)60mgpoq4hourstoreversevasospasm.Nicardipine:2mgIVbolusesfollowedbyanIVinfusionof4to15mg/hrisusedbysometotreatSubarachnoidHemorrhage.HemorrhagicCVAManagementHemo32IschemicCVAPathophysiology:ElevatedBloodPressurecanbethecauseofthecentralnervoussystemevent,OR,itmaybeanormalphysiologicresponse(Cushing’sReflex)IschemicCVAPathophysiology:33IschemicCVAManagementFavorsloweringMAP(meanarterialpressure)by20%.RecommendsIVLabetalolinsmalldosesof5mgincrementsIFDiastolicBloodPressureishigherthan140mmHg.(T.398)IschemicCVAManagement34HPTRetinopathyHPTRetinopathy35AVcrossingchangesAVcrossingchanges36HPTretinopathyHPTretinopathy37HPTretinopathyHPTretinopathy38CardiovascularHypertensiveEmergenciesAorticDissectionCongestiveHeartFailureAcuteMICardiovascularHypertensiveEm39CongestiveHeartFailurePathophysiology:IncreasedAfterloadwithdecreasedCardiacOutputCongestiveHeartFailurePathop40CHF/PulmonaryEdemaSymptoms:

ShortnessofBreath,Cough,ChestPainLowerExtremitySwellingSigns:

JugularVenousDistension,Rales,S3GallopHepatomegaly,PedalEdemaCHF/PulmonaryEdemaSymptoms:41CHF/PulmonaryEdemaTreatment:DiureticsNitroglycerinVasodilatorsDigitalisBeta-adrenoceptoragonistsOtherpositiveinotropicagentsCHF/PulmonaryEdemaTreatment42AcuteCoronarySyndromePathophysiology:-Increasedafterload,cardiacworkload,andmyocardialoxygendemand-DecreasedcoronaryarterybloodflowAcuteCoronarySyndromePathoph43

AcuteCoronarySyndrome/

AcuteMISymptoms:

ChestPain,Nausea/Vomiting,Diaphoresis,ShortnessofBreath

Signs:

CongestiveHeartFailureSigns,S4Gallop(duetodecreasedventricularcompliance)FewphysicalfindingsinmanypatientsClinicalHistoryisveryImportant

AcuteCoronarySyndrome/

Ac44AcuteCoronarySyndrome/

AcuteMIImmediateBloodPressurereductionisindicatedtopreventMyocardialDamageNospecificDefinedBPtarget

Management:NitroglycerinIVorSublingualBetaBlockers(Esmolol,Lopressor)NitroglycerinisDrugofChoiceAcuteCoronarySyndrome/

Acute45AorticDissectionPathophysiology:-AtheroscleroticVascularDisease,ChronicHypertension,increasedshearingforceonthethoracicaorta,leadingtointimaltear.-50%begininascendingaorta-30%ataorticarch-20%indescendingaortaAorticDissectionPathophysiolo46DissectionofThoracicAorta

Symptoms:Chestpainradiatingtotheback(classicpresentation)NeurologicalSymptoms(carotidarterydissection)Angina(coronaryarterydissection)Shortnessofbreath(aorticinsufficiency,cardiactamponade)Signs:-DifferentialBloodPressure(inUE)Bruit(interscapular)NeurologicalDeficitsAcuteCardiacTamponade(rare)DissectionofThoracicAorta 47DissectionofThoracicAortaOptimalBloodPressureinthesepatientsisundefinedandmustbetailoredforeachpatient,however,SBPof120-130mmHgmaybeaintialstartingpoint.(T.408)DissectionofThoracicAorta48AcuteRenalFailurePathophysiology:HypertensiveGlomerulonephropathy,AcuteTubularNecrosis-WorseningrenalfunctioninthesettingofseverehypertensionwithelevationofBUN/CR,proteinuria,orthepresenceofredcellsandredcellcastsintheurine.AcuteRenalFailurePathophysio49AcuteRenalFailureSymptoms:-ManytimestherearefewactualsymptomsFacialorPeripheralEdemaduetofluidoverloadorproteinuriamaybepresent,shortnessofbreathSigns:FewfindingsunlessedematousPulmonaryEdemaAcuteRenalFailureSymptoms:50AcuteRenalFailureManagement:NitroprussideisagentofchoiceDialysis(asneeded)LasixtoenhanceSodiumexcretion;AlsorecommendsNitroprussideorNifedipineNitroglycerinisalsoagoodagentinthissettingsinceitishepaticallymetabolizedandgastrointestinallyexcreted.AcuteRenalFailureManagement:51Preeclampsia/EclampsiaPathophysiology:Systemicarterialvasoconstriction(includingplacental,leadingtodecreaseduterinebloodflow).DefinedasSBP=140/90mmHgorgreater,ORa20mmHgriseinSBPor10mmHgriseinDBPfrombaselineandevidenceofHELLPSyndromePreeclampsia/EclampsiaPathop52Preeclampsia/EclampsiaSymptoms:lowerextremityswelling,headache,confusion,seizures,comaSigns:edema,hyperreflexia,elevationofbloodpressurerelatedtobaselineBPpriortopregnancy(elevationmaybemild125/75)Management:IVMagnesiumSulfate,Hydralazine.MayalsousenifedipineorlabetalolDeliveryofFetusisdefinitivetreatmentofpre-eclampsiaPreeclampsia/EclampsiaSympto53Treatmentofacuteseverehypertensioninpreeclampsia

Treatmentofacuteseverehype54PheochromocytomaPathophysiology:-AlphaandBetastimulationofthecardiovascularsystemduetoadrenergicexcessstatesSymptoms:EpisodicHeadaches,flushing,tremor,diaphoresis,diarrhea,hyperactivity,andpalpitationsSigns:Tachycardia,tachypnea,tremor,hyperdynamicstate(highoutputCHF)PheochromocytomaPathophysiolog55PheochromocytomaManagement:AlphaBlockerFIRST,followedbyaBetaBlockerPhentolamine(alpha)+Esmolol(beta)LabetalolIV(combinedalphaandbetablockade)PheochromocytomaManagement:56PharmacologicAgents

HypertensiveEmergenciesRapidOnsetRapidMaximaleffectRapidoffsetEaseofTitrationParenteralAgentsPharmacologicAgents

Hypertens57ParenteraldrugsfortreatmentofhypertensiveemergenciesParenteraldrugsfortreatment58OralRegimensforTreatmentofHypertensive

UrgencyintheED

Clonidine:0.1to0.2mgPO,repeat0.1mgqhourtodesiredBPreductionormaxof0.7mg.Labetalol:200to400mgPO,repeatevery2to3hoursCaptopril:25mgPOLosartan:50mgPO

OralRegimensforTreatm59KeyConcepts AcuteEnd-organdamagedetermineshypertensiveemergencyBefamiliarwiththeagentsofchoiceinspecificemergenciesGoalformostiscarefulreductionofMAPby20-25%overminutestohoursDBPnotlessthan100to110Except:Pregnancy,Dissection,MI,Patientswithoutacuteend-organischemiararelyrequireurgentinterventionKeyConcepts AcuteEnd-organd60高血压危象（英文版）PPT高血压危象（英文版）PPT61SCOPEofthePROBLEMHypertensionisanincreasinglyimportantmedicalandpublichealthissue.Theprevalenceofhypertensionincreaseswithadvancingagetothepointwheremorethanhalfofpeopleaged60to69yearsoldandapproximatelythree-fourthsofthoseaged70yearsandolderareaffectedDatafromobservationalstudiesinvolvingmorethan1millionindividualshaveindicatedthatdeathfrombothischemicheartdiseaseandstrokeincreasesprogressivelyandlinearlyfromBPlevelsSCOPEofthePROBLEMHypertensi62高血压危象(英文版)-课件63Definitionsandclassificationofbloodpressurelevels(mmHg)Definitionsandclassification64FactorsinfluencingprognosisFactorsinfluencingprognosis65FactorsinfluencingprognosisFactorsinfluencingprognosis66大家学习辛苦了，还是要坚持继续保持安静大家学习辛苦了，还是要坚持继续保持安静67高血压危象(英文版)-课件68High/VeryhighrisksubjectsHigh/Veryhighrisksubjects69BloodpressuremeasurementBloodpressuremeasurement70Positionstatement:AmbulatoryandhomeBPmeasurementPositionstatement:Ambulatory71JNC–VIIGuidelines

JNC–VIIGuidelines

72高血压危象(英文版)-课件73PatientcharacteristicsassociatedwithresistanthypertensionPatientcharacteristicsassoci74SecondarycausesofresistanthypertensionSecondarycausesofresistant75MedicationthatcaninterferewithbloodpressurecontrolMedicationthatcaninterfere76ConditionsfavouringuseofsomeantihypertensivedrugsversusothersConditionsfavouringuseofso77CompellingandpossiblecontraindicationstouseofantihypertensivedrugsCompellingandpossiblecontra78HypertensiveCrisisDefinitions-IsThis:ACrisis?AnEmergency?

AnUrgency?…ClinicalPresentationsTreatmentsHypertensiveCrisisDefinitions79OtherTerminologySeverelyelevatedBP(JNCVII)DefinedasBP>180/120“acceleratedHPT”termusedtodescribeindividualswithchronichypertensionwithassociatedgroup3Keith-Wagener-Bakerretinopathy“malignantHPT”describethoseindividualswithgroup4KWBretinopathychanges+papilledemaOtherTerminologySeverelyelev80Definitions

HypertensiveCrisisHypertensiveEmergency………1-2hoursRapid/progressiveendorgandamageHypertensiveUrgency………….24-48hrsInc.BPwithoutevidenceofendorgandamageUncontrolledHypertension……..1weekDonotrequireacuteinterventionShaynePH-AnnEmergMed-01-APR-2003;41(4):513-29Definitions

HypertensiveCrisi81HypertensiveEmergency

HypertensiveencephalopathyIntracerebralbleedAcuteMIAcuteCHFwithpulmedemaUnstableanginaAorticdissectionEclampsiaTx:parenteralagentBP>180/120withevidenceoftargetorgandysfunctionHypertensiveEmergency

Hyperte82CerebrovascularHypertensiveEmergenciesCerebralInfarctIntracerebralHemorrhageCerebralEdemaHypertensiveEncephalopathyCerebrovascularHypertensiveE83CerebralPerfusionPressureCerebralbloodflowafunctionofCPPAutoreg.Failsat25%ofMAPICP CPPVulnerableto MAPCBF=bloodflow;CPP=cerebralperfusionpressure;ICP=intracranialpressure;MAP=meanarterialpressure;TCA=totalcirculatoryarrest.CerebralPerfusionPressureCer84HypertensiveEncephalopathyPathophysiology:-LossofCerebralAutoregulationofbloodflowresultinginhyperperfusionofthebrain,lossofintegrityofthebloodbrainbarrier,andvascularnecrosis.LossofAutoregulationoccursataconstantcerebralbloodflowofaboveMAP150to160mmHg.AcuteOnsetReversibleHypertensiveEncephalopathyPat85HypertensiveEncephalopathySymptoms:Headache,Nausea/Vomiting,Lethargy,Confusion,Lateralizingneurologicalsymptomsthatarenotofteninananatomicaldistribution.Signs:Papilledema,RetinalHemorrhagesDecreasedlevelofconsciousness,ComaFocalneurologicalfindingsHypertensiveEncephalopathySym86HypertensiveencephalopathyClinicalmanifestationofcerebraledemaandmicrohemorrhagesseenwithdysfunctionofcerebralautoregulationDefinedasanacuteorganicbrainsyndromeordeliriuminthesettingofseverehypertensionHypertensiveencephalopathyCli87HPTEncephalopathyNotadequatelytreated–cerebralheamorrhage,comaanddeath.BUTwithpropertreatment–completely

reversibleClinicaldiagnoses(exclusion)HPTEncephalopathyNotadequate88ManagementofHypertensiveEncephalopathyReduceMeanArterialPressure(MAP)by20to25%(T.397)anddonotexceedthiswithinfirst30to60min.Rosenrecommendsreductionof30to40%(R.1759)MAP=1/3(SBP-DBP)+DBPTreatmentReducesvasospasmthatoccursatthesehighpressuresAvoidexcessiveBPreductiontopreventhypoperfusionofthebrainandfurthercerebralischemiaManagementofHypertensiveEnc89HypertensiveEncephalopathyCerebraloverperfusionMAPoverwhelmsautoregulationVasodilationandInc.Perm.CerebralEdemaHemorrhage,Coma,DeathTx:Nipride,Fenoldopam, Labatalol,NicardipineHypertensiveEncephalopathyCer90HemorrhagicCVA

causesHypertensiveVascularDiseaseArteriovenousAnomalies(AVM)ArterialAneurysmsTumorsTraumaHemorrhagicCVA

causesHyperten91HemorrhagicCVAManagementHemorrhagicCVA’scommonlyresultsinaprofoundreactiveriseinbloodpressureManagementisCONTROVERSIAL.SubarachnoidHemorrhage:oralnimodipine(nimotop)60mgpoq4hourstoreversevasospasm.Nicardipine:2mgIVbolusesfollowedbyanIVinfusionof4to15mg/hrisusedbysometotreatSubarachnoidHemorrhage.HemorrhagicCVAManagementHemo92IschemicCVAPathophysiology:ElevatedBloodPressurecanbethecauseofthecentralnervoussystemevent,OR,itmaybeanormalphysiologicresponse(Cushing’sReflex)IschemicCVAPathophysiology:93IschemicCVAManagementFavorsloweringMAP(meanarterialpressure)by20%.RecommendsIVLabetalolinsmalldosesof5mgincrementsIFDiastolicBloodPressureishigherthan140mmHg.(T.398)IschemicCVAManagement94HPTRetinopathyHPTRetinopathy95AVcrossingchangesAVcrossingchanges96HPTretinopathyHPTretinopathy97HPTretinopathyHPTretinopathy98CardiovascularHypertensiveEmergenciesAorticDissectionCongestiveHeartFailureAcuteMICardiovascularHypertensiveEm99CongestiveHeartFailurePathophysiology:IncreasedAfterloadwithdecreasedCardiacOutputCongestiveHeartFailurePathop100CHF/PulmonaryEdemaSymptoms:

ShortnessofBreath,Cough,ChestPainLowerExtremitySwellingSigns:

JugularVenousDistension,Rales,S3GallopHepatomegaly,PedalEdemaCHF/PulmonaryEdemaSymptoms:101CHF/PulmonaryEdemaTreatment:DiureticsNitroglycerinVasodilatorsDigitalisBeta-adrenoceptoragonistsOtherpositiveinotropicagentsCHF/PulmonaryEdemaTreatment102AcuteCoronarySyndromePathophysiology:-Increasedafterload,cardiacworkload,andmyocardialoxygendemand-DecreasedcoronaryarterybloodflowAcuteCoronarySyndromePathoph103

AcuteCoronarySyndrome/

AcuteMISymptoms:

ChestPain,Nausea/Vomiting,Diaphoresis,ShortnessofBreath

Signs:

CongestiveHeartFailureSigns,S4Gallop(duetodecreasedventricularcompliance)FewphysicalfindingsinmanypatientsClinicalHistoryisveryImportant

AcuteCoronarySyndrome/

Ac104AcuteCoronarySyndrome/

AcuteMIImmediateBloodPressurereductionisindicatedtopreventMyocardialDamageNospecificDefinedBPtarget

Management:NitroglycerinIVorSublingualBetaBlockers(Esmolol,Lopressor)NitroglycerinisDrugofChoiceAcuteCoronarySyndrome/

Acute105AorticDissectionPathophysiology:-AtheroscleroticVascularDisease,ChronicHypertension,increasedshearingforceonthethoracicaorta,leadingtointimaltear.-50%begininascendingaorta-30%ataorticarch-20%indescendingaortaAorticDissectionPathophysiolo106DissectionofThoracicAorta

Symptoms:Chestpainradiatingtotheback(classicpresentation)NeurologicalSymptoms(carotidarterydissection)Angina(coronaryarterydissection)Shortnessofbreath(aorticinsufficiency,cardiactamponade)Signs:-DifferentialBloodPressure(inUE)Bruit(interscapular)NeurologicalDeficitsAcuteCardiacTamponade(rare)DissectionofThoracicAorta 107DissectionofThoracicAortaOptimalBloodPressureinthesepatientsisundefinedandmustbetailoredforeachpatient,however,SBPof120-130mmHgmaybeaintialstartingpoint.(T.408)DissectionofThoracicAorta108AcuteRenalFailurePathophysiology:HypertensiveGlomerulonephropathy,AcuteTubularNecrosis-WorseningrenalfunctioninthesettingofseverehypertensionwithelevationofBUN/CR,proteinuria,orthepresenceofredcellsandredcellcastsintheurine.AcuteRenalFailurePathophysio109AcuteRenalFailureSymptoms:-ManytimestherearefewactualsymptomsFacialorPeripheralEdemaduetofluidoverloadorproteinuriamaybepresent,shortnessofbreathSigns:FewfindingsunlessedematousPulmonaryEdemaAcuteRenalFailureSymptoms:110AcuteRenalFailureManagement:NitroprussideisagentofchoiceDialysis(asneeded)LasixtoenhanceSodiumexcretion;AlsorecommendsNitroprussideorNifedipineNitroglycerinisalsoagoodagentinthissettingsinceitishepaticallymetabolizedandgastrointestinallyexcreted.Acut