单纯性高血压

1PrimaryHypertension

LianjunGao,MD,PhDFirstaffiliatedhospitalofDMU2Incidenceofprimaryhypertension(11.9%）IntroductionInChina3SeventhReportoftheJointNationalCommitteeonPrevention,Detection,Evaluation,andTreatmentofHighBloodPressure

JNC7(2003)fromUSA4IntroductionAwareRxControl200230.2%24.7%6.1%199126.6%12.2%2.9%InChina(FROMJNC7)5IncidenceinChinais6.62%;borderlinehypertension5.26%,total:11.9%,indevelopedwesterncountry–--morethan20%.Riskfactorfor---heart,cerebralvasculardiseasesAffectmanyimportantorgans---heart,brain,kidneyEpidemiology6UpdateDataEpidemiology:(2004)morbidityat18.8%.Totalat160million.Onepatient，inthreefamilies.3millionnewsuffering,everyyear.7UpdateDataHazardOneStrokeattackin3mins.OnepatientsdiedforAMIeach11mins.70%,cerebralstroke.20%,withCHD.10%,renaldamage.1.5milliondiedfromhemorrhagicorischemicstrokecausedbyhypertensionperyear.8Definition(WHO/ISH1999)TypeSystolic(mmHg)Diastolic(mmHg)ideal<120and<80normal<130and<85upperlimit130-139or85-89HypertensionGrade1(mild)140-159or90-99sub-group(critical)140-149or90-94Grade2(moderate)160-179or100-109Grade3(severe)≥180or≥110simplicitySBP≥140and<90sub-group(critical)140-149and<909ESH/ESC2003Guideline10ESH/ESC2003Guideline11ESH/ESC2003Guideline12GuidelinesinmeasuringBPPostureSittingpressures---adequateforroutinefollow-up.Ptshouldsitquietlywithbacksupportedfor5minandarmsupportedatlevelofheart

CircumstancesNocaffeineforprecedinghour.Nosmokingforpreceding15min.Noexogenousadrenergicstimulants,e.g.,phenylephrineinnasaldecongestantsoreyedrops.Quiet,warmsetting.

13GuidelinesinmeasuringBPCuffsize(12–13cmlongand35cmwide)Thebladder---encircleandcover2/3ofthelengthofthearm;ifnot,placethebladderoverthebrachialartery;ifbladderistoosmall,spuriouslyhighreadingsmayresult.

Manometer:amercurymanometerNumberofreadings

eachoccasion,takeatleast2readingsseparatedby1-2min.Ifreadingsvarybymorethan5mmHg,takeadditionalreadingsuntil2areclose.Fordiagnosis,obtainatleast3setsofreadingsatleastaweekapart.14GuidelinesinmeasuringBPMeasuringInflatethebladderquicklytoapressure20mmHgabovethesystolic,asrecognizedbydisappearanceoftheradialpulse.Deflatethebladder3mmHgeverysecond.RecordtheKorotkoffphaseV(disappearance).15EtiologyHeredityfactors60%ptshasfamilyhistoryofHTParentswithHT,46%childrendevelopHTEnvironmentalfactorsDiet:excessivesodium,K+intake,lowCa++intake,highproteinintake,alcohol,highlevelofsaturatedfattyacid.Emotionalstress:highbrainwork,noiseOtherfactorsOverweighted,centralobesityControceptivesOSAHS:obstructivesleepapneahypoventilationsydrome16Modulationofbloodpressure

ActivationofRenin-Angiotensin-Aldosteronesystem(RAAS)ActivationofsympatheticnervesystemRenalfluid,natriumretensionAbnormalitiesfunctionofvascularendotheliumInsulinresistance(IR)MechanismsMultiplefactorsareinvolvedinthepathogenesisofessentialhypertension.Severalhypothesesisproposedbutnonofthemcanexplainthemajorityofthehypertensivecases.17Pathogenesis18

Heart:

Concentrichypertrophy,DilatationofLVFinallyHF

Persistentspasmofarteriolesleadstothehypertrophyofitssmoothmusclecoatandeventuallyarterioscleroticchangesofthevessels.Pathophysiology19

Brain:

cerebralthrombosiscerebralinfarctionFormationofmiliaryaneurysmsofsmallarteriesofbrainincreasetheriskofcerebralhemorrhagePathophysiology20

Kidneys:

Renalarterioscleroticchangesimpairmentofrenalfunction,uremia.

Retina:edemahemorrhagePathophysiology21RetinopathyGradeI(Keith,Wagener,andBarker)MildnarrowingoftheretinalarteriesrelativetotheveinsGradeIIModeratesclerosiswithincreasedlightreflexandcompressionofveinsatcrossingsGradeIIIEdema,exudatesandhemorrhages,scleroticandmarkedlyspastic(“silver-wire”)arteriesGradeIVPapilledemaorchokeddisc,extensivehemorrhagesandexudates22Inmostpts----noclinicalmanifestationsotherthantheelevatedpressurefoundinphysicalexamination.Mostcommonsymptoms----Slowinprogressheadache,fatigue,dizziness,insomnia,tinnitus, epistaxis,orblurvision.Clinicalmanifestation23earlyevidencerelatedto‘targetorgans’：

decreasedexercisetoleranceandfatiguenocturiaSymptomsofcardiacawarenesspalpitationsandtachycaradia(maypersistinordinatelylongafterexertionorstress)Clinicalmanifestation24Physicalexaminations

AccentuatedA2,orwithmetallicqualityinelderlypts;S4duetodecreasedventricularcompliance;Systolicejectionsoundattheaorticvalve;LVhypertrophy;

signsandsymptomsofsecondaryHT25Malignant/rapidprogressingHT

Acuteonset,progressivelyDBP≥130mmHg,persistantlyheadache,blurvision,hemorrageofeyebase,edema,prominentrenalinjury:persistentprotein-urea,badprognosis:diedofrenalfailure,strokeorHFPathophysiololgy:fibrinosticnecrosisofrenalartery26

ComplicationsPressurecrisis

Significant↑BP(SBP>260mmHgorDBP>120mmHg)Symptoms:headache,nausea,vomiting,restless,palpitation,sweating,pallororflushappearance,eyeblurredHypertensiveencephalopathy

rapidelevationofBPSymtoms:headache,vomiting,restless,cloudingofconsciousness,epilepticattacks,convulsion,coma27

ComplicationsHeartfailureChronicrenalfailureAorticdissectionlifethreatening.MaybemisdiagnosisasAMIduetoseverechestpain.28TargetRelatedtoacceleratedRelatedtosystemic

organs

atherosclerosisHTitselfHeart anginapectoris,MI HeartfailureBrain TIA,CerebralthrombosisCerebralhemorrhageKidneysNephroateriosclerosisGlomerulosclerosisArteriesarteriosclerosisAorticdissectionComplications29

StratificationofAddedRiskto

QuantifyPrognosisBloodPresureRiskFactorsgrade1grade2grade30LowHigh1~2factorsModerateModerateextremely≥3,orDMHighextremelyortargetorgandamageAssociatedclinicalconditions

extremelyextremelyextremelyHighModerate30LevelsofsystolicanddiastolicBPAge:Men>55years,Women>65yearsSmokingDyslipidaemia

totalcholesterol>6.5mmol/l(250mg/dl)orLDL-cholesterol>4.0mmol/l(155mg/dl)orHDL-cholesterolM<1.0,F<1.2mmol/l(M<40,F<48mg/dl)Riskfactorsforcardiovasculardiseaseusedforstratification31Familyhistoryofprematurecardiovasculardisease

M<55years,F<65yearsAbdominalobesity

abdominalcircumferenceM>102cm,F>88cmC-reactiveprotein>1mg/dlRiskfactorsforcardiovasculardiseaseusedforstratification32LeftventricularhypertrophyElectrocardiogram/echocardiogramUltrasoundevidenceofarterialwallthickeningcarotidIMT>0.9mmoratheroscleroticplaqueSlightincreaseinserumcreatinineM115–133,F107–124μmol/l(M1.3–1.5,F1.2–1.4mg/dl)Microalbuminuria30–300mg/24h;albumin–creatinineratioM>22,F>31mg/g(M>2.5,F>3.5mg/mmol)Targetorgandamage(TOD)33Cerebrovasculardisease:ischaemicstrokecerebralhaemorrhagetransientischaemicattackHeartdisease:CHD----MI;angina;coronaryrevascularization;congestiveheartfailureAssociatedclinicalconditions(ACC)34Renaldisease:diabeticnephropathy;renalimpairment(SCr>133/124mol/l,1.5/1.4mg/dl)proteinuria(>300mg/24h)PeripheralvasculardiseaseAorticdissectionAdvancedretinopathy:haemorrhagesorexudates,papilloedemaAssociatedclinicalconditions(ACC)35Thetermslow,moderate,highandextremelyhighaddedriskarecalibratedtoindicate---anapproximateabsolute10-yearriskofcardiovasculardiseaseof<15%,15–20%,20–30%and>30%,respectively,accordingtoFraminghamcriteria.StratificationofAddedRisktoQuantifyPrognosis36GradeofBP1,2,3gradebasedonBPlevelRiskfactorsofCVDOthercardiacriskfactor:Age,>55(M),>65(F)CholesterolFamilyhistorySmokingObesityDiabetesMellitusTargetorgansdysfunctionAssociatedclinicalconditionsDiagnosis37

DBP≥

90mmHgand/orSBP≥

140mmHgonatleastthreeseparateoccasionsshouldberecordedbeforeclinicalevaluationandtreatmentareinitiated.DiagnosisWhenthediagnosisofHTisestablished----thepossibilityofsecondaryHTshouldbeexcluded

andtheseverityshouldbeassessed.38Oneshouldalwayscomparethefemoralandbrachialarterialpulsationsinasearchforadelayinthepropagationoftheaorticpulsewaveasamanifestationofcoarctationoftheaorta(particularlyinyoungpatients)orforevidenceofatheroscleroticocclusiveprocessesinolderpatients.Renalarterialbruitsonexaminationoftheabdomen,flanks,andbackprovideanimportantsignofrenovascularhypertension.Physicalexamination39Evenbeforecardiacstructureisaltered,palpationmayrevealahyperkineticapicalimpulseandafasterheartrateasevidenceofearlyfunctionalhyperdynamiccardiacchanges.PhysicalexaminationThesmallvesselsoftheopticfundusprovideanexcellentmeanstoassessthedegreeofsystemicvasoconstriction,itshouldbeperformedroutinely.40TheearliestclinicalindexofcardiacinvolvementinHTisleftatrialenlargement,whichmaybesuspectedbyanatrialdiastolicgallop(fourthheartsound).AsventricularhypertrophybecomesmoreevidentbyXray,ECG,orECHO,alouderA2isheard,thefourthheartsoundalmostalwayspresent,andthereispalpablesustainedleftventricularlift.Cardiacexamination41CompletebloodcountUrinalysisBloodsugar,serumelectrolyte(Na,K,Cl)concentsRenalfunction:Crand/orBUNCholesterolconcentrationXray,ECG,ECHOLaboratorystudies42SecondaryhypertensionAsecondarycauseispresentinroughly1-5%oftheHypertensivepopulation.Detectionofaconditionotherthanessentialhypertensionmaydrasticallyalterthepatient’ssubsequentcare.43SleepapneaDrug-inducedorrelatedcausesChronickidneydiseasePrimaryaldosteronismRenovasculardiseaseChronicsteroidtherapyandCushing’ssyndromePheochromocytomaCoarctationoftheaortaThyroidorparathyroiddiseaseSecondaryhypertension44HypertensionpresentingatanatypicalageSuddenappearanceofseverehypertensionatanyageApoorresponsetostandarddrugtreatmentSignificantsymptomsaccompanythehypertensionSecondaryhypertensionCluestothepresenceofasecondarycause45HypertensioninrenalparenchymaldiseaseHypertensionispresentatsomestageinapproximately85%patientswithchronicrenalfailureandisthemostcommonsecondaryhypertension.Itcanbetheinitialmanifestationofasymptomaticchronicrenalparenchymaldisease.Commoncauseofrenalfailure:chronicnephritis,diabeticnephropathy,repeatedurinarytractinfections,calculusformation.Uncommoncauseofrenalfailure:systemiclupuserythematosus,polyarteritisnodosa,scleroderma,polycyctickidney,postrenaltransplant.46HypertensioninrenalparenchymaldiseasePathophysiology:Itisincompletelyunderstoodandprobablyvarieswithdifferentetiologiesofchronicrenalfailure,volumeretention,andabnormalcontroloftherenin-angiotensinsystemappeartobethemostimportantfeatures.Laboratoryinvestigation:Azotemia,proteinuria,anabnormalurinesediment,and/oranemia.ECHO:excludetheobstructiveuropathy,cysticdiseaseofkidney,estimatekidneysizeTreatment:Volume-depletingmeasures(saltrestriction,diuretics,dialysis)arethemainstay.ACEI(captopril,enalapril):initiationoflowdose,usinginpatientswithmildandmoderaterenalfailure47SecondaryHypertension48RenovascularhypertensionEtiology:Atheroscleroticdiseaseoccurswithincreasingfrequencyinolderpatients,FibrousandTakayashu’sdiseaseoftherenalarteriesarecommoninyoungpatientsandthelaterismorecommoninorientalpatients(70%).Incontrastatheroscleroticdiseaseismorecommoninwesterncountry(65%).Pathophysiology:Therenin-angiotensinsystemplayanimportantrole.ItissuggestedbyhighperipheralPRAsandcontractedandnormalplasmavolume.

49RenovascularhypertensionClinicalpresentation:Thepresenceofbruitdeepwithintheabdomenisaparticularlyimportantcluetothepresenceofrenovascularhypertension.Systolicbruitsarecommonlydetected,especiallyinolderpatients,andmaynotbeassociatedwithocclusivearterialdisease;however,whenassociatedwithadiastoliccomponenttothebruitthereisamoresignificantrelationshiptorenalarterialdisease.Laboratoryinvestigation:PRAs,rapid-sequenceintravenouspyelogram,renalarteriographyTreatment:surgery,PTA,medicaltherapy:CCB50PrimaryaldosteronismEtiology:Unilateralaldosteronomaiscommon(60-90%),bilateralhyperplasiaoftheadrenalcortex(10-40%)Pathophysiology:

Thecontinuedsecretionofaldoseroneinthefaceofasaline-inducedinhibitionoftherenin-angiotensinsystempromotessodiumretentionandrenalpotassiumwasting.

51PrimaryaldosteronismClinicalpresentation:

Aninvestigationforprimaryaldosteronismisindicatedforhypertensivepatientswhohavespontaneoushypokalemia(<3mEq/liter)andtherelatedclinicalsymptoms,suchasweaknes