OfficialreprintfromUpToDate

www.uptodate.com2017UpToDate

Mechanisms,causes,andevaluationoforthostatichypotension

Authors: HoracioKaufmann,MD,NormanMKaplan,MD
SectionEditor: MichaelJAminoff,MD,DSc
DeputyEditor: JanetLWilterdink,MD

Alltopicsareupdatedasnewevidencebecomesavailableandourpeerreviewprocessiscomplete.
Literaturereviewcurrentthrough:Jun2017.|Thistopiclastupdated:Feb02,2015.

INTRODUCTIONWhenautonomicreflexesareimpairedorintravascularvolumeismarkedlydepleted,a
significantreductioninbloodpressureoccursuponstanding,aphenomenontermedorthostatichypotension.
Orthostatichypotensioncancausedizziness,syncope,andevenanginaorstroke.

Symptomaticfallsinbloodpressureafterstandingoreatingareafrequentclinicalproblem.Theprevalenceof
orthostatichypotensionvariesfrom5to20percentindifferentreports.Manydisorderscancauseorthostatic
hypotension,whichcanalsobeasymptomofacuteorchronicvolumedepletionaswellasasideeffectofdrugs,
particularlyantihypertensives.Arelatedproblem,postprandialhypotension(afallinbloodpressureoccurring15
to90minutesaftermeals)isalsocommoninoldersubjects.

Chronicorthostaticintolerancedescribestheassociationoflightheadedness,dizziness,faintness,orsyncope
thatoccurswithprolongedstandingoruprightposture.Thesesymptomsmaybesometimesassociatedwithan
exaggeratedtachycardiabutlittleornofallinbloodpressure,adisorderthatiscalledtheposturaltachycardia
syndrome(POTS).

Thistopicwillreviewthepathogenesisandcausesoforthostaticandpostprandialhypotension.Thetreatmentof
thesesyndromesisdiscussedseparately.POTSisalsodiscussedseparately(See"Treatmentoforthostaticand
postprandialhypotension"and"Posturaltachycardiasyndrome".)

NORMALBLOODPRESSURERESPONSETOSTANDINGAssumptionoftheuprightpostureresultsinthe
poolingof500to1000mLofbloodinthelowerextremitiesandsplanchniccirculation,whichinitiatesthe
followingsequence[1]:

Arapiddecreaseinvenousreturntotheheart

Theensuingreductioninventricularfillingresultsindiminishedcardiacoutputandbloodpressure

Thefallinbloodpressureandthoracicvolumeprovokesacompensatoryreflexinvolvingthecentraland
peripheralnervoussystemsthatincreasessympatheticandreducesparasympatheticoutflow(ie,
baroreceptorreflex).

Theincreaseinsympatheticoutflowraisesperipheralvascularresistance,venousreturn,andcardiacoutput,
therebylimitingthefallinbloodpressure.

Becauseofthesecompensatorymechanisms,normally,assumptionoftheerectpostureleadstoasmallfallin
systolicbloodpressure(5to10mmHg),anincreaseindiastolicbloodpressure(5to10mmHg)andanincrease
inpulserate(10to25beatsperminute).

Inpatientswithorthostatichypotension,oneormoreofthesecompensatorymechanismsfails,leadingtoa
declineinbloodpressurewithassumptionofuprightposture.(See'Diagnosis'below.)
EPIDEMIOLOGYANDRISKFACTORSThereportedprevalenceoforthostatichypotensionvarieswithage
andtheclinicalsetting[1].

Orthostatichypotensionismorecommonintheelderlydue,atleastinpart,toimpairedbaroreceptorsensitivity
[25].Epidemiologicsurveyshavefoundposturalhypotensioninasmanyas20percentofpatientsoverage65
[69].IntheCardiovascularHealthstudy,forexample,theprevalenceoforthostatichypotensionwas18percent
insubjectsage65yearsorolder,althoughonly2percentweresymptomatic(definedasdizzinesswithstanding)
[6].Therewasamodestassociation(oddsratio1.4to1.9)withsystolichypertensionwhensupine,carotid
stenosisgreaterthan50percent,andtheuseoforalhypoglycemicagents.Therewasonlyaweakassociation
withtheuseofbetablockersandnoassociationwithotherantihypertensivedrugs(includingdiuretics).

However,otherstudieshavefoundtheuseofantihypertensivemedicationstoberelatedtoposturalhypotension
intheelderly[7,10].Otherdrugsassociatedwithposturalhypotension,especiallyintheelderly,arevasodilators,
includingnitratesandcalciumchannelblockers,antidepressants(tricyclicsandphenothiazines),opiates,and
alcohol(table1).

Orthostatichypotensionisacommonreasonfor,orcontributorto,hospitalizationinelderlypatients.Areportfrom
theNationwideInpatientSampleestimatedanorthostatichypotensionhospitalizationrateof233per100,000
patientsover75yearsofage,withamedianlengthofstayofthreedaysandanoverallinhospitalmortalityrate
of0.9percent[2].Amongvariousinpatientseries,theprevalenceoforthostatichypotensioninelderlypatientsis
ashighas60percent[11,12].

Orthostatichypotensioncanalsooccurinyoungerandmiddleagesubjects,who,intheabsenceofvolume
depletion(duetodiuretics,hemorrhageorvomiting),usuallyhavechronicautonomicfailure.

ETIOLOGIESManydisorderscancauseposturalhypotension,withthetwomajormechanismsbeing
autonomicfailure(whichcanbecausedbymultipledisorders)andvolumedepletion.Inaddition,reflexsyncope
(alsoreferredtoasvasovagalorneurallymediatedsyncope)causesacuteposturalhypotensionduetoa
transient,paroxysmaldysfunctionoftheautonomicnervoussystem[13,14].(See"Reflexsyncopeinadults:
Clinicalpresentationanddiagnosticevaluation".)

Whenautonomicreflexesareimpaired,bloodpressurefallsprogressivelyafterstandingbecausethe
gravitationalpoolingofbloodinthelegscannotbecompensatedbysympatheticvasoconstriction.Patientswith
severeintravascularvolumedepletionmayexperienceorthostatichypotensiondespitenormalautonomic
reflexes.

Therelativefrequenciesofvariouscausesoforthostatichypotensionvaryaccordingtothesetting.Uptoforty
percentofpatientshavenodefinitecause[3,15].Inonestudyfromatertiarycenterof100consecutivepatients
withmoderatetosevereposturalhypotension[15]:

27percenthadprimaryautonomicfailure,includingmultiplesystematrophyandPAF
35percenthadsecondaryautonomicfailure,suchasdiabeticneuropathyorparaneoplasticautonomic
failure
38percenthadnoevidenceofgeneralizedautonomicdysfunction
Theuseofantidepressantdrugswasfoundtobeamajoroverlookedcause

AutonomicfailureAutonomicfailureisadisorderofnoradrenergicneurotransmissioninwhichpostganglionic
sympatheticneuronsdonotreleasenorepinephrineappropriately.Subnormalnorepinephrinereleaseresultsin
impairedvasoconstrictionandreducedintrathoracicvascularvolume,bothofwhichcontributetoorthostatic
hypotension.Theabsenceofanappropriatereflexinducedincreaseinheartrateasthebloodpressurefallsisa
usefulclinicalcluetothepresenceofautonomicfailurehoweverthepresenceofaheartrateincreasedoesnot
excludeautonomicfailure.(figure1).Heartrateusuallydecreasesduringreflexsyncope[13].(See'Reflex
syncope'below.)

Theneurodegenerativediseasesthatmostoftenproduceclinicallyimportantautonomicdysfunctionarethe
synucleinopathies,agroupofdiseaseswithabnormalaccumulationoftheproteinalphasynucleininneuronsand
glia.Severaltypesofneuropathymayalsocauseautonomicdysfunction.

NeurodegenerativediseaseAutonomicdysfunctionisacommonclinicalfeatureofthesynucleinopathies,
whicharecharacterizedpathologicallybycytoplasmicneuronal(Lewybodies)orglialinclusionscontainingalpha
synucleinfoundinthebrainandperipheralautonomicnervesofaffectedpatients[16].Theseincludethe
following:

Parkinsondisease(PD)presentswithmotorabnormalitiesandvaryingdegreesofautonomicfailure.(See
"ClinicalmanifestationsofParkinsondisease",sectionon'Autonomicdysfunction'.)

DementiawithLewybodies(DLB)presentswithcognitiveimpairmentwhichisaccompaniedby
parkinsonismandautonomicdysfunction.(See"ClinicalfeaturesanddiagnosisofdementiawithLewy
bodies",sectionon'Autonomicdysfunction'.)

Multiplesystematrophy(MSA,ShyDragersyndrome)affectsthecentralautonomicsystembutspares
peripheralautonomicneuronsandhastwophenotypes:parkinsonianandcerebellar,bothwithprominent
autonomicfailure[17].(See"Multiplesystematrophy:Clinicalfeaturesanddiagnosis".)

Pureautonomicfailure(PAF,BradbuyEgglestonsyndrome)presentswithidiopathicperipheralautonomic
failureasthesoleclinicalfinding.Whileorthostatichypotensionisthemostcommonpresentingfeature,
impotence,urinaryandgastrointestinalsymptomsmayoccuraswell.

SomesmallnumberofpatientswithPAFmayprogresstodevelopPDorDLB[18],butPAFusually
progressesgradually,respondswelltotherapy,andhasasubstantiallybetterprognosisthanPDorDLB
[19].

NeuropathiesAutonomicfailurecanresultfromperipheralneuropathiesorfromautoimmuneblockadeof
ganglionicautonomictransmission:

Smallfiberperipheralneuropathiescanaffectpostganglionicautonomicnervesandcauseautonomic
dysfunction[16].Orthostatichypotension,rarelythepresentingfeature,usuallydevelopsalongwithorafter
distalneuropathicpainand/orsensoryloss,erectiledysfunction,andurinaryorgastrointestinalsymptoms.

Diabetesisthemostcommoncauseofautonomicneuropathythedurationorseverityofdiabetesdoesnot
correlatewiththedevelopmentofthissyndrome.Amyloidosis,Sjogrensyndromeandothercollagen
vasculardisorders,renalfailure,B12deficiency,toxins,certaininfections(syphilis,Lyme,HIV,Chagas),
sarcoidosis,andporphyriaareothercausesofautonomicneuropathy[2022].(See"Clinicalmanifestations
anddiagnosisofdiabeticpolyneuropathy"and"Overviewofpolyneuropathy".)

Prominentautonomicsymptoms,includingorthostatichypotension,canbeafeatureofacuteinflammatory
demyelinatingpolyneuropathy(GuillainBarresyndrome)aswell.(See"GuillainBarrsyndromeinadults:
Clinicalfeaturesanddiagnosis".)

Autoimmuneautonomicimpairmentwithganglionicnicotinicacetylcholinereceptor(nAChR)autoantibodies
(autoimmuneautonomicganglionopathy)isusuallyassociatedwithsubacute(lessthanthreemonths)
clinicalonsetofdysautonomia.Inadditiontoorthostatichypotension,patientsalsohavedryeyesanddry
mouth,severeuppergastrointestinaldysautonomia,largepupilsthatreactpoorlytolightand
 accommodation,andneurogenicbladder[23,24].Thereisusuallynoobjectivesensorylossormotoror
reflexchanges.Patientsareyoungtomiddleagedadultsandaremorelikelytobefemalethanmale(ratio
2:1).Otherautoimmunedisordersmaybepresent.DetectionofthenAChRantibodiesconfirmsthe
diagnosis.Thisdisordermayimprovebutrarelyremitswithtreatment(plasmaexchange,intravenous
immunoglobulin).

ParaneoplasticautonomicneuropathyoccurscommonlyinassociationwithantiHuantibodies(alsoknown
astype1antineuronalnuclearantibodyANNA1),mostofteninpatientswithsmallcelllungcancer,butit
canbeseeninothermalignancies.AlsoassociatedwithparaneoplasticautonomicneuropathyarePurkinje
cellcytoplasmicantibodiestype2(PCA2)andantibodiestotheneuroncytoplasmicprotein,collapsin
responsemediatorprotein5(CRMP5).ThenAChRantibodiesdiscussedabovearesometimes
paraneoplasticaswell[25].Bowelhypomotility,intestinalobstruction,bladderdysfunction,orthostatic
hypotension,pupillomotorandsudomotordysfunctionandxerophthalmiaareprominentclinicalfindings.
(See"Paraneoplasticsyndromesaffectingperipheralnerveandmuscle",sectionon'Paraneoplastic
autonomicneuropathy'.)

Familialdysautonomia(RileyDaysyndrome)isahereditarysensoryandautonomicneuropathy(HSANtype
3)expressedatbirthwithimpairedpainandtemperaturesensation,alongwithautonomicdysfunctiondueto
afferentbaroreflexfailure.Patientsexperiencerecurrenthypertensiveepisodesandexcessivesweating
combinedwithorthostatichypotension.(See"Hereditarysensoryandautonomicneuropathies",sectionon
'HSAN3(Familialdysautonomia)'.)

VolumedepletionAcuteorsubacutevolumedepletion(duetodiuretics,hyperglycemia,hemorrhage,or
vomiting)isusuallyaneasilyrecognizablecauseoforthostatichypotension.

Chronichypovolemia,afrequentfeatureofautonomicfailureexacerbatesorthostaticsymptoms.Normally,
norepinephrineincreasessodiumreabsorptionintheproximaltubule[26].Thisisanappropriateresponseto
minimizesodiumlosseswhenreductionsineffectivecirculatingbloodvolumestimulatereflexsympathetic
activity.Thus,areductioninsympatheticactivity,asinautonomicfailure,willincreaseurinarysodiumexcretion
untilanewsteadystateisachievedatalowerplasmavolume[27].(See"Generalprinciplesofdisordersofwater
balance(hyponatremiaandhypernatremia)andsodiumbalance(hypovolemiaandedema)",sectionon
'Regulationofeffectivearterialbloodvolume'.)

MedicationsOrthostatichypotensionisacommonsideeffectofmedications.Manymedicationscancauseor
exacerbateorthostatichypotensionthroughavarietyofmechanisms,includingperipheralvasodilation,
autonomicdysfunction,andvolumedepletion.Apartiallistisprovidedinthetable(table1)[28].

AgingInadditiontotheaboveautonomicdisorders,adecreaseinbaroreceptorsensitivityisassumedtobe
involvedinthemilder,frequentformofposturalhypotensionseeninelderlypatients.

Onestudy,forexample,showedadiminishedresponseintheolderpatientstotilt(abaroreceptormediated
response)butnottononbaroreceptormediatedstimulisuchasthecoldpressortestorisometricexercise
[29].Thereducedbaroreceptorresponseintheelderly(whencomparedtoyoungercontrols)wasseenin
bothhypertensiveandnormotensivesubjects.

Anotherstudy,measuringbloodpressureandheartrateresponsestoValsalvamaneuver,foundthatboth
thevagalandadrenergiccomponentsofthebaroreceptorreflexbecamebluntedwithincreasingage,each
independentoftheother[4].

OthersOrthostatichypotensionmayalsobeaclinicalfeatureofcardiacpumpfailure(aorticstenosis,
pericarditis/myocarditis,arrhythmias)[28].
Theclinicalfeaturesofadrenalinsufficiency(andlesscommonlypheochromocytoma)mayalsoinclude
orthostatichypotension[28].(See"Clinicalmanifestationsofadrenalinsufficiencyinadults",sectionon
'Hypotension'.)

RELATEDCONDITIONS

PostprandialhypotensionInpostprandialhypotension,bloodpressurefallsoccurwithinonetotwohours
afterameal[1].

Postprandialhypotensionisalsocommoninoldersubjectsandinpatientswithdiabetesanddifferenttypesof
autonomicfailure[30].Amongelderlyresidentsofnursinghomes,forexample,24to36percenthavea20
mmHgorgreaterfallinsystolicbloodpressurewithin75minutesaftereatingameal[31].Inanotherseriesof
401consecutiveelderlypatientswithhypertensionreferredtoanoutpatientcardiologyclinic,73percentwere
foundtohavea20mmHgorgreaterfallinsystolicbloodpressurewithintwohoursafterameal[32].

Theetiologyofpostprandialhypotensionisnotunderstoodcompletely.Affectedpatientshaveinadequate
sympatheticcompensationtomealinducedpoolingofbloodinthesplanchniccirculation,leadingtoimpaired
maintenanceofcardiacoutputandsystemicvascularresistance[31].Otherpossiblecontributorsinclude
vasodilatationinducedbyinsulinorvasoactivegastrointestinalpeptides.

ReflexsyncopeOrthostatichypotensionoccursacutelyandtransientlyinreflexsyncope.Vasovagal,
neurocardiogenic,carotidsinushypersensitivity,andsyncopeassociatedwithmicturitionanddefecationare
examplesofreflexsyncope.

Theclinicalsyndromeofreflexsyncopediffersfromthatofautonomicfailure.Inthelatter,sympatheticefferent
activityischronicallyimpaired,anduponstanding,bloodpressurealwaysfalls.Incontrast,inreflexsyncope,the
failureofsympatheticefferentvasoconstrictortraffic(andhypotension)occursepisodicallyandtypicallyin
responsetoatrigger(emotionalstress,painfulornoxiousstimuli,etc).Duringreflexsyncope,concomitantwith
withdrawalofsympatheticefferentactivity,parasympathetic(vagal)activityincreases,slowingtheheart(figure1)
[13].Thepathogenesisandclinicalfeaturesofvasovagalandotherreflexsyncopesarediscussedseparately.
(See"Reflexsyncopeinadults:Clinicalpresentationanddiagnosticevaluation".)

PosturaltachycardiasyndromeandchronicorthostaticintoleranceChronicorthostaticintolerance(COI)
isthetermusedtodescribetheassociationoflightheadedness,dizziness,faintness,orsyncopethatoccurswith
prolongedstandingoruprightposture.

Youngerpatientshavebeendescribedwithchronicorthostaticintolerancewhodevelopavarietyofsymptoms
suchasfatigue,lightheadedness,exerciseintolerance,andcognitiveimpairmentwithassumptionoftheupright
position.Thesesymptomsareassociatedwithanexaggeratedtachycardiabutlittleornofallinbloodpressure.
Thisdisorderhasbeencalledtheposturaltachycardiasyndrome(POTS).POTSisdiscussedseparately.(See
"Posturaltachycardiasyndrome".)

SYMPTOMSSymptomsoforthostatichypotensiontypicallyoccurinresponsetosuddenposturalchange,but
alsoinassociationwithmeals,exertion,andprolongedstanding[16].Symptomsresultfromcerebral
hypoperfusionandincludegeneralizedweakness,sensationsdescribedasdizzinessorlightheadedness,visual
blurringordarkeningofthevisualfieldsand,inseverecases,lossofconsciousness(syncope).Lessfrequently,
orthostatichypotensionleadstoanginaorstroke.

Complaintslesseasilyrecognizedashypotensiveinorigin,suchasgeneralizedweakness,fatigue,cognitive
slowing,legbuckling,andvisualblurring,mayalsooccur.Neckpainandheadachelocalizedinthesuboccipital,
posteriorcervical,andshoulderregion(the"coathangerheadache"),arereportedbyin50to90percentof
patientsaccordingtodifferentcaseseries[3335].
Symptomsoforthostatichypotensionvaryinseverityfrommildtoincapacitatingseverelyafflictedpatientsare
unabletoleavethesupinepositionwithoutexperiencingpresyncopeorsyncope[36,37].Inrarecases,
orthostatichypotensionhasbeenlinkedtocardiovascularandcerebrovascularevents[6,38,39].Incontrast,
somepatientswithorthostatichypotensionareasymptomatic.

Manypatientswithposturalhypotension,particularlythosewhohaveunderlyingautonomicdysfunction,have
systolichypertensionwhenseatedorsupine[6,7,40].

DIAGNOSISPostural(orthostatic)hypotensionisdiagnosedwhen,withintwotofiveminutesofquietstanding
(afterafiveminuteperiodofsupinerest),oneorbothofthefollowingispresent[1]:

Atleasta20mmHgfallinsystolicpressure
Atleasta10mmHgfallindiastolicpressure

Theheartratenormallyrisesimmediatelyonstanding.Theabsenceofanappropriatereflexinducedincreasein
heartrateasthebloodpressurefallsisausefulclinicalcluetothepresenceofautonomicfailurehoweverthe
presenceofaheartrateincreasedoesnotexcludeautonomicfailure.Anincreaseinheartrateof>30bpm
suggestsposturaltachycardiasyndrome,whichusuallydoesnotincludeorthostatichypotension.(See"Postural
tachycardiasyndrome".)

Aphenomenonofdelayedorthostatichypotensionhasalsobeendescribed.Inonestudy,108of230patients
investigatedwithtilttabletestinghadabnormaltestresults[41].Inmorethanhalfofthese,orthostatic
hypotensionoccurredafterfiveminutesoftilt,andin40percentitoccurredafter10minutes.Thesepatientshad
milderabnormalitiesofsympatheticadrenergicfunction,suggestingthepossibilitythatthisphenomenonmaybe
amilderorearlierformofimpairment.

EVALUATIONAdiagnosticevaluationinpatientswithdocumentedorthostatichypotension(see'Diagnosis'
above)focusesonidentifyingtreatableconditionswhichmaybecausativeorcontributory.Importantfeaturesto
elicitinahistoryandexaminationinclude[42]:

Detailedmedicationlist,prescriptionandnonprescription.Someofthemedicationsassociatedwith
orthostatichypotensionareshownintheTable(table1)

Recentmedicalhistoryofpotentialvolumeloss(vomiting,diarrhea,fluidrestriction,fever).

Medicalhistoryofcongestiveheartfailure,malignancy,diabetes,alcoholism.

Evidenceonneurologichistoryandexaminationofparkinsonism,ataxia,peripheralneuropathyor
dysautonomia(eg,abnormalpupillaryresponse,historyofconstipationorerectiledysfunction)

Laboratorytesting(hematocrit,electrolytes,bloodureanitrogen,creatinine,glucose)andanelectrocardiogram
shouldbeobtainedinselectedpatientstoevaluateforunderlyinganemiaordehydrationorheartdisease,when
thereisreasontosuspecttheseconditions,orwhenthecauseoforthostatichypotensionisotherwiseunclear.

Whenthehistoryorexaminationsuggestsaneuropathy(distalsensoryloss,areflexia),electromyographyand
nerveconductionstudiesmaybeusefultocharacterizetheabnormality.However,normalnerveconduction
studiesdonotexcludeasmallfiberneuropathy,whichisassociatedwithautonomicdysfunction.Fastingblood
sugar,syphilisserology,serumproteinelectrophoresis,andothertestingmaybeusedtoidentifytheunderlying
cause.(See"Overviewofpolyneuropathy",sectionon'Diagnosticevaluation'.)

Noninvasiveautonomictesting,includingbeattobeatbloodpressureandheartratechangesinducedby
Valsalvamaneuverorotherstandardizedstimuli,aswellasmeasurementsofplasmanorepinephrineandits
responsetostanding,canbeobtainedtoascertainabnormalautonomicfunctioninpatientswithorthostatic
hypotension(thusdistinguishingthemfromthosewithvolumedepletionorseverephysicaldeconditioning)andto
localizethesiteofabnormality.Detailedautonomictestingisnotwidelyavailablebutcanbeusefulin
documentinganunderlyingdysautonomiaandestablishprognosis.Regardlessofthecause,treatmentof
orthostatichypotensionissymptomatic.(See"Treatmentoforthostaticandpostprandialhypotension".)

Evenafterextensiveevaluation,uptoonethirdofpatientswillhavenoidentifiedcause[3].

COMPLICATIONSAccordingtoseveralpopulationbasedstudies,orthostatichypotensionisariskfactorfor
cardiovascularandallcausemortality,usuallyduetounderlyingcausesandassociateddiseases[20,39,4349].
Aprospectivestudyusingambulatorybloodpressuremonitoringin374olderadults(age70.2+/8.5years)
foundthatsystolicorthostatichypotensionwasastrongpredictoroffuturecardiovascularevents(HR=2.4)[50].
Orthostatichypotensionhasalsobeenlinkedtoariskofcongestiveheartfailure[5153]andtoincidentalatrial
fibrillation[54].

Orthostatichypotension,particularlywhensymptomatic,cancausefalling,whichhassignificantassociated
morbidity,particularlyinafrailelderlypopulation[8,55].Inonestudyofoldernursinghomeresidentspatients,
orthostatichypotensionwasassociatedwithanincreasedriskofrecurrentfalls(RR=2.6)[56].

Someinvestigatorshavequestionedwhetherorthostatichypotensionproducescognitivedeclineintheabsence
ofanassociatedneurodegenerativecondition.Thepresumedmechanismisneuronalinjuryfromchronicor
repeatedepisodesofcerebralhypoperfusion.Onestudyfoundthatorthostatichypotensionwasassociatedwith
periventricularwhitematterlesionburden[57],whichinturnisamarkerofvascularcognitiveimpairmentinsome
studies.(See"Etiology,clinicalmanifestations,anddiagnosisofvasculardementia",sectionon'Whitematter
lesions'.)Studiesexamininganassociationbetweenorthostatichypotensionandcognitivedeclineordementia
havehadconflictingresults,perhapsasaresultofvaryinglengthsoffollowupandthedifferentcognitive
measuresusedintheirstudies[5862].

Orthostatichypotension,particularlywhendisabling,isassociatedwithimpairedqualityoflife.Whileanxiety,
depressionandotherpsychosocialproblemsappeartobeassociatedwithorthostatichypotension,thedirection
ofapossiblecausalrelationshipisunclearandmaybemediatedinpartbymedications[6365].

INFORMATIONFORPATIENTSUpToDateofferstwotypesofpatienteducationmaterials,TheBasicsand
BeyondtheBasics.TheBasicspatienteducationpiecesarewritteninplainlanguage,atthe5thto6thgrade
readinglevel,andtheyanswerthefourorfivekeyquestionsapatientmighthaveaboutagivencondition.These
articlesarebestforpatientswhowantageneraloverviewandwhoprefershort,easytoreadmaterials.Beyond
theBasicspatienteducationpiecesarelonger,moresophisticated,andmoredetailed.Thesearticlesarewritten
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Basicstopics(see"Patienteducation:Orthostatichypotension(TheBasics)")

SUMMARYANDRECOMMENDATIONS

Orthostatichypotensionismorecommoninolderpatientsandmayaffectupto20percentofpatientsover
theageof65years.(See'Epidemiologyandriskfactors'above.)

Orthostaticandpostprandialhypotensionarefeaturesofautonomicdysfunctionthatmayresultfromcertain
neurodegenerativediseasesaffectingthecentralandperipheralnervoussystemaswellascertain
 peripheralneuropathies.(See'Autonomicfailure'above.)

Orthostatichypotensionmayresultfromvolumedepletion(duetodiuretics,hemorrhageorvomiting).(See
'Volumedepletion'above.)

Theuseofantihypertensiveandothermedications(table1)oftencontributestoposturalhypotension,
particularlyintheelderly.(See'Medications'above.)

Patientswithreflexsyncope,outsidetheacuteevent,havenormalbloodpressureresponsetostanding.
Patientswithposturaltachycardiasyndromecomplainofsymptomsthataresimilartothoseoforthostatic
hypotension,butarenotassociatedwithposturalhypotensiononexamination.(See'Relatedconditions'
aboveand'Posturaltachycardiasyndromeandchronicorthostaticintolerance'above.)

Symptomsoforthostatichypotensionoccurinresponsetoposturalchange(sometimesexacerbatedby
recentmeal,heat,exertion)andincludegeneralizedweakness,sensationsdescribedasdizzinessor
lightheadedness,visualblurringordarkeningofthevisualfieldsand,inseverecases,lossofconsciousness
(syncope).Somepatientswithorthostatichypotensionareasymptomatic.(See'Symptoms'above.)

Postural(orthostatic)hypotensionisdiagnosedwhen,withintwotofiveminutesofquietstanding(afterafive
minuteperiodofsupinerest),oneortwoofthefollowingispresent:(See'Diagnosis'above.)

Atleasta20mmHgfallinsystolicpressure

Atleasta10mmHgfallindiastolicpressure

Adiagnosticevaluationinpatientswithdocumentedorthostatichypotensionfocusesonidentifyingtreatable
conditionswhichmaybecausativeorcontributory,inparticularmedicationsandpotentialvolumeloss.(See
'Evaluation'above.)

Orthostatichypotensionisariskfactorforcardiovascularandallcausemortality,cancausefallsand
attendantmorbidity,andisassociatedwithcomorbidpsychiatricsymptoms.(See'Complications'above.)

ACKNOWLEDGMENTTheeditorialstaffatUpToDate,Inc.wouldliketoacknowledgeDr.RoyFreeman,who
contributedtoanearlierversionofthistopicreview.

UseofUpToDateissubjecttotheSubscriptionandLicenseAgreement.

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Topic5103Version17.0
GRAPHICS

Examplesofdrugsthatcancauseorexacerbateorthostatichypotension

Alcohol

Alphablockers:Terazosin(eg)

Antidepressantdrugs:Selectiveserotoninreceptorreuptakeinhibitors,trazodone,monoamineoxidaseinhibitors,
tricyclicantidepressants

Antihypertensivedrugs:Sympatheticblockers(eg)

Antiparkinsonismdrugs:Levodopa,pramipexole,ropinirole(egs)

Antipsychoticdrugs:Olanzapine,risperidone(egs)

Betablockerdrugs:Propranolol(eg)

Diureticdrugs:Hydrochlorothiazide,furosemide(egs)

Musclerelaxantdrugs:Tizanidine(eg)

Narcoticanalgesicdrugs:Morphine(eg)

Phosphodiesteraseinhibitors:Sildenafil,tadalafil(egs)

Sedatives/hypnoticdrugs:Temazepam(eg)

Vasodilatordrugs:Hydralazine,nitroglycerin,calciumchannelblockers(egs)

Reproducedwithpermissionfrom:PerlmuterLC,SardaG,CasavantV,MosnaimAD.Areviewoftheetiology,associated
comorbidities,andtreatmentoforthostatichypotension.AmJTher201320:279.DOI:10.1097/MJT.0b013e31828bfb7f.
Copyright2013WoltersKluwerHealth,LippincottWilliams&Wilkins.Unauthorizedreproductionofthismaterialis
prohibited.

Graphic89955Version6.0
Heartrateandbloodpressurepatternsobservedinheaduptilttable
testing

Shownaretheheartrateandbloodpressureresponsesseenduringtilttabletestinginpatients
withvariousetiologiesofsyncope,includingautonomicfailure,neurallymediatedsyncope,and
posturaltachycardiasyndrome(POTS).Theabsenceofanappropriatereflexinducedincreasein
heartrateasthebloodpressurefallsisausefulcluetothepresenceofautonomicfailure.During
neurallymediatedsyncope,parasympathetic(vagal)activityincreasesasbloodpressure
declines,slowingtheheart.WithPOTS,tilttabletestingtypicallyreproducestheclinical
symptomsinassociationwithaheartrateincrease30beats/minoramaximumheartrate
120beats/minwithinthefirst10minutesthesechangesarenotassociatedwithhypotension.

Graphic56293Version2.0
Contributor Disclosures
Horacio Kaufmann, MD Grant/Research/Clinical Trial Support: Dysautonomia Foundation [Familial
dysautonomia]; National Institutes of Health [Parkinson disease]; US Food and Drug Administration [Multiple
system atrophy]. Consultant/Advisory Boards: Lundbeck [Neurogenic orthostatic hypotension]; AstraZeneca
[MSA]. Norman M Kaplan, MD Nothing to disclose Michael J Amino, MD, DSc Equity Ownership/Stock
Options: Trust, which is independently managed by a nancial company. The portfolio may include medical or
drug companies. Janet L Wilterdink, MD Nothing to disclose

Contributor disclosures are reviewed for conicts of interest by the editorial group. When found, these are
addressed by vetting through a multi-level review process, and through requirements for references to be
provided to support the content. Appropriately referenced content is required of all authors and must conform to
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