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1 CARDIOVASCULAR PATHOPHYSIOLOGY Hypertension - Sustained increase of systemic arterial (particularly systolic) blood pressure Clinical manifestation § Silent disease in early hypertension i.e. no signs or symptoms § Others have anatomic and physiological damage to brain, eyes, kidney, vessels, heart Diastolic (mmHg) Systolic (mmHg) Normal < 80 < 120 High Normal 80 - 89 120 - 139 Grade 1 (mild) 90 - 99 140 - 159 Grade 2(moderate) 100 - 109 160 - 179 Grade 3 (severe) >110 > 180 § Mean arterial BP = cardiac output x peripheral resistance o MAP = CO x TPVR § Increase BP due to: o Increased cardiac output (= HR x stroke volume) o Increased peripheral resistance (reduced vessel diameter and increased viscosity) § Peripheral resistance- opposition to flow that blood encounters in vessels away from the heart. Depends on two variables: o Blood viscosity “thickness” § RBC count and albumin concentration elevate viscosity the most § Decreased viscosity with anemia and hypoproteinemia speed flow § Increased viscosity with polycythemia and dehydration slow flow § Smoking increase viscosity o Vessel radius – most powerful influence over flow § Vasomotion- change in vessel radius • Vasoconstriction- by muscular effort that results in smooth muscle contraction • Vasodilation- by relaxation of smooth muscle § Two major types of baroreceptors o Arterial or high pressure baroreceptors- fast response – regulates heart rate and blood vessel diameter – located in carotid sinus and aortic arch o Low pressure baroreceptors- slower response – responds to change in blood volume – located in walls of major veins and right atrium of the heart which receives deoxygenated blood from the blood § Volume decreaseà Signals sent to hypothalamus leading to ADH release and water reabsorption

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Page 1: CARDIOVASCULAR PATHOPHYSIOLOGY Hypertension · 5 Etiology of Hypertension § Primary: diagnosis of primary hypertension is one of exclusion- if no secondary causes found o Multiple

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CARDIOVASCULARPATHOPHYSIOLOGYHypertension

- Sustainedincreaseofsystemicarterial(particularlysystolic)bloodpressure

Clinicalmanifestation§ Silentdiseaseinearlyhypertensioni.e.nosignsorsymptoms§ Othershaveanatomicandphysiologicaldamagetobrain,eyes,kidney,vessels,heart

Diastolic(mmHg)

Systolic(mmHg)

Normal <80 <120

HighNormal 80-89 120-139

Grade1(mild) 90-99 140-159

Grade2(moderate) 100-109 160-179

Grade3(severe) >110 >180

§ MeanarterialBP=cardiacoutputxperipheralresistance

o MAP=COxTPVR§ IncreaseBPdueto:

o Increasedcardiacoutput(=HRxstrokevolume)o Increasedperipheralresistance(reducedvesseldiameterandincreasedviscosity)

§ Peripheralresistance-oppositiontoflowthatbloodencountersinvesselsawayfromtheheart.Dependsontwovariables:

o Bloodviscosity“thickness”§ RBCcountandalbuminconcentrationelevateviscositythemost§ Decreasedviscositywithanemiaandhypoproteinemiaspeedflow§ Increasedviscositywithpolycythemiaanddehydrationslowflow§ Smokingincreaseviscosity

o Vesselradius–mostpowerfulinfluenceoverflow§ Vasomotion-changeinvesselradius

• Vasoconstriction-bymusculareffortthatresultsinsmoothmusclecontraction

• Vasodilation-byrelaxationofsmoothmuscle§ Twomajortypesofbaroreceptors

o Arterialorhighpressurebaroreceptors-fastresponse–regulatesheartrateandbloodvesseldiameter–locatedincarotidsinusandaorticarch

o Lowpressurebaroreceptors-slowerresponse–respondstochangeinbloodvolume–locatedinwallsofmajorveinsandrightatriumoftheheartwhichreceivesdeoxygenatedbloodfromtheblood

§ VolumedecreaseàSignalssenttohypothalamusleadingtoADHreleaseandwaterreabsorption

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§ Volumeincreaseàsecretionofatrialnatriureticpeptide(ANP)whichpromoteswaterandsodiumexcretionthroughtheurine

Juxtaglomerularapparatus

§ ifGFRrises:o flowoftubularfluid

increasesandmoreNaClisreabsorbedbythePCT

o maculadensastimulatesJGcellswithaparacrineo JGcellscontractwhichconstrictsafferentarteriole,reducingGFRtonormalOR

§ Mesangialcellsmaycontract,constrictingthecapillariesandreducingfiltration

§ IfGFRfalls:o Macularelaxesafferentarteriolesandmesangialcellso BloodflowincreasesandGFRrisesbacktonormalo ReleaseofreninfromJGcells

§ Myogenicresponse:intrinsicabilityofvascularsmoothmuscletorespondtopressurechanges

Renin-angiotensin-aldosteronepathway

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Atrialnatriureticpeptides

Arterial(HighPressure)Baroreceptors§ Mechanoreceptorthatdetectsthepressure

ofbloodflowingthroughthem,cansendmessagestoCNStoincreaseordecreasetotalperipheralresistanceandcardiacoutput

§ Thefrequencyofafferentimpulsesincreaseswhenthepressureisrisingduringsystoleanddecreaseswhenthepressureisfallingduringdiastole

Controlcentreàmedullaofbrainstem

§ Cardiostimulatorycentre:makestheheartbeatfasterandstrongeràincreasingbloodpressure

§ Cardioinhibitorycentre:slowstheheartdownàdecreasingbloodpressure

§ Vasomotorcentre:clusterofsympatheticneuronsinthemedullathatoverseeschangesinbloodvesseldiameter

o Maintainsbloodvesseltonebyinnervatingsmoothmusclesofbloodvessels,especiallyarterioles

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EtiologyofHypertension§ Primary:diagnosisofprimaryhypertensionisoneofexclusion-ifnosecondarycauses

foundo Multipleriskfactors:

§ Obesity,smoking,genetics(aging,hyperlipidaemia,sleepapnoea),increasebloodviscosity(increasesaltintake,oralcontraceptives)

§ Secondary:duetosystemicdiseasethatraisesperipheralresistanceo Renaldisease-decreasedurineformation,retentionofsodiumandwatero Renovascularhypertension-renalarterystenosis-reducedrenalbloodflowwhich

triggersrenin-angiotensin-aldosteronemechanismo Adrenalglandtumours-excessivealdosteroneproduction-increaseinwaterand

sodiumretentiono Pheochromocytoma-increaseadrenalineo Coarctationoftheaorta-narrowingoftheaorticarch–LVmustgenerategreater

pressureso Drugs-oralcontraceptives,corticosteroids

§ Malignant:morecommoninyoungeradults,esp.AfricanAmericanmen,duringpregnancyandpeoplewithkidneydisordersorcollagenvasculardisorders

o Intensespasmofarteriese.g.cerebralarteries,retinalvessels-swellingofopticnerves

o Suddenandrapiddevelopmentofextremelyhighbloodpressureàmedicalemergency

§ TreatmentofunderlyingcausereversehypertensionHealthconsequences

§ Bloodvessels§ Heart§ Kidneys§ Brain§ Eyes

§ Unmodifiableriskfactors:age,

genetics,gender,race,pregnancy§ Modifiableriskfactors:

§ Diet:reducesodiumintake§ Obesity:loseweight§ Stopsmoking§ Oralcontraceptives-previousstudiesshowedastrongassociationwithriskofstroke§ Treatment-medicationse.g.diuretics,ACEinhibitors,Cachannelblockers,betablockers

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Atherosclerosis§ Progressivedisease-thickeningandhardeningofarteriescausedbyformationoffibrofatty

plaquesthathardenwithtimeànarrowingbloodvesselàdecreaseinbloodflowSitesofsevereatherosclerosis:

CoronaryDisease

Coronaryarterydisease–mostcommoncauseisatherosclerosis

Transientischemia–cellstemporarilydeprivedofoxygen,manifestaspain–associatedwithstress/exercise

Myocardialischemia–cellstemporarilydeprivedofbloodandoxygen,manifestaspain,cardiacarrhythmiasthatmaybefatalàstroke.Embolimayform.

Myocardialinfarction–irreversiblemyocardialdamageandcelldeath(necrosis)duetoprolongedoxygenstarvation.Impairmentofheartandbrainfunction

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Plaque§ Acombinationofcholesterol,otherfattymaterials,calciumandbloodcomponentsthat

sticktothearterywalllining§ Ahardshellorscarcoverstheplaque

Twotypesofplaque§ Unstable-thinfibrouscaps

o Maycompletelyblockthearteryo Canruptureorformcloto Clotmaybreakfreeandbecomeanembolus(anydetached,travellingintravascular

masscarriedbycirculation,capableofcloggingarterialvesselsatasitedistantfromitspointoforigin)

§ Stable-thickfibrouscapso Partiallyblockvesselso Donottendtoformclotsoremboli

Initialtrigger

§ Hypertension:stressonbloodvesselwalls§ Diabetes:disruptionofendotheliumliningofbloodvesselsthatkeepsbloodflowing

smoothlybyproducingnitricoxide(NO)whichrelaxesthesmoothmusclesofthewallstopreventcellsfromstickingtowallsàincreasedformationofplaquesindiabetes

§ Turbulentbloodflow:duetoobstruction§ Smoking-nicotineàdecreaseinnitricoxidelevels§ Infection:e.g.chlamydiapneumoniaemaymanagewallandcausecholesterolaccumulation§ HighcholesterolandLDLlevels:increasefoamcells

Unmodifiableriskfactors

§ Ageandgender

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o Increasedincidenceinmalesandpost-menopausalwomeno Familyhistory-genetic

Modifiableriskfactors

§ Smoking§ Highalcoholintake§ Sedentarylifestyle§ Obesity§ Stress§ TypeIIdiabetes§ Hypertension§ Increasedcholesterol

Clinicalmanifestation-Angina

§ Stableanginao Predictablepatternofintermittentanginaduringexerciseorexcitementrelievedby

resto Usuallystableatheroscleroticplaque

§ Variantorprinzmetalanginao Unpredictablecourse,frequencyanddurationofpainatresto Atherosclerosisusuallypresentbutmaybeabsentand/orvasospasm-cause

unknownbuttheoriesincludehyperactivityofsympatheticsystem,increaseincalciumfluxinarterialsmoothmuscle,impairedproductionorreleaseofvasoconstrictor,disturbancesinproductionofNO

o Painrelievedbynitro-glycerineo Chestpainandshortnessofbreathoftennotpresentwhenwalking/exercising

§ Silentischemiao Nopainassociatedwithischemicevento Highincidenceinassociationwithmentalstresso Autonomicneuropathywithsensorydenervationo Detectedwithstressradionuclideimaging(Thallium201)andECG

§ Unstableanginao Myocardialischemiarangingbetweenstableanginatomyocardialinfarctiono Occursatrestandcanevenwakepeoplefromarestfulsleepo Suddenchestpaino Unpredictablecourse,frequencyanddurationofpaino Usuallyindicatorofatheroscleroticplaquewhichbecomesunstableàinfarctiono Symptomsoftenpersistformorethanafewminuteso Nitro-glycerinefailstorelievethepaino Causedbytheactualruptureofaplaqueinacoronaryartery

Diagnostictechniques

§ Electrocardiogramo STsegmentelevationordepressionandTwaveinversionindicationofMIdueto

tissuedamageleadingtoearlyrepolarisation§ Exercisestresstest

o GradedexercisewheresymptomsobservedplusHR,BPandECGrecorded


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