HD1Cardiology

TheCardiacCycle
I) TheCardiacCycle

A) Stepsinthecycle
1) TheSAnodedepolarizes,triggeringatrialcontraction
a ThisgeneratesthePwaveintheECG
b Thisgeneratestheawaveintheatrialpressurecurve
2) TheAVnodedepolarizes,andbeginstransmittinganimpulsethroughthebundleofHisand
Purkinjesystem
a DepolarizationoftheAVisnotregisteredintheECGduetothesmalltissuemass
3) Astheventriclesdepolarizeandcontract,ventricularpressurerises
a TheQRScomplexisgeneratedintheECG
i TheQRScomplexmasksatrialrepolarization
b Therisingventricularpressureclosesthemitralvalve,generatingthefirstheartsound(S1)
i Thepressureintheventricleissufficienttobulgethemitralvalveintotheleftatrium,
increasingthepressureofthelatterandgeneratingthecwaveintheatrialpressurecurve
c Isovolumiccontractionoccursuntiltheventricularpressurerisesabovetheaorticpressure,at
whichpointtheaorticvalveopensandrapidejectionensues
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4) Rapidejectioncontinuesuntiltheventricularpressurefallsbelowtheaorticpressure,atwhichpoint
theaorticvalvesclose
a Closureoftheaorticvalvesgeneratesthesecondheartsound(S2)
b VentricularrepolarizationgeneratestheTwaveintheECG
c Isovolumicrelaxationcontinuesuntiltheventricularpressurefallsbelowtheaorticpressure,at
whichpointthemitralvalveopensandrapidfillingensues
i Asthepressureintheleftatriumfalls(asaresultofbloodrapidlyflowingintotheleft
ventricle),thenotableydescentoftheatrialvwaveisgenerated
5) Rapidfillingcontinuesuntilthepressuresequalizeand/ordepolarizationoftheSAnoderestartsthe
cycle
B) FeaturesoftheECG
1) Electricalsignals(e.g.depolarization)precedemyocytecontraction,whichprecedesbloodflow
2) Becauseittakestimeforthemyocytestocontract/relax,theincreaseinleftventricularpressure
beginsslightlyaftertheQRScomplexandpersistsaftertheTwave
C) Featuresofthepressurecurves
1) Preloadisestimatedbytheenddiastolicpressureintheleftventricle
2) Afterloadisestimatedbytheaorticsystolicpressure
II) TheHeartSounds
A) S1
1) Representsclosureofthemitral/tricuspidvalves
2) Auscultatedbestattheapex
3) Intensitydependsonseveralfactors
a Leafletmobility
b Positionoftheleafletsattheonsetofcontraction
i Thefurtheraparttheleafletsareattheonsetofcontraction,thelouderS1willbe
o Indicatedinsomepathologies(e.g.shortPRintervalsandmitralstenosis)
c Rateatwhichpressurerisesintheleftventricle
B) S2
1) Representsclosureoftheaortic/pulmonicvalves
2) Auscultatedbestatthebase
3) Physiologicsplitting
a Duringexpiration,theaorticsound(A2)andthepulmonicsound(P2)areseparatedbylessthan
30millisecondsandareheardasasinglesound
b Duringinspiration,theincreasedvenousreturnincreasedfillingoftherightventricleincreased
strokevolumeprolongedrightventricularejectionS2splitting
i Inadults,A2islouderthanP2
4) Abnormallywidesplittingwithnormalrespiratoryvariationsuggestsdelayedpulmonicclosure
a Rightbundlebranchblock,causingdelayeddepolarizationoftherightventricle
b Pulmonarystenosis,mechanicallyprolongingrightventricularsystole
5) Abnormallywidesplittingthatisfixedsuggestsanatrialseptaldefect
6) Paradoxical(reversed)splittingisassociatedwithdelayedaorticvalveclosure
a Leftbundlebranchblock,causingdelayeddepolarizationoftheleftventricle
b Hypertensivecardiovasculardisease,mechanicallyprolongingleftventricularsystole
c Leftventricularfailure,mechanicallyprolongingleftventricularsystole
C) Gallopsounds(S3andS4)
1) S3occurswhenleftatrialpressuredipsbelowleftventricularpressurejustafterthemaximum
pressuregradient
a Associatedwithrapidventricularfilling
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2) S4occursatthepeakoftheawavewhenthereisasuddenincreaseinbloodfillingtheleftventricle
a Associatedwithdiastolicdysfunction(stiffness)oftheventricles
D) Additionalsounds
1) Systolicejectionclicks
a Earlysystole
i Bicuspidaorticvalve
ii Pulmonarystenosis
iii Dilationoftheaorta/pulmonaryartery
b Midsystole
i Systolicmitralvalveprolapse
2) Openingsnapofrheumaticmitralstenosis
a Causedbythestenoticvalvewhenitreachesmaximumexcursion
3) Murmursrepresentstatesofturbulentbloodflow
a Innocentstatesofhighbloodflow
b Aorticstenosis
c Mitralregurgitation
III) PhysicalExaminationoftheCardiacCycle
A) Distentionofjugularveins
1) JVPismeasuredwiththepatientsemisupine(tiltedto3045),takingthemeasurementvertically
fromtheangleofLouis
2) AnormalJVPismeasuredat<8cmofdistention
3) Thea,c,andvwavesoftheatrialpressurecurvecanbeexaminedintherightjugularvein
4) Associatedpathologies
a Aprominentawaverepresentsanincreasedresistancetoatrialflow
i Rightventricularhypertrophycreatesmoreresistanceduetoalesscompliantright
ventricle
ii Tricuspidstenosisresistanceismetatthevalve
b Aprominentvwaverepresentsatypicalventricularsystole
i Tricuspidinsufficiencyregurgitationofbloodthroughthetricuspidvalveincreasesright
atrialpressure
c Aprominentydescentrepresentsconstrictivepericarditis
B) Palpitationoftheprecordium
1) Apicalimpulse
a Normallocationisthe5thintercostalspace,justmedialtothemidclavicularline
b Correspondstothefirst1/3ofsystole
C) Auscultationoftheheart
1) Smaller/lighterbellisusedtohearlowpitchedsounds
a Diastolicmurmurofmitralstenosis
b Galloprhythms(S3andS4)
2) Larger/heavierdiaphragmisusedtohearhighpitchedsounds
a S1andS2
b Ejectionandmidsystolicclicks
c Murmurofaorticregurgitation
3) Murmurswillradiateinthedirectionofflow
a Aorticmurmurswillradiateintotheneck
b Pulmonicmurmurswillradiatetowardstheleftscapula
DistinguishingS1andS2
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S1
Firstoftwogroupedbeats
Precedescarotidpulse
Louderattheapex
Lowerpitchandlongerinduration

S2
Secondoftwogroupedbeats
Followscarotidpulse
Louderatthebase
Higherpitchandshorterinduration

Electrocardiography
I) TheECGLeadSystem
A) PolarityofECGwaveforms
1) Depolarizationmovingtowardsthepositiveterminalofaleadgeneratesapositivewave
a Thedepolarizationwillwritethelargestdeflectionintheleadmostparalleltoitspath
2) Depolarizationmovingawayfromthepositiveterminalofaleadgeneratesanegativewave
3) Depolarizationmovingperpendiculartothepositiveterminalofaleaddoesnotgeneratea
deflection,ratheritisisoelectric
a Thedepolarizationwillwritethesmallestdeflectionintheleadmostperpendiculartoitspath

B) TheQRScomplexanditsvariations

C) ECGelectrodes
1) Bipolarlimbelectrodes
a LeadIrightarmtoleftarm(+0)
b LeadIIrightarmtoleftleg(+60)
c LeadIIIleftarmtoleftleg(+120)

2) Unipolarlimbelectrodes
a aVL=augmentedvoltageattheleftarm(30)
b aVR=augmentedvoltageattherightarm(150)
c aVF=augmentedvoltageattheleftfoot(+90)

3) Thesixchestleads(V1V6)
a Duetoitsincreasedmass,themyocardiumoftheleftventricleisfeaturedmostprominentlyin
theRwaveoftheseleads
i RisnegativeinleadV1
ii RisroughlyequalinthepositiveandnegativedirectionsinV3
iii RispositiveinV6

II) InterpretingaNormalECG

A) Determinationofaxis
1) Theheartaxisshouldbebetween30and+90
2) IftheRwaveinleadsIandIIarebothupright,thentheaxisisnormal
a IftheRwaveineitherleadisnegative,thenthedirectionofthedepolarizationmustoffsetby
morethan90,placingitoutsidethenormalrange
3) Theleadwiththelargestpositivedeflectionisclosesttotheaxis
4) Theaxisis~90awayfromtheleadthatisclosesttoisoelectric
B) Determinationofrhythm
1) Normalsinusrhythm
a EveryPwaveisfollowedbyaQRScomplex
b ThePwaveispositiveinleadsIandII
c 60100cycles/min
i Sinusbradycardiais<60cpm
ii Sinustachycardiais>100cpm
C) Determinationofheartrate
1) Normalheartrateis60100beats/min
2) CalculationusingtheRRinterval
a
3) Estimationusingthenumberofboxes
a EachlargeboxontheECGrepresents200ms
i Eachlargeboxisfurtherdividedintofivesmallboxes,eachrepresenting40ms
b Divide300bythenumberoflargeboxesseparatingtheRRintervaltoarriveatanestimationof
heartrate
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i 3boxesofseparation100bpm
ii 4boxesofseparation75bpm
iii 5boxesofseparation60bpm
D) Measurementofintervals
1) PRinterval(120200ms)
a ProlongedinAVblock
b Shortenedinpreexcitation
2) QRScomplex(100ms)
a Prolongedinbundlebranchandinterventricularblocks
3) CorrectedQTinterval(QTc;<400ms)
a Prolongedinhypokalemia,hypocalcemia,congenitalchannelopathy,anddrugs

III) InterpretingAbnormalECGs
A) Pwaveabnormalities(e.g.leftatrialenlargement)
1) ClassifiedasanegativePwavegreaterthan0.1mVinmagnitude(1smallbox)inleadV1

B) QRSabnormalities
1) Rightventricularhypertrophy
a IncreasedRwaveinleadsoverlyingtherightventricle(i.e.V1andV2)
b Rightaxisdeviation

2) Leftventricularhypertrophy
a IncreasedRwaveinV5andV6
b MorenegativeSwaveinV1andV2
c STsegmentandTwavechangesindicatingstrain

3) Rightbundlebranchblock
a QRS>120ms
b Rightventriculardepolarizationisdelayed,whileleftventriculardepolarizationisunaffected
c RSRwaveforminV1V3(rabbitears)

4) Leftbundlebranchblock
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a
b

QRS>120ms
Leftventriculardepolarizationisdelayed,whilerightventriculardepolarizationisunaffected

5) PathologicQwaves
a Occurwhenascarfromapreviousmyocardialinfarctinpresent
i Infarctedtissuedoesnotgenerateelectricalforces,causingtheoverlyingelectrodetosee
theopposite,leftventricularwall

6) STsegmentandTwaveabnormalitiesfollowingacutemyocardialinfarction

Structure,Imaging,andHeartCatheterization
I) Imaging
A) ChestXray(CXR)
1) Typicallytakenposteriortoanterior(PAfilm)tomorefinelyresolvetheheartandavoidartificial
enlargement
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Rightheartborders
i Aorta(A)
ii Rightatrium
b Leftheartborders
i Aorticknob(AK)
ii Pulmonicartery
iii Leftventricle
o InPAfilms,thelarger,posteriorleftventricleobscuresthesmaller,anteriorright
ventricle
iv Iftheleftatriumisvisibleattheborders,thenitispathologicallyenlarged
c Cardiothoracicratio
i Thecardiothoracicratiocomparesthediameterofthehearttothatofthethoraciccavity
ii Theheartshouldoccupynomorethan50%ofthefield(i.e.,theratioshouldbe<0.5)
2) LateralCXRsareusefulinassessingtherightventricleandretrosternalairspace

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Iftherightventricleoccupiesmorethan1/3oftheretrosternalairspace,thenitis
enlarged/dilated
3) Pulmonaryedema
a Features

i Increasedheartsize(CTratio>0.5)
ii Fluidinpleuralspaceobscuresinferiorborders(liquidisdrawninferiorlybygravity)
iii Pooroxygenationinlowerlungfieldsconstrictsthearteriolesinthatregion,shuntingblood
superiorlyandenlargingvesselsintheupperlungfields
iv BronchiaretypicallyinvisibleonCXR,butmayappearwhenedematousandthickened
v Engorgedlymphaticsmaybepresent
b Etiologies
i Leftheartfailure
ii Mitralstenosisorinsufficiency
iii Increasedintravascularvolume(asseenwithrenalfailure)
B) Echocardiography
1) General
a Echocardiographyusesultrasoundtoconstructimagesbasedofacousticresponses
b Echoisthemostcommonlyusedtechniqueusedassesstheheart
c Dopplerechocanbeusedtoassessbloodflow,valvestenosis,regurgitation,etc.
2) Acousticwindows
a Densematerials(e.g.bone)totallyabsorbsoundwaves
b Airfilledstructures(e.g.lungs)totallyreflectsoundwaves
c Theheartmustbeassessedthroughsofttissuewindows
i Leftparasternalwindow(betweenribs)
ii Apical
iii Subcostal
3) Mmodeechocardiography
a Pulsesarereleasedinrapidsuccession,formingacompositeimageovertime(analogoustoa
video)
b CanrelateechotoECG

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4) Twodimensional(2D)echocardiography
a Alineararrayoftransducersscansasingleplanesimultaneously
b Routinelyusesthreeimagingplanes
i Longaxisplane(apextobase)
ii Shortaxisplane(crosssectionoftheheart)
o Theleftparasternalshortaxiscanbeusedtoviewtheaorticvalveanditsthreeleaflets
o Theleftparasternalshortaxiscanbeusedtoviewanteriorandposteriorpapillary
musclesintheleftventricle
iii Fourchamberplane(transverseview)

5) Calculationoftheejectionfraction
a
C) Singlephotonemissioncomputedtomography(SPECT)
1) Radioisotopesareusedassessmyocardialperfusion
a Thallium201
b Technitium99msestamibi
2) Imageunderseveralconditionstoassessfunctionalperfusion(infarct,inducibleischemia,etc.)
a Rest
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Statesinducingcoronaryvasodilation
i Exercise
ii Adenosineinfusion
Normal
Infarct
Ischemia

UptakeofRadioactiveIndicator
Rest
+

Vasodilated
+

D) Magneticresonanceimaging(MRI)
1) Features
a Asuperconductingmagnetdetectsrelaxinghydrogennuclei
b Doesnotuseionizingradiation
c Distinguishestissuecontrasts
i Canbeenhancedwithgadolinium
E) Computedtomography(CT)
1) Features
a MultipleXrayimagesareassembledintoacomposite
b Contrastcanbeusedtodistinguishbloodcontainingstructures
II) CardiacCatheterization
A) Normalheartcatheterizationpressures(mmHg)

B) Rightheartcatheterization
1) Catheterisplacedthroughtherightfemoralveinorjugularvein
2) Rightatrialpressurecanbeusedtoestimaterightventricularenddiastolicpressure
3) Pulmonarycapillarywedgepressurecanbeusedtoassessleftatrialpressure
a Aballooncatheterisplacedintheleftpulmonicarteryandinflatedtoblockflow
b Eventually,thepressuredistaltotheballoonwillequilibratewiththatoftheleftatrium,andthe
sensorcanregisterthispressure

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C) Leftheartcatheterization
1) Catheterisplacesthroughtherightfemoralartery
D) Catheterassessments
1) Cardiacoutput
a
i VO2isthetotaloxygenconsumption
ii AVO2isthedifferenceinarterialandvenousoxygensaturation
b Cardiacindexisoftenobtainedbydividingthecardiacoutputbybodysurfacearea
i
ii Normalcardiacindicesfallwithintherangeof2.54.2L/min/m2
2) Systemicvascularresistance(SVR)
a
b Normalrangeis7001600dynesseccm5
3) Pulmonaryvascularresistance(PVR)
a
b Normalrangeis20130dynesseccm5
c TheSVRandPVRareparticularlyusefulinassessingpatientsinintensivecare(e.g.sepsis,
shock,etc.)
IschemiaandAngina
I) CoronaryCirculation
A) Myocardiumisflowlimited
1) Myocardialoxygenextractionisnearmaximalatrest(7580%),leavinglittlecapacitytoincrease
extractionfurthertomeetthedemandsofexercise/stress
2) Therefore,theonlymechanismbywhichmyocardialenergydemandscanbemetisbyincreasing
coronaryflow
B)
1) Basalviscousresistance
2) Autoregulatoryresistance
a Coronaryreactivehyperemiareferstoamarked,compensatoryvasodilationfollowingperiodsof
ischemiaorincreasedresistance
b Mediatedbymetabolic,neurogenic,andendothelialvasodilationfactors
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Adenosinehypothesis
i Intimesofintenseworkorischemia,ATPstoresaredepletedand[AMP]rises
ii AMPisfurtherdegradedtoadenosine,whichfreelydiffusesoutofthecell
iii Adenosinethenactsasapotentarteriolarvasodilator,increasingperfusiontothestressed
tissue
3) Compressiveresistance
a Systolecompressesthecoronaryarteriesincreasedresistancedecreasedflow
b Inordertomaintainadequateperfusionoftheendocardialtissues,theresistanceofendocardial
arteriolesmustbelowerthanthatofepicardialarterioles
i Incoronaryarterydisease,coronaryarteriolesbegintodilate(inanefforttoincreaseflow)
ii However,dilationofendocardialarteriolesmaxesoutfirst,andfurtherdilationofthe
epicardialarteriolesbeginstostarvetheendocardium,leadingtosubendocardialischemia
C) Determinantsofoxygendemand
1) Walltension,estimatedby
a P=systolicleftventricularpressure
b d=cavitydiameter
c h=wallthickness
2) Heartrate
3) Contractility
4) Basalmetabolicneeds
II) AnginaPectoris
A) Clinicalfeatures
1) Characteristics
a Diffusevisceralpain(somewhatdifficulttopinpoint)
b 110minutesinduration
c Oftenlocatedinsubsternal,epigastric,orneckregions
d Radiationtoshoulders,innerarm,andjaw
2) Precipitatingevents
a Exercise
b Emotionalstress
3) Aggravatingfactors
a Meals(bloodflowtovisceraincreased)
b Coldtemperatures
c Timeofday
B) Examinationsequelaeofmyocardialischemia
1) Decreasedsystolicfunctiondyskineticapicalimpulse
2) DecreaseddiastoliccomplianceappearanceofS4heartsound,indicatingrapidventricularfilling
a Together,decreasedsystolicanddiastolicfunctionmayproducepulmonarycongestionrales
3) Papillarymuscledysfunctionmitralregurgitation,producingapansystolicmurmur
4) Increasedsympathetictonediaphoresisandtachycardia
5) STsegmentvariationsareevidentintheEKGasischemiaensues
a Iftheleadisoverlyingischemictissue,STsegmentelevationisobserved
b Iftheleadisoverlyinghealthytissuewithdeeperischemia,STsegmentdepressionisobserved
i Inearlycasesofsubendocardialischemia,allleadswillshowSTsegmentdepression
C) Threecategoriesofanginapectoris
1) Classical(Heberden)
a Precipitatedbystress
b Relievedbyrest
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c EKGshowsSTdepression
d Mostcasesareduetocoronaryarterydisease
2) Variant(Prinzmetal)
a Occursatrest(mayhavenormalexercisetolerance)
b Oftencyclicalinonset
c EKGshowsSTelevation
d Mostcasesareduetospontaneousvasospasm
D) Treatment
1) Correctremediablefactors
a Hypertension,smoking,anemia,obesity,aorticvalvedisease,etc.
2) Medicaltherapy
a Aspirin,antihyperlipidemics,nitrates,blockers,calciumchannelblockers
b Seerelevantpharmacologylecturesfordetails
3) Surgicaltherapy
a Revascularization
AcuteCoronarySyndromesI&II
I) EpidemiologyofMyocardialInfarction
A) Over16millionpeopleintheUSAhaveMI/angina
1) 785,000cases/yearwitharecurrencerateof470,000cases/year
2) Additional195,000silentMIcases/year
B) Heartdiseaseistheleadingcauseofmortality
C) Majorriskfactors
1) Hypertension
2) Hypercholesterolemia
3) Tobaccouse
4) Diabetes
5) Obesity
II) PathogenesisofMyocardialInfarction
A) Prerequisites
1) Endothelialinjury
2) Plateletactivation
3) Activationofclottingcascade
4) Failureofendogenousantithromboticmechanisms
5) Formationofatheroscleroticplaque
B) Plaquerupture
1) Triggers
a Stress
b Circadianrhythm(AMIpeaksinearlymorning)
c Sympatheticactivity(exercise,sex,anger,anxiety)
d Anesthesia/surgery
e Infection/inflammation
2) Instigators
a Macrophages(foamcells)
i Degradefibrouscaprupture
ii Producetissuefactor,apowerfulprocoagulant
b Tcells
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i Promotesmoothmusclecellapoptosis
ii Promotemacrophageproliferation
C) Plateletadhesion
1) Plateletsbindtotheexposedcollagenoftheendothelialbasementmembraneandactivate,releasing
severalfactors
a ADP
b Plateletderivedgrowthfactor(PDGF)
c Fibrinogen
d ThromboxaneA2
2) PlateletsaggregatetooneotherviaglycoproteinIIb/IIIa(GPIIb/IIIa)receptorsandfibrinogen
linkers
3) Aplateletplugforms,andthecoagulationcascadeensues
a Seepathologynotesforanoverviewoftheclottingcascade
D) Endogenousantithromboticmechanisms
1) Inactivationofclottingfactors
a AntithrombinIII
i AntithrombinIIIcoupleswithheparinsulfatetoirreversiblyinhibitthrombin
b ProteinCandproteinS
i JointogethertoinactivatefactorsVaandVIIIa
c Tissuefactorpathwayinhibitor
i GeneratedbyfactorXa
ii InhibitsfactorVII
2) Lysisoffibrinclots
a Tissueplasminogenactivator(tPA)
i tPAconvertsplasminogentoplasmin,whichdegradesthefibrinclotintofibrinsplitproducts
3) Endogenousplateletinhibitionandvasodilation
a Prostacyclin
b Endotheliumderivedrelaxationfactornitricoxide(EDRFNO)
E) Formationofcoronarythrombus

III) PathophysiologyofAMI
A) Causes
1) Coronaryatherosclerosis
2) Aorticdissectioninvolvingthecoronaryarteries
3) Vasculitis
4) Coronaryembolism
5) Increasedbloodviscosity(polycythemia,thrombocytosis)
B) Consequences
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1) Themoreextensivethedamage,themorelikelyoneistoexperienceQwaveabnormalities
C) Histologicalchanges

D) Grosspathology
1) TransmuralMI
a Spansthethicknessofthemyocardium
b TypicallyassociatedwithQwaveMI
2) SubendocardialMI
a Injuryislimitedtothesubendocardium
i Subendocardiumisatthegreatestriskforischemia
o Subjectedtothehighestpressurefromtheleftventricle
o Minimalcollateralflow
o Epicardialvesselsneedtopenetratethemyocardium
b TypicallyassociatedwithnonQwaveMI
3) Stunnedmyocardium
a Myocardiumexposedtohypoxicinsultthatcontinuestodemonstrateprolongedsystolic
dysfunctionevenaftercoronaryflowisrestored
b Myocardiumisreversiblyinjured,notnecrotic
4) Hibernatingmyocardium
a Hypocontractilemyocardiumfollowingchronichypoperfusion
b Involvesmultivesselcoronaryarterydisease,throughtheLADisparticularlyvulnerable
5) Ventricularremodeling
a Changeinshape/thicknessofleftventriclefollowingAMI
b Infarctwallexpansion
i Augmentswallstress
ii Impairssystolicfunction
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iii PredisposestoLVaneurysm
c Noninfarctwallexpansionandhypercontractility
i NoninfarctedmyocardiumcompensatesviaFrankStarlingmechanism
IV) DiagnosisofAMI
A) Symptoms
1) Diffusesubsternalchestpainthatisdifficulttolocalize
a Painmayradiatetojawandleftarm
2) Dyspnea
3) Diaphoresisandcool/clammyskin
4) Nausea,vomiting,andweakness
5) Fever
B) Physicalexamfindings
1) Vitalsigns
a Hypotensionandtachycardiamayindicateshock
b Bradycardiamayindicateinferiormyocardialinfarction
c Hypertensionmayresultfromthesympatheticresponse
2) Cardiovascular
a ElevatedjugularveinsinCHF
b Murmursmaybeauscultated
c Pericardialrub
d S4/S3gallopmayindicateCHF
e Dyskineticbulgemayindicateaneurysm
3) Pulmonary
a RalesmayindicateCHF
C) Differentialdiagnosisofchestpain
1) Vascular
a Aorticdissection
2) Myocardial
a Hypertrophiccardiomyopathy
b Dissection/rupture
3) Valvular
a Aortic/mitralstenosis
4) Pericardium
a Pericarditis
5) Coronaryartery
a STelevatedMI(STEMI)
b NonSTEMI
c Unstableangina
D) EKGpatterns
1) Ischemia
a STdepression
b Twaveinversion
2) Injury
a STelevation
3) Infarction
a PathologicQwaves
E) Serummarkers
1) Lactatedehydrogenase(LDH)andtransaminases
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2) CreatininekinaseMB(CKMB)andrelatedisoforms
3) Troponin
a MostspecificandlonglastingD i a g n o s i s o f A M
4) Myoglobin
A C S A lg o r ith m
F) Diagnosticalgorithm

A c u te C o r o n a r y S y n d r o m e

S T E le v a tio n

N o S T E le v a tio n

(+ ) T ro p o n in
(+ ) T ro p o n in

Q -w a v e M I

NQW MI

NSTEM I

( ) T r o p o n in

U n s ta b l e
a n g in a

A n d e r s o n J L , e t a l. A C C /A H A G u id e lin e s U A & N S T E M I. C ir c u la tio n 2 0 1 1 ; 1 2 3 : e 4 2 6 - e 5 7 9 .

P o s itiv e c a r d ia c b io m a r k e r s

A ll- C a u s e M o r ta l ity , N e w /
e c u r r e n t M I, R e c u r r e n t Is c h e m ia
e q u ir in g R e v a s c in 2 w e e k s (% )

G) Diagnosticclassificationscheme
1) Type1
a SpontaneousMIrelatedtoischemiaduetoprimarycoronaryevent
2) Type2
a MIsecondarytoischemiaduetoincreasedoxygendemandordecreasedsupply
3) Type3
D ia g n o s is o f A M I
a Sudden,unexpectedcardiacdeath
R is k S t r a tif ic a t io n f o r D e a t h / N o n fa t a l M I
4) Type4
a AMIassociatedwithpercutaneouscoronaryintervention
I n te r m e d i a t e R i s k
H ig h R is k
L o w R is k
b BMIassociatedwithstentthrombosis
S y m p to m s
A c c e le r a tin g te m p o o f
P r io r C A B G , C V A , P V D ,
is c h e m ic s y m p to m s in
M I, o r A S A u s e
5) Type5
p a s t 4 8 h o u rs
a MIassociatedwithCABG
C h a ra c te r o f O n g o in g (> 2 0 m in ) o f
P r o lo n g e d (> 2 0 m in ) r e s t
N e w o n s e t C C S C la s s III o r IV
P a in
r e s t p a in
a n g i n a , n o w r e s o l v e d , w i th a n g i n a i n t h e p a s t 2 w e e k s
m o d e r a te / h i g h l i k e l i h o o d
w ith o u t p r o lo n g e d (> 2 0 m in )
H) Imaging
o f C A D . R e s t a n g in a
r e s t p a in b u t w ith m o d e ra te
(
<
2
0
m
i
n
)
r
e
l
i
e
v
e
d
w
i
t
h
o r h ig h lik e lih o o d o f C A D
1) Noninvasive
re s t o r S L N T G .
P h y s ic a l
A g e > 7 5 , p u lm o n a r y r a le s ,
A ge > 70
a ECHO
n e w / w o rs e n in g M R , S 3 ,
h
y
p
o
t
e
n
s
i
o
n
,
b
r
a
d
y
c
a
r
d
i
a
,
b Nuclearimaging
ta c h y c a r d ia
2) Invasive
ECG
A n g in a a t r e s t w / tr a n s ie n t
T W I > 0 .2 m V
N o rm a l o r u n c h a n g e d E C G
S T - s e g m e n t d e v ia tio n
P a th o lo g ic Q w a v e s
d u r in g e p is o d e o f c h e s t
a Rightheartcatheterization
( 0 .0 5 m m ) . S u s t a i n e d V T .
d is c o m fo r t
N e w / p re s u m a b ly n e w B B B .
b Leftheartcatheterization
N o r m a l b io m a rk e r s
B io m a rk e rs
M a r k e d ly e le v a te d T p I, T p T ,
S lig h tly e le v a te d T p I o r
( > 0 .1 n g / m l )
T p T ( > 0 .0 1 & < 0 .1 n g / m l )
i Coronaryangiography
ii Leftventriculography
o Canassessejectionfraction
V) TreatmentofAMI
A) Pharmacological
1) Antiplatelettherapy
a Aspirin
D ia g n o s is o f A M I
i InhibitsCOX2inplatelets,preventingproductionofTXA
R i s k S t r a t i f i c a t i o n f o r U A / N S T E M I P a t i e2 n t s
ii UsedinconjunctionwithP2Y12inhibitorforincreasedeffect
b P2Y12inhibitors
c GPIIb/IIIainhibitors
C o u n t (1 p o in t e a c h )
A ge 65
2) Antithrombotictherapy
3 ris k fa c to rs fo r C A D
P r io r c o r o n a r y s te n o s is 5 0 %
a Heparin
S T s e g m e n t s h i f t o n i n i ti a l E C G
b Xainhibitors A S2 Aa ni ng ipnrai ol re p7 i ds oa dy se s in p a s t 2 4 h r s
20

3) Reperfusiontherapy
a Thrombolysis
b Primarycoronaryintervention
i Balloons
ii Stents
iii Thrombectomy
4) Cardioprotective
a Nitrates
i Donotreducemortality
b Betablockers
c ACEinhibitors
d Angiotensinreceptorblockers(ARBs)
e Aldosteroneblockers
5) Markersofsuccessfulreperfusion
a Resolutionofsymptoms
b ReturnofSTsegmentstobaseline
c Earlywashoutofcardiacmarkers
d Normalepicardialcoronaryflow
VI) ComplicationsofAMI
A) Flowchart

1) Hallmarksoftissuenecrosis
a Papillarymusclerupture
b Ventricularseptalrupture
c Myocardialrupture
B) Recurrentischemiaandreinfarction
1) Incidenceis~2030%
2) Balloonpumpsarecontraindicated
C) Congestiveheartfailure
1) Leftventriculardysfunctionisthesinglemostimportantpredictorofmortality
a Systolicdysfunction=depressionincardiacoutputandejectionfractions
b Diastolicdysfunction=elevatedventricularfillingpressure,pulmonaryhypertension,and
pulmonarycongestion
D) Cardiogenicshock
21

1) Systemichypoperfusionsecondarytodepressedcardiacoutput
E) Rightventricularinfarction
1) AlmostexclusivelyassociatedwithinferiorMI
F) Arrhythmias
1) Electricalinstability(ischemia)
a Prematureventricularcontractions(PVCs)
b Ventriculartachycardia
c Ventricularfibrillation
d Acceleratedidioventricularrhythm
2) Pumpfailure,pericarditis,pain,pressors
a Sinustachycardia
b Atrialfibrillation
c Atrialflutter
d Paroxysmalsupraventriculartachycardia(PSVT)
3) Parasympathetictone,damagedconduction
a Sinusbradycardia
b Junctionalescaperhythm
c AVblock
G) Leftventricularthrombusandarterialembolism
1) AnteriorMIisathigherrisk
CHFandCardiomyopathy
I) Introduction
A) Definitionsofheartfailure
1) Inabilityofthehearttopumpbloodforwardatasufficientratetomeatthemetabolicdemandsofthe
body(forwardfailure)
a Typicallyleadstoinadequatesystemicperfusion
2) Theabilitytopumpsufficientlyonlyifthecardiacfillingpressuresareabnormallyhigh(backwards
failure
a Thisvariantistreatedmorecommonlyinclinic
b Typicallyleadstopulmonarycongestion
B) Commoncausesofheartfailure
1) Myocardialischemia(e.g.,coronaryarterydisease)
2) Hypertension
3) Valvulardisease
4) Congenitalheartdisease
5) Cardiomyopathies
C) Determinantsofcardiacoutput
1) Remember,cardiacoutput=heartratexstrokevolume
2) Strokevolumeisdependentonpreload,contractility,andafterload
D) Classificationofheartfailure
1) Systolicheartfailure
a Impairedventricularcontractility
b Increasedafterload
2) Diastolicheartfailure
a Impairedventricularfilling
E) Recallthatthephysiologyofthecardiovascularsysteminvolvesneurohormonalcomponents
22

1) Adrenergicnervoussystem
2) Renin/angiotensin/aldosteronesystem
F) Classesofheartfailure
1) ClassInolimitationsofphysicalactivity
2) ClassIIslightlimitationofactivitywithdyspneaandfatigueuponmoderateexertion
3) ClassIIImarkedlimitationofactivitywithdyspneaandfatigueuponminimalexertion
4) ClassIVseverelimitationofactivitywithsymptomsevenatrest
II) PressureVolumeLoops
A) Normalpressurevolumeloop

B) Pathologicpressurevolumeloops

1) Thefirstimagerepresentsincreasingpreload
2) Themiddleimagerepresentsincreasingafterload
3) Thefinalimagerepresentsincreasingcontractility
III) AssessingHemodynamicStatus
A) Warmvs.cold
1) Referstothedegreeofsystemicperfusion
2) Thepresenceofthefollowingfindingsmayindicateinadequateperfusionanddemotethepatientto
acoldstatus
23

a Narrowpulsepressure
b Sleepy/obtundedstate
c Lowserumsodium
d Elevatedliverenzymes(LFTs)
e Coolextremities
f HypotensionwhilealreadytakinganACEinhibitor
g Renaldysfunction
h Pulsusalternans
B) Dryvs.wet
1) Referstothedegreeofcongestion
2) Thepresenceofthefollowingfindingsmayindicatecongestionsanddemotethepatienttothewet
status
a Orthopnea
b JVD
c Hepatomegaly
d Edema
e Rales(rarelyobservedinchronicheartfailure)
f Elevatedpulmonaryarterysystolicpressure
g Abdominojugularreflex
h PresenceofS3heartsound
C) Coldanddrymaybetheworstcombinationofstatus,asitoftenrepresentsendstagediseasewhere
theheartcannolongerfunctionwithanotherwisenormal/correctedpreload
IV) Treatment
A) Goals
1) Themostimportantcomponentoftreatmentistoidentify(andsubsequentlycorrect)theunderlying
causeofdisease
a Onlytreatingthesymptomsismerelypalliative,endstagecare...
2) Manageheartfailuresymptoms(e.g.congestion)
3) Modulateneurohormonalresponse
4) Improvelongtermsurvival
B) Treatingdiastolicdysfunction
1) Unfortunately,thereisnodrugcapableofimprovingtheabilityofthehearttorelax
2) Youneedtotreattheunderlyingcausesandsymptomsasadequatelyaspossible
C) Treatingsystolicdysfunction
1) ACEinhibitor
a Useinallpatientswithejectionfraction<40%
b Maycauserenalarterystenosis
c Contraindicatedinpregnancy
2) Betablocker
a Useinallpatientswithejectionfraction<40%
b Mayexacerbateasthmaandcausearrhythmias
c Contraindicatedinpatientswithvolumeoverload
3) Aldosteroneblockers
a Useinallpatientswithejectionfraction<30%andpersistentsymptomsdespiteothertherapies
4) Digoxin
5) Diuretics
V) Cardiomyopathies
A) Dilatedcardiomyopathy(DCM)
24

1) Allfourventriclesoftheheartdilateduetosomeintrinsicweaknesssystolicdysfunction
2) Symptomsresemblecongestiveheartfailure
3) Numerouscauses
a Idiopathic
b Familial(genetic)
i About40geneshavebeenidentifiedasbeingassociatedwithDCM
c Inflammatory
i E.g.,viralinfectious,connectivetissuedisorders,peripartum,sarcoidosis,etc.
d Toxicdrugs
i E.g.alcohol,chemotherapy,etc.
e Metabolic
f Neuromuscular
B) Hypertrophiccardiomyopathy(HCM)
1) Leftventriclehypertrophydiastolicdysfunction
2) Causedbymutationsinsarcomereproteins
3) Associatedwithleftventricularoutflowobstructionduetosystolicanteriormotion(SAM)ofthe
mitralvalve
a Thehighspeedflowthroughthenarrowedaorticoutflowtractlowersthepressureinthatregion,
drawingtheanteriorleafletofthemitralvalvetowardsthehypertrophicventricularseptum
b Iftheleafletcontactstheseptum,theaorticoutflowtractwillbeoccludedand,becausethemitral
valveisnowopen,bloodwillbeforcedintotheleftatrium
4) Othersymptoms
a Dyspnea(frequent)
b Angina
i Highoxygendemandofincreasedmusclemass
ii Narrowedbranchesofcoronaryarteries
c Syncope
i Arrhythmias
ii Outflowtractobstruction
5) Clinicalfindings
a SystolicmurmurthatvarieswithvenousreturninsuchawaythatHCMcanbedistinguished
fromaorticstenosis
i DuringtheValsalvamaneuver,venousreturnisreduceddecreasedpreloadcontractionof
theventriclestenosisworsensmurmurloudens
ii Whensquatting,venousreturnisincreasedincreasedpreloadexpansionoftheventricle
stenosisimprovesmurmursoftens
b Inaorticstenosis,thescenarioistheopposite
i DuringtheValsalvamaneuver,venousreturnisreduceddecreasedpreloadlessblood
movesthroughstenoticvalvemurmursoftens
ii Whensquatting,venousreturnisincreasedincreasedpreloadmorebloodmovesthrough
stenoticvalvemurmurloudens
C) Restrictivecardiomyopathy(RCM)
1) Characterizedbyanabnormallyrigid(andthickened)ventriclesdiastolicdysfunction
a Atriaenlargeasaresult
2) Causes
a Infiltrationofthemyocardium
i E.g.,amyloidosis,sarcoidosis,hemochromatosis,etc.
b Fibrosisoftheendomyocardium
25

i E.g.,metastatictumors,radiationtherapy,etc.
3) Clinicalfindings
a Rightheartfailure
i IncludingJVD,peripheraledema,ascites,etc.
b Arrhythmias
c Heartblock
i E.g.,exaggeratedxandydescentsonEKG
Atherosclerosis,RiskFactors,andHypertension
I) Atherosclerosis
A) Definition
1) Diseaseoftheaortaandmusculararteriesinwhichtheinnerlayersbecomethickenedbyfatty
depositsandfibroustissue
B) Pathogenesisp
1) Endothelialdysfunctionaccumulationoflipidsrecruitmentofleukocytesformationoffoamcells
depositionofECM(atheroscleroticplaque)
2) Endothelialdysfunction
a Causes
i Highshearstress(branchpointsofcirculation)
ii Toxins(e.g.,cigarettesmoke)
iii Adversemetabolicenvironment(e.g.,hyperlipidemia,diabetes)
iv Increasedoxidativestressactivatedendothelium
o Impairedpermeability
o DecreasedproductionofNOandprostaglandins
o Releaseofinflammatorycytokines
o Productionofcellsurfaceadhesionmolecules
o Interferencewithantithromboticmechanisms
b Results
i Monocyteinfiltrationdifferentiationintomacrophages
ii MacrophagesingestoxidizedLDLfoamcells
iii Foamcellspromotesmoothmusclecellmigrationintothesubintimalspace
iv Therecruitedsmoothmusclecellsthendepositcollagenfibrouscap
v Whilemacrophagesattempttodegradecollagen,thesmoothmusclecellscontinuallyreplace
itequilibrium
3) Plaquestability
a Stableplaque
i Smallpoolsofcholesterolesters
ii Thickfibrouscap
iii Fewinflammatorycells
b Vulnerableplaque
i Largepoolsofcholesterolesters
ii Thinfibrouscaps
iii Manyinflammatorycells
c Vulnerableplaquesgrowintwoways
i Steadyaccumulationoflipidsandgrowthofthefibrouscap
ii Growthburstsduetoplaqueruptureorhemorrhage
d Plaquerupture/hemorrhage
26

i Thrombusincorporation
ii Occlusivethrombusrecanalization
iii Intraplaquehemorrhagehealing
II) RiskFactors
A) Nonmodifiable
1) Age
a Aspeopleage,CObeginstofallwhileTRPbeginstorise
2) Gender(male)
3) Genetics(lipoproteinAmutations)
B) Modifiable
1) Dyslipidemia
a Totalcholesterol>200mg/dL
b Triglycerides>150mg/dL
c LDL>130mg/dL
i LDLhasthestrongestassociationwithatherosclerosis
d HDL<40mg/DL
2) Hypertension
a Bothsystolicanddiastolichypertensionincreasetheriskofcoronaryarterydisease
3) Diabetes
a Diabetesisacoronaryarterydiseaseequivalent,grantingdiabeticsthesameriskasnon
diabeticswhohavehadapriorMI
4) Smoking
a IntroductionofsmokefreeordinancesreducedtheincidenceofACSby~30%
5) Obesity
6) Metabolicsyndrome
a Dyslipidemia,hypertension,insulinresistance,obesity
b Diagnosticcriteria
i TGs>150mg/dL
ii HDL<40mg/dL
iii Waistcircumference>40in
iv Fastingglucose>100mg/dL
v BP>130/80mmHg
C) Riskfactorshaveacumulativeeffectonendothelialdysfunction
III) WorkupofHypertension
A) History
1) Durationofhypertension
2) Historyofcardiovasculardisease
3) Familyhistoryofcardiovasculardisease
4) Lifestylefactors
5) Medications
B) Physicalexam
1) Bloodpressure
2) Assesspulses
3) Fundoscopicexaminationofsmallvesselsofeye
4) Examinationofneck,heart,lungs,abdomen,andextremities
5) Neurologicalassessment
C) Laboratorytesting
1) Urinalysis
27

2) CBC
3) Bloodchemistry(potassium,sodium,creatinine,fastingglucose)
4) Lipidprofile
5) EKG
D) Targetorgandamageasaresultofhypertension
1) Heartdisease
a LVhypertrophy
i DiagnosebyvoltagecriteriainV5+V2andlookforstrain(STdepressionwithTwave
inversion)inV5
b AnginaandMI
c Heartfailure
2) Cerebrovasculardisease
3) Nephropathy
4) Peripheralarterydisease
5) Retinopathy
E) Treatment
1) Lifestylemodifications
a Exercise
b Loseweight
c Stopsmoking/drinking
d Reducesodium,fat,andcholesterolintake
2) Drugs
ValvularDisease
I) Overview
A) Pressureandvolumeoverloadbothstimulateadaptationsinthemyocardiumandpulmonaryvasculature
1) Physiologicadaptations
a Pregnancy
b Exercise
2) Pressureoverloadconcentrichypertrophy
a Aorticstenosis
b Hypertension(includingpulmonary)
c Pulmonicstenosis
3) Volumeoverloadeccentrichypertrophy
a Aortic/pulmonicinsufficiency
b Mitral/tricuspidregurgitation
c Shunts
II) AorticStenosis
A) Aorticstenosisreferstonarrowingoftheaorticvalve(andthusaorticoutflowtract)
B) Etiologies
1) Calcification
a Pathogenesisissimilar(butnotidentical)toatherosclerosis
b Osteopontinisdepositedinthevalvecusps
2) Bicuspidaorticvalve
a Congenitalanomalywheretwocuspsremainfusedbecauseacommissureneverformsbetween
them
3) Chronicrheumaticheartdisease
28

C) Pathophysiology
1) Stenosisoftheaorticvalverequiresthattheleftventricletoexpendmoreenergytoejectanadequate
amountofblood
2) Concentrichypertrophyresults,leadingtodiastolicdysfunction
D) Symptoms
1) Syncope
2) Angina
3) CHF
E) Physicalexam
1) Late,highpitched,systolicejectionmurmur
2) Smallandslowcarotidupstroke
3) S4heartsound
F) Treatment
1) Medical
a Diuretics,inotropes,vasodilators
2) Surgical
a Aorticvalvereplacementisrecommendedformanypatients
III) MitralStenosis
A) Mitralstenosisreferstonarrowingofthemitralvalveopening
B) Etiologies
1) Rheumaticheartdisease(mostcommon)
2) Mitralannularcalcification
3) Singlepapillarymuscle(congenital)
C) Pathophysiology
1) Duetothestenosis,anincreasedpressuregradientisrequiredtomovebloodacrossthemitralvalve
2) TheLVisunderfilledwhiletheLAmaintainsanelevatedpressure
a LAfibrillationmayresult
3) BecauseLVfillingisslow,alongdiastoleisimportant
a Highheartrates,whichshortendiastole,resultinacuteelevationsofLApressure
4) TheelevatedLApressureistransmittedtothepulmonaryvessels,whichbegintoconstrictinorder
tocompensatefortheincreasedpressure
a Rupturehemoptysis
b PulmonaryedemaKerleyBlines
5) SustainedelevationinpulmonarypressureleadstopulmonaryhypertensionandRVfailure
D) Physicalexamfindings
1) EKGfindingsareoftensubtle
a RVHisdifficulttoidentify
b BiphasicPwaveinV1
c BifidcamelhumpPwaveinleadsII,III,andaVF
2) ThehighLALVpressuregradientaccentuatestheopeningandclosingsoundsofthemitralvalve
a LoudS1(openingsnap)
b LoudP2(duetopulmonaryhypertension)
3) Lowpitcheddiastolicrumble
4) DilationofpulmonaryarteryandrightventriclepalpableleftpulmonaryarteryandRVlift
E) Treatment
1) Warfarin
a StasisintheenlargedLAleadstothrombusformationandembolization
2) Valvuloplasty
29

3) Mitralvalvereplacement
IV) VolumeOverload
A) Generalprinciples
1) Volumeoverloadstimulateseccentrichypertrophywithincreasedcompliance
2) Increasingchambersizeallowspressurestoremainnormal
3) Regurgitantvolumesarethosethatarepushedbackacrosstheirrespectivevalves
a Totalstrokevolume=forwardstrokevolume+regurgitantvolume
b Regurgitantfraction=regurgitantvolume/totalstrokevolume
B) Aorticregurgitation
1) Etiologies
a Acute
i Endocarditis
ii Aorticdissection
b Chronic
i Aorticdilation
ii Bicuspidaorticvalve
iii Rheumaticheartdisease
iv Syphiliticaorticaneurysm
2) Pathophysiology
a Chronic,compensatedaorticinsufficiency
i Inaorticregurgitation,theLVfillsfromboththeLAandtheaorta
ii TheextravolumecausestheLVtodilateinordertomaintainnormaldiastolicpressure
iii However,theLVisforcedtocompensatefortheaorticinsufficiencybypumpingout
additionalvolumesuchthatenoughbloodisstillreachingtheperiphery
iv Thisleadstoagradualincreaseinsystolicpressure,especiallyinelderlypatientswhose
aortasarelesscompliant
b Uncompensatedaorticinsufficiency
i Eventually,theLVbecomesfullydilatedandLVpressurebeginstorise
ii Thisismarkedbyasmall(butclinicallysignificant)decreaseinejectionfraction
c Acuteaorticinsufficiency
i Therapidchangeisdiastolicvolumecannotbefullycompensatedforbycompliance,sothe
LVpressurerises
ii Resemblesuncompensatedaorticinsufficiency,thoughtheLVpressureismuchhigher
iii EjectionfractiondecreasesbecausethepressuregradientbetweentheaortaandLVisgreatly
decreased
3) Symptoms
a HighLApressure
i Shortnessofbreath
ii Fatigue
b Lowaorticpressureand/orhighLVdiastolicpressure
i Angina
c DilatedLVwithincreasedpreload
i Heartpounding
4) Physicalexamfindings
a Duetotheregurgitantflow
i Diastolicmurmur
o Themurmurismoresubtleinacuteaorticinsufficiencybecausetheaortic/LVpressure
gradientissmaller
30

ii AustinFlintrumble
iii S3
b Duetothewidepulsepressure
i Quinkessign(pulsationofthecapillarybedsinthenails)
ii Corriganspulse(rapidupstrokeandcollapseofthecarotidpulse)
iii Duroziezssign(systolicanddiastolicmurmursofthefemoralartery)
5) Treatment
a Vasodilators,thoughtheirlongtermbenefitisuncertain
b Valvereplacement
C) Mitralregurgitation
1) Etiologies
a Acute
i Ruptureofpapillarymuscleorchordaetendinae
ii Perforation
b Chronic
i Myxomatousdegeneration
ii DilatedLVwithdistortedgeometry
iii Rheumaticfever
c SeverityincreasesasthepressuregradientbetweentheLAandLVincreases
2) Pathophysiology
a TheLVejectsexcessvolumebackintothelowpressureLA
b Again,theLVcompensatesforthisforwardstrokevolumelossbyincreasingthetotalstroke
volume
c Inchronicmitralregurgitation,boththeLAandLVdilateinresponsetotheincreasedvolumes,
whichkeepspressuresnormal
i PressureintheLAstillincreasesslightly,duetotheextravolumecomingbackfromtheLV
ii AsubtleVwavemaybeobservedintheEKG
d Inchronic,decompensatedmitralregurgitation,theLVcannolongerdilatetomaintainthe
ejectionfraction,andtheejectionfractiondeclines
e Inacutemitralregurgitation,theLAandLVdonothavetimetocompensateviadilation,so
pressuresrisedramatically
i AprominentVwaveisobservedintheEKG
3) Symptoms
a ElevatedLApressure
i Pulmonaryedema
ii Dyspneaonexertion
iii Severedyspneaindecompensatedmitralregurgitation
b Decreasedforwardstrokevolume
i Fatigue
c ChronicelevationinLApressure
i Rightheartfailure
ii Edema
iii Venousdistension
4) Physicalexamfindings
a Holosystolicmurmurthatcanbemanipulatedbyalteringtheaortic/LVandLV/LApressure
gradients
i Increasingaorticpressureincreasedmurmur
ii Decreasingaorticpressuredecreasedmurmur
31

iii IncreasedLApressuredecreasedmurmur
iv DecreasedLApressureincreasedmurmur
D) Mitralvalveprolapse
1) Occurswhenoneorbothofthemitralleafletsfallbackintotheleftatrium,losingcontactwitheach
other
a Thisprocessispotentiatedwhentheheart/LVissmallest(i.e.,duringsystole)
2) Physicalexamfindings
a DilatedLV
i Displaced/diffusecardiacimpulse
b Increasedflowacrossmitralvalve
i S3
c HighLVdiastolicpressure(increasedpreload)
i S4
V) InfectiveEndocarditis
A) Pathogenesis
1) Fibrinandplateletvegetationsformondamagedendotheliumorprostheticsurfaces
2) Bloodbornebacteriaseedthesedeposits
B) Diagnosis
1) Bloodculturesofbacteremicindividuals
2) Observationofvegetations(echocardiogram)
3) Presenceofnewmurmur/insufficiency
Arrhythmias
I) MechanismsofArrhythmias
A) Automaticity
1) Thereisnormallynoelectricalconnectionbetweentheatriaandtheventriclesexceptthroughthe
AVnode
2) BoththeSAandAVnodesdepolarizespontaneouslyatsomegivenrate,afeaturetermed
automaticity
3) Therateofautomaticitycanbeprolongedbythreemechanisms,eachresultinginbradycardia
a Slowingphase4depolarization
b Producingamorenegativediastolicrepolarizationvalue
c Establishingahigher(lessnegative)depolarizationthreshold
B) Overdrivesuppression
1) Afteraperiodofrapidstimulation,thenormalautomaticityoftheSAnodeisinhibited
a AfewsecondsareneededbeforetheSAnodewillbeginspontaneouslydepolarizingagain
2) Thiseffectcanbeexaggeratedindiseasestates
a E.g.,tachycardiabradycardiasyndrome

C) Reentranttheories
1) Reentrantarrhythmiasdependontwoitems
a Conductionvelocity
i Referstotheamountoftimeittakesforawaveformtotravelfromonepointtoanother
32

Refractoryperiod
i ReferstotheperiodoftimefollowinganactionpotentialduringwhichthevoltagegatedNa+
areinactivatedandthetissueisunabletogenerateanotheractionpotential
2) Reentrantarrhythmiasoccurwhenawaveformfindsawaytotravelaroundatissueinacyclical
manner

3) Forreentrytooccur,theconductiontimemustbegreaterthantherefractoryperiod
a Thatis,therefractoryperiodmustendbeforethepropagatingwavefrontreachesit
b Thisalsogivesrisetotwomechanismsbywhichreentrantarrhythmiascanbetreated
i Slowconductiontothepointofextinguishmentbyblockingsodiumchannels
o Ifconductionismerelyslowed(butnotextinguished),thiscanactuallypotentiate
arrhythmia
ii Prolongtherefractoryperiodbyblockingpotassiumchannels
4) WolfParkinsonWhite(WPW)syndromeisanexampleofareentrantarrhythmia
a InWPWsyndrome,thereisanaccessorypathwayoffastconductionbetweentheatriaand
ventriclesthatisseparatefromtheslowconductingpathwayoftheAVnode
b Ifconditionsarecorrect,areentrantarrhythmiacanbetriggeredduetotheconductiondisparity
betweenthesepaths
33

Clinically(anddiagnostically),thearrhythmiacanbecorrected(atleasttemporarily)witha
procainamidechallenge

5) Atrialflutterisanotherexampleofareentrantarrhythmia
a Here,thewaveformcyclesaroundthetricuspidvalve,passingbetweenitandtheinferiorvena
cava
b TheEKGshowsacharacteristicsawtoothappearance

D) Proarrhythmiceffectsofantiarrhymicmedications
1) Conductionvelocityinmyocardiumisverydependentonsodiumchannels
a TypeIantiarrhythmicdrugsslowconductionbyantagonizingsodiumchannels
2) Slowingconductionmayenhanceorstabilizeareentrantarrhythmia
E) Triggeredactivity
1) Mayoccurwhentherefractoryperiodisprolongedandheartrateisslowed
2) Whiletheexactmechanismremainsobscured,newactionpotentialsmayariseoutofprolonged
inactivationperiods(refractoryperiods)

3) Torsadesdepointesisanexample
34

ImpulseInitiation

ClassificationofArrhythmias
Bradycardia
Sinusnodedysfunction

ImpulsePropagation

AVblock

Tachycardia
Enhancedautomaticity
Triggeredactivity
Reentranttachycardia

II) ArrhythmiasandEKGs
A) Normalsinusrhythm
1) EveryPwaveisfollowedbyaQRScomplex
2) EveryPRintervalisidentical
3) Insinustachycardia,therhythmisnormalbuttherateis>100bpm

4) Insinusbradycardia,therhythmisnormalbuttherateis<60bpm

B) Prematurecontractions
1) Prematureventricularcontractions(PVCs)
a Prematureandwideventricularcontraction(QRS)
b AfterthePVC,thenextsinusbeatfireswhenitnormallyshouldhave
i AcompensatorypausebetweenthePVCandsubsequentsinusbeatrestoresthenormalpace

35

2) Prematureatrialcontractions(PACs)
a AnarrowQRScomplexfollowsapremature,ectopic(andlikelyinverted)Pwave
b Thereisnocompensatorypause,andanewrateisadopted

C) Escaperhythms
1) Junctionalrhythm
a Rate(~50bpm)issetbytheAVnodeinsteadoftheSAnode
b NarrowQRScomplexwithoutaprecedingPwave
c TheSAnodemayeventuallywakeupandregaincontrol

2) Ventricularrhythm
a Rate(~30bpm)issetbytheventriclesinsteadoftheSAnode
b WideQRScomplexeswithoutaprecedingPwave

36

D) AVblocks
1) Firstdegree
a PRinterval>200ms(oronelargeblock)

2) Seconddegree
a TypeI
i PRintervalprolongsaftereachbeatuntilaQRScomplexisdropped
ii Mayobservegroupedbeating

TypeII
i PRintervalsdonotprolong,andabeatisabruptlydropped
ii Mayobservegroupedbeating

3) Thirddegree
a ThereisnorelationshipbetweenPwavesandQRScomplexes
37

Ajunctionalorventricularescaperhythmmaypredominate

E) Atrialfibrillation
1) Characterizedbychaotic,highrateatrialdepolarization
a Astheatrianeverfullycontract,bloodpoolsintheleftatrialappendage
b Thisstasiscanleadtothrombosisandsystemicembolism,requiringanticoagulationtherapy
2) Sinusnodeissuppressed
3) AVnodemaybeabletofiltersomeoftheincomingactionpotentials
a Leadstoanirregularventricularbeat
4) Ratecontrolhasbeenshowntobemoreeffectiveinmanaginglongtermoutcomes
a Betablockers
b Calciumchannelblockers
c Digoxin
d Hisbundleablationandimplantationofapermanentpacemaker

F) Atrialflutter
1) Exampleofreentrantarrhythmia(seeabove)
2) Characteristicsawtoothappearance
3) ConductionpatternoftheAVnodecanvarygreatly(4:1and2:1patternsareoftenobserved)
a However,theAVnodeonlyfiltersatrialratesthatarelargerthanitsnativethroughputof250
bpm
b Iftherapydecreasestheatrialratebelow250bpm,theAVnodewillstopfilteringimpulsesand
transferthemalltotheventricles,leadingtopronouncedventriculartachycardia
c Thus,itisimperativethattheAVnodebeslowedbeforeslowingtheatrialrate

38

G) Supraventriculartachycardias
1) Therearemanydifferenttypes
a AVnodereentrytachycardia(AVNRT)
b AVbypasstracts
c Primaryatrialtachycardia(mayhaveectopicfocus)
2) RegularrhythmandfastratewithnarrowQRScomplexes

H) Ventriculartachycardia
1) FastratewithwideQRScomplexes
2) Includestorsadesdepointes
3) Treatmentthoughts
a Themajorityoffastandwidecasesareventriculartachycardia
b Treatingventriculartachycardiawillnothurtthepatient,evenifthearrhythmiais
supraventricularinorigin
c Treatingventriculartachycardiaasifitweresupraventricularinorigin,however,canbeharmful
d Tobesafe,justassumeallfastandwidecasesareventriculartachycardiaandtreataccordingly

39

I) Ventricularfibrillation(a.k.a.death)
1) Irregular,widewaveforms

CongenitalHeartDisease
I) Introduction
A) Definition
1) Acongenitalheartdiseaseisagrossstructuralabnormalityoftheheartorintrathoracicgreatvessels
thatisactuallyorpotentiallyoffunctionalsignificance
2) Excludes
a Normalvariationsofvenousanatomy
b Arrhythmias
c PDA<14daysofage
d Bicuspidaorticvalve
e Mitralvalveprolapse
B) Incidence
1) 8in1,000livebirths
2) 27.5in1,000stillbirths
C) Lesionfrequency
1) VSDisthemostcommon(30%)
2) Mostlesionsarediagnosedatbirth(36%)
3) Majorityoflesionsareidentifiedwithinthefirstyearoflife(85%)
II) FetalCirculation

40

A) Normalfetalflow
1) Oxygenatedbloodtravelsfromtheplacentatotheheartviathefetalvenoussystem
a PlacentaumbilicalveinductusvenosusIVCRAforamenovaleLALVBrain
2) Deoxygenatedbloodreturnstotheplacentaviatheaorta
a BodyRARVPAductusarteriosusaortaumbilicalarteriesplacenta
B) Transitionalcirculation
1) Atbirth,theLApressurerisesandflowbetweentheatria(viathePFO)ceases
2) Simultaneously,PGE1levelsfallasoxygentensionrisesandthePDAcloses
3) Problems
a Ifpulmonaryresistancefailstofall,therewillbepersistentfetalcirculationviathePDA
b IfthePDAcloseswhilethereisacriticalheartdefect,deathcanoccur
i Leftsidedobstructivelesions
o Aorticcoarctation
o Aorticatresia
o Hypoplasticleftheart
ii Rightsidedobstructivelesions
o Pulmonaryatresia
o Pulmonarystenosis
iii Parallelcirculations
o Dtranspositionofthegreatvessels
III) AorticCoarctation
A) Features
1) WithaPDA,muchofthebloodflowingtothelowerbodywillbedeoxygenated
41

2) ClosureofthePDAwillcausebloodflowtothelowerbodytocease
B) Diagnosis
1) Presentation
a Cardiogenicshock
i Pallor,tachycardia,tachypnea,hypotension
2) Physicalexam
a Diminishedfemoralpulses
b BPdifferentialbetweenarmsandlegs
c Lowerextremitycyanosis
d IncreasedS2
3) Imaging
a CXRshowscardiomegalyandpulmonaryedema
b Ultrasounddefinesthecoarctationandstatusoftheductusarteriosus
C) Treatment
1) Reopen/stabilizetheductusarteriosus(PGE1)
2) Inotropes
3) Surgicalrepair
IV) PulmonaryStenosis/Atresia
A) Features
1) Theincreasedpressureintherightheartmayforcedeoxygenatedbloodacrosstheforamenovale
2) ClosureofthePDAwillcausebloodflowtothelungstocease
B) Diagnosis
1) Presentation
a Profoundhypoxemiathatisunresponsivetooxygen
b Tachycardia
c Tachypnea
d Hepatomegaly
2) Physicalexam
a SingleS2(nosplitting)
b Systolicejectionmurmuratleftuppersternalborder
c Blowingpansystolicmurmuratleftlowersternalborder
3) Imaging
a CXRshowscardiomegalyandoligemia(lackofblood)oflungfields
b Ultrasoundsdefinesthepulmonaryobstructionandsizeoftherightventricle
C) Treatment
1) Reopen/stabilizetheductusarteriosus(PGE1)
2) Inotropes
3) Surgicalrepair
V) DTranspositionoftheGreatVessels
A) Features
1) Mostcommoncyanoticheartanomalyintheneonatalperiod
2) Incompatiblewithlifewithoutcommunicationbetweentheparallelcircuits
3) Associatedwithmaternaldiabetes
B) Diagnosis
1) Presentation
a Cyanosis
2) Physicalexam
a RVimpulseatlowersternalborder
42

b ProminentS2(nowduetopulmonicclosure)
3) Imaging
a CXRshowscardiomegaly,increasedpulmonarymarkings,andeggonastringappearance
4) Treatment(medicalemergency)
5) Reopen/stabilizetheductusarteriosus(PGE1)
6) Surgicalrepair
a Balloonseptostomy(Rashkind)permitsbloodmixingandsurvival
b Arterialswitchprocedure
VI) VentricularSeptalDefect
A) Features
1) Mostcommoncongenitalheartanomaly
a 5080%ofsmalltomoderateVSDswillclosebeforeage2
2) BloodflowsfromtheLVtotheRV
3) Leftventricularandleftatrialdilationresult
4) Associatedwithfetalalcoholsyndrome
B) Diagnosis
1) Presentation
a Symptomsaretypicallyabsentatbirth,butdevelopwithinthefirst23monthsoflife
b Failuretothrive
i Increasedcaloricneedduetoincreasedworkofbreathing
c Tachypnea
i Nasalflaring,ribretraction
d Tachycardia
2) Histologicalfindings
a Neonateshavemedialhypertrophyofthepulmonaryarteries
b Thishypertrophyregressesoverthefirst23monthsoflife,andpulmonaryresistancefalls
c Decreasedpulmonaryresistanceincreasedpulmonarybloodflowincreasedshuntingthrough
VSDRVHpulmonaryhypertensionreversalofshuntEisenmengersyndrome
3) Physicalexam
a Hepatomegaly
b Diaphoresiswithfeeding
c Holosystolicmurmuratleftlowersternalborder
d Middiastolicrumbleatapex(duetoincreasedmitralflow)
4) Imaging
a CXRrevealscardiomegaly,increasedpulmonaryvasculature,andleftatrialenlargement
b Ultrasoundvisualizesdefect
C) Treatment
1) TreatsymptomsofCHFwithdiuretics,digoxin,andACEinhibitors
2) Surgicalrepair
VII) AtrialSeptalDefect
A) Features
1) Directionofshuntingdependsonventricularcompliances(e.g.,whicheverventriclehasahigher
resistance)
a Lefttorightshuntingismorecommon
2) Types
a Secundum(includesPFO)
b Primum
c Sinusvenosus
43

3) AssociatedwithDownSyndrome(trisomy21)
B) Presentation
1) Symptoms
a Cyanosis
2) Physicalexam
a Systolicejectionmurmur
b Middiastolicmurmur
c Fixed,widelysplitS2
3) Imaging
a CXRshowscardiomegaly
b Ultrasoundscanvisualizeanomaly
C) Treatment
1) Surgicalrepair
VIII) PatentDuctusArteriosus(PDA)
A) Features
1) Lefttorightshuntwithvaryingmagnitude
a CrosssectionalareaofPDA
b LengthofPDA
c Relativepulmonaryandsystemicresistances
2) MayresultinCHF
3) Associatedwithcongenitalrubella
B) Diagnosis
1) Symptoms
a Failuretothrive
b Recurrentrespiratoryinfections
c Fatigue
d Dyspnea
e Atrialfibrillation
2) Physicalexam
a Continuousmurmur
b Abnormallywidepulsepressure
3) Imaging
a CXRrevealscardiomegaly
b UltrasoundcanvisualizePDA
C) Treatment
1) Newborns
a Indomethacin
b Fluidrestriction
2) Everyoneelse
a Surgicalrepair
IX) TetralogyofFallot
A) Features
1) Fourcharacteristicmalformations
a VSD
b Overridingaorta
c RVoutflowtractstenosis
d RVH
2) RighttoleftshuntingdependentupondegreeofPAobstruction
44

B) Diagnosis
1) Symptoms
a Periodiccyanosis(mayprogresstoconstantcyanosis)
b Tetspells
c Squatting
d NotableforthelackofCHF
2) Physicalexam
a Pulmonarysystolicejectionmurmur
3) Imaging
a CXRrevealsabootshapedheart
C) Treatment
1) Surgicalcorrection
a CloseVSD
b Relievepulmonarystenosis
Acyanotic
VSD(fetalalcoholsyndrome)
ASD(trisomy21)
PDA(congenitalrubella)
AVcanal(trisomy21)

SummaryofCongenitalHeartDefects
Cyanotic
Transposition(diabetes,22q11.2)
TetralogyofFallot(22q11.2)
Truncusarteriosus(22q11.2)
Tricuspidatresia
Coarctationoftheaorta(Turnersyndrome,bicuspidaorticvalve)

PericardialDiseases
I) Introduction
A) Thepericardiumisatwolayeredsac
1) Theparietal(outer)andvisceral(inner)layersareseparatedbyathinfilmoffluid
2) Functions
a Fixestheheartinthemediastinum
b Providesalowresistancesurface
c Limitsacutedilation
d Actsasabarriertoinfection
3) Congenitalabsenceofthepericardiumisgenerallywelltolerated
II) AcutePericarditis
A) Etiologies
1) Idiopathic
2) Infectious
a Viral
i CoxsackieBvirus
ii Echovirus
iii ParvovirusB19
b Tuberculoid
i Spreadfrommediastinallymphnodes
c Purulent(bacterial)
i PneumococcusorStaphylococcusmicrobes
ii Hematogenousspread
iii Extensionofpneumonia
iv Perforation(traumaorsurgical)
45

3) Noninfectious
a PostMI
i PericarditismayoccurearlyaftertransmuralMI
ii Dresslerssyndromeisanautoimmunephenomenonthatmaydevelopweekstomonthsafter
MI
b Uremiccauses
c Malignantcauses
B) Features
1) Relativelycommonandgenerallybenign
a Purulentetiologiescanbelethalifuntreated,andtypicallyrequiresurgicaldrainage
C) Diagnosis
1) Presentinghistory
a Pleuriticchestpain
b Pseudodyspnea
i Patientstakerapid,shallowbreathsbecausetakingfull/deepbreathsispainful
c Fever
d Symptomsofpulmonarydisease
2) Physicalexamfindings
a Pericardialfrictionrubsthatareheardbestduringtimeswhentheheartismoving
i Atrialsystole(latediastole)
ii Ventricularsystole(becausethisisthemostvigorousmovement,rubsarebestheardduring
thisphase)
iii Ventricularfilling(earlydiastole)
b Pericardialfrictionrubsmayalsoexhibitevanescence,beingheardbestwhilethepatientis
sittingupandleaningforward
3) Laboratoryfindings
a EKGabnormalities
i STsegmentelevation(concaveupwardssmile)
o STsegmentelevationinMIisaconcavedownwardsfrown
ii PRsegmentdepression(leadII)
iii Twavesinvertlate(aftertheSTsegmentsnormalize)

b Echomayrevealpericardialfluid
c Serologicaltestsforviralinfection
d PPDforTBinfection
D) Treatment
1) Painrelief
a NSAIDs
b Colchicine(approvedforgout,butusedofflabelforpericarditis)
2) Treatunderlyingillness
46

a Treatmalignancieswithchemotherapy
b Treatpurulentinfectionswithdrainageandantimicrobialtherapy
c Treatconnectivetissuedisorderswithsteroids(avoidsteroidsifpossible)
d Treaturemiawithdialysis
3) Prognosisdependsontheunderlyingdisease
a Recurrenceandtamponadearerare
III) PericardialEffusionandTamponade
A) Etiology
1) Acutepericarditis
2) Increasedcapillarypermeability(e.g.,myxedema)
3) Increasedcapillaryhydrostaticpressure(e.g.,CHF)
4) Decreasedplasmaoncoticpressure(e.g.,cirrhosis,nephroticsyndrome)
5) Lymphaticobstruction(e.g.,chylopericardium)
B) Pathophysiology
1) Chronicaccumulationsoffluidovertimewillgivethepericardiumtimetoincreasecompliancesuch
thatpericardialpressurerisesslowly(onlyaftervastvolumeshaveaccumulated)
2) Acuteaccumulationoffluidwillcauserapidincreasesinpericardialpressuretamponade
a Duringinspiration,venousreturnincreasesandRVvolumeincreases
b Theheartcannormallyexpandtoaccommodatethistransientincreaseinvolume
c Incardiactamponade,theheartcannotexpandandtheincreaseinRVsizecomesattheexpense
ofadecreaseinLVsize
d ThisreducesLVfillingandstrokevolumepulsusparadoxus
3) Pulsusparadoxus
a Whentheheartcannotexpandtoaccommodatetheincreasedvenousreturnassociatedwith
inspiration,LVstrokevolumewillfall
b Thedecreasedstrokevolumelowersaorticbloodpressureduringinspiration,whichcanbe
measured
c PressurizethebloodpressurecuffuntilKorotkoffsoundsareheardonlyonexpiration,andnote
thispressure
d Decreasethepressureuntilsoundsareheardthroughouttherespiratorycycleandnotthis
pressure
e Ifthepressuredifferentialis>10mmHg,thenpulsusparadoxusispresent
C) Diagnosis
1) Clinicalfeatures
a Sinustachycardia
b Hypotension
c Pulsusparadoxus
d JVD
e Diminishedheartsounds
2) Imaging
a CXRmayshownonspecificfindingssuchascardiomegaly
b CTmayshowpericardialfluid
c Echo
i Pericardialeffusion
ii DiastoliccollapseoftheRVfreewall
iii LatediastoliccompressionoftheRA
iv Swingingheartinpericardialfluid
3) EKG
47

Electricalalternans
i QRScomplexesalternateinintensity(observableinleadsIIorV3)
4) Cardiaccatheterizationwillrevealthatdiastolicpressurehasequalizedinallfourchambersofthe
heart
a Thisisdiagnosticofcardiactamponade
D) Treatment
1) Medical
a Maintainadequateintravascularbloodvolume(decreasedvolumemaycausefatalheartcollapse)
b Treatunderlyingdisease
2) Percutaneouspericardiocentesis(drainthefluid)
a Numerouscomplications,butanecessaryprocedurenonetheless
3) Surgicalwindowing
IV) ConstrictivePericarditis
A) Features
1) Theheartbecomesencasedinarigid(sometimescalcified)pericardialshell
2) Ventriclefillsinearlydiastoleandthenabruptlystopswhenthenoncompliantpericardiumis
stretchedtoitslimit
3) Presentswithfindingsofrightheartfailure
4) Insidiousonsetdelaysdiagnosis
B) Etiologies
1) Idiopathic(>50%)
2) Postinfectious(e.g.,TB,viral,bacterial,fungal)
3) Postchestirradiation
4) Postoperative
C) Diagnosis
1) Clinicalpresentation
a Lowcardiacoutput(fatigue,malaise,weightloss,hypotension,restingtachycardia)
b Elevatedvenouspressure(ascites,hepatomegaly,anorexia,edema)
i Maymimichepaticcirrhosisinthisregard
2) Physicalexam
a ElevatedJVP
i ProminentYdescentinearlydiastole
ii Kussmaulssign
o Normally,venouspressurefallsduringinspirationasintrathoracicpressurefalls
o Kussmaulssignisaparadoxicalriseinvenouspressureduringinspiration
Thisoccursbecausethewithdrawnbloodhasnowheretogo,seeingastheheart
cannotexpandtoaccommodatetheincomingvolume
b Pericardialknock
i Highfrequencysoundthatcomes90120msafterS2
ii Causedbybloodenteringanoncompliantventricleandcomingtoanabruptstop
3) Labtesting
a CXR
i Pericardialcalcifications(>50%)
ii Pulmonaryvenousdistention
iii Pleuraleffusions
b EKG(rarelydiagnostic)
i Lowvoltages
ii DiffuseSTsegmentchanges
48

c MRIandCTmayrevealthethickenedpericardium
D) Treatment
1) Medical
a Diuretics
2) Surgicalpericardiectomy
a Extensiveprocedurewithvariableresults
PeripheralVascularDisease
I) Introduction
A) Functionsoftheperipheralvessels
1) Deliveryofoxygenandnutrients
2) Synthesisofbioactivemolecules
a Vasoactivesubstances(NO,endothelin)
b Antithromboticsubstances(prostaglandins)
3) Transportofimmunecells
II) DiseasesoftheAorta
A) Aneurysm
1) Definedasanincreaseindiameter>50%
2) Trueaneurysms
a Fusiform
i Symmetricaldilationoftheentirecircumferenceofthevesselwall
b Saccular
i Localizeddilationofaportionofthevesselwall
3) Falseaneurysms
a Containedrupturesofthevesselwall
b Causedbyinfectionandtrauma
4) Etiologies
a Ascendingaorta
i Cysticmedialnecrosis
ii Hypertension
iii Bicuspidaorticvalve
iv Connectivetissuediseases(Marfanssyndrome,EhlersDanlossyndrome)
b Descendingaorta
i Atherosclerosis
5) Riskofruptureisrelatedtosize
a Surgicaltreatmentisavailablewhenaneurysmsreachcriticalsizes
B) Dissection
1) Atearintheintimacreatesanaccessorypathofbloodflowthroughthemedia
2) Clinicalfeatures
a History
i Abruptonsetofsevereripping/tearingpainintheanteriorchestthatmigratesasthe
dissectionproceeds
ii Historyofhypertension,bicuspidaorticvalve,and/orconnectivetissuedisorder
b Presentation
i Hypertension
ii Occlusionofaorticbranchvessels
iii Aorticregurgitation
49

iv Shock(ifrupture)
c Imaging
i LargeaorticdilationonCXRandCT
3) Treatment
a Stopprogressionofthedissection
i ReducesystolicBPto100120mmHg
ii DecreaseLVejectionforce(blockade)
b TypeAdissection
i Earlysurgery
c TypeBdissection
i Treatmedically
ii Percutaneouscatheterbasedrepair
4) Complications
a Ruptureintoadjacentbodycavity(pericardium,mediastinum,thorax,peritoneum)
b Occlusionofaorticbranchvessels
c Aorticregurgitation
III) OcclusiveArterialDiseases
A) Peripheralatheroscleroticocclusion(peripheralarterydisease)
1) Features
a Occurspredominantlyinthepelvicandlegvessels
b Impairsoxygensupply/demandrelationship
c Riskfactorsresemblethoseforatherosclerosis
2) Manifestationsofdisease
a Asymptomatic
i Noclinicalcomplaint
ii Minimalfunctionalimpairment
b Classicclaudication
i Lowerextremitymusclesymptoms
ii Reproducibleonsetwithexercise
iii Reliefwithrest
c Atypicallegpain
i Lowerextremitydiscomfort
ii Inconsistentreproducibilitywithexercise
iii Incompleteresolutionwithrest
3) Clinicalfeatures
a History
i Exertionallimitationoflowerextremitymuscles
ii Localizedpaininlowerleg/foot
iii Poorlyhealinglegwounds
iv Abdominalpainaftereating(aversiontoeating,weightloss)
v FamilyhistoryofAAA
b Physicalexam
i Anklebrachialindex(ABI)
o ABI=anklesystolicpressure/brachialsystolicpressure
o ABR<0.90indicatesdisease
ii Criticallimbischemia
o Nonhealingwound
o Gangrene
50

Imaging
i Duplexultrasonographyshowsabnormalbloodvelocity/waveform
ii MRAandCTAvisualizedefect
4) Treatment
a Managemodifiableriskfactors
i Smokingcessation
ii Treathypertension
iii Treathyperlipidemia
iv Treatdiabetesmellitus
b Pharmacologicaltherapy
i Antiplatelettherapy
ii Cilostazol
B) Vasculitis
1) Inflammatorydamagetovessels
a Myoccludevessellumen
2) Primarydiseases
a Takayasusarteritis(pulselessdisease)
i Carotidorlimbpulsesdiminishedin80%ofpatients
b Giantcellarteritis(temporalarteritis)
c Thromboangiitisobliterans(Buergersdisease)
i Superficialveinthrombosisand/orarterialocclusion
ii Frequentlyaffectsmalesmokers
3) Secondarydiseases
a Immunecomplexdisorders
IV) AterialSpasm
A) Raynaudsphenomenon
1) Coldinducedvasospasmofdigitalarteries
2) Triphasicresponse
a Blanching
b Cyanosis
c Rubor(redness)withrewarming
3) Classifications
a Primary(Raynaudsdisease)
b Secondary(duetootherpathology)
i Connectivetissuediseases(scleroderma,SLE)
ii Vibrationorthermalinjury
iii Bodydyscrasias
4) Treatment
a Avoidcoldanddresswarmly
b Pharmacologicagents
i Calciumchannelblockers
ii adrenergicreceptorblockers
V) VenousDisease
A) Varicoseveins
1) Primarydisease
a Affectsfemalesmuchmorethanmales
b Pathyphysiology
i Vesselwallweakness
51

ii Valvularinvompetence(failureofvalvestocoapt)
iii Increasedintraluminalpressure
2) Secondarydisease
a OftenoccursafterDVTwhentheveinsarerecanalized(whichdestroysthevalves)
B) Hypertensioninmicrocirculation
1) Edema
2) Stasisdermatitis
3) Ulceration
C) Treatment
1) Elevatelegs
2) Compressionstockings
3) Occlusivedressing
4) Surgery

52