Heart WaLL, cHambers, and VaLVes · The pericardium is a tough, fibrous, double-walled sac that...
Transcript of Heart WaLL, cHambers, and VaLVes · The pericardium is a tough, fibrous, double-walled sac that...
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C H A P T E R
19 Heart and Neck Vessels
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NeckVesselandHeart
num.Theheartextendsfromthesecondtothefifthintercos-talspaceandfromtherightborderofthesternumtotheleftmidclavicularline.
Thinkoftheheartasanupside-downtriangleinthechest.The“top”oftheheartisthebroaderbase,andthe“bottom”is the apex, which points down and to the left (Fig. 19-3).Duringcontraction,theapexbeatsagainstthechestwall,pro-ducing an apical impulse. This is palpable in most people,normallyatthefifthintercostalspace,7to9cmfromthemid-sternalline.
Insidethebody,theheartisrotatedsothatitsrightsideisanterior and its left side is mostly posterior. Of the heart’sfourchambers,therightventricleformsthegreatestareaof
O u T l i n E
Structure and Function
PositionandSurfaceLandmarksHeartWall,Chambers,andValvesDirectionofBloodFlowCardiacCycleHeartSoundsConductionPumpingAbilityTheNeckVessels
Subjective Data
HealthHistoryQuestions
Objective Data
PreparationTheNeckVesselsThePrecordiumSummaryChecklist:HeartandNeckVesselsExam
Documentation and Critical Thinking
Abnormal Findings
Abnormal Findings for Advanced Practice
STruCTure AND FuNCTiON
Thecardiovascularsystemconsistsoftheheart(amuscularpump)andtheblood vessels.Thebloodvesselsarearrangedin twocontinuous loops, thepulmonary circulationandthesystemic circulation (Fig.19-1).Whentheheartcontracts, itpumpsbloodsimultaneouslyintobothloops.
Position and surface Landmarks The precordium is the area on the anterior chest directlyoverlying the heart and great vessels (Fig. 19-2). The greatvesselsarethemajorarteriesandveinsconnectedtotheheart.Theheartandthegreatvesselsarelocatedbetweenthelungsinthemiddlethirdofthethoraciccage,calledthemediasti-
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anterior cardiac surface. The left ventricle lies behind therightventricleandformstheapexandslenderareaoftheleftborder.Therightatriumliestotherightandabovetherightventricleandformstherightborder.Theleftatriumislocatedposteriorly,withonlyasmallportion,theleftatrialappend-age,showinganteriorly.
Thegreat vesselsliebunchedabovethebaseoftheheart.The superior and inferior vena cava return unoxygenatedvenousbloodtotherightsideoftheheart.Thepulmonary artery leaves the right ventricle, bifurcates, and carries thevenousbloodtothelungs.Thepulmonary veinsreturnthefreshlyoxygenatedbloodtotheleftsideoftheheart,andtheaortacarriesitouttothebody.Theaortaascendsfromtheleftventricle,archesbackatthelevelofthesternalangle,anddescendsbehindtheheart.
Heart WaLL, cHambers, and VaLVesThe heart wall has numerous layers. The pericardium is atough, fibrous, double-walled sac that surrounds and pro-tectstheheart(seeitscutedgeinFig.19-4).Ithastwolayersthatcontainafewmillilitersofserouspericardial fluid.Thisensuressmooth,friction-freemovementoftheheartmuscle.Thepericardiumisadherenttothegreatvessels,esophagus,sternum,andpleuraeandisanchoredtothediaphragm.Themyocardium is the muscular wall of the heart; it does thepumping.Theendocardium isthethinlayerofendothelialtissuethatlinestheinnersurfaceoftheheartchambersandvalves.
Thecommonmetaphoristothinkoftheheartasapump.Butconsiderthattheheart isactually twopumps;therightsideoftheheartpumpsbloodintothelungs,andtheleftsideoftheheartsimultaneouslypumpsbloodintothebody.Thetwopumpsareseparatedbyanimpermeablewall,theseptum.
19-2 ©PatThomas,2006.
PRECORDIUM
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2
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5
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Apex
Base
7
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19-1 Twoloops—separatebutindependent.
Systemicarteries
Systemicveins
Pulmonaryarteries
Pulmonary circulation
Systemic circulation
Rightventricle
Leftventricle
PulmonaryveinsSt
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CHAPTer 19 Heart and Neck Vessels 457
Eachsidehasanatriumandaventricle.Theatrium(Latinfor“anteroom”)isathin-walledreservoirforholdingblood,and the thick-walled ventricle is the muscular pumpingchamber. (It is common to use the following abbreviationstorefertothechambers:RA,rightatrium;RV,rightventricle;LA,leftatrium;andLV,leftventricle.)
The four chambers are separatedby swinging-door–likestructures, called valves, whose main purpose is to preventbackflow of blood. The valves are unidirectional; theycan open only one way. The valves open and closepassively in response to pressure gradients in the movingblood.
19-3 ©PatThomas,2006.
Common carotid arteries
Aorta (arch)
Pulmonary artery
Left atrial appendage
Left ventricle
Internal jugular veins
Superior vena cava
Right atrium
Right atrial appendage
Right ventricle
Inferior vena cava
Aorta (thoracic)Apex
Base
19-4 ©PatThomas,2006.
Cut edge of pericardium
Aorta (arch)
Pulmonary veins
Left atrium
Chordae tendineae
Papillary muscle
Left ventricle
Endocardium
Myocardium
Superior vena cava
Right atrium
Pulmonary artery
Pulmonary veins
Right ventricle
Inferior vena cava
Aortic valve
Mitral (AV) valve
Tricuspid (AV) valve
Pulmonic valve
Structu
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to abdomen and lowerextemities
to head and neck
to armsto arms
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2
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Therearefourvalvesintheheart(seeFig.19-4).Thetwoatrioventricular(AV)valvesseparatetheatriaandtheven-tricles. The rightAV valve is the tricuspid, and the leftAVvalve is the bicuspid or mitral valve (so named because itresemblesabishop’smitredcap).Thevalves’thinleafletsareanchoredbycollagenousfibers(chordae tendineae)topapil-larymusclesembeddedintheventriclefloor.TheAVvalvesopenduringtheheart’sfillingphase,ordiastole,toallowtheventricles tofillwithblood.During thepumpingphase,orsystole,theAVvalvesclosetopreventregurgitationofbloodbackupintotheatria.Thepapillarymusclescontractatthistime, so that the valve leaflets meet and unite to form aperfectsealwithoutturningthemselvesinsideout.
Thesemilunar (SL)valvesaresetbetweentheventriclesandthearteries.Eachvalvehasthreecuspsthatlooklikehalfmoons.TheSLvalvesarethepulmonicvalveintherightsideoftheheartandtheaorticvalveintheleftsideoftheheart.Theyopenduringpumping,orsystole,toallowbloodtobeejectedfromtheheart.
Note:Therearenovalvesbetweenthevenacavaandtherightatriumnorbetween thepulmonaryveinsand the leftatrium.Forthisreason,abnormallyhighpressureintheleftside of the heart gives a person symptoms of pulmonarycongestion,andabnormallyhighpressureintherightsideoftheheartshowsintheneckveinsandabdomen.
direction of bLood fLoWThink of an unoxygenated red blood cell being draineddownstream into the vena cava. It is swept along with theflow of venous blood and follows the route illustrated inFig.19-5.1. Fromlivertorightatrium(RA)throughinferiorvenacava
Superiorvenacavadrainsvenousbloodfromtheheadandupperextremities
FromRA,venousbloodtravelsthroughtricuspidvalvetorightventricle(RV)
2. FromRV,venousbloodflowsthroughpulmonicvalvetopulmonaryarteryPulmonaryarterydeliversunoxygenatedbloodtolungs
3. LungsoxygenatebloodPulmonaryveinsreturnfreshbloodtoleftatrium(LA)
4. FromLA,arterialbloodtravelsthroughmitralvalvetoleftventricle(LV)LVejectsbloodthroughaorticvalveintoaorta
5. AortadeliversoxygenatedbloodtobodyRemember that the circulation is a continuous loop. Thebloodiskeptmovingalongbycontinuallyshiftingpressuregradients.Thebloodflows fromanareaofhigherpressuretooneoflowerpressure.
cardiac cycLeThe rhythmicmovement ofblood through the heart is thecardiac cycle. It has two phases, diastole and systole. Indiastole, the ventricles relax and fill with blood. This takesuptwothirdsofthecardiaccycle.Theheart’scontractionissystole.Duringsystole,bloodispumpedfromtheventricles
and fills the pulmonary and systemic arteries. This is onethirdofthecardiaccycle.
Diastole. In diastole, the ventricles are relaxed and theAVvalves(i.e.,thetricuspidandmitral)areopen(Fig.19-6).(Openingofthenormalvalveisacousticallysilent.)Thepres-sureintheatriaishigherthanthatintheventricles,sobloodpours rapidly into the ventricles. This first passive fillingphaseiscalledearlyorprotodiastolic filling.
Toward the end of diastole, the atria contract and pushthelastamountofblood(about25%ofstrokevolume)intotheventricles.Thisactivefillingphaseiscalledpresystole,oratrial systole,orsometimesthe“atrialkick.”Itcausesasmallriseinleftventricularpressure.(Notethatatrialsystoleoccursduringventriculardiastole,aconfusingbutimportantpoint.)
Systole. Nowsomuchbloodhasbeenpumpedintotheventriclesthatventricularpressureisfinallyhigherthanthatintheatria,sothemitralandtricuspidvalvesswingshut.TheclosureoftheAVvalvescontributestothefirstheartsound(S1)andsignalsthebeginningofsystole.TheAVvalvesclosetopreventanyregurgitationofbloodbackupintotheatriaduringcontraction.
For a very brief moment, all four valves are closed. Theventricularwallscontract.Thiscontractionagainstaclosedsystemworkstobuildpressureinsidetheventriclestoahighlevel(isometric contraction).Considerfirst the left sideoftheheart.Whenthepressureintheventriclefinallyexceedspressure in the aorta, the aortic valve opens and blood isejectedrapidly.
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CHAPTer 19 Heart and Neck Vessels 459
19-6
DIASTOLE
Pressure Changes in Left Heart
Aortic pressure
Aortic valve closes
Aortic valve opens
AV valve opensAV valve closes
Atrial pressure
Ventricular pressure
Heart Sounds
Electrocardiogram
THE CARDIAC CYCLE
R
P
Q
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S3 S4 S1 S2
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mm Hg 0
Rapidfilling
(protodiastolic)
Slowfilling
SYSTOLEEjection
DIASTOLERapidfilling
Presystole
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After the ventricle’s contents are ejected, its pressurefalls.Whenpressure fallsbelowpressure in theaorta, somebloodflowsbackwardtowardtheventricle,causingtheaorticvalve to swing shut. This closure of the semilunar valvescauses the second heart sound (S2) and signals the end ofsystole.
Diastole Again. Now all four valves are closed and theventriclesrelax(calledisometricorisovolumic relaxation).Meanwhile, the atria have been filling with blood deliveredfromthelungs.Atrialpressureisnowhigherthantherelaxedventricular pressure. The mitral valve drifts open, and dia-stolicfillingbeginsagain.
Events in the Right and Left Sides. The sameeventsarehappeningatthesametimeintherightsideoftheheart,butpressures in the right sideof theheart aremuch lowerthan those of the left side because less energy is needed topump blood to its destination, the pulmonary circulation.Also, events occur just slightly later in the right side of theheartbecauseoftherouteofmyocardialdepolarization.Asaresult,twodistinctcomponentstoeachoftheheartsoundsexist, and sometimes you can hear them separately. In thefirst heart sound, the mitral component (M1) closes justbefore the tricuspid component (T1). And with S2, aorticclosure(A2)occursslightlybeforepulmonicclosure(P2).
Heart soundsEventsinthecardiaccyclegeneratesoundsthatcanbeheardthrough a stethoscope over the chest wall. These includenormal heart sounds and, occasionally, extra heart soundsandmurmurs(Fig.19-7).
Normal Heart Sounds
The first heart sound (S1) occurs with closure of the AVvalvesand thus signals thebeginningof systole.Themitral
componentofthefirstsound(M1)slightlyprecedesthetri-cuspidcomponent(T1),butyouusuallyhearthesetwocom-ponents fused as one sound. You can hear S1 over all theprecordium,butusuallyitisloudestattheapex.
The second heart sound (S2)occurswith closureof thesemilunar valves and signals the end of systole. The aorticcomponent of the second sound (A2) slightly precedes thepulmoniccomponent(P2).Althoughit isheardoveralltheprecordium,S2isloudestatthebase.
Effect of Respiration. Thevolumeofrightandleftven-tricularsystoleisjustaboutequal,butthiscanbeaffectedbyrespiration.Tolearnthis,considerthephrase:
Mo e to the ight heart
ess to the eft
R R
L L
,
Thatmeansthatduringinspiration,intrathoracicpressureisdecreased. This pushes more blood into the vena cava,increasingvenousreturntotherightsideoftheheart,whichincreases right ventricular stroke volume. The increasedvolume prolongs right ventricular systole and delays pul-monicvalveclosure.
Meanwhile,ontheleftside,agreateramountofbloodissequestered in the lungs during inspiration. This momen-tarily decreases the amount returned to the left side of theheart,decreasingleftventricularstrokevolume.Thedecreasedvolumeshortensleftventricularsystoleandallowstheaorticvalve tocloseabitearlier.Whentheaorticvalveclosessig-nificantlyearlier thanthepulmonicvalve,youcanhear thetwocomponentsseparately.ThisisasplitS2.
Extra Heart Sounds
Third Heart Sound (S3). Normally, diastole is a silentevent.However,insomeconditions,ventricularfillingcreatesvibrationsthatcanbeheardoverthechest.ThesevibrationsareS3.TheS3occurswhentheventriclesareresistanttofilling
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S3 S4 S1 S2
DIASTOLE DIASTOLERapidfilling
(protodiastolic)
Slowfilling
Presystole
Heart Sounds
SYSTOLE
Isom
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cont
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Ejection
Isom
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Rapidfilling
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CHAPTer 19 Heart and Neck Vessels 461
during the early rapid filling phase (protodiastole). Thisoccurs immediately after S2, when the AV valves open andatrial blood first pours into the ventricles. (See a completediscussionofS3inTable19-7onpp.490-491.)
Fourth Heart Sound (S4). The S4 occurs at the end ofdiastole,atpresystole,whentheventricleisresistanttofilling.Theatriacontractandpushbloodintoanoncompliantven-tricle. This creates vibrations that are heard as S4. The S4occursjustbeforeS1.
Murmurs
Blood circulating through normal cardiac chambers andvalves usually makes no noise. However, some conditionscreate turbulent blood flow and collision currents. Theseresultinamurmur,muchlikeapileofstonesorasharpturninastreamcreatesanoisywaterflow.Amurmurisagentle,blowing, swooshing sound that can be heard on the chestwall.Conditionsresultinginamurmurareasfollows:
1. Velocity of blood increases (flow murmur) (e.g., inexercise,thyrotoxicosis)
2. Viscosityofblooddecreases(e.g.,inanemia)3. Structuraldefectsinthevalves(narrowedvalve,incom-
petentvalve)orunusualopeningsoccurinthecham-bers(dilatedchamber,walldefect)
Characteristics of Sound
Allheartsoundsaredescribedby:1. Frequency(pitch)—heartsoundsaredescribedashigh
pitchedorlowpitched,althoughthesetermsarerela-tive because all are low-frequency sounds, and youneedagoodstethoscopetohearthem
2. Intensity(loudness)—loudorsoft3. Duration—veryshort forheartsounds;silentperiods
arelonger4. Timing—systoleordiastole
conductionOfallorgans, thehearthas auniqueability—automaticity.Theheartcancontractby itself, independentofanysignalsorstimulationfromthebody.Theheartcontractsinresponsetoanelectricalcurrentconveyedbyaconductionsystem(Fig.19-8).Specializedcells in the sinoatrial (SA)nodenear thesuperiorvenacavainitiateanelectricalimpulse.(BecausetheSAnodehasanintrinsicrhythm,itisthe“pacemaker.”)Thecurrentflowsinanorderlysequence,firstacrosstheatriatothe AV node low in the atrial septum. There it is delayedslightly so that the atria have time to contract before theventricles are stimulated. Then the impulse travels to thebundleofHis,therightandleftbundlebranches,andthenthroughtheventricles.
Theelectricalimpulsestimulatesthehearttodoitswork,whichistocontract.Asmallamountofelectricityspreadstothebodysurface,whereitcanbemeasuredandrecordedontheelectrocardiograph(ECG).TheECGwavesarearbitrarilylabeledPQRST,whichstandforthefollowingelements:
P wave—depolarizationoftheatriaPR interval—from the beginning of the P wave to the
beginningoftheQRScomplex(thetimenecessaryforatrialdepolarizationplustimefortheimpulsetotravelthroughtheAVnodetotheventricles)
QRS complex—depolarizationoftheventriclesT wave—repolarizationoftheventricles
19-8 ©PatThomas,2006.
Bundle of HisSA node
AV node
CONDUCTION SYSTEMELECTROCARDIOGRAPH
(ECG) WAVE
PQ
R
S
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Electricaleventsslightlyprecedethemechanicaleventsintheheart.TheECGjuxtaposedonthecardiaccycleisillustratedinFigure19-6.
PumPing abiLityIntherestingadult,theheartnormallypumpsbetween4and6Lofbloodperminutethroughoutthebody.Thiscardiac outputequalsthevolumeofbloodineachsystole(calledthestroke volume)timesthenumberofbeatsperminute(rate).Thisisdescribedas:
CO SV R= ×
Theheartcanalter itscardiacoutputtoadapttothemeta-bolic needs of the body. Preload and afterload affect theheart’sabilitytoincreasecardiacoutput.
Preload is thevenousreturnthatbuildsduringdiastole.Itisthelengthtowhichtheventricularmuscleisstretchedattheendofdiastolejustbeforecontraction(Fig.19-9).
When the volume of blood returned to the ventricles isincreased (as when exercise stimulates skeletal muscles tocontractandforcemorebloodbacktotheheart),themusclebundles are stretched beyond their normal resting state toaccommodate.Theforceofthisswitchisthepreload.Accord-ing to the Frank-Starling law, the greater the stretch, thestrongeristheheart’scontraction.Thisincreasedcontractil-ityresultsinanincreasedvolumeofbloodejected(increasedstrokevolume).
Afterloadistheopposingpressuretheventriclemustgen-eratetoopentheaorticvalveagainstthehigheraorticpres-sure. It is the resistance against which the ventricle mustpump itsblood.Once theventricle isfilledwithblood, theventricularenddiastolicpressureis5to10mmHg,whereasthatintheaortais70to80mmHg.Toovercomethisdiffer-ence,theventricularmuscletenses(isovolumiccontraction).Aftertheaorticvalveopens,rapidejectionoccurs.
tHe neck VesseLsCardiovascular assessment includes the survey of vascularstructures in the neck—the carotid artery and the jugular
veins (Fig. 19-10). These vessels reflect the efficiency ofcardiacfunction.
The Carotid Artery Pulse
Chapter9describesthepulseasapressurewavegeneratedbyeachsystolepumpingbloodintotheaorta.Thecarotidarteryisacentralartery—thatis,itisclosetotheheart.Itstimingcloselycoincideswithventricularsystole.(AssessmentoftheperipheralpulsesisfoundinChapter20,andbloodpressureassessmentisfoundinChapter9.)
The carotid artery is located in the groove between thetracheaandthesternomastoidmuscle,medialtoandalong-sidethatmuscle.Notethecharacteristicsofitswaveform(Fig.19-11):asmoothrapidupstroke,asummitthat isroundedandsmooth,andadownstrokethatismoregradualandthathas a dicrotic notch caused by closure of the aortic valve(markedDinthefigure).
Jugular Venous Pulse and Pressure
The jugular veins empty unoxygenated blood directly intothe superior vena cava. Because no cardiac valve exists toseparate the superior vena cava from the right atrium, thejugularveinsgiveinformationaboutactivityontherightsideof the heart. Specifically, they reflect filling pressure andvolumechanges.Becausevolumeandpressureincreasewhentherightsideoftheheartfailstopumpefficiently,thejugularveinsexposethis.
Twojugularveinsarepresentineachsideoftheneck(seeFig.19-10).Thelargerinternal jugularliesdeepandmedialtothesternomastoidmuscle.Itisusuallynotvisible,althoughitsdiffusepulsationsmaybeseeninthesternalnotchwhenthepersonissupine.Theexternal jugularveinismoresuper-ficial; it lies lateral to the sternomastoid muscle, above theclavicle.
Althoughanarterialpulseiscausedbyaforwardpropul-sionofblood,thejugularpulseisdifferent.Thejugularpulseresults from a backwash, a waveform moving backwardcausedbyeventsupstream.Thejugularpulsehasfivecom-ponents,asshowninFig19-12.
19-9
AFTERLOADPRELOAD
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CHAPTer 19 Heart and Neck Vessels 463
19-10
Superiorvena cava
Aorta
Right external jugular vein
Right common carotid artery
Sternomastoid muscle
Left external jugular vein
Left internal jugular vein
Left common carotid artery
Sternomastoid muscleand clavicle cut
NECK VESSELS
19-11
Phonocardiogram (apex)
Carotid artery pulse tracing
ECG
S1 S2
QRS
D
P T U
S1 S2
QRS
P T U
D
ARTERIAL PULSE
The five components of the jugular venous pulse occurbecauseofeventsintherightsideoftheheart.TheAwavereflects atrial contraction because some blood flows back-wardtothevenacavaduringrightatrialcontraction.TheCwave,orventricularcontraction,isbackflowfromthebulgingupwardofthetricuspidvalvewhenitclosesatthebeginningof ventricular systole (not from the neighboring carotidarterypulsation).Next,theXdescentshowsatrialrelaxation
whentherightventriclecontractsduringsystoleandpullsthebottom of the atria downward. The V wave occurs withpassiveatrialfillingbecauseoftheincreasingvolumeintheright atria and increased pressure. Finally, the Y descentreflects passive ventricular filling when the tricuspid valveopensandbloodflowsfromtheRAtotheRV.
19-12
Phonocardiogram
Jugular venous pulse
ECG
S1 S2
A2P2
QRS
A
C
X
V
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TP
QRS
TP
A
C
X
V
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S1 S2
VENOUS PULSE
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DevelopmentalCompetenCe
Infants and Children
Thefetalheartfunctionsearly;itbeginstobeatattheendof3weeks’gestation.Thelungsarenonfunctional,butthefetalcirculation compensates for this (Fig. 19-13). Oxygenationtakesplaceattheplacenta,andthearterialbloodisreturnedto the right side of the fetal heart. There is no point inpumpingallthisfreshlyoxygenatedbloodthroughthelungs,so it isreroutedintwoways.First,abouttwothirdsof it isshuntedthroughanopeningintheatrialseptum,theforamen ovale,intotheleftsideoftheheart,whereitispumpedoutthroughtheaorta.Second,therestoftheoxygenatedbloodis pumped by the right side of the heart out through thepulmonaryartery,butitisdetouredthroughtheductus arte-riosustotheaorta.Becausetheyarebothpumpingintothesystemiccirculation,therightandleftventriclesareequalinweightandmusclewallthickness.
19-13
Ductus arteriosus
Aorta
Maternalblood
Umbilicus
Placenta
Foramenovale
Superiorvena cava
Inferiorvena cava
FETAL CIRCULATION
Inflationandaerationofthelungsatbirthproducescir-culatorychanges.Nowthebloodisoxygenatedthroughthelungs rather than through the placenta. The foramen ovalecloseswithinthefirsthourbecauseofthenewlowerpressureintherightsideoftheheartthanintheleftside.Theductusarteriosuscloseslater,usuallywithin10to15hoursofbirth.Nowtheleftventriclehasthegreaterworkloadofpumpinginto the systemic circulation, so that when the baby hasreached 1 year of age, the left ventricle’s mass increases toreachtheadultratioof2:1,leftventricletorightventricle.
Theheart’spositioninthechestismorehorizontalintheinfantthanintheadult;thustheapexishigher,locatedatthefourthleftintercostalspace(Fig.19-14).Itreachestheadultpositionwhenthechildreachesage7years.
The Pregnant Woman
Blood volume increases by 30% to 40% during pregnancy,withthemostrapidexpansionoccurringduringthesecond
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CHAPTer 19 Heart and Neck Vessels 465
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19-14
5th interspace
4th interspace
HEART'S POSITION IN THE CHEST
ChildInfant
trimester. This creates an increase in stroke volume andcardiacoutputandanincreasedpulserateof10to15beatsper minute. Despite the increased cardiac output, arterialbloodpressuredecreasesinpregnancyasaresultofperiph-eralvasodilation.Thebloodpressuredropstoitslowestpointduring the second trimester and then rises after that. Thebloodpressurevarieswiththeperson’sposition,asdescribedonp.509.
The Aging Adult
Itisdifficulttoisolatethe“agingprocess”ofthecardiovascu-lar system per se because it is so closely interrelated withlifestyle,habits,anddiseases.Wenowknowthatlifestyleisamodifying factor in the development of cardiovasculardisease; smoking, diet, alcohol use, exercise patterns, andstresshaveaninfluenceoncoronaryarterydisease.Lifestylealsoaffectstheagingprocess;cardiacchangesoncethoughttobeduetoagingarepartiallyduetothesedentarylifestyleaccompanyingaging(Fig.19-15).Whatislefttobeattributedtotheagingprocessalone?
Hemodynamic Changes with Aging• Withaging,thereisanincreaseinsystolicbloodpressure
(BP).6Thisisduetostiffeningofthelargearteries,whichinturnisduetocalcificationofvesselwalls(arterioscle-rosis). This stiffening creates an increase in pulse wavevelocity because the less compliant arteries cannot storethevolumeejected.
• The overall size of the heart does not increase with age,but left ventricular wall thickness increases. This is an
adaptivemechanismtoaccommodatethevascularstiffen-ingmentionedearlierthatcreatesanincreasedworkloadontheheart.
• Nosignificantchangeindiastolicpressureoccurswithage.A rising systolic pressure with a relatively constant dia-stolicpressureincreasesthepulsepressure(thedifferencebetweenthetwo).
• Nochangeinrestingheartrateoccurswithaging.• Cardiacoutputatrestisnotchangedwithaging.• Thereisadecreasedabilityofthehearttoaugmentcardiac
output with exercise. This is shown by a decreasedmaximumheart ratewithexerciseanddiminished sym-patheticresponse.Noncardiacfactorsalsocauseadecreasein maximum work performance with aging: decrease inskeletal muscle performance, increase in muscle fatigue,increasedsenseofdyspnea.Chronicexerciseconditioningwillmodifymanyoftheagingchangesincardiovascularfunction.32
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DiseaseLifestyle
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Dysrhythmias. The presence of supraventricular andventriculardysrhythmiasincreaseswithage.Ectopicbeatsarecommoninagingpeople;althoughtheseareusuallyasymp-tomatic in healthy older people, they may compromisecardiacoutputandbloodpressurewhendiseaseispresent.
Tachydysrhythmiasmaynotbetoleratedaswell inolderpeople.Themyocardiumis thickerand lesscompliant,andearlydiastolicfillingisimpairedatrest.Thusitmaynottoler-ateatachycardiaaswellbecauseofshorteneddiastole.Also,tachydysrhythmias may further compromise a vital organwhosefunctionhasalreadybeenaffectedbyagingordisease.For example, a ventricular tachycardia produces a 40% to70% decrease in cerebral blood flow. Although a youngerpersonmaytoleratethis,anolderpersonwithcerebrovascu-lardiseasemayexperiencesyncope.48
ECG. Age-relatedchangesintheECGoccurasaresultofhistologicchangesintheconductionsystem.Thesechangesinclude:
• Prolonged P-R interval (first-degree AV block) andprolonged Q-T interval, but the QRS interval isunchanged
• Leftaxisdeviationfromage-relatedmildLVhypertro-phyandfibrosisinleftbundlebranch
• IncreasedincidenceofbundlebranchblockAlthough the hemodynamic changes associated with agingalonedonotseemsevereorportentous,thefactremainsthatthe incidence of cardiovascular disease increases with age.The incidence of coronary artery disease increases sharplywithadvancingageandaccountsforabouthalfofthedeathsofolderpeople.Hypertension(systolic>140mmHgand/ordiastolic >90mmHg) and heart failure also increase withage.Certainly,lifestylehabits(smoking,chronicalcoholuse,lackofexercise,diet)playasignificantroleintheacquisitionofheartdisease.Also,increasingthephysicalactivityofolderadults—even at a moderate level—is associated with areducedriskofdeathfromcardiovasculardiseasesandrespi-ratory illnesses.Bothpointsunderscore theneed forhealthteachingasanimportanttreatmentparameter.
CultureanDgenetiCs
Prevalence is an estimate of how many people in a statedgeographic locationhaveadiseaseatagivenpoint in time.In theUnitedStates, anestimated81millionpeople (morethan1in3)haveoneormoreformsofcardiovascularheartdisease(CVD).3TheannualratesoffirstCVDeventincreasewithage.Forwomen,comparableratesoccur10years laterinlifethanformen,butthisgapnarrowswithadvancingage.
CausesofCVDincludeaninteractionofgenetic,environ-mental,andlifestylefactors.However,evidenceshowspoten-tially modifiable risk factors attribute to the overwhelmingmajorityofcardiacrisk.Forexample,myocardialinfarction(MI)isanimportanttypeofCVD.TheINTERHEARTstudycovering52countriesindicatedthatninepotentiallymodifi-ableriskfactorsaccountedfor90%ofthepopulationattrib-utableriskforMIinmenand94%inwomen!47Theseninemodifiable risk factors include abnormal lipids, smoking,hypertension, diabetes, abdominal obesity, psychosocial
factors, consumption of fruits and vegetables, alcohol use,andregularphysicalactivity.
High Blood Pressure (HBP). Although all adults havesomepotentialCVDrisk,somegroups(definedbyrace,eth-nicity,gender,socioeconomicstatus,educationallevel)carryanexcessburdenofCVD.Hypertension isa systolicbloodpressure (SBP) of ≥140mmHg or diastolic blood pressure(DBP)of≥90mmHgor takingantihypertensivemedicine.Ahigherpercentageofmenthanwomenhavehypertensionuntilage45years.Fromage45to64years, thepercentagesare similar; after age 64 years, women have a much higherpercentageofhypertensionthanmenhave.3Also,hyperten-sionis2to3timesmorecommonamongwomentakingoralcontraceptives (especially among obese and older women)thaninwomenwhodonottakethem.Amongracialgroups,theprevalenceofhypertensioninblacksisamongthehighestintheworldanditisrising.Theprevalenceofhypertensionis 31.8% for African Americans, then 25.3% for AmericanIndians or Alaska natives, 23.3% for whites, and 21% forHispanics and Asians.3 Compared with whites, AfricanAmericansdevelopHBPearlierinlifeandtheiraverageBPsaremuchhigher.ThisresultsinAfricanAmericanshavingagreater rate of stroke, death due to heart disease, and end-stagekidneydisease.
Smoking. In the 40+ years from 1965 to 2004, U.S.smoking rates declinedby50.4% amongadults18years ofageandolder.33Thisresultsin2008with23.1%ofmenand18.3%ofwomenbeingsmokers.NicotineincreasestheriskofMIandstrokebycausingthefollowing:increaseinoxygendemand with a concomitant decrease in oxygen supply; anactivationofplatelets,activationoffibrinogen;andanadversechangeinthelipidprofile.
Serum Cholesterol. Highlevelsoflow-densitylipopro-teingraduallyaddtothelipidcoreofthrombusformationinarteries, which results in MI and stroke. The current cut-points for cholesterol risk in adults are the following: totalcholesterollevelsof≥240mg/dLarehighrisk;andlevelsfrom200to239mg/dLareborderline–highrisk.Theage-adjustedprevalence of total cholesterol levels over 200mg/dL areasfollows:51.1%ofMexican-Americanmenand49%ofMex-ican-American women; 45% of white men and 48.7% ofwhite women; and 40.2% of African American men and41.8%ofAfricanAmericanwomen.3
Obesity. TheepidemicofobesityintheUnitedStatesiswellknownandisreferenced inmanychaptersof this text.AmongAmericansages20yearsandolder,theprevalenceofoverweightorobesity(bodymassindex[BMI]of≥25kg/m2foroverweightand≥30.0forobesity)isasfollows:74.8%ofMexican-American men and 73% of Mexican-Americanwomen; 73.7% of African American men and 77.7% ofAfrican American women; and 72.4% of white men and57.5%ofwhitewomen.
Type 2 Diabetes Mellitus. TheriskofCVDis twofoldgreater among persons with diabetes mellitus (DM) thanwithoutDM.TheincreasedprevalenceofDMintheUnitedStatesisbeingfollowedbyanincreasingprevalenceofCVDmorbidity and mortality.3 Diabetes causes damage to thelargebloodvesselsthatnourishthebrain,heart,andextremi-
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CHAPTer 19 Heart and Neck Vessels 467
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1. Chestpain2. Dyspnea3. Orthopnea4. Cough
5. Fatigue6. Cyanosisorpallor7. Edema8. Nocturia
9. Pastcardiachistory10. Familycardiachistory11. Personalhabits(cardiacrisk
factors)
examiner Asks rationale
1. Chest pain. Anychest painortightness? • Onset:Whendiditstart?Howlonghaveyouhaditthistime?Hadthis
typeofpainbefore?Howoften? • Location:Wheredidthepainstart?Doesthepainradiatetoanyother
spot? • Character: How would you describe it? Crushing, stabbing, burning,
viselike?(Allowthepersontoofferadjectivesbeforeyousuggestthem.)(Noteifusesclenchedfisttodescribepain.)
Angina,animportantcardiacsymptom,occurs when heart’s own blood supplycannot keep up with metabolic demand.Chest pain also may have pulmonary,musculoskeletal,orgastrointestinalorigin;itisimportanttodifferentiate.
Asqueezing“clenchedfist”signischar-acteristic of angina, but the symptomsbelow may be anginal equivalents in theabsenceofchestpain.39a
• Pain brought on by: Activity—what type; rest; emotional upset; aftereating;duringsexualintercourse;withcoldweather?
• Anyassociatedsymptoms:Sweating,ashengrayorpaleskin,heartskipsbeat,shortnessofbreath,nauseaorvomiting,racingofheart?
Diaphoresis, cold sweats, pallor,grayness.
Palpitations, dyspnea, nausea, tachy-cardia,fatigue.
• Painmadeworsebymovingthearmsorneck,breathing,lyingflat? Try to differentiate pain of cardiacversusnoncardiacorigin.
• Painrelievedbyrestornitroglycerin?Howmanytablets?
2. Dyspnea. Anyshortnessofbreath? • Whattypeofactivityandhowmuchbringsonshortnessofbreath?How
muchactivitybroughtiton6monthsago? • Onset:Doestheshortnessofbreathcomeonunexpectedly? • Duration:Constantordoesitcomeandgo? • Seemtobeaffectedbyposition:Lyingdown? • Awakenyoufromsleepatnight?
Dyspneaonexertion(DOE)—quantifyexactly(e.g.,DOEafterwalkingtwo levelblocks).
Paroxysmal.Constantorintermittent.Recumbent.Paroxysmal nocturnal dyspnea (PND)
occurs with heart failure. Lying downincreases volume of intrathoracic blood,andtheweakenedheartcannotaccommo-date the increased load. Classically, thepersonawakensafter2hoursofsleepwiththeperceptionofneedingfreshair.
• Doestheshortnessofbreathinterferewithactivitiesofdailyliving?
3. Orthopnea. Howmanypillowsdoyouusewhensleepingorlyingdown? Orthopnea is the need to assume amoreuprightpositiontobreathe.Notetheexactnumberofpillowsused.
ties;thisresultsinstroke,coronaryarterydisease,andperiph-eralvasculardisease.
About13%ofAfricanAmericans20yearsofageandolderhaveDM.Between11.8%and13.1%ofMexican-AmericanshaveDM,comparedwith6.4%ofwhites.3Themostpowerfulpredictoroftype2DMisobesity,withabdominal(visceral)fatposingagreaterriskthanlowerbodyobesityposes.Evi-
dence from epidemiologic studies shows a strong geneticfactor for DM, but no specific antigen type has yet beenidentified.Inthepast,type2DMwasdiagnosedinadults40yearsofageandolder,butnowwearefindingmorechildrenwithtype2DM.Thesechildrenareusuallyoverweightorobese,have a family history of DM, and identify with AmericanIndian,AfricanAmerican,Hispanic,orAsiangroups.3
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468 uNiT iii Physical examination
examiner Asks rationale
4. Cough. Doyouhaveacough? • Duration:Howlonghaveyouhadit? • Frequency:Isitrelatedtotimeofday? • Type:Dry,hacking,barky,hoarse,orcongested? • Doyoucoughupmucus?Color?Anyodor?Bloodtinged? Sputum production, mucoid or puru-
lent.Hemoptysisisoftenapulmonarydis-order but also occurs with mitralstenosis.
• Associatedwith:Activity,position(lyingdown),anxiety,talking? • Doesactivitymakeitbetterorworse(sit,walk,exercise)? • Relievedbyrestormedication?
5. Fatigue. Doyouseemtotireeasily?Abletokeepupwithyourfamilyandco-workers?
• Onset:Whendidfatiguestart?Suddenorgradual?Hasanyrecentchangeoccurredinenergylevel?
• Fatiguerelatedtotimeofday:Allday,morning,evening? Fatigue fromdecreasedcardiacoutputis worse in the evening, whereas fatiguefromanxietyordepressionoccursalldayorisworseinthemorning.
6. Cyanosis or pallor. Evernotedyourfacialskinturnblueorashen? Cyanosis or pallor occurs with myo-cardial infarction or low cardiac outputstates as a result of decreased tissueperfusion.
7. Edema. Anyswellingofyourfeetandlegs? • Onset:Whendidyoufirstnoticethis? •Anyrecentchange?
edema is dependent when caused byheartfailure.
• What timeofdaydoes the swellingoccur?Doyour shoes feel tightattheendofday?
Cardiacedemaisworseateveningandbetter in morning after elevating legs allnight.
• Howmuchswellingwouldyousaythereis?Arebothlegsequallyswollen? Cardiac edema is bilateral; unilateralswellinghasalocalveincause.
• Doestheswellinggoawaywith:Rest,elevation,afteranight’ssleep? • Any associated symptoms, such as shortness of breath? If so, does the
shortnessofbreathoccurbeforelegswellingorafter?
8. Nocturia. Do you awaken at night with an urgent need to urinate? Howlonghasthisbeenoccurring?Anyrecentchange?
Nocturia—Recumbency at night pro-motes fluid reabsorption and excretion;thisoccurswithheartfailureinthepersonwhoisambulatoryduringtheday.
9. Cardiac history. Any past history of: Hypertension, elevated cholesterolortriglycerides,heartmurmur,congenitalheartdisease,rheumaticfeverorunexplainedjointpainsaschildoryouth,recurrenttonsillitis,anemia?
• Everhadheartdisease?Whenwasthis?Treatedbymedicationorheartsurgery?
• LastECG,stressECG,serumcholesterolmeasurement,otherhearttests?
10. Family cardiac history. Anyfamily historyof:Hypertension,obesity,dia-betes,coronaryarterydisease(CAD),suddendeathatyoungerage?
11. Personal habits (cardiac risk factors). • Nutrition:Pleasedescribeyourusualdailydiet.(Noteifthisdietisrep-
resentativeofthebasicfoodgroups,theamountofcalories,cholesterol,
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CHAPTer 19 Heart and Neck Vessels 469
examiner Asks rationale
and any additives such as salt.) What is your usual weight? Has therebeenanyrecentchange?
• Smoking:Doyousmokecigarettesorothertobacco?Atwhatagedidyoustart?Howmanypacksperday?Forhowmanyyearshaveyousmokedthisamount?Haveyouevertriedtoquit?Ifso,howdidthisgo?
• Alcohol:Howmuchalcoholdoyouusuallydrinkeachweek,oreachday?Whenwasyourlastdrink?Whatwasthenumberofdrinksthatepisode?Haveyoueverbeentoldyouhadadrinkingproblem?
risk factors for CAD—Collect dataregarding elevated cholesterol, elevatedblood pressure, blood sugar levels above130mg/dL or known diabetes mellitus,obesity, cigarette smoking, low activitylevel,andlengthofanyhormonereplace-menttherapyforpostmenopausalwomen.
• Exercise:Whatisyourusualamountofexerciseeachdayorweek?Whattype of exercise (state type or sport)? If a sport, what is your usualamount(light,moderate,heavy)?
• Drugs: Do you take any antihypertensives, beta-blockers, calciumchannel blockers, digoxin, diuretics, aspirin/anticoagulants, over-the-counterorstreetdrugs?
Additional History for Infants
1. How was the mother’s health during pregnancy: Any unexplained fever,rubellafirsttrimester,otherinfection,hypertension,drugstaken?
2. Haveyounotedanycyanosiswhilenursing,crying?Isthebabyabletoeat,nurse,orfinishbottlewithouttiring?
To screen for heart disease in infant,note fatigue during feeding. Infant withheart failure takes fewer ounces eachfeeding; becomes dyspneic with sucking;may be diaphoretic, then falls intoexhaustedsleep;awakensafterashorttimehungryagain.
3. Growth:Has thisbabygrownasexpectedbygrowthchartsandabout thesameassiblingsorpeers?
Poorweightgain.
4. Activity:Werethisbaby’smotormilestonesachievedasexpected?Isthebabyable to play without tiring? How many naps does the baby take each day?Howlongdoesanaplast?
Additional History for Children
1. Growth:Hasthischildgrownasexpectedbygrowthcharts? Poorweightgain.
2. Activity:Isthischildabletokeepupwithsiblingsoragemates?Isthechildwillingorreluctanttogoouttoplay?Isthechildabletoclimbstairs,rideabike,walkafewblocks?Doesthechildsquattorestduringplayortowatchtelevision,orassumeaknee-chestpositionwhilesleeping?Haveyounoted“bluespells”duringexercise?
Fatigue.Recordspecificlimitations.
Cyanosis.
3. Hasthechildhadanyunexplainedjointpainsorunexplainedfever?
4. Doesthechildhavefrequentheadaches,nosebleeds?
5. Does the child have frequent respiratory infections? How many per year?How are they treated? Have any of these proved to be streptococcalinfections?
6. Family history:Doesthechildhaveasiblingwithheartdefect?Isanyoneinthechild’sfamilyknowntohavechromosomalabnormalities,suchasDownsyndrome?
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470 uNiT iii Physical examination
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Additional History for the Pregnant Woman
1. Haveyouhadanyhighbloodpressureduringthisorearlierpregnancies? • What was your usual blood pressure level before pregnancy? How has
yourbloodpressurebeenmonitoredduringthepregnancy? • Ifhighbloodpressure,whattreatmenthasbeenstarted? • Anyassociatedsymptoms:Weightgain,proteininurine,swellinginfeet,
legs,orface?
2. Haveyouhadanyfaintnessordizzinesswiththispregnancy?
Additional History for the Aging Adult
1. Doyouhaveanyknownheartorlungdisease:Hypertension,CAD,chronicemphysema,orbronchitis?
• Whateffortstotreatthishavebeenstarted? • Usualsymptomschangedrecently?Doesyourillnessinterferewithactivi-
tiesofdailyliving?
2. Doyoutakeanymedicationsforyourillnesssuchasdigitalis?Awareofsideeffects?Haveyourecentlystoppedtakingyourmedication?Why?
Noncompliancemayberelatedtosideeffectsorlackoffinances.
3. environment:Doesyourhomehaveanystairs?Howoftendoyouneedtoclimbthem?Doesthishaveanyeffectonactivitiesofdailyliving?
ObjeCTiVe DATA
PrePArATiON eQuiPMeNT Nee DeDTo evaluate the carotid arteries, the person can be sitting up. To assess thejugularveinsandtheprecordium,thepersonshouldbesupinewiththeheadandchestslightlyelevated.
Stand on the person’s right side; this will facilitate your hand placement,viewingoftheneckveins,andauscultationoftheprecordium.
The room must be warm—chilling makes the person uncomfortable, andshivering interferes with heart sounds. Take scrupulous care to ensure quiet;heartsoundsareverysoft,andanyambientroomnoisemasksthem.
Ensurethefemale’sprivacybykeepingherbreastsdraped.Thefemale’sleftbreastoverridespartoftheareayouwillneedtoexamine.Gentlydisplacethebreastupward,oraskthewomantoholditoutoftheway.
Whenperformingaregionalcardiovascularassessment,usethisorder:1. Pulseandbloodpressure(seeChapter9)2. Extremities(seePeripheralVascularAssessmentinChapter20)3. Neckvessels4. PrecordiumThelogicofthisorderisthatyouwillbeginobservationsperipherallyandmoveintowardtheheart.Forchoreographyof thesesteps inthecompletephysicalexamination,seeChapter27.
MarkingpenSmallcentimeterrulerStethoscopewithdiaphragmandbell
endpiecesAlcoholwipe(tocleanendpiece)
Normal range of Findings Abnormal Findings
tHe neck VesseLs
Palpate the Carotid Artery
Locatedcentraltotheheart,thecarotidarteryyieldsimportantinformationoncardiacfunction.
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CHAPTer 19 Heart and Neck Vessels 471
Normal range of Findings Abnormal Findings
Palpateeachcarotidarterymedialtothesternomastoidmuscleintheneck(Fig. 19-16).Avoid excessive pressure on the carotid sinus area higher in theneck;excessivevagalstimulationherecouldslowdowntheheartrate,especiallyinolderadults.Takecaretopalpategently.Palpateonlyonecarotidarteryatatimetoavoidcompromisingarterialbloodtothebrain.
Carotid sinus hypersensitivity is thecondition in which pressure over thecarotid sinus leads to a decreased heartrate,decreasedBP,andcerebralischemiawith syncope. This may occur in olderadults with hypertension or occlusion ofthecarotidartery.
Feelthecontourandamplitudeofthepulse.Normallythecontourissmoothwitharapidupstrokeandslowerdownstroke,andthenormalstrengthis2+ormoderate(seeChapter20).Yourfindingsshouldbethesamebilaterally.
Diminishedpulsefeelssmallandweak(decreasedstrokevolume).
Increasedpulsefeelsfullandstronginhyperkineticstates(seeTable20-1,Varia-tionsinArterialPulse,onp.549).
Auscultate the Carotid Artery
Forpersonsmiddle-agedorolderorwhoshowsymptomsorsignsofcardio-vasculardisease,auscultateeachcarotidarteryforthepresenceofabruit(pro-nounced bru′-ee) (Fig. 19-17). This is a blowing, swishing sound indicatingbloodflowturbulence;normallynoneispresent.
A bruit indicates turbulence due to alocalvascularcause,suchasatheroscle-roticnarrowing.
Keeptheneckinaneutralposition.Lightlyapplythebellofthestethoscopeoverthecarotidarteryatthreelevels:(1)theangleofthejaw,(2)themidcervicalarea,and(3)thebaseoftheneck(seeFig.19-17).Avoidcompressingthearterybecausethiscouldcreateanartificialbruit,anditcouldcompromisecirculationif thecarotidartery is alreadynarrowedbyatherosclerosis.Ask theperson totakeabreath,exhale,andholditbrieflywhileyoulistensothattrachealbreathsoundsdonotmaskormimica carotidarterybruit. (Holding thebreathoninhalationwillalsotensethelevatorscapulaemuscles,whichmakesithardtohear thecarotids.)Sometimesyoucanhearnormalheart sounds transmittedtotheneck;donotconfusethesewithabruit.
A carotid bruit is audible when thelumenisoccludedby 1
2 to 23 .Bruitloud-
ness increases as the atherosclerosisworsensuntilthelumenisoccludedby 2
3 .Afterthat,bruitloudnessdecreases.Whenthe lumen is completely occluded, thebruitdisappears.Thusabsenceofabruitdoes not ensure absence of a carotidlesion.
19-16
19-17
1
2
3
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472 uNiT iii Physical examination
Normal range of Findings Abnormal Findings
Amurmursoundsmuchthesamebutis caused by a cardiac disorder. Someaortic valve murmurs (aortic stenosis)radiate to the neck and must be distin-guishedfromalocalbruit.
Inspect the Jugular Venous Pulse
Fromthejugularveinsyoucanassessthecentral venous pressure(CVP)andthus judge the heart’s efficiency as a pump. Stand on the person’s right sidebecausetheveinstherehaveadirectroutetotheheart.Traditionallywehavebeen taught to use the internal jugular vein pulsations for CVP assessment.However,youmayuseeithertheexternalortheinternaljugularveinsbecausemeasurementsinbotharesimilar.27Youcanseethetopoftheexternaljugularvein distention overlying the sternomastoid muscle or the pulsation of theinternaljugularveininthesternalnotch.
Positionthepersonsupineanywherefroma30-toa45-degreeangle,wher-everyoucanbest see the topof theveinorpulsations. Ingeneral, thehigherthevenouspressureis,thehigherthepositionyouneed.Removethepillowtoavoidflexingtheneck;theheadshouldbeinthesameplaneasthetrunk.Turntheperson’sheadslightlyawayfromtheexaminedside,anddirectastronglighttangentiallyontothenecktohighlightpulsationsandshadows.
Notetheexternaljugularveinsoverlyingthesternomastoidmuscle.Insomepersons, the veins are not visible at all, whereas in others they are full in thesupineposition.Asthepersonisraisedtoasittingposition,theseexternaljugu-larsflattenanddisappear,usuallyat45degrees.
Unilateraldistentionofexternaljugularveins is due to local cause (kinking oraneurysm).
Full distended external jugular veinsabove 45 degrees signify increased CVPaswithheartfailure.
Nowlookforpulsationsoftheinternaljugularveinsintheareaofthesupra-sternal notch or around the origin of the sternomastoid muscle around theclavicle.You must be able to distinguish internal jugular vein pulsation fromthat of the carotid artery. It is easy to confuse them because they lie closetogether.UsetheguidelinesshowninTable19-1.
TABLE 19-1 | Characteristics of jugular Versus Carotid Pulsations
InternalJugularPulse CarotidPulse
1. Location Lower,morelateral,underorbehindthesternomastoidmuscle
Higherandmedialtothismuscle
2. Quality Undulantanddiffuse,twovisiblewavespercycle
Briskandlocalized,onewavepercycle
3. Respiration Varieswithrespiration;itsleveldescendsduringinspirationwhenintrathoracicpressureisdecreased
Doesnotvary
4. Palpable No Yes
5. Pressure Lightpressureatthebaseoftheneckeasilyobliterates
Nochange
6. Positionofperson Levelofpulsedropsanddisappearsasthepersonisbroughttoasittingposition
Unaffected
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CHAPTer 19 Heart and Neck Vessels 473
Normal range of Findings Abnormal Findings
Estimate the Jugular Venous Pressure
ThinkofthejugularveinsasaCVPmanometerattacheddirectlytotherightatrium.Youcan“read”theCVPatthehighestlevelofpulsations(Fig.19-18).Use the angle of Louis (sternal angle) as an arbitrary reference point, andcompareitwiththehighestlevelofthedistendedveinorvenouspulsation.
Holdaverticalruleronthesternalangle.AlignastraightedgeontherulerlikeaT-square,andadjustthelevelofthehorizontalstraightedgetothelevelofpulsation.Readthelevelofintersectionontheverticalruler;normaljugularvenouspulsationis2cmorlessabovethesternalangle.Alsostatetheperson’sposition,forexample,“internaljugularveinpulsations3cmabovesternalanglewhenelevated30degrees.”
Elevatedpressureisalevelofpulsationthat ismorethan3cmabovethesternalangle while at 45 degrees. This occurswithheartfailure.
Ifyoucannotfindthe internal jugularveins,usetheexternal jugularveinsandnote thepointwhere they lookcollapsed.Beawarethat thetechniqueofestimatingvenouspressureisdifficultandisnotalwaysareliablepredictorofCVP.Consistencyingradingamongexaminersisdifficulttoachieve.
Ifvenouspressureiselevatedorifyoususpectheartfailure,performhepa-tojugular reflux (Fig. 19-19). Position the person comfortably supine, andinstructhimorhertobreathequietlythroughanopenmouth.Holdyourrighthandontherightupperquadrantoftheperson’sabdomenjustbelowtheribcage.Watchthelevelofjugularpulsationasyoupushinwithyourhand.Exertfirmsustainedpressurefor30seconds.Thisdisplacesvenousbloodoutoftheliversinusoidsandaddsitsvolumetothevenoussystem.Iftheheartisabletopumpthisadditionalvolume(i.e., ifnoelevatedCVP ispresent), the jugularveinswillriseforafewsecondsandthenrecedebacktopreviouslevel.
If heart failure is present, the jugularveinswillelevateandstayelevatedaslongasyoupush.
tHe Precordium
Inspect the Anterior Chest
Arrangetangentiallightingtoaccentuateanyflickerofmovement. A heave or lift is a sustained forcefulthrustingoftheventricleduringsystole.Itoccurs with ventricular hypertrophy as aresultofincreasedworkload.Arightven-tricularheaveisseenatthesternalborder;aleftventricularheaveisseenattheapex(seeTable19-8,AbnormalPulsationsonthePrecordium).
Pulsations. You may or may not see the apical impulse, the pulsationcreatedastheleftventriclerotatesagainstthechestwallduringsystole.Whenvisible,itoccupiesthefourthorfifthintercostalspace,atorinsidethemidcla-vicularline.Itiseasiertoseeinchildrenandinthosewiththinnerchestwalls.
19-18
19-19
Hepatojugularreflux.
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474 uNiT iii Physical examination
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Palpate the Apical Impulse
(This used to be called the point of maximal impulse, or PMI. Because someabnormalconditionsmaycauseamaximalimpulsetobefeltelsewhereonthechest,usethetermapical impulsespecificallyfortheapexbeat.)
Localizetheapicalimpulsepreciselybyusingonefingerpad(Fig.19-20,A).Askingthepersonto“exhaleandthenholdit”aidstheexaminerinlocatingthepulsation.Youmayneedtoroll thepersonmidwayto the left tofind it;notethatthisalsodisplacestheapicalimpulsefarthertotheleft(Fig.19-20,B).
Note:• Location—Theapicalimpulseshouldoccupyonlyoneinterspace,thefourth
orfifth,andbeatormedialtothemidclavicularline• Size—Normally1cm×2cm• Amplitude—Normallyashort,gentletap• Duration—Short,normallyoccupiesonlyfirsthalfofsystole
Cardiacenlargement:• Leftventriculardilation(volumeoverload)
displacesimpulsedownandtoleftandincreasessizemorethanonespace.
• A sustained impulse with increasedforce and duration but no change inlocation occurs with left ventricularhypertrophy and no dilation (pressureoverload)(seeTable19-8).
Theapical impulse ispalpable inabouthalfofadults. It isnotpalpable inobese persons or in persons with thick chest walls.With high cardiac outputstates(anxiety,fever,hyperthyroidism,anemia),theapicalimpulseincreasesinamplitudeandduration.
Not palpable with pulmonary emphy-semaduetooverridinglungs.
Palpate Across the Precordium
Usingthepalmaraspectsofyourfourfingers,gentlypalpatetheapex,theleftsternal border, and the base, searching for any other pulsations (Fig. 19-21).Normallynoneoccur.Ifanyarepresent,notethetiming.Usethecarotidarterypulsationasaguide,orauscultateasyoupalpate.
A thrill isapalpablevibration. It feelslike the throat of a purring cat. The thrillsignifiesturbulentbloodflowandaccom-paniesloudmurmurs.Absenceofathrill,however,doesnotnecessarilyruleoutthepresenceofamurmur.
Accentuated first and second heartsoundsandextraheartsoundsalsomaycauseabnormalpulsations.
19-21
19-20 Theapicalimpulse.
A B
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CHAPTer 19 Heart and Neck Vessels 475
Normal range of Findings Abnormal Findings
Percussion
Percussion isused tooutline theheart’sborders,but ithasbeendisplacedbythechestx-rayorechocardiogram.Evidenceshowsthesearemoreaccurateindetectingheartenlargement.Whentherightventricleenlarges,itdoessointheanteroposteriordiameter,which isbetter seenonx-rayfilm.Numerouscom-parisonstudiesshowthepercussedcardiacbordercorrelates“onlymoderately”withthetruecardiacborder.27Also,percussionisoflimitedusefulnesswiththefemalebreast tissueor inanobesepersonorapersonwithamuscular chestwall.
Cardiacenlargementisduetoincreasedventricular volume or wall thickness; itoccurs with hypertension, CAD, heartfailure,andcardiomyopathy.
Auscultation
Identify the auscultatory areas where you will listen. These include the fourtraditional valve“areas” (Fig. 19-22). The valve areas are not over the actualanatomiclocationsofthevalvesbutarethesitesonthechestwallwheresoundsproducedbythevalvesarebestheard.Thesoundradiateswiththedirectionofbloodflow.Thevalveareasare:
• Secondrightinterspace—aorticvalvearea• Secondleftinterspace—pulmonicvalvearea• Leftlowersternalborder—tricuspidvalvearea• Fifthinterspaceataroundleftmidclavicularline—mitralvalvearea
Donotlimityourauscultationtoonlyfourlocations.Soundsproducedbythevalvesmaybeheardallovertheprecordium.(Forthisreason,manyexpertsevendiscouragethenamingofthevalveareas.)ThuslearntoinchyourstethoscopeinaroughZpattern,fromthebaseoftheheartacrossanddown,thenovertotheapex.Orstartattheapexandworkyourwayup.IncludethesitesshowninFigure19-22.
19-22
Tricuspid area
Aortic area Pulmonic area
Erb’s point
Mitral area
Revised
AUSCULTATORY AREAS
Traditional
1
2
3
4
5
1AO
PA
LV
LA
RV
RA
2
3
4
5
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476 uNiT iii Physical examination
Normal range of Findings Abnormal Findings
Recall the characteristicsof a good stethoscope (seeChapter8).Clean theendpieceswithanalcoholwipe;youwillusebothendpieces.Althoughallheartsoundsarelowfrequency,thediaphragmisforrelativelyhigherpitchedsoundsandthebellisforrelativelylowerpitchedones.
Beforeyoubegin,alerttheperson:“Ialwayslistentotheheartinanumberofplacesonthechest.JustbecauseIamlisteningalongtime,itdoesnotneces-sarilymeanthatsomethingiswrong.”
Afteryouplacethestethoscope,tryclosingyoureyesbrieflytotuneoutanydistractions.Concentrate,andlistenselectivelytoone sound at a time.Considerthatat least two,andperhapsthreeor four,soundsmaybehappening in lessthan 1 second. You cannot process everything at once. Begin with the dia-phragmendpieceandusethefollowingroutine:(1)notetherateandrhythm,(2) identifyS1andS2,(3)assessS1andS2 separately,(4) listenforextraheartsounds,and(5)listenformurmurs.
Note the Rate and Rhythm. Theraterangesnormallyfrom50to90beatsperminute.(ReviewthefulldiscussionofthepulseinChapter9andthenormalratesacrossage-groups.)Therhythmshouldberegular,althoughsinus arrhyth-miaoccursnormallyinyoungadultsandchildren.Withsinusarrhythmia,therhythmvarieswiththeperson’sbreathing,increasingatthepeakofinspirationand slowing with expiration. Note any other irregular rhythm. If one occurs,checkifithasanypatternorifitistotallyirregular.
Premature beat—an isolated beat isearly, or apatternoccurs inwhicheverythirdorfourthbeatsoundsearly.
Irregularly irregular—no pattern to thesounds;beatscomerapidlyandatrandomintervals.
Whenyounoticeany irregularity,check forapulse deficitbyauscultatingtheapicalbeatwhilesimultaneouslypalpatingtheradialpulse.Countaserialmeasurement (one after the other) of apical beat and radial pulse. Normally,everybeatyouhearattheapexshouldperfusetotheperipheryandbepalpable.The two counts should be identical. When different, subtract the radial ratefromtheapicalandrecordtheremainderasthepulsedeficit.
Apulse deficitsignalsaweakcontrac-tionof theventricles; itoccurswithatrialfibrillation, premature beats, and heartfailure.
Identify S1 and S2. ThisisimportantbecauseS1isthestartofsystoleandthus serves as the reference point for the timing of all other cardiac sounds.Usually,youcan identifyS1 instantlybecauseyouhearapairof soundsclosetogether(lub-dup),andS1 isthefirstofthepair.Thisguidelineworks,exceptinthecasesofthetachydysrhythmias(rates>100perminute).Thenthediastolicfilling time is shortened, and the beats are too close together to distinguish.OtherguidelinestodistinguishS1fromS2are:
• S1islouderthanS2attheapex;S2islouderthanS1atthebase.• S1coincideswiththecarotidarterypulse.Feelthecarotidgentlyasyouaus-
cultateattheapex;thesoundyouhearasyoufeeleachpulseisS1(Fig.19-23).• S1coincideswiththeRwave(theupstrokeoftheQRScomplex)iftheperson
isonanECGmonitor.
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CHAPTer 19 Heart and Neck Vessels 477
Normal range of Findings Abnormal Findings
Listen to S1 and S2 Separately. Notewhethereachheartsoundisnormal,accentuated,diminished,orsplit.Inchyourdiaphragmacrossthechestasyoudothis.
First Heart Sound (S1). CausedbyclosureoftheAVvalves,S1signalsthebeginningofsystole.Youcanhearitovertheentireprecordium,althoughitisloudestattheapex(Fig.19-24).(Sometimesthetwosoundsareequallyloudattheapex,becauseS1islowerpitchedthanS2.)
Causes of accentuated or diminishedS1 (see Table 19-3, Variations in S1, onp.487).
Bothheartsoundsarediminishedwithconditionsthatplaceanincreasedamountof tissue between the heart and yourstethoscope: emphysema (hyperinflatedlungs),obesity,pericardialfluid.
You can hear S1 with the diaphragm with the person in any position andequally well in inspiration and expiration.A split S1 is normal, but it occursrarely.A splitS1meansyouarehearing themitraland tricuspidcomponentsseparately.Itisaudibleinthetricuspidvalvearea,theleftlowersternalborder.Thesplitisveryrapid,withthetwocomponentsonly0.03secondapart.
Second Heart Sound (S2). TheS2isassociatedwithclosureofthesemilu-nar valves. You can hear it with the diaphragm, over the entire precordium,althoughS2isloudestatthebase(Fig.19-25).
Accentuated or diminished S2 (seeTable 19-4, Variations in S2, onp.488).
Splitting of S2. AsplitS2isanormalphenomenonthatoccurstowardtheendofinspirationinsomepeople.Recallthatclosureoftheaorticandpulmonicvalvesisnearlysynchronous.Becauseoftheeffectsofrespirationontheheartdescribedearlier,inspirationseparatesthetimingofthetwovalves’closure,andthe aortic valve closes 0.06 second before the pulmonic valve. Instead of oneDUP, you hear a split sound—T-DUP (Fig. 19-26). During expiration, syn-chronyreturnsandtheaorticandpulmoniccomponentsfusetogether.AsplitS2isheardonlyinthepulmonicvalvearea,thesecondleftinterspace.
19-24
APEX
LUB — dup
S1 S2
19-25
S1 S2
BASE
lub — DUP
19-26
EXPIRATION INSPIRATION
SPLITTING OF THE SECOND HEART SOUND
A2-P2 A2 P2
S1 S2
lub — DUP
S1 S2
lub — T-DUP
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Normal range of Findings Abnormal Findings
WhenyoufirsthearthesplitS2,donotbetemptedtoaskthepersontoholdhisorherbreathsothatyoucanconcentrateonthesounds.Breathholdingwillonlyequalizeejectiontimesintherightandleftsidesoftheheartandcausethesplittogoaway.Instead,concentrateonthesplitasyouwatchtheperson’schestriseupanddownwithbreathing.ThesplitS2occursabouteveryfourthheart-beat,fadinginwithinhalationandfadingoutwithexhalation.
Afixed split isunaffectedby respira-tion;thesplitisalwaysthere.
Aparadoxical split is theoppositeofwhatyouwouldexpect; thesounds fuseoninspirationandsplitonexpiration(seeTable19-5,VariationsinSplitS2).
Focus on Systole, Then on Diastole, and Listen for any Extra Heart Sounds. Listenwiththediaphragm,thenswitchtothebell,coveringallaus-cultatoryareas(Fig.19-27).Usuallythesearesilentperiods.Whenyoudodetectan extra heart sound, listen carefully to note its timing and characteristics.During systole, the midsystolic click (which is associated with mitral valveprolapse) is the most common extra sound (see Table 19-6). The third andfourthheartsoundsoccurindiastole;eithermaybenormalorabnormal(seeTable19-7).
A pathologic S3 (ventricular gallop)occurswithheartfailureandvolumeover-load;apathologicS4(atrialgallop)occurswithCAD(seeTable19-7,DiastolicExtraSounds,forafulldescription).
Listen for Murmurs. Amurmurisablowing,swooshingsoundthatoccurswithturbulentbloodflowintheheartorgreatvessels.Exceptfortheinnocentmurmursdescribed,murmursareabnormal.Ifyouhearamurmur,describeitbyindicatingthesefollowingcharacteristics:
Murmurs may be due to congenitaldefects and acquired valvular defects.StudyTables19-9and19-10 foracom-pletedescription.
Timing. It is crucial to define the murmur by its occurrence in systole ordiastole.You must be able to identify S1 and S2 accurately to do this. Try tofurtherdescribethemurmurasbeinginearly,mid-,orlatesystoleordiastole;throughoutthecardiacevent(termedpansystolicorholosystolic/pandiastolicorholodiastolic);andwhetheritobscuresormufflestheheartsounds.
A systolic murmur may occur with anormalheartorwithheartdisease;adia-stolic murmur always indicates heartdisease.
Loudness. Describe the intensity in terms of six “grades.” For example,recordagradeiimurmuras“ii/vi.”
Grade i—Barelyaudible,heardonlyinaquietroomandthenwithdifficultyGrade ii—Clearlyaudible,butfaintGrade iii—Moderatelyloud,easytohearGrade iv—Loud,associatedwithathrillpalpableonthechestwallGrade v—Veryloud,heardwithonecornerofthestethoscopeliftedoffthechest
wallGrade vi—Loudest, stillheardwith entire stethoscope lifted justoff the chest
wall
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Normal range of Findings Abnormal Findings
Pitch. Describe the pitch as high, medium, or low. The pitch depends onthepressureandtherateofbloodflowproducingthemurmur.
Pattern. The intensity may follow a pattern during the cardiac phase,growinglouder(crescendo),taperingoff(decrescendo),orincreasingtoapeakandthendecreasing(crescendo-decrescendo,ordiamondshaped).Becausethewholemurmurisjustmillisecondslong,ittakespracticetodiagnoseanypattern.
Quality. Describethequalityasmusical,blowing,harsh,orrumbling. Themurmurofmitralstenosis is rum-bling, whereas that of aortic stenosis isharsh(seeTable19-10).
Location. Describetheareaofmaximumintensityofthemurmur(whereitisbestheard)bynotingthevalveareaorintercostalspaces.
Radiation. Themurmurmaybetransmitteddownstreaminthedirectionofbloodflowandmaybeheardinanotherplaceontheprecordium,theneck,theback,ortheaxilla.
Posture. Some murmurs disappear or are enhanced by a change inposition.
Some murmurs are common in healthy children or adolescents and aretermed innocentor functional.innocent indicateshavingnovalvularorotherpathologiccause;functionalisduetoincreasedbloodflowintheheart(e.g.,inanemia, fever,pregnancy,hyperthyroidism).Thecontractile forceoftheheartisgreaterinchildren.Thisincreasesbloodflowvelocity.Theincreasedvelocityplusasmallerchestmeasurementmakesanaudiblemurmur.
The innocent murmur is generally soft (grade ii), midsystolic, short, cre-scendo-decrescendo, and with a vibratory or musical quality (“vooot” soundlikefiddlestrings).Also,theinnocentmurmurisheardatthesecondorthirdleftintercostalspaceanddisappearswithsitting,andtheyoungpersonhasnoassociatedsignsofcardiacdysfunction.
Althoughitisimportanttodistinguishinnocentmurmursfrompathologicones,itisbesttosuspectallmurmursaspathologicuntiltheyareprovedoth-erwise.Diagnostic tests suchasECG,phonocardiogram,andechocardiogramareneededtoestablishanaccuratediagnosis.
Change Position. Afterauscultatinginthesupineposition,rollthepersontowardhisorherleftside.Listenwiththebellattheapexforthepresenceofanydiastolicfillingsounds(i.e.,theS3orS4)(Fig.19-28).
S3 and S4, and the murmur of mitralstenosis sometimes may be heard onlywhenontheleftside.
19-28
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Normal range of Findings Abnormal Findings
Ask theperson to situp, lean forward slightly, andexhale.Listenwith thediaphragmfirmlypressedat thebase, right,and left sides.Check for thesoft,high-pitched,earlydiastolicmurmurofaorticorpulmonicregurgitation(Fig.19-29).
Murmur of aortic regurgitation some-timesmaybeheardonlywhenthepersonisleaningforwardinthesittingposition.
DevelopmentalCompetenCe
Infants
The transition from fetal to pulmonic circulation occurs in the immediatenewbornperiod.Fetalshuntsnormallyclosewithin10to15hoursbutmaytakeup to48hours.Thusyou shouldassess the cardiovascular systemduring thefirst24hoursandagainin2to3days.
Failureofshunts toclose (e.g.,patentductus arteriosus [PDA], atrial septaldefect[ASD]);seeTable19-9.
Noteanyextracardiacsignsthatmayreflectheartstatus(particularlyintheskin),liversize,andrespiratorystatus.Theskincolorshouldbepinktopinkishbrown,dependingontheinfant’sgeneticheritage.Ifcyanosisoccurs,determineitsfirstappearance—atorshortlyafterbirthversusafter theneonatalperiod.Normally, the liver isnot enlargedand the respirationsarenot labored.Also,notetheexpectedparametersofweightgainthroughoutinfancy.
Cyanosis at or just after birth signalsoxygen desaturation of congenital heartdisease(Table19-9).
The most important signs of heartfailureinaninfantarepersistenttachycar-dia, tachypnea, and liver enlargement.Engorgedveins,galloprhythm,andpulsusalternans also are signs. Respiratorycrackles (rales) are an important sign inadultsbutnotininfants.
Failure to thrive occurs with cardiacdisease.
Palpate theapical impulse todetermine the sizeandpositionof theheart.Because the infant’shearthasamorehorizontalplacement,expect topalpatetheapicalimpulseatthefourthintercostalspacejustlateraltothemidclavicularline.Itmayormaynotbevisible.
Theapexisdisplacedwith:• Cardiacenlargement,shiftstotheleft• Pneumothorax, shifts away from
affectedside• Diaphragmatichernia,shiftsusually to
rightbecause thisherniaoccursmoreoftenontheleft
• Dextrocardia,a rareanomaly inwhichthe heart is located on right side ofchest
19-29
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CHAPTer 19 Heart and Neck Vessels 481
Normal range of Findings Abnormal Findings
The heart rate is best auscultated because radial pulses are hard to countaccurately.Usethesmall(pediatricsize)diaphragmandbell(Fig.19-30).Theheartratemayrangefrom100to180perminuteimmediatelyafterbirth,thenstabilize to an average of 120 to 140 per minute. Infants normally have widefluctuationswithactivity, from170perminuteormorewithcryingorbeingactiveto70to90perminutewithsleeping.Variationsaregreatestatbirthandareevenmoresowithprematurebabies(seeTable9-3).
Persistent tachycardia is >200 perminuteinnewborns,or>150perminuteininfants.
Bradycardiais<90perminuteinnew-bornsor <60 inolder infantsor children.This causes a serious drop in cardiacoutputbecausethesmallmusclemassoftheirheartscannotincreasestrokevolumesignificantly.
Expecttheheartrhythmtohavesinusarrhythmia,thephasicspeedinguporslowingdownwiththerespiratorycycle.
Investigateanyirregularityexceptsinusarrhythmia.
Rapidratesmakeitmorechallengingtoevaluateheartsounds.Expectheartsounds to be louder in infants than in adults because of the infant’s thinnerchestwall.Also,S2hasahigherpitchandissharperthanS1.SplittingofS2justafter the height of inspiration is common, not at birth, but beginning a fewhoursafterbirth.
Fixed split S2 indicates atrial septaldefect(seeTable19-9).
Murmursintheimmediatenewbornperioddonotnecessarilyindicatecon-genital heart disease. Murmurs are relatively common in the first 2 to 3 daysbecause of fetal shunt closure. These murmurs are usually grade i or ii, aresystolic,accompanynoothersignsofcardiacdisease,anddisappear in2 to3days.ThemurmurofPDAisacontinuousmachinerymurmur,whichdisap-pearsby2to3days.Ontheotherhand,absenceofamurmurintheimmediatenewborn period does not ensure a perfect heart; congenital defects can bepresentthatarenotsignaledbyanearlymurmur.Itisbesttolistenfrequentlyandtonoteanddescribeanymurmuraccordingtothecharacteristicslistedonp.504.
Persistent murmur after 2 to 3 days,holosystolic murmurs or those that lastintodiastole,andthosethatareloud—allwarrantfurtherevaluation.
Children
Note any extracardiac or cardiac signs that may indicate heart disease: poorweight gain, developmental delay, persistent tachycardia, tachypnea, dyspneaon exertion, cyanosis, and clubbing. Note that clubbing of fingers and toesusually does not appear until late in the 1st year, even with severe cyanoticdefects.
19-30
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482 uNiT iii Physical examination
Normal range of Findings Abnormal Findings
The apical impulse is sometimes visible in children with thin chest walls.Noteanyobviousbulgeoranyheave—thesearenotnormal.
A precordial bulge to the left of thesternumwithahyperdynamicprecordiumsignals cardiac enlargement. The bulgeoccursbecausethecartilaginousribcageismorecompliant.
A substernal heave occurs with rightventricular enlargement, and an apicalheave occurs with left ventricularhypertrophy.
Palpatetheapical impulse: inthefourth intercostalspacetothe leftof themidclavicularlineuntilage4years;atthefourthinterspaceatthemidclavicularlinefromage4to6years;andinthefifthinterspacetotherightofthemidcla-vicularlineatage7years(Fig.19-31).
Theapicalimpulsemoveslaterallywithcardiacenlargement.
Thrill(palpablevibration).
Theaverageheartrateslowsasthechildgrowsolder,althoughitisstillvari-ablewithrestoractivity(seeTable9-2).
Theheartrhythmremainscharacterizedbysinusarrhythmia.PhysiologicS3iscommoninchildren(seeTable19-7).Itoccursinearlydiastole,justafterS2,andisadullsoftsoundthatisbestheardattheapex.
A venous hum—due to turbulence of blood flow in the jugular venoussystem—iscommoninhealthychildrenandhasnopathologicsignificance.Itis a continuous, low-pitched, soft hum that is heard throughout the cycle,although it is loudest indiastole.Listenwith thebellover thesupraclavicularfossaatthemedialthirdoftheclavicle,especiallyontheright,orovertheupperanteriorchest.
The venous hum is usually not affected by respiration, may sound louderwhenthechildstands,and iseasilyobliteratedbyoccludingthe jugularveinsintheneckwithyourfingers.
Thislattermaneuverhelpsdifferentiatethe venous hum from other cardiacmurmurs(e.g.,PDA).
Heartmurmursthatareinnocent(orfunctional)inoriginareverycommonthroughchildhood.Someauthors say theyhavea30%occurrence,andsomeauthorssaynearlyallchildrenmaydemonstrateamurmuratsometime.Mostinnocentmurmurshavethesecharacteristics:soft,relativelyshortsystolicejec-tionmurmur;mediumpitch;vibratory;bestheardatthe left lowersternalormidsternalborder,withnoradiationtotheapex,base,orback.
Distinguish innocent murmurs frompathologicones.Thismayinvolvereferraltoanotherexaminerortheperformanceofdiagnostic tests such as the ECG orultrasonography.
For the child whose murmur has been shown to be innocent, it is veryimportant that the parents understand this completely. They need to believethatthismurmurisjusta“noise”andhasnopathologicsignificance.Otherwise,theparentsmaybecomeoverprotectiveand limitactivity for thechild,whichmayresultinthechilddevelopinganegativeself-concept.
19-31
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CHAPTer 19 Heart and Neck Vessels 483
Normal range of Findings Abnormal Findings
The Pregnant Woman
Thevitalsignsusuallyyieldanincreaseinrestingpulserateof10to15beatsperminuteandadropinbloodpressurefromthenormalprepregnancylevel.TheBPdecreasestoitslowestpointduringthesecondtrimesterandthenslowlyrisesduringthethirdtrimester.TheBPvarieswithposition.Itisusuallylowestinleftlateralrecumbentposition,abithigherwhensupine,andhighestwhensitting.10
Suspectpregnancy-inducedhyperten-sion with a sustained rise of 30mmHgsystolic or 15mmHg diastolic underbasalconditions.
Inspectionoftheskinoftenshowsamildhyperemiainlight-skinnedwomenbecause the increased cutaneous blood flow tries to eliminate the excess heatgeneratedbytheincreasedmetabolism.Palpationoftheapicalimpulseishigherandlateralcomparedwiththenormalposition,astheenlarginguteruselevatesthediaphragmanddisplaces theheartupandto the leftandrotates iton itslongaxis.
Auscultation of the heart sounds shows changes caused by the increasedbloodvolumeandworkload:• Heartsounds
ExaggeratedsplittingofS1andincreasedloudnessofS1
Aloud,easilyheardS3
• HeartmurmursAsystolicmurmurin90%,whichdisappearssoonafterdeliveryAsoft,diastolicmurmurheardtransientlyin19%Acontinuousmurmurfrombreastvasculaturein10%.10
Thelast-mentionedmurmuristermedamammary souffle(pronouncedsoof ′f ′l),whichoccursneartermorwhenthemotherislactating;itisduetoincreasedbloodflowthroughtheinternalmammaryartery.Themurmurisheardinthesecond,third,orfourthintercostalspace;itiscontinuous,althoughitisaccentedinsystole.Youcanobliterateitbypressurewiththestethoscopeoronefingerlateraltothemurmur.
Murmursofaorticvalvediseasecannotbeobliterated.
The ECG has no changes except for a slight left axis deviation due to thechangeintheheart’sposition.
The Aging Adult
A gradual rise in systolic blood pressure is common with aging; the diastolicbloodpressurestaysfairlyconstantwitharesultingwideningofpulsepressure.Someolderadultsexperienceorthostatic hypotension,asuddendropinbloodpressurewhenrisingtositorstand.
Usecautioninpalpatingandauscultatingthecarotidartery.Avoidpressureinthecarotidsinusarea,whichcouldcauseareflexslowingoftheheartrate.Also,pressureonthecarotidarterycouldcompromisecirculationifthearteryisalreadynarrowedbyatherosclerosis.
When measuring jugular venous pressure, view the right internal jugularvein.Theaortastiffens,dilates,andelongateswithaging,whichmaycompresstheleftneckveinsandobscurepulsationsontheleftside.15a
Thechestoftenincreasesinanteroposteriordiameterwithaging.ThismakesitmoredifficulttopalpatetheapicalimpulseandtohearthesplittingofS2.TheS4oftenoccursinolderpeoplewithnoknowncardiacdisease.Systolicmurmursarecommon,occurringinover50%ofagingpeople.15a
TheS3 isassociatedwithheart failureandisalwaysabnormaloverage35years(seeTable19-7).
Occasional premature ectopic beats are common and do not necessarilyindicate underlying heart disease. When in doubt, obtain an ECG. However,consider that theECGrecords foronlyone isolatedminute in timeandmayneedtobesupplementedbyatestof24-hourambulatoryheartmonitoring.
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484 uNiT iii Physical examination
Promoting a HealtHy lifeStyle: Women and Heart attackThe Heart Truth: Women and Heart Attacks
When someone complains of chest pain or pain radiating down the left arm, we think heart attack. After all, these are the symp-toms that typically occur, aren’t they? Well, yes and no. They are the most “typical” symptoms men have when having a myocar-dial infarction (MI), but not women. For women, symptoms can be quite different. A woman’s “atypical” symptoms may be one of the reasons that more women are dying from heart disease than men these days. According to the Women’s Heart Founda-tion, almost a third of women experience no chest pain at all when having a heart attack. Instead, 71% of women report flu-like symptoms, including extreme fatigue, for up to a month before the attack. Women are more likely to feel a hot or cold burning sensation or a tenderness to touch in their back, shoulders, arms, or jaw—not sharp pain. Women’s symptoms often include nausea, vomiting, indigestion, and shortness of breath, which are easy to attribute to something other than the heart. The evidence now shows that women tend to minimize their symptoms or attribute them to something else. This may be due to a lack of awareness.
The Heart Truth® is a national awareness and prevention campaign about heart disease in women sponsored by the National Heart, Lung, and Blood Institute (NHLBI). The campaign includes three components: (1) professional education, (2) patient education, and (3) public awareness. At The Heart Truth® website, health professionals can access both clinical and patient educa-tion resources. Of particular interest are the clinical assessment tools, including a Risk Status, LDL, and Drug-Therapy Guide; a 10-year heart attack calculator; and a body mass index (BMI) calculator, which are either available online or as an applications for a pocket PC. For patients, there is the Heart Truth E-zine, the NHBLI quarterly electronic publication that provides new informa-tion about heart disease research and heart-healthy recipes. Patients can also download the The Healthy Heart Handbook for Women.
The Red Dress® is the centerpiece of The Heart Truth® and the primary message of the campaign is Heart Disease Doesn’t Care What You Wear—It’s the #1 Killer of Women®. The idea behind using a red dress as the symbol was to draw attention to the idea that heart disease was not only a man’s issue. National Wear Red Day® is the first Friday in February. Plan to wear red and raise awareness. You may save a life!
®, ™ The Heart Truth, its logo, The Red Dress, and Heart Disease Doesn’t Care What You Wear—It’s the #1 Killer of Women are trademarks of NHBLI/ HHS. ®National Wear Red Day is a regis-tered trademark of NHBLI/HHS and AHA.
ResourcesAmerican Heart Association. Website: www.americanheart.org.National Institutes of Health National Heart, Lung, and Blood Institute.
Website: www.nhlbi.nih.gov. The Healthy Heart Handbook for Women. Website: www.nhlbi.nih.
gov/health/public/heart/other/hhw/index.htm.The Heart Truth: Awareness and Prevention. Website: www.women-
shealth.gov/hearttruth/.The Heart Truth E-zine. Website: www.nhlbi.nih.gov/educational/
hearttruth/materials/newsletter.htm.Women’s Heart Foundation. Website: www.womensheart.org/.
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D O CuMeNTATiON AND CriTiCAl THiNkiNG
Sample Charting
subjectiVe No chest pain, dyspnea, orthopnea, cough, fatigue, or edema. No history of hypertension, abnormal blood tests, heart
murmur, or rheumatic fever in self. Last ECG 2 yrs. PTA, result normal. No stress ECG or other heart tests.Family history: Father with obesity, smoking, and hypertension, treated c diuretic medication. No other family history sig-
nificant for cardiovascular disease.Personal habits: Diet balanced in 4 food groups, 2 to 3 c. regular coffee/day; no smoking; alcohol, 1 to 2 beers occasionally
on weekend; exercise, runs 2 miles, 3 to 4 ×/week; no prescription or OTC medications or street drugs.
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CHAPTer 19 Heart and Neck Vessels 485
objectiVeNeck: Carotids 2+ and = bilaterally. Internal jugular vein pulsations present when supine and disappear when elevated to a
45° position.Precordium: Inspection. No visible pulsations, no heave or lift.Palpation: Apical impulse in 5th ics at left midclavicular line, no thrill.Auscultation: Rate 68 beats per minute, rhythm regular, S1-S2 are normal, not diminished or accentuated, no S3, no S4 or
other extra sounds, no murmurs.
assessmentNeck vessels healthy by inspection and auscultationHeart sounds normal
Focused Assessment: Clinical Case Study
Mr. N.V. is a 53-year-old white male woodcutter admitted to the CCU at University Medical Center (UMC) with chest pain.
subjectiVe1 year PTA—N.V. admitted to UMC with crushing substernal chest pain, radiating to L shoulder, accompanied by nausea,
vomiting, diaphoresis.Diagnosed as MI, hospitalized 7 days, discharged with nitroglycerin prn for anginal pain.Did not return to work. Activity included walking 1 mile/day, hunting. Had occasional episodes of chest pain with
exercise, relieved by rest.1 day PTA—had increasing frequency of chest pain, about every 2 hours, lasting few minutes, saw pain as warning to go to
MD.Day of admission—severe substernal chest pain (“like someone sitting on my chest”) unrelieved by rest. Saw personal MD,
while in office had episode of chest pain as last year’s, accompanied by diaphoresis, no N & V or SOB, relieved by 1 nitro-glycerin. Transferred to UMC by paramedics. No further pain since admission 2 hours ago.
Family hx—mother died of MI at age 57.Personal habits—smokes 11
2 pack cigarettes daily × 34 years, no alcohol, diet—trying to limit fat and fried food, still high in added salt.
objectiVeExtremities: Skin pink, no cyanosis. Upper extrem.—capillary refill sluggish, no clubbing. Lower extrem.—no edema, no hair
growth 10 cm below knee bilaterally.Pulses—Carotid brachial radial femoral popliteal P.T. D.P.2+ 2+ 2+ 2+ 0 0 1+ all = bilaterally
B/P R arm 104/66 mm HgNeck: External jugulars flat. Internal jugular pulsations present when supine and absent when elevated to 45°.Precordium: Inspection. Apical impulse visible 5th ics, 7 cm left of midsternal line, no heave.Palpation: Apical impulse palpable in 5th and 6th ics. No thrill.Auscultation: Apical rate 92 bpm regular, S1-S2 are normal, not diminished or accentuated, no S3 or S4, grade iii/vi systolic
murmur present at left lower sternal border.
assessmentSubsternal chest painSystolic murmurIneffective tissue perfusion R/T interruption in flowDecreased cardiac output R/T reduction in stroke volume
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AbNOrMAl FiNDiNGS
TABLE 19-2 | Clinical Portrait of Heart Failure
Anxiety, gasping frompulmonary congestion
Falling O2 saturation
Confusion, unconsciousnessfrom decreased O2 to brain
Jugular vein distention fromvenous congestion
Infarct, may be cause ofdecreased cardiac output
Fatigue, weakness fromdecreased cardiac output
S3 gallop, tachycardia
Enlarged spleen and liver fromvenous congestion, which causespressure on breathing
Decreased urine output askidneys compensate fordecreased CO by retainingsodium and H2O
Weak pulseCool, moist skin as peripheralvasoconstriction shunts blood
to vital organs
Dilated pupils, a sympatheticnervous system response
Skin pale, gray, or cyanotic
Dyspnea, SOBOE is earlysymptom from pulmonary
congestionOrthopnea, cannot breathe
unless sitting upCrackles, wheeze are
adventitious breath soundsCough, frothy pink or white
sputum
Decreased blood pressure stimulates sympathetic nervoussystem, which acts on heart to
increase rate and increase forceof contraction
Nausea and vomiting asperistalsis slows and bile and
fluids back up into stomach
Ascites, fluid in peritoneal cavity
Dependent, pitting edema in sacrum, legs
Decreased cardiac outputoccurswhentheheartfailsasapump,andthecirculationbecomesbackedupandcongested.Signs and symptomsofheartfailurecomefromtwobasicmechanisms:(1)theheart’sinabilitytopumpenoughbloodtomeetthemetabolicdemandsofthebody;and(2)thekidney’scompensatorymechanismsofabnormalretentionofsodiumandwatertocompensateforthedecreasedcardiacoutput.Thisincreasesbloodvolumeandvenousreturn,whichcausesfurthercongestion.Onsetofheartfailuremaybe:(1)acute,asfollowingamyocardialinfarctionwhendirectdamagetotheheart’scontractingabilityhasoccurred;or(2)chronic,aswithhypertension,whentheventriclesmustpumpagainstchronicallyincreasedpressure.
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CHAPTer 19 Heart and Neck Vessels 487
AbNOrMAl FiNDiNGS FOr ADVANCeD PrACTiCe
TABLE 19-3 | Variations in S1
TheintensityofS1dependsonthreefactors:(1)positionofAVvalveatthestartofsystole,(2)structureofthevalveleaflets,and(3)howquicklypressurerisesintheventricle.
Factor Examples
loud (Accentuated) S1
S1 S2 1. PositionofAVvalveatstartofsystole—wideopenandnotimetodrifttogether
Hyperkineticstateswherebloodvelocityisincreased:exercise,fever,anemia,hyperthyroidism
2. Changeinvalvestructure—calcificationofvalve,needsincreasingventricularpressuretoclosethevalveagainstincreasedatrialpressure
Mitralstenosiswithleafletsstillmobile
Faint (Diminished) S1
S1 S2 1. PositionofAVvalve—delayedconductionfromatriatoventricles.Mitralvalvedriftsshutbeforeventricularcontractionclosesit
First-degreeheartblock(prolongedPRinterval)
2. Changeinvalvestructure—extremecalcification,whichlimitsmobility
Mitralinsufficiency
3. Moreforcefulatrialcontractionintononcompliantventricle;delaysordiminishesventricularcontraction
Severehypertension—systemicorpulmonary
Varying intensity of S1
S1 S2 S1 S2 1. PositionofAVvalvevariesbeforeclosingfrombeattobeat
Atrialfibrillation—irregularlyirregularrhythm
2. Atriaandventriclesbeatindependently CompleteheartblockwithchangingPRinterval
Split S1
S1 S2
MT
Mitralandtricuspidcomponentsareheardseparately
Normalbutuncommon
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TABLE 19-4 | Variations in S2
Condition Example
Accentuated S2
S1S2 1. Higherclosingpressure Systemichypertension,ringingorboomingS2
2. Exerciseandexcitementincreasepressureinaorta
3. Pulmonaryhypertension Mitralstenosis,heartfailure4. Semilunarvalvescalcifiedbutstillmobile Aorticorpulmonicstenosis
Diminished S2
S1 S2 1. Afallinsystemicbloodpressurecausesadecreaseinvalvestrength
Shock
2. Semilunarvalvesthickenedandcalcified,withdecreasedmobility
Aorticorpulmonicstenosis
TABLE 19-5 | Variations in Split S2
Normal Splitting
S1 S2
A2
S2
P2
S1
EXPIRATION INSPIRATION
A2-P2
Condition Example
Fixed Split
S1
A2
S2
P2A2
S2
P2
S1
EXPIRATION INSPIRATION Afixedsplitisunaffectedbyrespiration;thesplitisalwaysthere.
AtrialseptaldefectRightventricularfailure
Paradoxical Split
S1 S2S1
P2
S2
A2
EXPIRATION INSPIRATION Conditionsthatdelayaorticvalveclosurecausetheoppositeofanormalsplit.Ininspiration,P2isnormallydelayedsowithaparadoxicalsplit,thesoundsfuse.Inexpiration,youhearthesplit,intheorderofP2A2.
AorticstenosisLeftbundlebranchblockPatentductusarteriosus
Wide Split
S1
A2
S2
P2
S1
EXPIRATION INSPIRATION
A2
S2
P2
MT
Whentherightventriclehasdelayedelectricalactivation,thesplitisverywideoninspirationandisstillthereonexpiration.
Rightbundlebranchblock(whichdelaysP2)
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CHAPTer 19 Heart and Neck Vessels 489
TABLE 19-6 | Systolic extra Sounds
Earlysystolic:EjectionclickAorticprostheticvalvesounds
Mid-/latesystolic:Midsystolic(mitral)click
S1 S2
Ej
S1 S2
Ej
EXPIRATION INSPIRATION
Aortic ejection click(apex and base)
S1 S2
Ej
S2S1
Ej
Pulmonic ejection click(base only)
Ejection Click
Theejectionclickoccursearlyinsystoleatthestartofejectionbecauseitresultsfromopeningofthesemilunarvalves.Nor-mally,theSLvalvesopensilently,butinthepresenceofstenosis(e.g.,aorticstenosis,pulmonicstenosis),theiropeningmakesasound.Itisshortandhighpitched,withaclickquality,andisheardbetterwiththediaphragm.
Theaorticejectionclickisheardatthesecondrightinterspaceandapexandmaybeloudestattheapex.Itsintensitydoesnotchangewithrespiration.Thepulmonicejectionclickisbestheardinthesecondleftinterspaceandoftengrowssofterwithinspiration.
“Ball-in-cage”AO = aortic opensAC = aortic closes
S1 S2
SEMAO
AC
Aortic Prosthetic Valve Sounds
Asasequelaofmoderntechnologicinterventionforheartproblems,somepeoplenowhaveiatrogenicallyinducedheartsounds.Theopeningofamechanicalaorticball-in-cageprosthesisproducesanearlysystolicsound.Thissoundislessintensewithatiltingdiskprosthesisandisabsentwithabiologictissueprosthesis(e.g.,porcine).
S1S2C S1S2C S2C
ApexC = click
S1
Midsystolic Click
Althoughitissystolic,thisisnotanejectionclick.Itisassociatedwithmitral valve prolapse,inwhichthemitralvalveleafletsnotonlyclosewithcontractionbutballoonbackupintotheleftatrium.Duringballooning,thesuddentensingofthevalveleafletsandthechordaetendineaecreatestheclick.
Thesoundoccursinmid-tolatesystoleandisshortandhighpitched,withaclickquality.Itisbestheardwiththedia-phragm,attheapex,butalsomaybeheardattheleftlowersternalborder.Theclickusuallyisfollowedbyasystolicmurmur.Theclickandmurmurmovewithposturalchange;whenthepersonassumesasquattingposition,theclickmaymoveclosertoS2,andthemurmurmaysoundlouderanddelayed.TheValsalvamaneuveralsomovestheclickclosertoS2.
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TABLE 19-7 | Diastolic extra Sounds
Earlydiastole:OpeningsnapMitralprostheticvalvesound
Mid-diastole:ThirdheartsoundSummationsound(S3+S4)
Latediastole:FourthheartsoundPacemaker-inducedsound
EXPIRATION INSPIRATION
S1 S2
A2
S2
P2
S1
OS OS
Opening Snap
NormallytheopeningoftheAVvalvesissilent.Inthepresenceofstenosis,increasinglyhigheratrialpressureisrequiredtoopenthevalve.Thedeformedvalveopenswithanoise:theopeningsnap.Itissharpandhighpitched,withasnappingquality.ItsoundsafterS2andisbestheardwiththediaphragmatthethirdorfourthleftinterspaceatthesternalborder,lesswellattheapex.
Theopeningsnapusuallyisnotanisolatedsound.Asasignofmitralstenosis,theopeningsnapusuallyushersinthelow-pitcheddiastolicrumblingmurmurofthatcondition.
“Ball-in-cage”
MO = mitral prosthesis opensMC = S1
S2
SEM
S1
MOMC
Mitral Prosthetic Valve Sound
Aniatrogenicsound,theopeningofaball-in-cagemitralprosthesisgivesanearlydiastolicsound:anopeningclickjustafterS2.Itisloud,isheardoverthewholeprecordium,andisloudestattheapexandleftlowersternalborder.
S1 S2 S2S1S3 S3
LUB – duppa LUB – duppa
Third Heart Sound
TheS3isaventricularfillingsound.Itoccursinearlydiastoleduringtherapidfillingphase.YourhearingquicklyaccommodatestotheS3,soitisbestheardwhenyoulisteninitially.ItsoundsafterS2butlaterthananopeningsnapwouldbe.Itisadull,softsound,anditislowpitched,like“distantthunder.”Itisheardbestinaquietroom,attheapex,withthebellheldlightly(justenoughtoformaseal),andwiththepersonintheleftlateralposition.
TheS3canbeconfusedwithasplitS2.UsetheseguidelinestodistinguishtheS3:• Location—TheS3isheardattheapexorleftlowersternalborder;thesplitS2atthebase.• Respiratory variation—TheS3doesnotvaryintimingwithrespirations;thesplitS2does.• Pitch—TheS3islowerpitched;thepitchofthesplitS2staysthesame.TheS3maybenormal(physiologic)orabnormal(pathologic).Thephysiologic S3isheardfrequentlyinchildrenandyoungadults;itoccasionallymaypersistafterage40years,especiallyinwomen.ThenormalS3usuallydisappearswhenthepersonsitsup.
Inadults, theS3 isusuallyabnormal.Thepathologic S3 isalsocalledaventricular galloporanS3gallop,anditpersistswhensittingup.TheS3indicatesdecreasedcomplianceoftheventricles,asinheartfailure.TheS3maybetheearliestsignofheartfailure.TheS3mayoriginatefromeithertheleftortherightventricle;aleft-sidedS3isheardattheapexintheleftlateralposition,andaright-sidedS3isheardattheleftlowersternalborderwiththepersonsupineandislouderininspiration.
TheS3occursalsowithconditionsofvolumeoverload,suchasmitralregurgitationandaorticortricuspidregurgitation.The S3 is also found in high cardiac output states in the absence of heart disease, such as hyperthyroidism, anemia, andpregnancy.Whentheprimaryconditioniscorrected,thegallopdisappears.
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CHAPTer 19 Heart and Neck Vessels 491
S1 S2 S2S1S4 S4
daLUB – dup daLUB – dup
Fourth Heart Sound
TheS4isaventricularfillingsound.Itoccurswhentheatriacontractlateindiastole.ItisheardimmediatelybeforeS1.Thisisaverysoftsound,ofverylowpitch.Youneedagoodbell,andyoumustlistenforit.Itisheardbestattheapex,withthepersoninleftlateralposition.
Aphysiologic S4mayoccurinadultsolderthan40or50yearswithnoevidenceofcardiovasculardisease,especiallyafterexercise.
Apathologic S4istermedanatrial galloporanS4gallop.Itoccurswithdecreasedcomplianceoftheventricle(e.g.,coro-nary artery disease, cardiomyopathy) and with systolic overload (afterload), including outflow obstruction to the ventricle(aorticstenosis)andsystemichypertension.Aleft-sidedS4occurswiththeseconditions.Itisheardbestattheapex,intheleftlateralposition.
Aright-sidedS4islesscommon.Itisheardattheleftlowersternalborderandmayincreasewithinspiration.Itoccurswithpulmonarystenosisorpulmonaryhypertension.
S1 S2 S2S1S3 S3S4 S4
S1 S2 S2S1S3andS4
S3andS4
Summation Sound
WhenboththepathologicS3andS4arepresent,aquadruplerhythmisheard.Often,incasesofcardiacstress,oneresponseistachycardia.Duringrapidrates,thediastolicfillingtimeshortensandtheS3andS4moveclosertogether.Theysoundsuper-imposedinmid-diastole,andyouhearoneloud,prolonged,summatedsound,oftenlouderthaneitherS1orS2.
eXtracardiac sounds
S1 S2 S1
Pericardial Friction Rub
Inflammationof thepericardiumgives rise toa frictionrub.The sound ishighpitchedand scratchy, like sandpaperbeingrubbed. It is best heard with the diaphragm, with the person sitting up and leaning forward, and with the breath held inexpiration.
Africtionrubcanbeheardanyplaceontheprecordiumbutusuallyisbestheardattheapexandleftlowersternalborder,placeswherethepericardiumcomesinclosecontactwiththechestwall.Timingmaybesystolicanddiastolic.Thefrictionrubofpericarditisiscommonduringthe1stweekafteramyocardialinfarctionandmaylastonlyafewhours.
TABLE 19-7 | Diastolic extra Sounds—cont’d
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TABLE 19-8 | Abnormal Pulsations on the Precordium
Base Left Sternal Border
Athrillinthesecondandthirdrightinterspacesoccurswithsevereaorticstenosisandsystemichypertension. Athrillinthesecondandthirdleftinterspacesoccurswithpulmonicstenosisandpulmonichypertension.
A lift (heave) occurs with right ventricular hypertrophy, asfoundinpulmonicvalvedisease,pulmonichypertension,andchroniclungdisease.Youfeeladiffuseliftingimpulseduringsystoleat the left lower sternalborder. Itmaybeassociatedwithretractionattheapexbecausetheleftventricleisrotatedposteriorlybytheenlargedrightventricle.
Apex Apex
Cardiac enlargement displaces the apical impulse laterallyandoverawiderareawhenleftventricularhypertrophyanddilation are present. This is volume overload, as in mitralregurgitation,aorticregurgitation,andleft-to-rightshunts.
Theapicalimpulseisincreasedinforceanddurationbutisnot necessarily displaced to the left when left ventricularhypertrophyoccursalonewithoutdilation.Thisispressure overload,asfoundinaorticstenosisorsystemichypertension.
Images © Pat Thomas, 2006.
TABLE 19-9 | Congenital Heart Defects
Description ClinicalData
Patent Ductus Arteriosus (PDA)Persistenceofthechanneljoining
leftpulmonaryarterytoaorta.Thisisnormalinthefetusandusuallyclosesspontaneouslywithinhoursofbirth.
S:Usuallynosymptomsinearlychildhood;growthanddevelopmentarenormal.
O:Bloodpressurehaswidepulsepressureandboundingperipheralpulsesfromrapidrunoffofbloodintolow-resistancepulmonarybedduringdiastole.Thrilloftenpalpableatleftuppersternalborder.Thecontinuousmurmurheardinsystoleanddiastoleiscalledamachinery murmur.
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CHAPTer 19 Heart and Neck Vessels 493
Description ClinicalData
Atrial Septal Defect (ASD)Abnormal opening in the atrial
septum, resulting usually in left-to-right shunt and causing largeincrease in pulmonary bloodflow.
S:Defectisremarkablywelltolerated.Symptomsininfantarerare;growthanddevelopmentnormal.ChildrenandyoungadultshavemildfatigueandDOE.
O:Sternalliftoftenpresent.S2hasfixedsplit,withP2oftenlouder than A2. Murmur is systolic, ejection, mediumpitch,bestheardatbaseinsecondleftinterspace.Murmurcaused not by shunt itself but by increased blood flowthroughpulmonicvalve.
Ventricular Septal Defect (VSD)Abnormal opening in septum
between the ventricles, usuallysubaorticarea.Thesizeandexactpositionvaryconsiderably.
S: Small defects are asymptomatic. Infants with largedefects have poor growth, slow weight gain; later lookpale, thin, delicate. May have feeding problems; DOE;frequent respiratory infections;andwhen theconditionissevere,heartfailure.
O: Loud, harsh holosystolic murmur, best heard at leftlowersternalborder,maybeaccompaniedbythrill.Largedefects also have soft diastolic murmur at apex (mitralflow murmur) due to increased blood flow throughmitralvalve.
Tetralogy of FallotFour components: (1) right ven-
tricularoutflowstenosis,(2)VSD,(3)rightventricularhypertrophy,and (4) overriding aorta. Result:shunts a lot of venous blooddirectlyintoaortaawayfrompul-monary system, so blood nevergetsoxygenated.
S:Severecyanosis,notinfirstmonthsof lifebutdevelopsasinfantgrowsandRVoutflow(i.e.,pulmonic)stenosisgetsworse.Cyanosiswithcryingandexertionatfirst,thenatrest.Usessquattingpostureafterstartswalking.DOEcommon.Developmentisslowed.
O:Thrillpalpableatleftlowersternalborder.S1normal;S2has A2 loud and P2 diminished or absent. Murmur issystolic,loud,crescendo-decrescendo.
Coarctation of the AortaSevere narrowing of descending
aorta, usually at the junction ofthe ductus arteriosus and theaortic arch, just distal to theorigin of the left subclavianartery.Resultsinincreasedwork-loadonleftventricle.
Associated with defects of aorticvalve in most cases, as well asassociatedpatentductusarterio-sus; and associated ventricularseptaldefect.
S:Ininfantswithassociatedlesionsorsymptoms,diagnosisoccurs infirst fewmonthsassymptomsofheart failuredevelop. For asymptomatic children and adolescents,growth and development are normal. Diagnosis usuallyincidental due to blood pressure findings. Adolescentsmaycomplainofvaguelowerextremitycrampingthatisworsewithexercise.
O: Upper extremity hypertension over 20mmHg higherthanlowerextremitymeasuresisahallmarkofcoarcta-tion.Anotherimportantsignisabsentorgreatlydimin-ishedfemoralpulses.Asystolicmurmurisheardbestattheleftsternalborder,radiatingtotheback.
S, Subjective data; O, objective data. Images © Pat Thomas, 2006.
TABLE 19-9 | Congenital Heart Defects—cont’d
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TABLE 19-10 | Murmurs Due to Valvular Defects
Midsystolic ejection Murmurs Duetoforwardflowthroughsemilunarvalves
SYSTOLE DIASTOLE
S1 S1S2 S2 S1 S2
Description ClinicalData
Aortic StenosisCalcification of aortic valve cusps
restricts forward flow of bloodduring systole; LV hypertrophydevelops.
S: Fatigue, DOE, palpitation, dizziness, fainting,anginalpain.
O:Pallor,slowdiminishedradialpulse,lowbloodpressure, and auscultatory gap are common.Apical impulse sustained and displaced to left.Thrill in systole over second and third rightinterspaces and right side of neck. S1 normal,often ejection click present, often paradoxicalsplitS2, S4presentwithLVhypertrophy.
Murmur: Loud, harsh, midsystolic, crescendo-decrescendo, loudestatsecondright interspace,radiateswidelytosideofneck,downleftsternalborder,orapex.
Pulmonic StenosisCalcification of pulmonic valve
restrictsforwardflowofblood.O:Thrillinsystoleatsecondandthirdleftinter-
space,ejectionclickoftenpresentafterS1,dimin-ishedS2andusuallywithwidesplit,S4commonwithRVhypertrophy.
Murmur: Systolic, medium pitch, coarse,crescendo-decrescendo (diamond shape), bestheardatsecondleftinterspace,radiatestotheleftandneck.
S, Subjective data; O, objective data. Images © Pat Thomas, 2006.Continued
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Midsystolic ejection Murmurs Duetoforwardflowthroughsemilunarvalves
SYSTOLE DIASTOLE
S1 S1S2 S2 S1 S2
Description ClinicalData
Pansystolic regurgitant MurmursDuetobackwardflowofbloodfromareaofhigherpressuretooneoflowerpressure
SYSTOLE DIASTOLE
S1 S1S2 S2 S1 S2
Description ClinicalData
Mitral RegurgitationStreamofbloodregurgitatesbackinto
LAduringsystolethroughincompe-tent mitral valve. In diastole, bloodpassesbackintoLVagainalongwithnewflow;resultsinLVdilationandhypertrophy.
S:Fatigue,palpitation,orthopnea,PND.O: Thrill in systole at apex. Lift at apex. Apical
impulse displaced down and to left. S1 dimin-ished,S2accentuated,S3atapexoftenpresent.
Murmur: Pansystolic, often loud, blowing, bestheardatapex,radiateswelltoleftaxilla.
Tricuspid RegurgitationBackflowofbloodthroughincompe-
tenttricuspidvalveintoRA.O:Engorgedpulsatingneckveins, liverenlarged.
LiftatsternumifRVhypertrophypresent,oftenthrillatleftlowersternalborder.
Murmur: Soft, blowing, pansystolic, best heardat left lower sternal border, increases withinspiration.
CHAPTer 19 Heart and Neck Vessels 495
S, Subjective data; O, objective data. Images © Pat Thomas, 2006.
TABLE 19-10 | Murmurs Due to Valvular Defects—cont’d
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Midsystolic ejection Murmurs Duetoforwardflowthroughsemilunarvalves
SYSTOLE DIASTOLE
S1 S1S2 S2 S1 S2
Description ClinicalData
Diastolic rumbles of AV ValvesFillingmurmursatlowpressures,bestheardwithbelllightlytouchingskin
SYSTOLE DIASTOLE
S1
OS OS OS
S1S2 S2 S1 S2
Description ClinicalData
Mitral StenosisCalcified mitral valve will not open
properly, impedes forward flow ofblood into LV during diastole.ResultsinLAenlargedandLApres-sureincreased.
S: Fatigue, palpitations, DOE, orthopnea, occa-sionalPNDorpulmonaryedema.
O:Diminished,oftenirregulararterialpulse.Liftat apex, diastolic thrill common at apex. S1accentuated; opening snap after S2 heard overwideareaofprecordium,followedbymurmur.
Murmur: Low-pitched diastolic rumble, bestheardatapex,withpersoninleftlateralposition;doesnotradiate.
Tricuspid StenosisCalcification of tricuspid valve
impedes forward flow into RVduringdiastole.
O:Diminishedarterialpulse,jugularvenouspulseprominent.
Murmur:Diastolicrumble;bestheardatleftlowersternalborder;louderininspiration.
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S, Subjective data; O, objective data. Images © Pat Thomas, 2006.
TABLE 19-10 | Murmurs Due to Valvular Defects—cont’d
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Images © Pat Thomas, 2006.
Midsystolic ejection Murmurs Duetoforwardflowthroughsemilunarvalves
SYSTOLE DIASTOLE
S1 S1S2 S2 S1 S2
Description ClinicalData
early Diastolic MurmursDuetoSLvalveincompetence
SYSTOLE DIASTOLE
S1 S1S2 S2 S1 S2
Description ClinicalData
Aortic RegurgitationStreamofbloodregurgitatesback
throughincompetentaorticvalveintoLVduringdiastole.LVdilationandhypertrophyduetoincreasedLVstrokevolume.Rapidejectionoflargestrokevolumeintopoorlyfilledaorta,thenrapidrunoffindiastoleaspartofbloodpushedbackintoLV.
S:Onlyminorsymptomsformanyyears,thenrapiddeterioration:DOE,PND,angina,dizziness.
O:Bounding“water-hammer”pulseincarotid,brachial,andfemoralarteries.Bloodpressurehaswidepulsepressure.Pulsationsincervicalandsuprasternalarea,apicalimpulsedisplacedtoleftanddown,apicalimpulsefeelsbrief.
MurmurstartsalmostsimultaneouslywithS2:softhighpitched,blowingdiastolic,decrescendo,bestheardatthirdleftinterspaceatbase,aspersonsitsupandleansforward,radiatesdown.
Pulmonic RegurgitationBackflowofbloodthrough
incompetentpulmonicvalve,frompulmonaryarterytoRV.
Murmurhassametimingandcharacteristicsasthatofaorticregurgitation,andishardtodistinguishonphysicalexamination.
S, Subjective data; O, objective data.
CHAPTer 19 Heart and Neck Vessels 497
TABLE 19-10 | Murmurs Due to Valvular Defects—cont’d
Summary Checklist: Heart and Neck Vessels exam
ForaPDA-downloadableversion,gotohttp://evolve.elsevier.com/Jarvis/.
Neck1. Carotid pulse—Observe and
palpate2. Observejugularvenouspulse3. EstimatejugularvenouspressurePrecordium
Inspection and palpation1. Describelocationofapicalimpulse2. Noteanyheave(lift)orthrill
Auscultation1. Identifyanatomicareaswhereyou
listen2. Noterateandrhythmofheartbeat3. Identify S1 and S2 and note any
variation4. Listen in systole and diastole for
anyextraheartsounds
5. Listen in systole and diastole foranymurmurs
6. Repeatsequencewithbell7. Listen at the apex with person in
leftlateralposition8. Listen at the base with person in
sittingposition
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498 uNiT iii Physical examination
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