heart wall, chambers, and valves - … · heart wall, chambers, and valves direction of blood flow...

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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-

Jarvis_1517_Chapter 19_main.indd 455 1/6/2011 4:57:07 PM

456 uNiT iii Physical examination

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

1

2

3

4

5

6

Apex

Base

7

8

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.


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


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

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19-5

to abdomen and lowerextemities

to head and neck

to armsto arms

41

2

5

3

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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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

120

100

80

60

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mm Hg 0

Rapidfilling

(protodiastolic)

Slowfilling

SYSTOLEEjection

DIASTOLERapidfilling

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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

19-7

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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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


Bundle of HisSA node

AV node

CONDUCTION SYSTEMELECTROCARDIOGRAPH

(ECG) WAVE

PQ

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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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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

Y

TP

QRS

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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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19-13

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

19-15

Aging

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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SubjeCTiVe DATA

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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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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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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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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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.

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19-17

1

2

3

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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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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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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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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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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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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

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S1 S2

BASE

lub — DUP

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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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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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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.

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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

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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.

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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.

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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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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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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.



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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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


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


A2

S2

P2

MT

Whentherightventriclehasdelayedelectricalactivation,thesplitisverywideoninspirationandisstillthereonexpiration.

Rightbundlebranchblock(whichdelaysP2)

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TABLE 19-6 | Systolic extra Sounds

Earlysystolic:EjectionclickAorticprostheticvalvesounds

Mid-/latesystolic:Midsystolic(mitral)click

S1 S2

Ej

S1 S2

Ej


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


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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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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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


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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SYSTOLE DIASTOLE

S1 S1S2 S2 S1 S2


Pansystolic regurgitant MurmursDuetobackwardflowofbloodfromareaofhigherpressuretooneoflowerpressure

SYSTOLE DIASTOLE

S1 S1S2 S2 S1 S2


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.



TABLE 19-10 | Murmurs Due to Valvular Defects—cont’d

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SYSTOLE DIASTOLE

S1 S1S2 S2 S1 S2


Diastolic rumbles of AV ValvesFillingmurmursatlowpressures,bestheardwithbelllightlytouchingskin

SYSTOLE DIASTOLE

S1

OS OS OS

S1S2 S2 S1 S2


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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Images © Pat Thomas, 2006.


SYSTOLE DIASTOLE

S1 S1S2 S2 S1 S2


early Diastolic MurmursDuetoSLvalveincompetence

SYSTOLE DIASTOLE

S1 S1S2 S2 S1 S2


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.



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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heart wall, chambers, and valves - … · heart wall, chambers, and valves direction of blood flow...

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