455 CHAPTER 19 Heart and Neck Vessels http://evolve.elsevier.com/Jarvis/ • Animations • Audio Heart and Lung Sounds • Audio Key Points • Case Studies Chest Pain Shortness of Breath • Health Promotion Guide Heart Disease • Bedside Assessment Summary Checklist • Quick Assessments for Common Conditions Congestive Heart Failure (CHF) Hyperlipidemia Myocardial Infarction • Physical Examination Summary Checklist • Video—Assessment Neck Vessel and Heart num. The heart extends from the second to the fifth intercos- tal space and from the right border of the sternum to the left midclavicular line. Think of the heart as an upside-down triangle in the chest. The “top” of the heart is the broader base, and the “bottom” is the apex, which points down and to the left (Fig. 19-3). During contraction, the apex beats against the chest wall, pro- ducing an apical impulse. This is palpable in most people, normally at the fifth intercostal space, 7 to 9 cm from the mid- sternal line. Inside the body, the heart is rotated so that its right side is anterior and its left side is mostly posterior. Of the heart’s four chambers, the right ventricle forms the greatest area of OUTLINE Structure and Function Position and Surface Landmarks Heart Wall, Chambers, and Valves Direction of Blood Flow Cardiac Cycle Heart Sounds Conduction Pumping Ability The Neck Vessels Subjective Data Health History Questions Objective Data Preparation The Neck Vessels The Precordium Summary Checklist: Heart and Neck Vessels Exam Documentation and Critical Thinking Abnormal Findings Abnormal Findings for Advanced Practice STRUCTURE AND FUNCTION The cardiovascular system consists of the heart (a muscular pump) and the blood vessels. The blood vessels are arranged in two continuous loops, the pulmonary circulation and the systemic circulation (Fig. 19-1). When the heart contracts, it pumps blood simultaneously into both loops. POSITION AND SURFACE LANDMARKS The precordium is the area on the anterior chest directly overlying the heart and great vessels (Fig. 19-2). The great vessels are the major arteries and veins connected to the heart. The heart and the great vessels are located between the lungs in the middle third of the thoracic cage, called the mediasti- Jarvis_1517_Chapter 19_main.indd 455 1/6/2011 4:57:07 PM
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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
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-
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.
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.
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.
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
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.)
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.
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
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)
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.
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 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.
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.
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.
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
• Nosignificantchangeindiastolicpressureoccurswithage.A rising systolic pressure with a relatively constant dia-stolicpressureincreasesthepulsepressure(thedifferencebetweenthetwo).
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
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
• 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-
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
occurs with heart failure. Lying downincreases volume of intrathoracic blood,andtheweakenedheartcannotaccommo-date the increased load. Classically, thepersonawakensafter2hoursofsleepwiththeperceptionofneedingfreshair.
3. Orthopnea. Howmanypillowsdoyouusewhensleepingorlyingdown? Orthopnea is the need to assume amoreuprightpositiontobreathe.Notetheexactnumberofpillowsused.
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
• 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.
• 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?
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?
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.
4. Activity:Werethisbaby’smotormilestonesachievedasexpected?Isthebabyable to play without tiring? How many naps does the baby take each day?Howlongdoesanaplast?
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?
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.
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.
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.
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.
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
ThinkofthejugularveinsasaCVPmanometerattacheddirectlytotherightatrium.Youcan“read”theCVPatthehighestlevelofpulsations(Fig.19-18).Use the angle of Louis (sternal angle) as an arbitrary reference point, andcompareitwiththehighestlevelofthedistendedveinorvenouspulsation.
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.
(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).
• 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.
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:
Recall the characteristicsof a good stethoscope (seeChapter8).Clean theendpieceswithanalcoholwipe;youwillusebothendpieces.Althoughallheartsoundsarelowfrequency,thediaphragmisforrelativelyhigherpitchedsoundsandthebellisforrelativelylowerpitchedones.
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:
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.
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.”
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).
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.
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.
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
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.
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.
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.
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.
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.
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
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.
When measuring jugular venous pressure, view the right internal jugularvein.Theaortastiffens,dilates,andelongateswithaging,whichmaycompresstheleftneckveinsandobscurepulsationsontheleftside.15a
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.
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/
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
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
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.
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.
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.
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.
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.
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.
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.
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.
O:Diminished,oftenirregulararterialpulse.Liftat apex, diastolic thrill common at apex. S1accentuated; opening snap after S2 heard overwideareaofprecordium,followedbymurmur.
5.Armbrister, K. A. (2008). Self-management: improving heartfailureoutcomes.The Nurse Practitioner,33(11),20-28.
6.Aronow, W. S. (2006). Heart disease and aging. The Medical Clinics of North America,90(1),849-862.
7.Braveman,P.A.,Cubbin,C.,Egerter,S.,etal.(2010).Socioeco-nomicdisparities inhealthintheUnitedStates:whatthepat-terns tellus.American Journal of Public Health,100(Suppl.1),S186-S196.
8.Brown,D.W.,Giles,W.H.,&Croft,J.B.(2009).Associationofcardiacauscultatoryfindingswithcoronaryheartdiseasemor-tality.North American Journal of Medical Sciences,1,327-332.
9.Conn,R.D.,&O’Keefe,J.H.(2009).Cardiacphysicaldiagnosisinthedigitalage:animportantbutincreasinglyneglectedskill(from stethoscopes to microchips). The American Journal of Cardiology,104(4),590-595.
13.Dracup, K., et al. (2008). Acute coronary syndrome: what dopatientsknow?Archives of Internal Medicine,168(10),1049-1054.
14.Dressler,D.K.(2009).Deathbyclot:acutecoronarysyndromes,ischemicstroke,pulmonaryembolism,anddisseminatedintra-vascular coagulation. AACN Advanced Critical Care, 20(2),166-176.
15.Eslick,G.D.(2005).Usefulnessofchestpaincharacterandloca-tion as diagnostic indicators of an acute coronary syndrome.The American Journal of Cardiology,95(1),1228-1231.
15a. Fleg,J.L.(1990).Diagnosticevaluations.InW.B.Abrams&R.Berkow (Eds.), The Merck manual of geriatrics. Rahway, NJ:Merck,Sharp,&Dohme.
16.Fleiner, S. (2006). Recognition and stabilization of neonateswith congenital heart disease. Newborn and Infant Nursing Reviews,6(3),137-150.
17.Grossman,V.G.A.,&McGowan,B.A.(2008).Posturalortho-static tachycardia syndrome.The American Journal of Nursing,108(8),58-60.
18.Hartas,G.,Tsounias,E.,&Gupta-Malhotra,M.(2009).Approachtodiagnosingcongenitalcardiacdisorders.Critical Care Nursing Clinics of North America,21(1),27-36.
20.Klein,D.G.(2005).Thoracicaorticaneurysms.The Journal of Cardiovascular Nursing,20,245-250.
21.Kliegman,R.M.etal.(2007).Nelson textbook of pediatrics(18thed.).Philadelphia:Saunders.
22.Klieman,L.,Hyde,S.,&Berra,K.(2006).Cardiovasculardiseaserisk reduction in older adults. The Journal of Cardiovascular Nursing,21,527-539.
23.Kumar,A.,&Cannon,C.P.(2009).Acutecoronarysyndromes:diagnosis and management, Part I. Mayo Clinic Proceedings,84(10),917-938.
24.Lembo,N.J.,etal.(1988).Bedsidediagnosisofsystolicmurmurs.The New England Journal of Medicine,318(24),1572-1578.
25.Lloyd-Jones,D.M.,etal.(2010).Definingandsettingnationalgoals for cardiovascular health promotion and disease reduc-tion: the American Heart Association’s strategic impact goalthrough2010andbeyond.Circulation,121(1),586-613.
26.Matthews,K.A.,Crawford,S.L.,Chae,C.U.,etal.(2009).Arechangesincardiovasculardiseaseriskfactorsinmidlifewomendue to chronological aging or to the menopausal transition?Journal of the American College of Cardiology,54,2366-2373.
27.McGee, S. (2007). Evidence based physical diagnosis (2nd ed.).Philadelphia:Saunders.
28.Moe,G.W.,&Tu,J.(2010).Heartfailureintheethnicminori-ties.Current Opinion in Cardiology,2,124-130.
29.Mosack,V.,&Steinke,E.E. (2009).Trends in sexualconcernsafter myocardial infarction. The Journal of Cardiovascular Nursing,24(2),162-170.
30.Mosley, W., & Lloyd-Jones, D. M. (2009). Epidemiology ofhypertensionintheelderly.Clinics in Geriatric Medicine,25(2),179-189.
31.Moulton,S.A.(2009).HypertensioninAfricanAmericansanditsrelatedchronicdiseases.Journal of Cultural Diversity,16(4),165-170.
32.Muster,A.J.,etal.(2009).Ten-yearecho/Dopplerdeterminationof the benefits of aerobic exercise after the age of 65 years.Echocardiography,27(1),5-10.
33.National Center for Health Statistics. (2009). Health, United States, 2008 with chartbook.Hyattsville,MD:Author.RetrievedMay20,2010,fromwww.cdc.gov/nchs/data/hus/hus08.pdf.
34.Overbaugh,K.J.(2009).Acutecoronarysyndrome.The Ameri-can Journal of Nursing,109(5),42-52.
35.Perloff,J.K.(2000).Physical examination of the heart and circu-lation(3rded.).Philadelphia:Saunders.
42.Tanaka, H. (2009). Habitual exercise for the elderly. Family & Community Health,32(Suppl.1),S57-S65.
43.Thompson, J. (2006). Psychological and physical etiologies ofheartpalpitations.The Nurse Practitioner,31(2),14-25.
44.Tilkian, A. G., & Conover, M. B. (2001). Understanding heart sounds and murmurs with an introduction to lung sounds (4thed.).Philadelphia:Saunders.
45.Turris,S.A.(2009).Women’sdecisionstoseektreatmentforthesymptomsofpotentialcardiacillness.Journal of Nursing Schol-arship,41(1),5-12.
46.Wei, J.Y. (1992).Ageand thecardiovascular system.The New England Journal of Medicine,327,1735-1739.
47.Yusuf,S.,Hawken,S.,Ounpuu,S.,etal.(2004).Effectofpoten-tiallymodifiableriskfactorsassociatedwithmyocardialinfarc-tion in 52 countries (the INTERHEART study). Lancet, 364,937-952.
48.Zipes,D.,etal.(2008).Braunwald’s heart disease: a textbook of cardiovascular medicine(8thed.).Philadelphia:Saunders.