1-7 Levick and Dwight - Cardiovascular

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Expert Review Examination of the Cardiovascular System

C Levick and J Dwight……………………………………………………………………………………………………………………………………..

The Journal of Clinical Examination 2007; 3: 8-14

Abstract Examination of the cardiovascular system is a vital part of every general examination. This papersuggests an examination routine in a logical order consistent with The Principles of Clinical Examination [1] onwhich more individualised examinations can be developed. The routine for the cardiovascular examination isbased on the methods of examination described in textbooks [2-7] and peer reviewed journals as well as theexperiences of the authors. The common and important signs of cardiovascular pathology are described andweight given to their diagnostic value. This paper is aimed at medical students and junior doctors. Word count:3108 (excluding figures, tables and references)

Key words: Clinical examination, cardiovascular system

Add ress fo r correspondence: [email protected]

Authors ’ aff il iat ions : *Final year medical student, University of Oxford. #Consultant Cardiologist, John RadcliffeHospital, Oxford.

……………………………………………………………………………………………………………………………………..

IntroductionThe cardiovascular examination is one of the mostimportant and frequently used examinations inmedical practice, so it is essential that all doctorshave a routine of examination that reliably detectsthe common and serious cardiovascular

pathologies. Very few physical signs are specific fora given pathology. Mistakes are often made whentoo greater reliance is put on a single physical sign.The key to the cardiovascular examination is theability to put together the findings on clinicalexamination to give a probable diagnosis. Theexamination routine described here includes thecore elements of the physical examination andadheres to the conventional inspect, palpate,percuss, auscultate order of examination (whereapplicable) as it follows a path from the end of thebed, up the arm to the face, down to the chest andfinally the feet. The purpose of this rather

regimented approach is simply to avoid missingpotentially useful clinical information. However thecardiovascular clinical examination should not bemechanical. At each stage in the examination theclinician should assess the significance of thefindings to date and try to put them into context.Where the findings do not appear to be consistentwith the proposed diagnosis there is every reason tore examine the patient to try to resolve anydiscrepancies. The examination may not always beconclusive and occasionally one is still left withnumber of potential diagnoses.

General inspectionLike all physical examinations, the cardiovascularexamination begins with the examiner introducing

him/herself, obtaining consent and washing his/herhands. The patient should ideally have their chestfully exposed and be positioned at a 45º angle.

Observe the patient and their surroundings from theend of the bed. Does the patient look well or

unwell? If they appear unwell, try to think why thatis. Pay attention to their colour, respiratory rate andbody habitus. The rest of the examination is carriedout from the left of the bed.

The handsFirst inspect the fingernails from the side and abovefor clubbing and splinter haemorrhages. Clubbingdescribes an angle between the nail and nail fold ofover 180º, increased nail curvature and nail bedbogginess. Clubbing is a highly significant sign, buthas a wide range of causes (see Table 1). Splinterhaemorrhages occur along the longitudinal axis of

the nail bed. They are often caused by trauma butare also a classical sign of infective endocarditis.

Table 1 Causes of clubbing

Cardiovascular Cyanotic heart diseaseInfective endocarditis Atrial myxoma

Respiratory Suppurative lung diseasesBronchial carcinomaPulmonary fibrosis

Gastrointestinal Inflammatory bowel disease

CirrhosisOther Hereditary



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Next, look and feel along the finger tendons andpalms for xanthomata (cholesterol deposits fromhyperlipidaemia), fingers for tar-staining fromcigarettes, pulps of the fingers for Osler nodes(tender nodules) and palms for Janeway lesions(blanchable, erythematous macules). Clubbing,splinter haemorrhages, Osler nodes and Janewaylesions are all signs of infective endocarditis, but itshould be remembered that these signs are rare inmodern medicine and their absence does notexclude the diagnosis. Inspect the colour of the skinfor peripheral cyanosis and the palmer creases forthe pallor of anaemia. Feel the skin and check thecapillary refill time by firmly squeezing the fingertipfor 5 seconds then recording the time taken for theskin to return from white to pink. A capillary refilltime of over 2 seconds is abnormal, but be awarethat a cold environment may be the cause. Askyourself, is the patient warm and well-perfused or isthe patient cool, clammy and peripherallyshutdown?

The radial pulseThe radial pulse can either be assessed during orafter the examination of the hands. This pulse ispalpated using three fingertips over the radial artery,situated just medial to the radius. When feeling thepulse determine the rate and rhythm over at least a15 second period, multiplying the number of beatsby 4 to get the heart rate in beats per minute.Normal heart rate is 60-100 beats per minute. Anabnormal pulse rate has low specificity, but is oftenan early and sensitive sign of pathology. Decide ifthe rhythm is regular (sinus rhythm), irregularlyirregular (atrial fibrillation) or regularly irregular. Dueto variations in stroke volume when the pulse isirregular, assessment of heart rate using the radialartery may be inaccurate and the heart rate is moreaccurately assessed by listening with thestethoscope over the apex [6].

Next hold the flats of your fingers across theanterior aspect of the forearm so that the radialpulse is impalpable, check that the patient has nopain in their shoulder and then lift their arm abovetheir head whilst keeping your hand on theirforearm. A forceful impulse felt throughout theforearm is characteristic of aortic regurgitation andis sometimes called a muscle knock.

At this stage in the examination, the radial pulse ofthe right arm can be compared with the femoralpulse in young patients to check for a delay causedby coarctation of the aorta (patients rarely survive

with untreated coarctation beyond the age of 40). Alternatively, this could be left until the end of theexamination. Some sources recommend checking

for radio radial delay, but as this is present in only2% of patients with coarctation [4], checking for radiofemoral delay is advised for a higher diagnosticyield. Now, check for equality of the radial pulses.Some patients with atherosclerosis develop diseaseof the subclavian vessels, giving rise to aninequality in the radial pulses. Unequal arm pulsesmay also indicate aortic dissection and so should bechecked in patients complaining of chest pain [8].Positive findings warrant measurement of the bloodpressure in all four limbs, but note that a 10 mmHgdiscrepancy in systolic BP between arms and a 20mmHg higher systolic BP in the legs is normal.

The blood pressureNext, measure the blood pressure (BP) using anappropriately sized blood pressure cuff on the leftarm. First, palpate the radial artery and inflate theBP cuff until the pulse is no longer palpable. Thepressure at which the pulse is lost is an estimate ofthe systolic blood pressure. Deflate the cuff thenposition the bell of your stethoscope over thebrachial artery in the antecubital fossa. Reinflate thecuff 20-30 mmHg above the estimated systolic BPbefore deflating the cuff at a maximal rate of 2mmHg per second. Record the pressure to thenearest 2 mmHg at which the pulse is first audible(Korotkoff I) and the sound disappears (Korotkoff V)[9]. These correspond to the systolic and diastolicpressures respectively. Normal systolic BP is 100-140 mmHg and normal diastolic BP is 60-90 mmHg.These readings can also be used to calculate thepulse pressure (difference between the systolic anddiastolic BPs), which is wide in aortic regurgitationand narrow in aortic stenosis.

Pulsus paradoxicus is the variation in systolic bloodpressure which occurs with respiration and can bepresent in normal subjects. It can only be measuredmanually. Normally the systolic pressure falls ininspiration by a maximum of 10 mmHg or 10% ofthe systolic blood pressure due to a fall inintrathoracic pressure. In cardiac tamponade andsevere asthma there is a greater fall. To measureparadox deflate the cuff slowly until you hear thefirst Korotkoff sound, initially this may be intermittentwith the phases of respiration indicating thepresence of paradox, note the pressure. Deflate thecuff further until the systolic sound is heardthroughout respiration. The difference in pressure atthis point and the first measurement is the amountof paradox in mmHg.

If indicated by the history, check for postural

hypotension by comparing the lying BP with astanding BP measurement made within 1 minute of



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standing up. A fall of 15 mmHg systolic or 10 mmHgdiastolic is significant.

The face and eyesInspect the face for syndromic faces such asDown’s syndrome, which may increase yoursuspicion for particular cardiovascular anomalies.Look for cholesterol deposits around the eyes(xanthelasmata) and the iris (senile arcus), whichmay indicate hyperlipidaemia or be a normaldevelopment with age. Gently pull down the bottomeyelid whilst the patient looks up to inspect for theconjunctival pallor of anaemia. Fundoscopy ishelpful in confirming features of end organ damagein hypertension (a-v nipping, hard exudates andhaemorrhages etc) and endocarditis (Roth spots

due to embolic retinal damage). Look for a malarflush across the nose and cheeks caused by mitralstenosis, then, inspect the mouth for the high-arched palate of Marfan’s syndrome, dentalhygiene, petechiae from infective endocarditis andcentral cyanosis.

The neckMost students find assessment of the JVP the mostdifficult part of the cardiovascular examination. Twocommon errors are made. The first is to have theneck turned too far to the left. In patients withprominent sternocleidomastiod muscles this oftenmakes the internal jugular pulse more difficult tosee. Often it is easier to see the JVP simply byasking the patient to extend their neck directly back.The second is to fail to look for the JVP at areasonable distance from the patient, a high JVPcan often be seen more readily from end of the bedrather than close up. Try to outline the JVPwaveform against the pillow with an oblique lightshining on the neck. The height of the JVP in theinternal jugular vein provides an estimate of thecentral venous pressure and thus the intravascularvolume status and right heart function. Look for theJVP along the line of the internal jugular vein whichlies deep to sternocleidomastoid and follows a pathfrom below the earlobe to enter the thorax betweenthe two heads of sternocleidomastoid. When theJVP is low it may simply appear as a diffuseintermittent swelling in the root of the neck. The JVPhas an impalpable, double impulse, that varies withrespiration and position and rises transiently withcompression of the upper abdomen. These factorsallow it to be differentiated from the carotid pulse,which has a single, sharp palpable impulse.

With the patient at 45º, measure the highest point ofthe JVP in centimetres vertical from the sternalangle. The maximal normal JVP is 4cm. If the top of

the JVP cannot be seen, it may either be high orlow. Flicking of the earlobe is suggestive of a raised

JVP. To bring the top of the JVP into view, changethe angle of the patient appropriately. The height ofthe JVP is a reliable indicator of the central venouspressure if high or low, but a normal JVP does notrule out an abnormal central venous pressure [10]. An elevated JVP indicates fluid overload or heartfailure, whilst a low JVP indicates an underfilledvascular compartment. In practical terms if the JVPis easily seen it is usually elevated!

Ask the patient about abdominal pain, then applyfirm pressure to the upper abdomen for 20 secondswhilst observing the JVP. A persistent rise in theJVP throughout the period of compression is apositive abdominojugular reflex sign, indicating rightventricular failure. The area of compression does

not have to be over the liver as was previouslybelieved.

Now interpret the JVP waveform. The normal JVPwaveform is shown in relation to the cardiac cycle inFigure 1 and common abnormalities of the JVP aresummarised in Table 2. It is often very difficult todistinguish the wave forms of the JVP.Simultaneous palpation of the contralateral carotidpulse can help in the recognition of the v wave.Prominent v waves are characteristic of tricuspidregurgitation where the timing of the v wavecoincides with the carotid pulse (normally the peakof the v wave occurs slightly before the carotidpulse). a waves are absent in atrial fibrillation andirregular, large a waves (cannon waves) arecharacteristic of complete heart block. An importantsign of cardiac tamponade and constrictivepericarditis is Kussmaul’s sign, a paradoxical rise inthe JVP on inspiration.

Table 2 Causes of abnormalities of the JVP.

Elevation: Heart failure, fluid overload, corpulmonale, superior vena cava obstruction

Rises on inspiration: Cardiac tamponade,constrictive pericarditis (Kussmaul’s sign)

Absent a waves: Atrial fibrillation

Giant v waves: Tricuspid regurgitation

Cannon waves: Complete heart block

Next, palpate the carotid pulse, found deep andalong the medial aspect of sternocleidomastoid toassess the character and volume of the pulse. Thebrachial artery can also be felt for this purpose, butany smaller arteries cannot be interpretedaccurately [7]. A slow rising, small volume pulse is areliable indicator of aortic stenosis [12], a double orsometimes triple impulse pulse is often found inhypertrophic cardiomyopathy and a bounding pulseis caused by CO2 retention, sepsis or liver failure.



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The precordiumFirst inspect the precordium

for skeletal abnormality, scars,pacemakers, visible heaves orapex beats. The tick of amechanical heart valve mayalso be audible. Next, palpatethe apex beat. This is locatedin the mid-clavicular line in thefifth intercostal space, justbelow the left nipple in men.Find this location by palpatingthe sternal angle, moving yourfingers laterally to the secondintercostals space, then

counting down the intercostalsspaces in the mid-clavicularline. The apex beat cannot befelt in 50% of patients, butbefore deciding that yourpatient falls into this category,feel laterally and inferiorly. Alaterally of inferiorly deviatedapex beat suggestscardiomegaly [7]. Simultaneouspalpation of the carotid pulsemay reveal apical carotiddelay, a sign of aortic stenosis[12]. Place the flats of yourfingers across the chest to note

thecharacter of the impulse.

This can be quite subjective, so the simplest andarguably most useful classification of apex beatcharacters is into normal, volume overloaded,pressure overloaded or a combination of the two. Anormal apex beat is felt as the apex of the heartpressing into one or two of your fingers and fallingaway. A volume overloaded or dilated left ventriclegives rise to an apex beat which is more diffuse anddisplaced laterally and/or inferiorly. This is a featureof aortic regurgitation, mitral regurgitation, dilatedcardiomyopathies and ventricular damage due toischaemic heart disease. A pressure overloaded leftventricle due to aortic stenosis or hypertension ishypertrophied and has a forceful, heaving quality.The location of the apex beat is often normal unlessthe ventricle has also dilated. Other descriptions ofthe apex beat include tapping (a palpable firstsound in mitral stenosis) or double impulse(hypertrophic cardiomyopathy).

Palpate over the lower left sternal edge with theheel of your hand for a right ventricular heave, felt

as a push against your hand. This signifies rightventricular hypertrophy. Next palpate for thrills(transmitted murmurs) using the flats of your fingers

over the apex (mitral area), lower left sternal edge(tricuspid area), right 2nd intercostals space (aorticarea) and left 2nd intercostals space (pulmonaryarea). These areas are shown in Figure 2.

By this stage in the examination, you should have agood idea of what to expect on auscultation giventhe clues from the peripheral examination. It isimportant for beginners to time the heart soundswith the carotid pulse in order to differentiate systoleand diastole. Assess and concentrate on each ofthe components of the cardiac cycle in turn (heartsounds, added sounds, systole, diastole). Listenfirst with the diaphragm of the stethoscope over thefour valve areas as indicated in Figure 2. Repeatthe auscultation now using the bell of thestethoscope to allow easier detection of low pitchedmurmurs and sounds (particularly a third or fourthheart sound). In each area, determine the presenceand relative intensity of heart sounds one (S1) andtwo (S2) before listening for additional sounds. S1and S2 are produced by closing of the heart valves

(see Figure 1). A loud pulmonary S2 is caused bypulmonary hypertension and a loud aortic S2 bysystemic hypertension. Muffled heart sounds are

Mitral v.opens

Mitral v.closes

Aor ti c v . opens

Aorti c v .closes

I s o v o l u m

e t r i c

c o n t r a c t i o n

I s o v o l u m e t r i c

r e l a x a t i o nVentricular

ejectionVentricular filling

Ventricular filling

Ventricular diastoleVentricular systole At rialsystole

120

80

40

0

Aorta

JVP

Leftventricle

Y descent

V wave

X descent

C wave A wave

P r e s s u r e

( m m H g )

4 1 2 3

A P

Phono-cardiogram

Figure 1. The cardiac cyc le. Adapted from JR Levick [11].



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caused by cardiac tamponade. It is normal foraudible splitting of the S2 to occur, which increasesduring inspiration, but wide splitting is due todelayed emptying of the right ventricle and fixedsplitting is due to an atrial septal defect.

Figure 2 A reas of auscultation.

Now listen between the heart sounds. There may beadditional heart sounds, opening clicks from valves,pericardial friction rubs or murmurs. Time thesesounds with the cardiac cycle by simultaneouspalpation of the carotid pulse. Third (S3) and fourth(S4) heart sounds are low-pitched and heard bestover the apex. S3 occurs just after S2 and is causedby passive filling of the ventricles. This may bephysiological in young people, but may be due to ahigh output state or dilated left ventricle in olderpeople. S4 is always pathological. It occurs justbefore S1 and is caused by atrial contraction

against a noncompliant ventricle. Ejection systolicclicks occur in aortic stenosis or a bicuspid aorticvalve, a diastolic opening snap occurs in mitralstenosis and a mid-systolic click is caused by mitralvalve prolapse and may be accompanied by a latesystolic murmur. Pericarditis causes a pericardialfriction rub classically described as sounding likefootsteps crunching in fresh snow, not confined tosystole or diastole.

For a murmur, characterise it in terms of timing inrelation to the cardiac cycle, character, pitch, sitewhere loudest, peak intensity and radiation. Out of

these factors, the timing in relation to the cardiaccycle is the most diagnostic [12]. The intensity of amurmur is divided into 6 grades, shown in Table 3.

Intensity tends not to correlate well with the severityof valvular dysfunction, but a change in intensity isan important sign of progression. The common sitesof radiation are to the carotids (aortic stenosis) andto the left axilla (mitral regurgitation), so these areasshould be auscultated in all CVS examinations.Listen over both carotid arteries using the bell whilstthe patient comfortably holds a breath. The bruit ofcarotid stenosis can be differentiated from theradiation of aortic stenosis by determining thelocation of the peak intensity of the sound. Carotidbruits tend to be louder above the thyroid cartilage,whereas a systolic murmur is loudest over theprecordium [13].

Grade 1 Audible to an expert under optimumconditions

Grade 2 Audible to non-experts under optimumconditions

Grade 3 Easily audible, no thrill

Grade 4 Loud, with a thrill

Grade 5 Very loud or over a wide area, with athrill

Grade 6 Audible without a stethoscope

Table 3 Grades of murmur intensity

Special manoeuvres may be used to increase theintensity and improve the detection of murmurs. The

following two manoeuvres should be performed inall patients in order to detect the two most commondiastolic murmurs. Turn the patient into the leftlateral position with their breath held in expirationand auscultate the apex with the bell to listen formitral stenosis. Next, listen with the diaphragm ofthe stethoscope at the lower left sternal edge withthe patient sitting forward with their breath held inexpiration for the murmur of aortic regurgitation.This manoeuvre often also makes aortic stenosiseasier to characterise. Inspiration increases theintensity of right-sided murmurs, whilst expirationincreases the intensity of left-sided murmurs. Otherspecial manoeuvres include the Valsalvamanoeuvre, standing and squatting and isometricexercise, but these are not routine.

It is not necessary to limit yourself to the fourstandard areas. Many systolic murmurs are heardboth in the aortic and mitral areas. Where this is thecase track the murmur from the aortic area to themitral area to see if the intensity changes helping todifferentiate between aortic stenosis and mitralregurgitation, or the character changes indicatingthat both valve lesions exist. Table 4 shows thedifferential diagnosis of different timed murmurs andTable 5 shows the clinical findings of the mostcommon valve dysfunctions.



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Pathology Peripheralfeatures

Apex beat Heart sounds Murmurtiming

Murmursite

Murmurcharacter

Murmurradiation

Aorticstenosis

Slow rising,smallvolumepulse

Pressureoverloaded

Quiet A2 ± S4 Ejectionsystolic

Aorticarea

Harsh Carotids

Aorticregurgitation

Collapsing,largevolumepulse

Volumeoverloaded

Normal ± S3 Diastolic Lower leftsternaledge

Blowing Apex ifsevere

Mitralstenosis

Malar flush Tapping Opening snap,loud S1

Mid-latediastolic

Apex Rumbling ±pre-systolicaccentuation

Axilla

Mitral

regurgitation

Nil Volume

overloaded

Quiet S1 ± S3 Pan

systolic

Apex Blowing Axilla

Mitralprolapse

Nil Volumeoverloaded

Normal Latesystolic

Apex Crescendo-decrescendowithprecedingmid-systolicclick

Axilla

Tricuspidregurgitation

Prominent vwaves onJVP,pulsatileliver

Normal ±rightventricularheave

Normal Pansystolic

Tricuspidarea

Very soft Nil

Table 5. Summary table of examination findings in the common cardiac valve dysfunctions.

The back, abdomen and legsWhilst the patient is sitting forward, examine thebases of the lungs for the crackles of pulmonaryoedema or pleural effusions in heart failure. Withone finger press firmly on the sacrum for 15seconds then release to check for sacral pittingoedema. If pitting oedema is present, theindentation of your finger will be left in the skin.Next, lie the patient flat and palpate the liver forenlargement in heart failure and pulsatility intricuspid regurgitation. Finally, check the ankles forpitting oedema, progressing up the leg to record thelevel at which the oedema ends. In severe cases,this may extend up to the abdomen. Examination ofthe peripheral vascular system should beperformed, but the description of this is beyond thescope of this review.

Bedside investigationsTo complete the assessment of the patient, thefollowing bedside tests should be performed. Takethe patient’s temperature, oxygen saturations,electrocardiogram and urinalysis. Thank the patientand help them to dress, then present or record yourfindings.

Timing Causes

Ejection systolic Flow Aortic stenosisPulmonary stenosisCoarctation of the aortaHypertrophiccardiomyopathy

Pan systolic Mitral regurgitationTricuspid regurgitationVentricular septal defect

Late systolic Mitral valve prolapse

Early diastolic Aortic regurgitationPulmonary regurgitation

Mid-late diastolic Mitral stenosis

Table 4 Differential diagnosis of murmurs.

DiscussionThe order of examination and the techniquesdescribed in this paper are largely due to tradition

and the experiences of the authors. There havebeen relatively few attempts to validate one style of



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examination over another or to quantify theinterobserver or intraobserver reproducibility ofphysical signs. More research is necessary into theaccuracy of examination findings and their practicalimportance.

ConclusionThis paper has described a routine of examinationthat will enable the detection of most cardiovasculardiseases. It can be used as a framework on whichcardiovascular examinations can be tailored to aparticular patient and their condition or which can bealtered to suit your personal style. A summary of theimportant steps in the CVS examination is shown inTable 6.

Table 6 Examination checklist.

IntroductionInspection from the end of the bedExamination of the handsPalpation of the radial pulse Assessment for a muscle knockMeasurement of the blood pressureInspection of the face, eyes and mouthExamination of the JVPPalpation of the carotid pulseInspection, palpation and auscultation of theprecordium

Auscultation of the lung basesPalpation of the liverPalpation for dependent oedema Ask for temperature, oxygen saturations,electrocardiogram and urinalysisThank the patient

The cardiovascular examination is by no meanseasy as the signs can often be subtle or difficult todifferentiate. Just remember to be methodical andthink about your findings at every step of theexamination. As always, practice makes perfect.

Conflicts of interestNone declared

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[2] Douglas G, Nicol F, Robertson C. Macleod’sclinical examination. 11th edition. Elsevier ChurchillLivingstone. 2005.

[3] Longmore M, Wilkinson IB, Rajagopalan S.Oxford Handbook of Clinical Medicine. 6th edition.Oxford University Press. 2004.

[4] Ryder REJ, Freeman EA. An aid to the MRCPPACES. Volume 1: Stations 1, 3 and 5. 3rd edition.Blackwell Publishing. 2003.

[5] Talley NJ, O'Connor S. Clinical Examination, 5thEdition. 2005. Churchill Livingstone.

[6] Timmis AD, Nathan AW, Sullivan ID. EssentialCardiology. 3rd edition. Blackwell Publishing. 1997.

[7] Yusuf S, Cairns J, Camm J, Fallen E, Gersh B.Evidence Based Cardiology. 2nd edition. BlackwellBMJ Books. 2002.

[8] Klompas M. The Rational Clinical Examination.Does this patient have an acute thoracic aorticdissection? JAMA 2002. 287; 17: 2262-72.

[9] Reeves RA. The Rational clinical Examination.Does this patient have hypertension? How tomeasure blood pressure. JAMA 1995. 273; 15:1211-18.

[10] Cook DJ, Simel DL. The Rational clinicalExamination. Does this patient have abnormalcentral venous pressure? JAMA 1996. 275; 8: 630-634.

[11] Levick JR. An Introduction to CardiovascularPhysiology. Arnold Publishers. 2003.

[12] Etchells E, Bell C, Robb K. The Rational clinicalExamination. Does this patient have an abnormalsystolic murmur? JAMA 1997. 277; 7: 564-571.

[13] Sauvé JS, Laupacis A, østbye T, Feagan B,Sackett DL. The Rational Clinical Examination.Does this patient have a clinically important carotidbruit? JAMA 1993. 270; 23: 2843-45.

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