Editorial

See related article on page 10.

“The troublewith doctors is not that they don’t knowenough, but that they don’t see enough.”—Sir Dominic J. Corrigan (1802-1880)

“Where is the jugular venous pressure?” Failure to identify the height of the jugular venous

pulsations most commonly results from failure to lookfor it. Once a cardinal aspect of the clinical cardiovas-cular examination, jugular venous pulsations areunlikely to be sought by contemporary physiciansunless we can convince them of three principles: (1) Itis important to be able to assess cardiac filling pres-sures. (2) Jugular venous pressure often reflects cardiacfilling pressures. (3) Jugular venous pressure can bereliably assessed at the bedside.

The importance of assessing volumestatus

Abnormalities in the regulation of volume status playa central role in the progression of heart failure andaccount for the majority of the symptoms leading tohospitalization for heart failure. Although the review byMcGee1 on page 10 of this issue and most related arti-cles focus on heart failure, abnormalities of volume sta-tus can influence and be influenced by failure of mostorgan systems, such as the pulmonary, renal, andhepatic systems. In addition, other noncardiac crisessuch as hemorrhage and sepsis may often be suspectedand monitored by their effects on apparent volume sta-tus. The fundamental importance of volume status tomost areas of medicine is further enhanced by itsamenability to therapy. As in the old adage describingdermatology, we can usually intervene to make the drybecome wet and the wet become dry. For heart failurein particular, this amenability is of growing importancebecause it has been demonstrated that the majority ofpatients do well with intracardiac filling pressures thatare near normal levels.2-4

Circulating volume expansion leads to centralvenous pressure elevation.5 The relation between ele-vated central volume and elevated central venouspressures is complex, particularly in patients withalterations in vascular tone, such as in chronic heartfailure. As McGee emphasizes in his review, increasedvenous tone contributes to the elevated central venouspressures in heart failure. Initial therapy to reducethese pressures usually includes both diuretics andvasodilators, whereas in patients already receivingeffective vasodilator regimens, alteration in diureticsalone is often adequate to restore normal jugularvenous pressure. While recognizing that both volumeand vascular tone contribute to the cardiac filling pres-sures, for simplicity the distinction will be allowed toblur in this review.

If cardiac filling pressures are important, how shouldthey best be assessed? In the technologically richUnited States, there are many options for electronicmonitoring of patients lying supine in intensive careunits with nursing ratios of 1 to 1 or higher. Thesepatients constitute the minority requiring medical atten-tion, however. Outpatient clinics and urgent care andemergency centers provide the usual interfaces withdisease. The questions: Is there a problem? What is theproblem? Is treatment working? are most often askedoutside an intensive care unit, where the technologicalsupport immediately available has not advanced veryfar beyond the stethoscope and sphygmomanometer.The portable ability to answer the fundamental ques-tions is vital and requires knowledge and practice inthe skills of physical examination and history taking.

Where to look at volume status inheart failure

History yields multiple clues about cardiac fillingpressures in heart failure. Orthopnea is perhaps themost sensitive symptom suggesting elevated left-sidedfilling pressures and usually total volume overload,6

which can also be suggested by patient recognition ofedema or ascites, or early satiety and right abdominaldiscomfort. A symptom often elicited but rarely volun-teered is the feeling of head and neck fullness whenbending over. In diseases characterized by chronicfluid retention such as heart and kidney failure, the

The jugular veins: Knowing enough to lookEvagoras Economides, MD,a and Lynne Warner Stevenson, MDb Albany, N.Y., and Boston, Mass.

From the aDepartment of Internal Medicine, Albany Medical College, and the bDivi-sion of Cardiology, Brigham and Women’s Hospital.Reprint requests: Lynne Warner Stevenson, MD, Brigham and Women’sHospital/Cardiovascular Division, 75 Francis St., Boston, MA 02115.E-mail: lwstevenso@bics.bwh.harvard.eduAm Heart J 1998;136:6-9.0002-8403/98/$5.00 + 0 4/1/90220

American Heart JournalVolume 136, Number 1 Economides and Stevenson 7

symptom of thirst is relatively less helpful because itmay also be seen when volume is high. Symptoms ofrelative volume depletion generally appear first whenthe patient is in the upright position, in which he orshe can describe the typical dizziness or light-headed-ness, which can also be perceived as weakness orwobbly legs.

The physical examination yields its best direct cluesto volume status in acute illness of an otherwisehealthy patient, such as the appearance of rales withnew myocardial infarction, in which there has been notime for compensation. In chronic heart failure, how-ever, the expected rales are seldom encounteredbecause of the remarkable facility of the pulmonarylymphatics to hypertrophy to handle the excessextravascular water.6 Rales are, on the other hand, theonly physical sign that reflects solely left-sided fillingpressures. A third heart sound, which may arise fromeither or both ventricles, provides a clue that cardiacdisease is present; but once that is known, its presenceis not very sensitive or specific for estimation of vol-ume status. For an individual patient, however,changes in the intensity of the third heart sound mayparallel changes in volume status over time.

The remaining common signs of fluid overloadreflect primarily elevated right-sided filling pressuresand thus may reflect multiple sites of elevated pres-sures proximal to the left ventricle, such as mitralstenosis, pulmonary hypertension, or primary rightventricular disease. It is actually surprising, and fortu-nate for clinical cardiologists, that the chronic eleva-tion of left-sided pressures is transduced as frequentlyand reliably as it is through the pulmonary circulationand the right ventricle, with changes qualitatively con-current in approximately 70% of 1000 patients withchronic heart failure (Drazner M, personal communica-tion, 1997). Of the other signs of elevated right-sidedfilling pressures, peripheral edema is less than 30%sensitive. Although fairly specific in adults whose onlyknown diagnosis is cardiopulmonary disease, edemawithout elevated central venous pressures occurs com-monly in patients with obesity, peripheral venous dis-ease, and advancing age. In the absence of noncardiacdisease, pulsatile hepatomegaly with or without ascitesis a helpful sign of elevated central venous pressure.

Jugular venous pressure remains the most reliable“dipstick” for detection of central venous pressure ele-vation because a patent jugular vein must reflect cen-tral venous pressure, independent of the forces gov-erning extravascular fluid accumulation elsewhere in

the body. As discussed in the accompanying reviewarticle, assessment of the jugular venous pressurebecame an objective end point frequently used fordiagnosis and adjustment of therapy in chronic heartfailure.1,6,7 It should be noted that severe elevation ofright-sided pressures in chronic heart failure is almostalways accompanied by significant tricuspid regurgita-tion, waves of which emphasize the elevated meanvenous pressures. The identification of jugular venouspressures can be enhanced by the abdominojugulartest.8 Currently, clinicians such as Jay Cohn, Gary Fran-cis, Barry Massie, and many others involved in theactual daily care of patients with heart failure wouldconfirm their regular reliance on jugular venous pres-sure estimation. (Further embellishments such as theValsalva response are useful in specialized practice butless generalizable.)9

Can jugular venous pressure bereliably assessed?

The main focus of the current review is whether andhow jugular venous pressure can accurately beassessed by the clinician at the bedside. Several stud-ies indicate the poor reliability of such assessment incritically ill patients in intensive care units.10,11 Admis-sion to an intensive care unit itself already selects agroup of patients in whom diagnosis and therapy areunusually complex. For those studies, invasive moni-toring was not a random event but deemed to be nec-essary on a clinical basis. The decision to monitor apatient invasively is highly influenced by physicianuncertainty regarding the clinical assessment of hemo-dynamic status and by failure of clinical response totherapies guided by the noninvasive assessment. Inac-curate assessment of the jugular venous pressuredescribed in the current review and by previousauthors is particularly common in patients receivingmechanical ventilation.10,11 As suggested previously,such patients frequently warrant invasive hemody-namic monitoring for multiple reasons.

The primary population in whom clinical assessmentof the jugular venous pressure is important is insteadthat encountered in the office, the emergency room,and routine hospital floors. In patients with chronicheart failure outside intensive care units, clinicalassessment has been more encouraging when per-formed by clinicians experienced in the assessment ofheart failure.6,9,12 As discussed by McGee, this mea-surement can be very useful to guide diagnosis andtherapy when appropriately performed. Nonetheless,

there is currently widespread skepticism about the useof learning this skill. The most common error seen isunderestimation of the elevation of jugular venouspressure.

How can we improve?The current review focuses first on the importance

of defining the sternal angle as an external referencepoint. The multiple inaccuracies that may result fromthis are clearly minor compared with the importanceof having a uniform standard that is easily identified.The authors also focus on the vital concept of the ver-tical distance, which is critical. The angle of the bed isirrelevant as long as the top of the venous column canbe identified and the vertical distance to the sternalangle determined. Too many eager young clinicianshave been deterred from jugular vein examination bythe impossibility of establishing the precise angle ofbed elevation without a protractor. Once the verticaldistance has been visualized, the next common error isto underestimate its actual height in centimeters,because this is not a familiar unit in the United States.Because most clinicians do not carry rulers, it is valu-able to substitute the extended span of their ownhand, which need only be measured once.

Perhaps the most useful clinical point emphasizedby McGee, however, is the necessity to examine thepatient while he or she is in the supine position. Wehave found that many inconsistencies between exam-iners in jugular venous assessment result from thetemptation, as rounds accelerate, to examine the neckveins as a patient sits in a chair to eat or returns fromthe bathroom. The reason for the exaggerated posturaldependence in chronic heart failure remains complex.On the one hand, a patient with decreased venouscompliance might be expected to have less fall whenblood pools upon standing. On the other hand, somepatients with heart failure have been shown to haveinappropriate vasodilation while standing, whichwould tend to cause a greater decline in filling pres-sures. The latter seems to be most commonlyobserved. An additional useful clinical point raisedhere is the frequent occurrence of Kussmaul’s sign ofincreased jugular venous pressure with inspiration inpatients with severely volume-loaded right ventricles.

McGee has done the jugular venous examinationconsiderable service by clarifying the way in which itshould be performed. The major limitation to currentuse, however, is lack of practice. Few people seekopportunities to do what they do not do well. Looking

American Heart JournalJuly 1998Economides and Stevenson8

for the jugular veins only when their message is likelyto be crucial will further diminish accuracy. Examina-tion of the jugular veins should be an integral part ofevery physical examination, just as we routinely listento the chest despite the low yield of positive findings.Concerted effort should be made to calibrate an indi-vidual’s examination on every patient in whom a cen-tral venous pressure will be invasively measured. Thismay be of infinitely more value than, for instance,competing for the opportunity to perform occasionalintubation “to keep one’s hand in.”

Medical education has changed radically but contin-ues to rely on apprenticeship. The responsibility toencourage skillful jugular venous examination remainswith the attending physicians, particularly where inva-sive monitoring is frequently performed. Challenges toguess the pressures and cardiac output have honedthis skill in academic environments, where it mightotherwise have been lost. There are certainly patientsin whom the jugular venous pressure is not possiblefor most clinicians to assess because of body habitus,tortuous carotids, bandages, or mechanicalventilation.13 It is important to identify honestly thedegree of uncertainty and the degree of relevance todecide when invasive monitoring is indicated.

How good can we get?McGee indicates that the first priority is to identify

whether jugular venous pressures are elevated, normal,or indeterminate. This is a good starting place and maybe all that is vital for triage of a patient in an emer-gency room. However, even there it may be helpful toknow when the filling pressures are very high in heartfailure or very low in hemorrhage. There is clearly agreater need, however, for sequential evaluation in theoutpatient clinic and in the hospital wards where diure-sis or other vasoactive therapy is being adjusted. Per-haps the most compelling argument for the consistentstruggle to discern degrees of jugular venous pressureelevation is that we become confident in our abilityonly at a level lower than that to which we aspire.

To know enough to lookThere thus exists strong rationale for assessing car-

diac filling pressures, among which is the jugularvenous pressure. McGee has given us reason tobelieve that we can restore the art of jugular veinassessment. To answer the rebuke of Sir Corrigan, thisreview has helped us to know enough. It is now ourchallenge to look enough to see.

American Heart JournalVolume 136, Number 1 Economides and Stevenson 9

References1. McGee SR. Physical examination of venous pressure: a critical

review. Am Heart J 1998;136;10-8.2. Stevenson LW, Tillisch JH. Maintenance of cardiac output with normal

filling pressures in dilated heart failure. Circulation 1986;5:175-7.3. Stevenson LW, Tillisch JH, Hamilton MA, Luu M, Chelimsky-Fallick

C, Moriguchi J, et al. Importance of hemodynamic response to ther-apy in predicting survival with ejection fraction ≤20%. Am J Cardiol1990;66:1348-54.

4. Steimle AE, Stevenson LW, Chelimsky-Fallick C, Fonarow GC,Hamilton MA, Moriguchi JD, et al. Sustained hemodynamic effi-cacy of therapy tailored to reduce filling pressures in survivors withsustained heart failure. Circulation 1997;96:1165-72.

5. Cohn JN. Central venous pressure as a guide to volume expansion.Ann Int Med 1967;66:1283-6.

6. Stevenson LW, Perloff JK. The limited reliability of physical signs for esti-mating hemodynamics in chronic heart failure. JAMA 1989;261:884-8.

7. Badgett RG, Lucey CR, Mulrow CD. Can the clinical examinationdiagnose left-sided heart failure in adults? JAMA 1977;288:1712-9.

8. Butman SM, Ewy GA, Standen JR, Kern KB, Haha E. Bedside car-diovascular examination in patients with severe chronic heart fail-ure: importance of rest or inducible jugular venous distention. J AmColl Cardiol 1993;22:968-74.

9. Zema MJ, Restivo B, Sos T, Sniderman KW, Kline S. Left ventriculardysfunction—bedside Valsalva maneuver. Br Heart J 1980;44:560-9.

10. Eisenberg PR, Jaffe AS, Schuster DP. Clinical evaluation comparedto pulmonary artery catheterization in the hemodynamic assessmentof critically ill patients. Crit Care Med 1984;12:549-52.

11. Connors AF, McCaffree DR, Gray BA. Evaluation of right-heartcatheterization in the critically ill patient without acute myocardialinfarction. New Engl J Med 1983;308:263-7.

12. Davison R, Cannon R. Estimation of central venous pressure byexamination of jugular veins. Am Heart J 1974;87:279-83.

13. Cook DJ, Simel DL. Does this patient have abnormal central venouspressure? JAMA 1996;275:630-4.