jugular venous - postgraduate medical journalit falls to a lowerlevel in the neck. pulsation that is...

389

THE JUGULAR VENOUS PULSEBy D. S. SHORT, M.D., M.R.C.P.*

The Institute of Clinical Research and Experimental Medicine, theMiddlesex Hospital, and the Cardiac Department, the London Hospital

" Study of the veins still suffers an unfortunateneglect; in these vessels are to be found some -of themost valuable signs we possess in managing heartcases."-Sir Thomas Lewis, I948.

Although the neglect ofwhich Sir Thomas Lewisspoke has since been partially remedied, there is nodoubt that the value of the jugular pulse is stillinsufficiently realized. Important information canbe obtained both from the form of the venouspulse and the level of venous distension by simpleobservation without the aid of any instrument.

This paper is based on a careful inspection of thejugular pulse in over 3,000 patients with congenitalor acquired heart disease aged between five and80o years and ioo healthy men aged between 20o and6o years.

Until recently clinical interest has been focusedexclusively on either the wave form or the venouspressure. It is only in the past decade, due largelyto the observations of Wood (I950, 1956), thatboth have found their proper recognition.Venous pulsation was occasionally recorded in

the I8th century, notably by Lancisi (1728), butno important contribution to the subject was madeuntil the introduction of sphygmography, whichpermitted the taking of actual tracings (Friedreich,i866; Potain, 1867). Mackenzie (I893) recordedthe jugular and arterial pulses simultaneously andmade a systematic analysis of the clinical sig-nificance of the venous pulse. He recognized thewaves and designated them in accordance withthe events in the cardiac cycle, which he believedthey reflected. At first the chief clinical applicationof the venous pulse lay in the diagnosis of arrhyth-mias, but in this it was soon to be superseded bythe electrocardiogram. Interest in the venouswaves then waned until the advent of cardiaccatheterization and cardiac surgery led to moreprecise diagnosis of congenital heart disease and aconsequent reappraisal of physical signs (Wood,I950).In I733 Hales measured the jugular venous

pressure in a mare by inserting a glass tube into thevein. This procedure cannot readily be applied to

* Holding a ILeverhulme Scholarship.

man, but Moritz and Tabora (I9Io) showed thatthe venous pressure could be recorded by insertinga needle into'the median cubital vein and attachingit to a manometer filled with sodium citrate. Thismethod has been widely used in the past, but it istoo complicated for routine use; it measures theperipheral rather than the central venous pressureand an equally accurate estimate can be obtainedmuch more simply. Lewis (I930) showed that thejugular veins could be regarded as natural mano-meters connected to the right atrium, and that thecentral venous pressure could be determined byobserving the height of the venous column abovethe sternal angle.The Anatomy of the Jugular VeinsThere are three main veins running down-

wards on each side of the neck: the external, theanterior and the internal jugular veins (Fig. I).The external and anterior jugular veins are

covered only by skin, superficial fascia and thethin platysma muscle, so that when distended theyare visible throughout most of their course. Theexternal jugular vein runs from the angle of themandible to the middle of the clavicle, where itenters the subclavian vein. Its size varies in in-verse proportion to the other veins of the neck.The anterior jugular vein begins near the hyoidbone, runs downwards between the anterior borderof the sternomastoid and the midline,'and turnslaterally in the lower part of the neck to enterthe external jugular or the subclavian vein. Thetwo anterior jugular veins are united just above thesternum by a transverse trunk called the jugulararch.The internal jugular vein lies within the carotid

sheath, deep to the sternomastoid muscle. It runsfrom the jugular foramen of the skull to a pointbehind the sternal end of the clavicle, where itunites with the subclavian vein to form theinnominate vein. Near its termination it dilatesto form the inferior jugular bulb.The external jugular vein has two pairs of

valves, both of which are incompetent; an upperpair situated about 4 cm. above the clavicle, and alower pair immediately above its termination. The

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390 POSTGRADUATE MEDICAL JOURNAL August I957

Sternamastoid m.

Trapezius m. External Carotid a.

ANTERIOR JUGULAR. V

INTERNAL JUGULAR V.EXTERNAL JUGULAR V.

Common carotid a.

/___ JUGULAR ARCHClavicle INFERIOR JUGULAR

BULBSUBCLAVIAN V.FIG. I.-The anatomy of the jugular veins. Note the position of the valves in the external jugular, internal jugular,

and subclavian veins. Those in the external jugular vein are incompetent. Veins running superficially are shownin solid black.

anterior jugular vein has no valves. The internaljugular vein has a pair of valves immediately aboveits inferior bulb. The only valves in the subclavianvein lie on the lateral side of the external jugularopening. There are no valves in the innominateveins or in the superior vena cava. Thus there areno competent valves between the right atrium andthe upper ends of the external and anterior jugularveins, or between the heart and the inferior jugularbulb. The internal jugular valves readily becomeincompetent in the presence of a raised right atrialpressure.

Keith (i908) believed that during atrial con-traction the openings of the caval veins becameoccluded by a band of muscle fibres. The experi-mental evidence is, however, wholly against thisview (Wiggers, 1928). The pressure curverecorded from a cannula in the superior vena cavacorresponds to that recorded in the right atriumitself, and this still holds true when all the tribu-taries of the superior vena cava are ligated.The Normal Jugular Venous Pulse

Pulsation in the superficial jugular veins is anormal phenomenon, and so is pulsation over theinferior jugular bulb. Observations of pressure arebest made in the external jugular vein. The venouswaves, on the other hand, are most accuratelyreproduced in the internal jugular vein, which is indirect line with the right atrium. In the externaljugular vein the undulations, although visible, aresomewhat delayed and flattened.

In order to observe the jugular pulse, thepatient should lie almost flat, and be completelyrelaxed. If no pulsation can be seen, this is prob-

ably because the top of the column of blood is toolow and lies within the chest, or too high and lieswithin the head (Fig. 2). Veins that are fullydistended cannot pulsate appreciably, neither canthose that are collapsed. The next step, therefore,is to place a finger lightly over the lower end of theexternal jugular vein and wait 15 seconds to see ifthe vein fills. If it does not, the. same procedureshould be applied to the anterior jugular vein. Ifeither vein fills, it indicates that the venouspressure is too low to be recorded with the patientin his present position and the jugular pulse may beassumed to be normal. If the veins are not ren-dered visible by occluding their lower ends, it ispossible that they are, in fact, full. The patientshould therefore be instructed to sit upright when,unless the venous hypertension is extreme, the topof the column of blood will come into view.A full and tense external jugular vein on one

side only is due to local obstruction and the swell-ing can often be released by a little rotation of theneck. Attention should be directed to the vein inwhich the pressure is lowest and where free pulsa-tion is visible. Less commonly the veins on bothsides are full and motionless; they may be made tocollapse by a change of position or by sitting thepatient up. Rarely, in spite of the greatest care, itis impossible to demonstrate the venous pulse.The jugular pulse consists of three main waves,

named by Mackenzie (I902) a, c and v, the sum-mits of which are presystolic, systolic and diastolicin time, and two troughs, x and y (Fig. 3). Thea wave is due to atrial systole; the c wave, oftenjust a notch on the descending portion of the awave, is caused by the impact of the, underlying



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August 1957 SHORT: TheJugular Venous Pulse 391

LYNG.ST.TIN

NORMAL

VENOUS,, ,

PRESSURE

Vein partly distended Vein collapsedPuilsation visible No pulsatio

RAISED 4;

VENOUS

PRESSURE

Vein fully distended Vein partly distendedNo pulsation Pulsation visible

FIG. 2.-rThe effect of posture on filling and pulsation ofthe external jugular vein. The broken lines markthe level of the sternal angle (after Lewis).

carotid artery, and the x trough is due to atrialrelaxation. The v wave, which appears towardsthe end of the systole, is due to refilling of theatrium and its peak coincides with the opening ofthe tricuspid valve. They trough is caused by thefall in atrial pressure which follows the entry ofblood into the ventricle.

Wiggers (I949) studied phlebograms from 8oohealthy students and classified them into threegroups, which he called the atrial, the modifiedimpact type and the transitional. In the first,which was the most numerous, the a wave wasdominant; in the second there was a large c wave,while the third group was intermediate betweenthese two. By inspection it is rarely possible todetect more than two waves, since a and c cannotusually be separated. In a personal series of Ioohealthy men two waves could generally be seen inthe external jugular vein, and in 65 of them thelarger could be measured and timed; in 47 of thesethe main wave was atrial.

Differentiation ofVenous from ArterialPulsation

It is important to be sure that the pulsationwhich is observed is venous and not arterial. Thereis no difficulty if the external jugular vein is dis-tended, and the level of filling varies with respira-

NORMA. ABORMA

CI

" I

x I

5r IAs

Car C

FIG. 3.-Normal and abnormal forms of the jugularpulse:

I. Normal dominant a wave 4. Giant a wave2. Normal dominant c wave 5. Ventricular pulse of3. Sinus tachycardia: tricuspid incom-

summation of v and a petencewaves 6. Exaggerated y des-

cent of constrictivepericarditis

Note.-This figure depicts the rise and fall of bloodin the veins, i.e. volume changes. The brokenlines indicate the times of the carotid beats.

tion, change of position or abdominal compression;or if there are two waves to every heart beat, or asingle wave which is slow rather than sudden anddoes not synchronize with the carotid pulse. Butthe distinction is not always easy and venous isoften mistaken for arterial pulsation.

Arterial pulsation is usually maximal in thecarotid triangle and it increases when the erectposture is assumed. Venous pulsation may also beseen in this situation, but when the patient sits upit falls to a lower level in the neck. Pulsation thatis maximal in the subclavian triangles is almostalways venous, though the possibility of a kinkedcarotid must be considered if the pulsation is con-fined to the right side in a woman. Arterial pul-sation that is visible is always readily palpable.Venous pulsation is very rarely strongly palpableand only occasionally can be felt. If the jugularveins are compressed at the root of the neck, venouspulsation ceases above this level, whereas thecarotids continue to beat. When the radial pulsesare small, striking pulsation in the neck is almostinvariably venous. Conversely, if the radial pulses



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are large, striking pulsation in the neck is generallyarterial.When, as during congestion, the venous pul-

sation tends to lose its undulatory character andbecomes more sustained, and sometimes plainlypalpable, the direct distinction between it andarterial pulsation may be very difficult; but in suchcases the remaining signs of a congested venoussystem are always apparent.

Measurement of the Jugular VenousPressureThe pressure which is recorded in the jugular

veins is actually the right atrial pressure andsimultaneous measurement of pressures in theright atrium by cardiac catheterization and in thejugular vein by Lewis's method has shown that thetwo are almost identical.

Pressure must be measured with reference to afixed point or level. Various reference points havebeen suggested and there is still no agreement asto which is the best. The ideal reference pointwould be the centre of the right atrium, but inpractice it is impossible to determine this inrelation to the surface of the chest; moreover, itvaries with respiration and the heart beat. Bloom-field et al. (I946), from a study of lateral chestradiographs, found that the centre of the rightatrium in healthy subjects lay on an average 5.8cm. below the sternal angle. When the heart wasenlarged the distance was a little less (5.6 cm.) andin emphysema a little more (6.9 cm.). The distancevaried with the phase of the respiratory and cardiaccycles and there was also considerable individualvariation. Bloomfield et dl. concluded that anyattempt to predict the position of the centre of theright atrium in relation to the surface of the chestwould only be accurate to within 2 or 3 cm.American and Continental workers commonly

take as their zero level a horizontal line 5 cm. belowthe sternal angle, or o cm. anterior to the backwhen the patient is recumbent, but in Englandthe sternal angle is still the most widely usedreference point. As Lewis (I930) showed, itrepresents approximately the level of normalpressure whether the body is horizontal or verticalor in any intermediate position. Normally all veinslying higher than the sternal angle are collapsed;all lying below it are distended.The jugular venous pressure is expressed in

terms of the vertical distance between the top ofthe column of blood and the sternal angle duringquiet respiration. It is best to record the highestand the lowest points in the cycle; if the excursionis great, this is essential. If the patient cannot lieflat, he should be made to lie as low as he canwithout distress. If the venous pressure is greatlyelevated, he should be propped up in a semi-

sitting position so that the top of the venous columnlies approximately halfway up the neck.

Borst and Molhuysen (I952) have insisted that avalid venous pressure can be recorded only duringinspiration and in the part of the cycle duringwhich the atrial pressure is falling, because thenthe venous valves are knowvn to be open. Thisprecaution is, however, unnecessary, since thereare no competent valves in the superficial jugularveins.Wood (I956) states that the normal jugular

venous pressure ranges between 3 cm. above and7 cm. below the level of the sternal angle when thepatient is horizontal. In a personal series of Ioohealthy men the venous pressure could bemeasured in all but one. The average level was-I cm. and 93 fell within the range -3 to +I.The pressure was a little lower in summer than inwinter. Approximately half the cases wereexamined during the months May to Septemberand the remainder between October and March.The mean pressure during the warm months was-I.5 cm. and in the cold months -0.5 cm. Thevenous pressure is increased by exercise, but itusually returns to normal or lower within a minuteafter its cessation (Szekely, I94I). Borst and Mol-huysen (i952) observed no measurable change inpressure under the influence of emotion.

It is often stated that pressure over the livercauses a rise of blood in the jugular veins in heartfailure, but not in health. This so-called hepato-jugular reflux is, in fact, a normal phenomenonand may be produced by pressure on any portionof the abdominal wall (Wood, 1956).Jugular Venous HypertensionA raised pressure in the jugular veins is the

earliest evidence of general systemic congestionand precedes signs in the legs or abdomen. Later,if heart failure persists and increases, venous dis-tension will be followed by hepatic engorgementand the appearance of oedema. Similarly, whenthe heart improves, the venous pressure falls tonormal before the oedema disappears.A raised venous pressure at rest may be found

in many conditions besides heart failure. Wood(1956) lists hyperkinetic circulatory states, in-creased blood volume, bradycardia, increased intra-pericardial, intrathoracic or intra-abdominal pres-sure, partial obstruction of the superior vena cava,tricuspid stenosis and space-filling lesions affectingthe right side of the heart. The diseases whichcause most difficulty in practice are chronicanaemia, acute nephritis, emphysema and thyro-toxicosis. Congestive heart failure should not bediagnosed in the presence of any of these diseasesunless the venous pressure is considerably elevatedor the liver is engorged. The possibility of a raised



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August 1957 SHORT: The Jugular Venous Pulse 393

venous pressure being due to constrictive clothingor bandages around the waist should not be over-looked.

Persistent jugular venous engorgement withoutdyspnoea suggests constrictive pericarditis, tri-cuspid stenosis or superior vena caval obstruction.In superior caval obstruction the liver is not con-gested. Some jugular pulsation persists while theobstruction is partial, but once it becomes com-plete all pulsation is lost, anastomotic veins appearover the chest, and the face becomes congested andcyanosed.Abnormal Jugular PulsationThe commonest and most important abnormality

in the form of the venous pulse is an exaggerationof the normal a wave (Fig. 3). The peak of thiswave rises until in extreme instances its amplitudemay exceed Io cm. It is best seen with the patientsitting upright and usually increases during in-spiration. In the internal jugular vein its abruptrise and fall resembles the carotid pulsation ofaortic incompetence, for which it is sometimesmistaken. The a wave can be distinguished by thefact that the carotid pulse is small and follows theonset of the venous wave. Sometimes suddensystolic collapse of the vein is more striking thanits protrusion.

Laubry and Pezzi (1913) first described a largea wave as a sign of congenital pulmonary stenosis;and Abrahams and Wood (I95I) showed that thesize of this wave broadly reflects the degree of rightventricular hypertension in this disease. An ex-aggerated a wave is also found in pulmonaryhypertension and in tricuspid stenosis. The a waveis not always abnormally large in pulmonarystenosis or hypertension, but, provided the patientis in sinus rhythm, it is invariably the dominantwave. It declines in right heart failure and dis-appears with the onset of auricular fibrillation.

Another common and important abnormality ofthe venous pulse is the ventricular form due totricuspid incompetence (Fig. 3). At the onset ofventricular systole, blood regurgitates into the rightatrium and the caval veins and the distension ofthe jugular veins is maintained until the ventriclerelaxes. This pansystolic or cv wave is even morestriking than the exaggerated a wave because ofthe great distension of all the jugular veins whichoccurs with every heart beat. The start of the cvwave is a little later than that of the a, synchron-izing with the carotid impulse; it is more sustainedand it persists in auricular fibrillation. The cvwave does not necessarily indicate organic tricuspiddisease; the incompetence is more often tem-porary and due to dilatation of the tricuspid valvering resulting from right ventricular failure. Whenfailure subsides the competence of the valve returns

and the abnormal wave disappears. The earliestsign of tricuspid incompetence is prematureappearance of the v wave from accelerated fillingof the right atrium (Mackenzie, I902).Another striking and important abnormality of

the jugular pulse is that described by Friedreich(i866) in constrictive pericarditis (Fig. 3). Themain feature of this pulse is a steep dip in diastole,an exaggeration of the normal y descent. Thisrecession, which is immediately preceded by asimilar recession in the right ventricular pressurecurve, has been shown to be due to a high-pressuregradient between the right auricle and ventricle(Mounsey, I955). Although characteristic of con-strictive pericarditis, it is not pathognomonic of it,and it may be found in other conditions, such ascardiac myopathy, in which there is an unusuallyhigh venous filling pressure.

In the diagnosis of arrhythmias the electro-cardiogram is unrivalled. There are, however,emergencies when this instrument is not available,and then inspection of the venous pulse may pro-vide valuable information. It is frequently possibleto distinguish complete heart block from sinusbradycardia by observing the position of the awave in the cardiac cycle. In sinus bradycardiait precedes the carotid impulse, as in health,whereas in complete heart block its position iscontinually changing and periodically, when atrialand ventricular systole coincide, a wave of ex-ceptional amplitude (the so-called cannon wave)appears. The jugular pulse may likewise enableauricular flutter to be differentiated from fibrilla-tion. In flutter, rapid regular a waves are seen, butin fibrillation these are absent.

ConclusionInspection of the jugular veins deserves to take

its place beside palpation of the radial artery inthe clinical examination of a patient suspected ofcardiovascular disease. The one procedure is assimple as the other and yields information ofequal if not greater value. It tells at once whetheroedema is due to heart failure and when congestivefailure has developed provides an accurate indexof its progress. It gives warning of overloading ofthe circulation during intravenous infusion ortreatment with salt-retaining hormones and pro-vides a vital clue to the diagnosis of pulmonaryhypertension, pulmonary stenosis, tricuspid valvedisease, constrictive pericarditis and superior venacaval obstruction.Acknowledgments

I am indebted to Dr. William Evans, Dr. EvanBedford and Professor Kekwick for a number ofvaluable suggestions and to Dr. Russell Bearn foradvice on the anatomical details.Bibliography continued on next page



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BIBLIOGRAPHYABRAHAMS, D. G., and WOOD, P. (I95 ), Brit. Heart`Y., I3, 519.BLOOMFIELD, R. A., LAUSON, H. D., COURNAND, A.,

BREED, E. S., and RICHARDS, D. W., jun. (I946), J. clin.Invest., 25, 639.

BORST, J. G. G., and MOLHUYSEN, J. A. (I952), Lancet, ii, 304.FRIEDREICH, N. (i866), Dtsch. Arch. klin. Med., I, 241.HALES, S. (x733), 'Statical Essays: Containing Haemastaticks;

or, an account of some Hydraulic and Hydrostatical Experi-ments, made on the Blood and Blood-Vessels of Animals.'W. Innys and R. Manby, London.

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Rome.LEWIS, T. (193o), Brit. med. Y., i, 849.

LEWIS, T. (I948), Diseases of the Heart,' Macmillan & Co. Ltd.,London, 4th Edition.

MACKENZIE, J. (I893), J. Path. Bact., 2, 84 and 273.MACKENZIE, J. (1902), 'The Study of the Pulse,' Young J.

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Med., 98, 475.MOUNSEY, J. P. D. (I955)j Brit. Heart J., x7, I43.POTAIN, P. C. E. (I867), Bul . Soc. Mid. Paris, 4, 3.SZEKELY, P. (I94I), Amer. Heart J., 22, 360.WIGGERS, C. J. (1928), 'The Pressure Pulses in the Cardio-

vascular System,' Longmans Green & Co., London.WIGGERS, C. J. (1949), 'Physiology in Health and Disease,'

Henry Kimpton, London, 5th Edition, p. 685.WOOD, P. (I950), Brit. Med. J., 2, 639 and 693.WOOD, P. (1956), 'Diseases of the Heart and Circulation,' Eyre

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and LJUNGGREN, H. (I956), Amer. J. Med., 2I, 728.MALLARD, J. R., MCKINNELL, A., and FRANCOIS, P. E.

(1956), Nature, 178, I240.MATSON, D. D. (1956), Symposium on Hypophysectomy, Sloan-

Kettering Institute. To be published.MCKENZIE, A. (1955), Lanret, ii, 1129.NATHANSON, I. R., RICE, C., and MEIGS, J. V. (I940), Amer.

j. Obstet. Gynec., 40, 936.NICKSON, J. J. (1956), Symposium on Hypophysectomy, Sloan-

Kettering Institute. To be published.NORTHFIELD, D. W. C. (I949), Proc. roy. Soc. Med., 42, 845.NORTHFIELD, D. W. C. ('957), Discussion Roy. Soc. Med.,

March, 1957.NOTTER, G. (I957), Personal communication.PATTI SON, A. R. D., and SWAN, W. G. A. (1938), Lanct, i, 1265.PEARSON, O. H. (i956), Proceedings of the Fourth Conference in

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PEARSON, O. H, WEST, C. D., LI, M. C., MACLEAN, J. P.,and TREVES, N. (I955a), A.M.A. Arch. Int. Med., 95, 357.

PEARSON, O. H., WEST, C. D., MACLEAN, J. P., LI, M. C.,and LIPSETT, M. B. (I955b), Amer. Surgeon, 21, 1075.

PEARSON, O. H., RAY, B. S, HAROLD, C. C., LI, M. C.,MACLEAN, J. P., and LIPSETT M. B. (t956), J.A.M.A.,I6I, I7.

PERLIA, C. P., KOFMAN, S., NAGAMANI, D., and TAYLOR,S. G. (I956), Ann. Int. Med., 45, 989.

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I8, 319STRONG, J. A, BROWN, J. B., BRUCE, J., DOUGLAS, M.,

KLOPPER, A. I., and LORAINE, J A. (1956), Lancet, ii, 955.TAYLOR, S. G , LI, M. C., ECKLES, N., SLAUGHTER, D. P.,

and MCDONALD, J. H. (1953), Cancer, 6, 907.TREVES, N. (1956), Proceedings of the Fourth Conference in

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References from page ?88: Anticoagulants in Reconstructive SurgervREFERENCES

i. DEGNI, II., and LANFRANCHI, W. (1954), HeparinizacaoRegional: Vantagens o Desvantagens-Anais do SegundoCongresso Latino-Americano de Angiologia.

2. FREEMAN, L. E., WYLIE, E. J., and GILFILLAN, R. (I950),'Regional Heparinization in Vascular Surgery,' Slrg. Gynec.Obst., 90, 406, 412.

3. FREEMAN, N. E., and GILFILLAN, R. (1952), 'RegionalHeparinization after Thromboendarterectomy in the Treatmentof Obliterative Arterial Disease,' Surgery, 31, I 15.

4. MURRAY, D. NIV., and BEST (1938), 'Use of Heparin inThrombosis,' Ann. SuIrg., Io8, I63, I77.

5. MURRAY, D. WV., GORDON, and JAMES, J. M. (I940),Prevention of Acute Failure of Circulation Following Injuries

to Large Arteries,' Brit. med. J., ii, 6, 7.

6. WYLIE, E. J., GARDNER, R., JOHANSEN, R:, andMcCORKLE, H. (I950), 'An Experiment of RegionalHeparinization,' Surgery, 28, 29, 35.

zaeA o

SUMMER EXHIBITION

July II to August 23, 1957Although the Ilford Department of Radiography

and Medical Photography is well known as a placeof interest to the many visitors who enter itsdoors, this year a special effort is being made toadd to its technical appeal by holding a summerexhibition.The exhibition will include many attractive

features embracing a wide range of radiographs

of technical and diagnostic interest, practicaldemonstrations of some of the more unusual tech-nical procedures and items of special photographicappeal.Well-known members of the technical staff will

be available for discussions and for the specialdemonstration features.The exhibition, to be held at Tavistock House

North, Tavistock Square, will be for all users ofX-ray and photographic materials and visitors cananticipate a cordial welcome.



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