Jugular, hepatic, andpraecordial pulsations in ... · with less evident Cwaves. The latter were...

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British Heart Journal, I971, 33, 305-3I2. Jugular, hepatic, and praecordial pulsations in constrictive pericarditis A. El-Sherif and G. El-Said From the Cardiac Department, Cairo University Hospitals, U.A.R. A study of the pulsatile features in constrictive pericarditis has been attempted in ii cases. The diagnosis was confirmed in 5 cases at operation. The expected increase in the frequency of the condition in certain localities is put forward. Venous neck pulsations with particular reference to the pathogenesis of the x and y descents are discussed. Hepatic pulsations previously not suffici- ently stressed in this disease are described and are graphically documented. They are found to conform, though to a lesser magnitude, with the venous neck pulsations. Apex cardiography has been utilized to study praecordial pulsations. A reproducible curve was obtained from the prae- cordium in all cases. The curve appears characteristic of the condition and consists of a small isometric contraction phase, low E point, a wide systolic trough, a small isometric relaxation phase, a steep rapid filling wave (RFW), and a rebound wave, which is followed by a diastolic plateau without or including an ill-defined A wave. The curve is characteristically biphasic and the rebound wave rather than the E point forms its summit. Restoration of the abnormal cardio- gram to a normal pattern follows successful pericardiectomy. The genesis of the abnormal curve is discussed. The incidence of constrictive pericarditis of tuberculous aetiology is expected to be high in countries where this infection is still prevalent. Data from our department indicate that before the era of chemotherapy many patients with tuberculous pericarditis used to die in the active stage before the development of constriction. An early diagnosis is essential for successful operation and the addition of new diagnostic techniques to those already used may be of help. Of the various criteria, jugular venous pulsations have received the greatest attention (Gimlette, I959; Wood, I96I; Sorour et al., I963). Some studies on apical pulsations have also been made, utiliz- ing electrokymography (McKusick, I952), accelerator ballistocardiography (Mounsey, I957, 1959), and impulse cardiography (Boi- court, Nagle, and Mounsey, I965). Hepatic pulsations, on the other hand, have not received much attention. The present work aims at a detailed study of the hepatic and praecordial movements in conjunction with the jugular pulsations in constrictive pericarditis. The simplicity of apex cardiography and its reliability in the diagnosis of several cardiac disorders have stimulated us to use it in the diagnosis of this Received 22 May 1970. condition. Apex cardiography refers to the low-frequency displacement curve in the range of o io-20oo cycles per second recorded at the point of maximum impulse in mid- expiration, in the left lateral position (Benchi- mol and Dimond, I963). The technique has recently been extended to the study of other pulsations and has been termed the praecor- dial cardiogram (El-Sherif, Saad, and El- Said, I969). Subjects and methods Nine men and two women were studied. Except in one case there was no residual pericardial effu- sion or active inflammation. The diagnosis was made clinically, radiologically, and electrocardio- graphically according to established criteria (White, 1951; Gimlette, 1959; Wood, I96I; Sorour et al., I963). The diagnosis was confirmed haemodynamically through right-sided catheter- ization in 6 cases and at operation in the remaining 5. No case with annular constriction, such as that described by Mounsey (1959), was encountered. Pericardial calcification and atrial fibrillation were present each in three cases. Clinical examination was made by each author separately, then by both together for the final decision and before the graphic recordings of the jugular, hepatic, and praecordial movements were undertaken. Jugular phlebograms and external hepatograms were recorded while the patients were in the sit- on April 5, 2020 by guest. Protected by copyright. http://heart.bmj.com/ Br Heart J: first published as 10.1136/hrt.33.2.305 on 1 March 1971. Downloaded from

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British Heart Journal, I971, 33, 305-3I2.

Jugular, hepatic, and praecordial pulsations inconstrictive pericarditis

A. El-Sherif and G. El-SaidFrom the Cardiac Department, Cairo University Hospitals, U.A.R.

A study of the pulsatile features in constrictive pericarditis has been attempted in ii cases. Thediagnosis was confirmed in 5 cases at operation. The expected increase in the frequency of thecondition in certain localities is put forward. Venous neck pulsations with particular reference tothe pathogenesis of the x and y descents are discussed. Hepatic pulsations previously not suffici-ently stressed in this disease are described and are graphically documented. They are found toconform, though to a lesser magnitude, with the venous neck pulsations. Apex cardiography hasbeen utilized to study praecordial pulsations. A reproducible curve was obtained from the prae-cordium in all cases. The curve appears characteristic of the condition and consists of a smallisometric contraction phase, low E point, a wide systolic trough, a small isometric relaxationphase, a steep rapid filling wave (RFW), and a rebound wave, which is followed by a diastolicplateau without or including an ill-defined A wave. The curve is characteristically biphasic andthe rebound wave rather than the E point forms its summit. Restoration of the abnormal cardio-gram to a normal pattern follows successful pericardiectomy. The genesis of the abnormal curve

is discussed.

The incidence of constrictive pericarditis oftuberculous aetiology is expected to be highin countries where this infection is stillprevalent. Data from our department indicatethat before the era of chemotherapy manypatients with tuberculous pericarditis used todie in the active stage before the developmentof constriction. An early diagnosis is essentialfor successful operation and the addition ofnew diagnostic techniques to those alreadyused may be of help. Of the various criteria,jugular venous pulsations have received thegreatest attention (Gimlette, I959; Wood,I96I; Sorour et al., I963). Some studies onapical pulsations have also been made, utiliz-ing electrokymography (McKusick, I952),accelerator ballistocardiography (Mounsey,I957, 1959), and impulse cardiography (Boi-court, Nagle, and Mounsey, I965). Hepaticpulsations, on the other hand, have notreceived much attention.The present work aims at a detailed study

of the hepatic and praecordial movements inconjunction with the jugular pulsations inconstrictive pericarditis. The simplicity ofapex cardiography and its reliability in thediagnosis of several cardiac disorders havestimulated us to use it in the diagnosis of thisReceived 22 May 1970.

condition. Apex cardiography refers to thelow-frequency displacement curve in therange of o io-20oo cycles per second recordedat the point of maximum impulse in mid-expiration, in the left lateral position (Benchi-mol and Dimond, I963). The technique hasrecently been extended to the study of otherpulsations and has been termed the praecor-dial cardiogram (El-Sherif, Saad, and El-Said, I969).

Subjects and methodsNine men and two women were studied. Except

in one case there was no residual pericardial effu-sion or active inflammation. The diagnosis wasmade clinically, radiologically, and electrocardio-graphically according to established criteria(White, 1951; Gimlette, 1959; Wood, I96I;Sorour et al., I963). The diagnosis was confirmedhaemodynamically through right-sided catheter-ization in 6 cases and at operation in the remaining5. No case with annular constriction, such as thatdescribed by Mounsey (1959), was encountered.Pericardial calcification and atrial fibrillation werepresent each in three cases. Clinical examinationwas made by each author separately, then byboth together for the final decision and beforethe graphic recordings of the jugular, hepatic, andpraecordial movements were undertaken.

Jugular phlebograms and external hepatogramswere recorded while the patients were in the sit-

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306 El-Sherif and El-Said

ting, semirecumbent, or recumbent position,whichever brought maximum pulsations. Thegraphs were analysed and compared with thepressure curves obtained during cardiac catheter-ization from the superior vena cava, inferior venacava, and hepatic veins.

Praecordial movements were recorded duringheld expiration over areas where pulsations couldbe detected as described by Benchimol and Di-mond (I963) and Ginn et al. (I967). Lead II ofthe electrocardiogram and a phonocardiogramwere simultaneously recorded for timing. Beforerecording each tracing it was ascertained on anoscilloscope to fulfil the following criteria: (a) anupward deflection approximately synchronouswith the R wave of a simultaneously recordedelectrocardiogram; (b) a sharp nadir (O point)occurring after the T wave of the electrocardio-gram and followed by the diastolic filling waves.

Several successive tracings were obtained on amultichannel Elema Mingograph 42 B, at a paperspeed of 25 and 50 mm./sec. Good postoperativerecords were obtained in only 3 cases. Persistenttenderness of the chest wall after operation andthe development of postoperative scar tissue maderecording difficult in the rest of the cases.The records were studied in the light of the

criteria given by Benchimol, Dimond, and Carson(i96i), Benchimol and Dimond (i963), and Ta-fur, Cohen, and Levine (I964) for the normalcurve. A normal curve (Fig. i) shows: (i) A sys-tolic wave that forms an out-thrust throughoutsystole, which begins with a rapid rise correspond-ing to the isometric contraction phase, reaches asharp tent-like peak (E point or beginning of ven-tricular ejection), and descends at first steeply(maximum ventricular ejection) then gradually toa plateau (reduced ventricular ejection). (2) Adiastolic wave that begins after the second soundwith a steep downward deflection (isometric re-laxation) to the 0 point (opening of the AVvalve) after which it rises first rapidly then slowly(rapid and slow filling waves) till the presystolicor A wave of the next cycle. The latter wave iscaused by displacement of the ventricular wall byatrial contraction.

E

/ SFW\ RFW

ic istoic

FIG. I Normal apex cardiogram with simul-taneously recorded electrocardiogram. a, pre-systolic wave; E, ejection; 0, o point; RFW,rapid filling wave; SFW, slow filling wave.

ResultsJugular pulsations Jugular venous pulsa-tions were observed in all the cases in oneposition or the other. In 4 cases with markedvenous congestion the pulsations were seenonly in the sitting position in 3 and in thestanding position in the fourth. A diastolicdip immediately after the radial pulse wasseen in all cases, and an additional descent ofa variable degree was seen during systole inmost of them.

x Y

h

(\. .V

FIG. 2 jugular phlebograms with simultane-ously recorded electrocardiogram from threecases showing both the x andy descents. In theupper tracing the x is equal to the y; in themiddle with atrial fibrillation the x is smallerand in the lower tracing with sinus rhythm itis deeper. In the middle tracing the reboundor 'h' wave is shown.

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Yugular, hepatic, and praecordial pulsations in constrictive pericarditis 307

External phlebograms were obtained fromall the cases and uniformly showed both x andy descents (Fig. 2). In 3 cases the y wasdeeper than the x descent, in 5 both were

equal, and in the remaining 3 the x descentwas more prominent. Cases in which the ydescent was deeper were the 3 cases withatrial fibrillation in the series. No relation wasfound between the depth of the differentwaves and the age of the patient, duration ofthe illness, degree of venous congestion, rightatrial pressure, or presence of pericardialcalcification. Comparison of the external phle-bograms with the superior vena caval andright atrial tracings of the 6 cases catheterizedshowed exactly similar configurations.

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Hepatic pulsations Liver pulsations werefelt in 6 patients, prominent in 4 and faint in2. They were felt better in the recumbentthan in the semirecumbent position. Twocases with free pulsations had pericardial cal-cification. In 5 patients the pulsation was feltas a diastolic dip after the radial pulse, andcoincided with the third heart sound. In thesixth patient it was felt as a systolic dipsimultaneously with the radial pulse.

Hepatic tracings (Fig. 3) recorded from the6 cases showed x and y descents. Both waveswere equal in 3 cases. The y descent wasdeeper in 2, while the x descent was moreprominent in one. The latter case was the onewith hepatic pulsation felt as systolic collapse.The configuration of the hepatic tracings wassimilar to the phlebograms and to the inferiorvena caval and hepatic venous tracings of thecorresponding cases, except that the externalhepatograms were of smaller magnitude andwith less evident C waves. The latter werebetter identified in the external phlebogramsand internal tracings.

Praecordial pulsations Inspection andpalpation showed systolic retraction over andinside the region of the supposed apex fol-lowed by a diastolic out-thrust in IO out of theii cases. No forward movement was presentduring systole in the neighbourhood of thesystolic retraction or parasternally. In theremaining case no pulsations were visible orpalpable.

Praecordial cardiograms were obtained for9 cases only, and no pulsations could be re-corded in the remaining 2. Pulsations wererecorded from the cases with pericardial cal-cification and from the one in the active stage.Mapping of the whole praecordium wasattempted and any praecordial movement wasrecorded. Measurement studies of Benchimoland Dimond (I963) were difficult, but thefollowing alterations characterized the re-cords in all the cases (Fig. 4 and 5).

(i) The individual components of the car-diogram were less demarcated than those ofthe normal heart.

(2) The total amplitude of the record wassmall. This was confirmed by the increasewhich occurred after operation.

(3) The systolic configuration recordedfrom all the cases consisted of a small iso-metric contraction component that rose to alow E point, which was followed by a steepdescent ending in a wide trough throughoutsystole. Near the end of this trough and coin-ciding with the second heart sound a smallpositive wave was usually identifiable.

(4) The diastolic configuration found in all

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308 El-Sherif and El-Said

the cases consisted of a short continuation ofthe trough during the isometric relaxationfrom the second sound to an ill-defined 0point. The curve thereafter showed the rapidfilling wave (RFW) as a steep rise to a highsummit, from which it continued commonlyafter a slight drop as a series of shallow oscilla-tions or plateau with no well-defined slowfilling or A waves. The combination of thesystolic trough and the high diastolic plateaugives the praecordial curve a characteristic'biphasic appearance'. Such a curve was uni-formly recorded over any praecordial pulsa-tions present. The rise or overshoot ofthe rapidfilling wave above the level of the plateaucorresponds by measurement to the 'h'wave of the corresponding right atrial andventricular tracing. The latter is analogous to

FIG. 4 Apex cardiogram of two cases ofconstrictive pericarditis with simultaneouslyrecorded electro- and phonocardiograms. DP,onset of diastolic plateau. Coinciding with theR wave of the electrocardiogram and with thefirst sound is the small isometric contractioncomponent and the low E point, followed bythe steep descent and the wide trough. Withthe second sound, S2, a small positive wavecan be identified on the trough. The steepRFW is especially noticeable in the uppertracing and the overshoot or 'h' wave isnoticeable especially in the lower tracing. Theshallow oscillations following the overshoot areshown in the lower tracing, but no SFW or awaves can be observed.~~~~~~~~~~~~~~~~~~~~~~~~~~~~.. . ..

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trough, and the diastolic plateau. The over-shoot 'h' wave is shown in the lower tracing toconstitute its summit. The combination of thesystolic trough and the high diastolic plateaugives the curve its biphasic appearance (lowertracing).

the one described in the jugular pulse byHirschfelder (I907) in subjects with loudthird sound. The third heart sound is usuallyregistered along the rapid filling wave (RFW).

Postoperative cardiograms Restorationof the curve after pericardiectomy towards thenormal pattern has been striking. The totalamplitude increased and the systolic anddiastolic components regained their normnalpattern with an A wave, isometric contractionphase, high E point, rapid and slow ejectionphases, isometric relaxation phase, sharp 0point., and rapid and slow filling waves(Fig. 6).

DiscussionJugular pulsations are invariably present inconstrictive pericarditis (Gimlette, I959;Wood, I96I; Sorour et al., I963). Hepaticpulsations received little attention and Fried-berg (I966) stated that the liver did not pulsatein systole.

In our cases jugular pulsations were presentin all the patients. In 4 cases, however, venouscongestion was so severe that the pulsationswere only demonstrable in the sitting orstanding positions.

According to Sawyer et al. (I952) there isno obstruction at the mouths of the venaecavae in constrictive pericarditis. This allowsthe characteristic changes in the right atriumto be faithfully transmitted to the superior

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jugular, hepatic, and praecordial pulsations in constrictive pericarditis 309

-A-_

..wXo:.i 4.

71: I~~~~~~~~~~~I

FIG. 6 Postoperative cardiograms from threecases in the series. The upper and lower trac-ings are of the two cases in Fig. 5. They showincrease ifl amplitude, the well-defined pre-systolic a wave., the E and 0 points, and thediastolic wave are apparent. No overshoot orh'wave is present and the E point represents

the summit o the tracing.

,and inferior venae cavae (Fig. 2). Thesechanges were detailed by Hansen, Eskildsen.,and Gotzsche (1951), Wilson et al. (I954),Wood (1961., and Sorour et al. (1963).In all the cases an early diastoic dip fol-

lowing the radial pulse was seen and coincidedwith the third heart sound. This sign wasdescribed long ago by Friedreich in 1864 butgained popularity after its emphasis by Wood

in I96I. This diastolic dip coincides with they descent in the external phlebograms,superior vena caval, and right atrial tracings.Its steepness is attributed to the rapid dropof the high venous pressure through a non-obstructed tricuspid valve. Because of thefixed capacity of the ventricle, maximal ven-tricular filling occurs rapidly during the firstpart of diastole and the y descent is followedby an acute rise which may create a reboundor 'h' wave that travels up the right atriumand superior vena cava. The latter wave wasseen in the right atrial and superior venacaval tracings but was not recorded in all theexternal jugular phlebograms. It is the highrapid ascent after the y and the rebound or'h' wave that imparts depth to the diastolictrough.Among our cases another descent in the

jugular pulse was visualized during systolein most of the cases but was recorded in all.This wave coincided with the correspondingx descent in the superior caval and right atrialtracings. The presence of x descent in rightatrial tracings in constrictive pericarditis hasbeen described repeatedly and forms with they descent a characteristic M- or W-shapedappearance (Hansen et al., I95I; Wilson etal., 1954; Wood, I96I; Sorour et al., I963).The transmitted M- or W-shaped pulsationin the neck observed in our cases has beenreported also by Gimlette (I959).The relative amplitude of x and y descents

in our patients was variable. In the 8 caseswith sinus rhythm the x descent was equal tothe y in 5 cases and deeper in 3. In the 3cases with atrial fibrillation the x was lessprominent than the y. Various explanationswere given for the prominent x descent.Gibson (i959) considered it an atypical fea-ture and ascribed it to the rapid ejection ofblood from within the rigid pericardium re-sulting in lowering of the subsequent V waveand the AV gradient. Absence of the thirdheart sound in his cases was taken as evidenceto support his explanation. Wood (I96I)attributed the x descent to exceptional de-scent of the base during systole when thelateral walls of the ventricles have difficulty inmoving inwards. We favour Wood's explana-tion and consider the presence of a prominentx descent equal to or greater than the y acommon feature if sinus rhythm is present.Though Gibson (I959) reported that the deepx descent occurs irrespective of the cardiacrhythm we only encountered it in cases withsinus rhythm. That the x descent becomesless prominent in the presence of atrialfibrillation can be explained by loss of atrial

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3IO El-Sherif and El-Said

contraction which is required for the normalclosure of the atrioventricular valves (Little,I95i) or by the absence of atrial relaxation(Nixon and Polis, I962).Wood in I96I has described the deep x

descent in cases with active disease but itoccurred in quiescent cases among our series.

Conspicuous congestion of the neck veinsmay occur in both constrictive pericarditis andtricuspid regurgitation. The presence or ab-sence of an x descent in such cases would be ahelpful sign in differentiating one conditionfrom the other especially if sinus rhythm is pre-sent. The x descent is characteristically absentin cases of severe tricuspid regurgitation.

Hepatic pulsations detectable clinically in acase of constrictive pericarditis were reportedby us in a previous publication (Sorour et al.,I963). In the present series pulsations weredetected in 6 cases (Fig. 3). They were felt asa diastolic collapse in 5 cases and as a systoliccollapse in the sixth. They were better felt inthe recumbent than in the semirecumbentposition, when liver congestion became less.The discussion on the neck venous pulsationsapplies equally to the hepatic pulsations.Tracings comparable to those of the rightatrium and superior vena cava were obtainedfrom the hepatic veins. The inability to detecthepatic pulsations in all cases and the dampedexternal hepatograms without clear C wavescan be explained by the greater amount ofhepatic congestion especially in the semi-recumbent position.From the above discussion it appears that

the configuration of the neck and hepaticvenous pulsations rather than the degree ofcongestion is more important in diagnosis.

In nearly all our cases inspection of thepraecordium showed replacement of the nor-mal cardiac impulse by an evident systolicretraction followed by a diastolic bulge overand medial to the region of the supposed apex.White (i95i) and Gimlette (i959) did notrefer to any cardiac pulsations in constrictivepericarditis, while Evans (I956) described theapical impulse as either 'not visible' or 'im-properly defined'. Wood et al. (I95i) de-scribed 'a diastolic heart beat' in constrictivepericarditis characterized by an apical dia-stolic thrust and a loud protodiastolic sound.

'Apical' pulsations in constrictive pericar-ditis were repeatedly studied by differentmethods by McKusick (I952), Mounsey(I957, I959), and Boicourt et al. (I965), butnot by apex cardiography before the presentstudy. The earlier studies entailed only fewcases from which no definite conclusionscould be made. Our series is larger, and prae-cordial cardiograms were obtained from most

of the cases, including those with pericardialcalcification.A curve with a constant characteristic pat-

tern was regularly obtained from over thepulsatile area in the praecordium (Fig. 4 and5). Medial to this area pulsations were eitherabsent or weak but of the same pattern. Thesystolic component of the cardiogram showeddeviations from normal in the form of a smallisometric contraction phase, a low E pointdescending rapidly to a wide trough whichwas maintained throughout systole.The diastolic component also showed

characteristic changes. The isometric relaxa-tion phase did not appear as the normal down-ward deflection but as almost a horizontalline. It terminated at the 0 point, after whichthe curve ascended abruptly with an over-shoot which corresponds to the 'h' wave oftheright ventricular pulse. This wave is mostprobably the cause of the early praecordialtap, 'knock', or 'shock' described by Schna-bel (I966) and Friedberg (I966). The diastolicovershoot, and not the E point, characteristic-ally represents the summit of the tracing.After the overshoot the tracing continued as aplateau at the time interval of the slow fillingwave. The A wave is absent as a separate waveand is submerged in the diastolic plateau.Boicourt et al. (I965), using impulse cardio-graphy, reported a diastolic bulge followingthe systolic retraction over and medial to theapex, but no individual components weredescribed.

In three of our cases praecordial cardio-grams were repeated after pericardiectomy.The increase in amplitude and the normaliza-tion of the curve with the appearance of itsvarious components were striking (Fig. 6).This fact adds weight to the diagnostic signifi-cance of the preoperative cardiograms.

Boicourt et al. (I965) attributed the systolicretraction to the probable existence of ad-hesions between the pericardium and theanterior chest wall. They ascribed the diastolicimpulse in their cases associated with annularconstriction to the abnormally large outwardmovement of the free portion of the anteriorright ventricular wall as a result of tetheringof the heart over the AV groove and rightventricular outflow tract. Our findings makesuch explanation unlikely. In 5 of our caseswith definite diastolic bulge seen in praecor-dial tracings the constriction was seen atoperation to be of the generalized and not ofthe annular type.The praecordial cardiogram in constrictive

pericarditis can be readily explained in thelight of the origin of its various componentsand the haemodynamic disturbances that

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jugular, hepatic, and praecordial pulsations in constrictive pericarditis 311

occur in the disease. According to Luisadaand Magri (I952), the low frequency tracingsof the apex cardiogram are the result of severalfactors, of which the main ones are: (i) Move-ment of the heart and especially the apextowards the chest wall during cardiac con-traction. (2) Volume change of the heart withdecrease of the ventricular mass during ejec-tion and its increase during diastole.

Tafur et al. (I964) consider the apex cardio-gram to record motions of the chest wall pro-duced by movements of the heart and intrinsicvolume pressure changes in its chambers.Coulshed and Epstein (I963) consider theinitial upstroke of the apex cardiogram (iso-metric contraction phase) to be probably pro-duced by increase in the tension of the cardiacmuscle leading to alteration of its shape andforward rotation of the apex. When left ven-tricular volume decreases with ejection ofblood the plateau part of the curve is formed.In constrictive pericarditis the dense peri-cardial sac and the adhesions between itsvisceral and parietal layers diminish or pre-vent cardiac movements in systole and diastole(White, I951). This has been demonstratedby fluoroscopy and roentgenkymography(Stewart, Carty, and Seal, 1943). The prae-cordial cardiogram in such cases will recordmainly the part due to volume changes. Thisexplains the small isometric contraction phase,the low E point, and the small isometricrelaxation phase, which are mainly the resultof movement. The volume changes in systole,on the other hand, together with the absenceof forward rotation of the apex, explain thesystolic retraction and trough.The diastolic events also reflect exactly the

volume changes produced by the pathophysio-logical alterations present in the disease. En-casement of the ventricles allows maximalfilling in the first part of diastole. The fillingabruptly ends when the fixed capacity of thenondistensible ventricle is rapidly reached,and this explains the abrupt ascent of theRFW. The rapid halting of blood creates therebound or 'h' wave in the atrial, ventricular,and sometimes the pulmonary artery pressurecurve (Sorour et al., I963) and the overshootof the RFW in the praecordial cardiogram.Comparison of the intracardiac and the exter-

'--nal cardiographic tracings demonstrated thatthe 'h' wave in the intracardiac tracings coin-cided with the overshoot of the externalcardiograms. After the overshoot no furthersignificant filling occurs and a diastolic plateauis recorded. The absence of the a wave, whichrepresents further ventricular filling as a resultof atrial contraction, can be readily explainedby the inability of the maximally filled ven-

tricle to accept any extra blood in late diastole.Gillick (i959) described characteristic electro-kymographic changes in constrictive pericar-ditis due to the abrupt halting of the diastolicfilling process by the mechanical restriction ofthe lateral motion of the ventricle and inter-ference with the waves of both the isometriccontraction and relaxation phases.That these changes are merely the result

of the mechanical hindrance offered by thefibrous and calcified pericardium is evidentfrom the restoration of the cardiogram to nor-mal pattem (Fig. 6) after successful peri-cardiectomy.The diagnosis of constrictive pericarditis is

not always easy, and difficulties may arisewith such conditions as myocarditis and myo-cardiopathies. It remains to be settled wheth-er this praecordial cardiogram will be ofhelp in differentiating these disorders. Prae-cordial cardiograms, by offering a characteris-tic curve, will no doubt add to our means ofdiagnosing constrictive pericarditis.

ReferencesBenchimol, A., and Dimond, E. G. (I963). The normal

and abnormal apexcardiogram. Its physiologicvariation and its relation to intracardiac events.American journal of Cardiology, 12, 368.

, , and Carson, J. C. (I96I). The value of theapexcardiogram as a reference tracing in phono-cardiography. American Heart Journal, 6I, 485.

Boicourt, 0. W., Nagle, R. E., and Mounsey, J. P. D.(I965). The clinical significance of systolic retrac-tion of the apical impulse. British Heart Journal,27, 379.

Coulshed, N., and Epstein, E. J. (I963). The apex-cardiogram: its normal features explained by thosefound in heart disease. British Heart Journal, 25,697.

El-Sherif, A., Saad, Y., and El-Said, G. (i969). Prae-cordial tracings of myocardial aneurysms. BritishHeart Journal, 31, 357.

Evans, W. (1956). Cardiology, 2nd ed., p. 220. Butter-worth, London.

Friedberg, C. K. (i966). Diseases of the Heart, 3rd ed.,p. 971. Saunders, Philadelphia and London.

Friedreich, N. (i864). Zur Diagnose der Herzbeutel-verwachsungen. Virchows Archiv fur pathologischeAnatomie und Physiologie undfur klinische Medicin,29, 296.

Gibson, R. (I959). Atypical constrictive pericarditis.In Proceedings of the British Cardiac Society.British HeartJournal, 21, 583.

Gillick, F. G. (I959). Electrokymography in pericar-ditis and constrictive pericarditis. In Cardiology,Vol. 3, pp. 8-56. Ed. by A. A. Luisada. McGraw,Hill, New York, Toronto, and London.

Gimlette, T. M. D. (I959). Constrictive pericarditis.British Heart3Journal, 21, 9.

Ginn, W. M., Sherwin, R. W., Harrison, W. K., andBaker, B. M. (I967). Apexcardiography: use incoronary heart disease and reproducibility. Ameri-can Heart Journal, 73, i68.

Hansen, A. T., Eskildsen, P., and G6tzsche, H. (I95I).Pressure curves from the right auricle and the rightventricle in chronic constrictive pericarditis. Circu-lation, 3, 88i.

on April 5, 2020 by guest. P

rotected by copyright.http://heart.bm

j.com/

Br H

eart J: first published as 10.1136/hrt.33.2.305 on 1 March 1971. D

ownloaded from

Page 8: Jugular, hepatic, andpraecordial pulsations in ... · with less evident Cwaves. The latter were better identified in the external phlebograms andinternal tracings. Praecordial pulsations

312 El-Sherif and El-Said

Hirschfelder, A. D. (I907). Some variations in theform of the venous pulse. A preliminary report.Bulletin of the Johns Hopkins Hospital, I8, 265.

Little, R. C. (i95I). Effect of atrial systole on ventricu-lar pressure and closure of the A-V valves. Ameri-can Journal of Physiology, I66, 289.

Luisada, A. A., and Magri, G. (I952). The low fre-quency tracings of the precordium and epigastriumin normal subjects and cardiac patients. AmericanHeart Journal, 44, 545.

McKusick, V. A. (1952). Chronic constrictive peri-carditis. II. Electrokymographic studies and cor-relations with roentgenkymography, phonocardio-graphy, and right ventricular pressure curves.Bulletin of the Johns Hopkins Hospital, 90, 27.

Mounsey, P. (I957). Praecordial ballistocardiography.British Heart_Journal, 19, 259.-(959). Annular constrictive pericarditis; with

an account of a patient with functional pulmonary,mitral, and aortic stenosis. British Heart J'ournal,2I, 325.

Nixon, P. G. F., and Polis, 0. (I962). The left atrialX descent. British Heart J'ournal, 24, I73.

Sawyer, C. G., Burwell, C. S., Dexter, L., Eppinger,E. C., Goodale, W. T., Gorlin, R., Harken, D. E.,and Haynes, F. M. (I952). Chronic constrictivepericarditis: Further consideration of the patho-logic physiology of the disease. American HeartJournal, 44, 207.

Schnabel, T. G., Jr. (I966). Constrictive (restrictive)pericarditis. Medical Clinics of North America, 50,123I.

Sorour, A., El-Sherif, A., El-Ramly, Z., Sallam, F.,Saad, Y., and El-Said, G. (I963). The diagnosis ofconstrictive pericarditis. Bulletin of the EgyptianSociety of Cardiology, 4, 3.

Stewart, H. J., Carty, J. R., and Seal, J. R. (1943).Contributions of roentgenology to diagnosis ofchronic constrictive pericarditis. American J'ournalof Roentgenology, Radium Therapy, and NuclearMedicine, 49, 349.

Tafur, E., Cohen, L. S., and Levine, H. D. (I964).The normal apexcardiogram. Its temporal relation-ship to electrical, acoustic, and mechanical cardiacevents. Circulation, 30, 38I.

White, P. D. (i95i). Chronic constrictive pericarditis.Circulation, 4, 288.

Wilson, R. H., Hoseth, W., Sadoff, C., and Dempsey,M. E. (I954). Pathologic physiology and diagnosticsignificance of the pressure pulse tracings in theheart in patients with constrictive pericarditis andpericardial effusion. American Heart Journal, 48,671.

Wood, F. C., Johnson, J., Schnabel, T. G., Kuo, P. T.,and Zinsser, H. F. (I95i). The diastolic heart beat.Transactions of the Association of American Physi-cians, 64, 95.

Wood, P. (I96I). Chronic constrictive pericarditis.American Journal of Cardiology, 7, 48.

on April 5, 2020 by guest. P

rotected by copyright.http://heart.bm

j.com/

Br H

eart J: first published as 10.1136/hrt.33.2.305 on 1 March 1971. D

ownloaded from