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Antstht\ioll>h~1999;91 .40(7 - 130 999 Am r i i w i Socitty of Ancsrhesiologists, Inc.Lippincott Williams & Wilkins, Inc.

Diaphragmatic Activity after LaparoscopicCholecystectomyRajiv R. Sharma, M.B.B.S., F.R.C.A.,* Hans Axelsson, M.D.,t Ake Oberg, M.D. , t Erica Jansson, E.C.C.P.,SFrancois Clergue, M.D., Goran Johansson, M.S.,II Sebastian Reiz, M.D., Ph.D.#

Background Laparoscopic cholecystecto my is presumed toinduce a reduction in diaphragmatic activity. Ind irect indices ofdiaphragmatic function based on tidal changes in pressures andcross-section area m easurements can be unreliable in the post-operative phase. The present study evaluates diaphragmaticactivity by directly record ing diaphragmatic EMG (EMG,,,) data,along with indirect indices.

Methods: Thirteen adult patients (American Society of Anes-thesiologists physical status I or Ir) undergoing laparoscopiccholecystectomy were examined preoperatively for inspiratorytidal changes in gastric (Pgas.inep)nd esophageal (Peso.insp) res-sures , and tidal changes in ribcage (V,,,,) and abdominal (Vabd)cross-section areas and th en again at 1, 6, and 24 h p ostopera-tively combined with EMG,,, recordings. Variations in inspira-tory gastric (APpas.insp) and inspiratory transdiaphragmaticCAPdiResults: Laparoscopic cholecystectomy induced a significantreduction in mean APgas.i,,sp, mean APdi.insp, and mean Vindicating a reduction of diaphrag matic activity postopera-tively. APdi decreased from 11.8 f 4.0 cm H,O preopera-tively to 5.7 f 5.7 cm H,O at 1 h and 6.6 f 5.1 cm H,O at 6 hpostoperatively (m ean f SD; P < 0.05). V, decreased from

pressures were derived from th e above.

* Consultant Anaesthetist, Department of Anesthesiology and Inten-

t Consultant Surgeon, Ikpartment o f Surgery, IJmea IJniversity Hos-* Research Technical Assistant, Department of Cardiothoracic Anes-

sive Care Medicine, IJmei IJniversity Hospital, IJ mei, Sweden.

pital, LJmei, Sweden.

thesia, Ume i University Hospital, LJmeb, Sweden.versitaircs de Genbve, Geneva, Switzerland.

Professor, Medicin-chef, Division dAnes thbs iolo ~~ie ~iipitaux IJni-

/I Research Technical Assistant, Department of Anesthesiology and4 Professor, Department of Anesthesia, Centre Hospitalier IJniversi-

Intensive Care Medicine, Umei University Hospital, IJmei, Sweden.

taire Vandois, Lausanne, Switzerland.Received from the Department of Anesthesiology and Intensive Care

Medicine, Iline i IJniversity Hospital, IlineP, Sweden. Submitted for pub-lication November 13, 1997. Accepted for publication April 1, 1999.Supported by the Medical Faculty of the IJniversity of llmei, Umea,Sweden. The preliminary studywiw presented at the European Society ofAnesthesiologists Congress at Brussels,Belgiiun, February 1 2 , 1994.

Address reprint reques ts to Dr. Sharma: Department of Anesthesiol-ogy and Intensive Care Medicine, IJmei IJniversity Hospital, UmeiS-90185. Sweden. Address elect ronic mail to: [email protected];goran .joh;insson@anestrsi.~imu.se

327.0 ? 113.0 ml preoperatively to 174.0 f 65.0 ml at 1 h and175.0 & 98.0 ml at 6 h postoperatively (mean f SD;P


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Table 1. PatientCharacteristics and Surgical DetailsPatient Numb er Age (vr) Se x Operation Time (min)

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10111213

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907012513513514510018019510560

195135

scopic cholecystectomy (table 1). Patients who had pul-monary disease or morbid obesity (i.e., body massindex >30) were excluded from the study. The patientsgave their informed consent to participate in the inves-tigation, which was approved by the Ethics Committeeof the University Hospital, Urn&, Sweden.

Gastric and Esophageal PressuresPrior to premedication, a triple lumen nasogastric cath-

eter with its distal orifice located 3 cm from the tip andthe other two orifices located 10 and 20 cm proximal tothe distal orifice (PVC, esophageal manometric catheter,3.6 mm OD, 90 cm long, Synectics AB , Stockholm, Swe-den) was inserted through one of the nostrils and placedinitially with all three orifices in the stomach. Each lu-men was connected to a pressure transducer (Ohmeda,DT-XX, Hatfield, Herts, United Kingdom), which wasplaced at the mid-axillary level and calibrated to theatmospheric pressure and a hydrostatic pressure of 10cm and flushed thoroughly with normal saline solutionto remove air bubbles from the system. The cathe ter waskept patent by a continuous infusion of normal saline at3 ml/h. Initially all recorded pressures were the same,i.e., rom the stomach. The ca theter was then pulled outin a stepwise fashion, noting the recording from themiddle hole. The arrival of the middle orifice at thelower esophageal region was marked by a sudden rise inpressure due to t he presence of the resting lower esoph-ageal sphincter tone, followed by a trace exhibitingcardiac artifacts and a negative deflection with inspira-tion. At this point the distal hole was in th e stomach andthe proximal hole in the esophagus 10 cm proximal tothe lower esophageal region. The trace obtained fromthe distal hole revealed a positive pressure with inspira-tion and the trace from the proximal hole revealed car-

diac artifacts and a negative deflection with inspirationfurther confirming that the distal and proximal holeswere in the stomach and mid-esophagus, respectively.The catheter was then marked at the nasal entry pointand secured to the nose by tape. The validation of fluid-filled catheter system for pleural and gastric pressuremeasurement is described elsewhere.'310 The pressurechanges with quiet tidal respiration were recorded on amultichannel strip chart recorder (Mingograph 8 2 , Sie-mens-Elema, Solna, Sweden) which was adjusted to givea 2- or 4-mm deflection for each mmHg pressure changeusing a test signal. All calibration procedures and thealignment of the fluid jet pens were checked before andafter each set of measurements. The changes in gastricpressure (P,,,) and esophageal pressure (P,,,,) with quiettidal respiration were recorded from the distal and theproximal hole respectively on a strip chart at threedifferent speeds: 10 mm/s, 25 mm/s, and 50 mm/s.These measurements were obtained preoperatively be-fore preniedication and at 1,6,and 24 h postoperatively,all in the supine position. Tracings recorded at higherspeed and with minimal cardiac artifacts were used formeasurements as far as possible. Three consecutive pres-sure curves (and three rib cage and abdominal volume-motion curves recorded parallel to the pressure curves atthe Same time and on the same paper) were selected andanalyzed over the same time period (fig. 1). The begin-ning and the end of each inspiration was determinedafter inspection of both the pressure and motion signals.The following measurements we re derived from the Pga,and P,,,, values: transdiaphragmatic pressure (Pc,i, thedifference between simultaneously recorded Pgas andP,,,, values, calculated by manual subtraction technique),gastric pressure variation with inspiration (APgas.insprhedifference in Pgas between the start and the end ofinspiration), esophageal pressure variation with inspira-tion (APrso.insp, he difference in P,,,, between the startand the end of inspiration), the ratio of changes in gastricto esophageal pressure variations during inspiration(APFas.i,~sp/APr~r,-insp).nd changes in transdiaphrag-matic pressure variation during inspiration (APcli.insl,,APga,.insp- APcso.insp). n addition, loops of PRnS ersusP,,, were plotted to provide dynamic information oftransdiaphragmatic pressure changes over time.

Rib Cage and Abdominal DimensionsTidal changes in rib cage and abdominal cross-section

areas were measured using a respiratory inductive ple-thysmograph (RIP, Ambulatory Monitoring, Ardsley,Ny)and inductor band transducers that were applied circum-

Ane'dhesiology, V 91, No 2 , Aug I999


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SHARMA ET AL.

VtiiorV a b d /

I 1 -/-V t o t a lC 6h Postop D 24h Postop

3 s c c Vt0l;d -/-l --'"or\- Vtlior --c-- /-----/Vabd-Vabd -Fig. 1. Traces of tidal changes in ribcage (V,,,$ and abdominal(Va& cross-sectionareas and esophageal(P,J andgastric (P& pressuresas recorded on a multichannel strip chartrecorderpreoperatively01)and 1 h (B), 6 h (C), and24 h (D )postoperativelyina single patient.ferentially over the chest and abdominal wall. The ribcage inductor band w d S applied with its upper borderjust below the axillae and the abdominal inductor bandwas applied with its upper border at the level of umbi-licus. Both levels were circumferentially marked on thepatient's body with a permanent marker, and the size ofinductor band was noted for subsequent measurements.The apparatus was zeroed, adjusted for unity gain usingreference voltage, and volume motion coefficients forabdominal and thoracic excursions calcukdted using theleast square method with patients breathing in and outof a fixed volume spirobag in both supine and standing

position (before and 6 and 24 h after surgery) and supineand semirecumbent position (1 h after surgery). Thecalibration procedure, which was repeated before eachset of measurements, has been described previously."The multichannel recorder was adjusted to record 10mm deflection/volt at each channel. The rib cage andabdominal cross-sectional area changes that corre-sponded to respective tidal volume changes to quietrespiration were recorded along with and at the sametime interval as pressure measurements on the Mingo-graph 82 for approximately 6-8 min, following 5 min ofquiet tidal respiration. Tidal volume (Vt) was calculated

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Table 2. Basic Ventilatorv Measurements and Rib Cage and Abdominal Dimensions (n =13)Measurements ControlVt (ml)Vabd (ml)vabd(%)vthofiabdRespiratory rate (breathdmin)Minute volume (Vmin)lnspiratory timekotal respiratory time

421O ? 125.0327.0 t 113.076.9 2 11O0.33 ? 0.2213.8 i 4.55.60 t 1.810.38 2 0.04

1 h Postoperation344.0 2 84.0174.0 5 65.0*51O 2 16.2'1.1 5 5 0.68*14.3 2 3.94.76 5 1.200.34 2 0.09

6 h Postoperation347.0 ? 143.0175.0 t 98.0*49.3 2 16.6*1.31 ? 0.94*14.7 2 3.05.16 t 2.690.35 2 0.05

24 h Postoperation420.0 2 168.0260.0 t 138.059.8 t 18.80.89 2 0.8115.1 t 4.16.15 i 2.880.33 t 0.05

Values are mean 2 SD.Vt = tidal volume; Vabd abdominal volume: V = thoracic volume.' i.05 versus control (ANOVA for repeated measures followed bypost hoc Tukey's honestly significant difference test)from the instantaneous sum of ribcage (Vthor)and ab-dominal (V;,hd)volumes. Relative contribution of VahrloVt w a s calculated as Val,,%. The ratio of Vthc,r o Vabd(Vthor/Vabd)as also calculated. Konno-Mead plots'' ofVthor versus Vabdwere plotted in all patients.

Diaphragmatic ElectromyogramsA bipolar myocardial electrode (TME-642, 60 cm, Dr.

Osypka GmbH, Grenzach-Wyhlen, Germany) was in-serted laparoscopically in the muscular part of the cu-pola of the right hemidiaphragm (n = 13) by the surgeonat the end of surgery. The electrode in its preinsertionstate terminates with a needle at each end; its distal endhas two bare contact points that are 5 mm and 10-50mm wide with a gap of 10 mm in between. The 10-50mm contact point is zigzag-shaped to allow for satisfac-tory anchoring of the electrode in the muscle mass. Thedistal end with bare contact points was buried into themuscle, whereas the proximal end was exteriorizedthrough the abdominal wall, sutured in place, and itsidentification marked. The presence of needles at bothends of the electrode facilitates its insertion with thehelp of laparoscopy forceps. EMG,,, data were filteredand amplified (PS 101 and ISO-2104, Braintronics BV,h e r e , The Netherlands) and recorded on the Mingo-graph 82 along with and at the same time interval as thepressure and volume changes postoperatively. The bandpass filter (20 -2,000 Hz) and amplification were identi-cal at all measurement periods. A qualitative study of theraw EMG,,,, amplitude was carried out. The electrodewas easily withdrawn after the study with minimal dis-comfort to the patient.

AnesthesiaPrernedication consisted of 10 nig oral diazepam, and

general anesthesia was induced with thiopental (4 - 6mg/kg) and maintained with fentanyl (3-4 pg/kg),isoflurane, nitrous oxide (70%), nd oxygen (30%).En-

dotracheal intubation was facilitated with suxametho-nium (1 mg/kg), and further muscle relaxation was pro-vided with vecuronium (0.1 nig/kg). The degree ofmuscle relaxation was monitored with a peripheralnerve stimulator (Microstim plus, P/N7 106, Neuro Tech-nology, Houston, TX), and incremental doses of vecuro-nium (1-2 mg) were given depending on the adductorpollicis response to a train-of-four stimulus. The abdo-men was inflated with CO, to a pressure of 1 5 mmHgduring the surgery, and as much gas as possible wasremoved toward the end of surgery. The residual musclerelaxation was antagonized with neostigmine (2.5 mg)and atropine (0.5 mg) at the end of the surgery in allpatients. Ketorolac and cetobemidone hydrochloridewere used for postoperative pain relief. Patients received10 -30 mg Ketorolac intravenously as the first line anal-gesic. Cetomebidone hydrochloride was reserved forthose who had pain despite Ketorolac.

Sta tistical AnalysisResults are reported as mean ? SD . Analysis of Vdri-

ance (one- way ANOVA) for repeated measures followedby Tukey honestly significant difference test were ap-plied where appropriate for comparison between thepreoperative and postoperative values. All differenceswere considered significant at the P


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Rib Cage and Abdominal DimensionsThe changes in rib cage and abdominal dimensions

with quiet tidal respiration are represented in figure 1and table 2.

During the 1- and 6-h postoperative period, there wasa significant reduction in the abdominal component oftidal volume (VLIhdnd V,,,) and an increase in theVtllor/Vclhclatio, both indicating a shift toward a thoracicpattern of breathing. Vnhcl nd V, , , , values returned to atleast the control value in 4 of 13 patients at 1 h and 3 of13 patients at 24 11. Konno-Mead plots of VthoruersusV.ll,rlalso displayed a shift toward a thoracic breathingduring the postoperative phase in all patients (fig. 2 ) .This pattern of Konno-Mead plot again shifted to pre-dominantly abdominal breathing at 24 h in 5 of 13patients.

Gastric and Esophugeal PressuresThe changes in gastric and esophageal pressures are

represented in figure 1 and table 3.Plots of AP,,,, uersus AP,,, showed a shift to the left of

the vertical line at I h and 6 h postoperatively in 8 of 13patients and at only 1 h postoperatively in 2 of 13patients. At 24 h postoperatively all loops were to theright of the vertical line (fig. 3). APgas.insp,which w d Snegative (and therefore positive value for APRJb.lnsp/APc.~,.illsl,)n 10 of 13 patients at 1 h and 8 of 13 patientsat 6 h postoperatively, had recovered to a positive valuein all patients at 24 h. The change in mean APpas.inspromcontrol is plotted in figure 4 . APgas.inspvalues were re-duced in 12 of 13 patients a t 1 h and 6 h postoperatively.A t 24 h postoperatively it had recovered to within 20%of control value in five patients and within 50% of con-trol value in an additional five patients. Mean APdiwassignificantly reduced at 1 h and 6 h postoperatively. APc,ihad returned at least to the preoperative value in 9 of 13patients at 24 h.

Plots of V;lhcluersus APgas in all patients at the mea-surement periods previously mentioned reflected twobroad patterns. In 8 of 13 patients at 1 h and 6 h and in2 of 13 patients at 1 h after surgery, the loop was shiftedto the left of the vertical line (i.e., decrease in PRaswithincrease in abdominal volume during inspiration; fig. 5 )compared with the preoperative loop. In 3 of 13patientsthe loops remained to the right of the vertical line at allmeasurement periods (i.e., increase in Pgaawith increasein abdominal volume during inspiration; fig. 6). In allpatients the loops were seen to the right of the verticalline at 24 h after surgery.

Diuphrugmutic ElectromyogruphyDiaphragmatic electromyographic data were lacking in

2 of 13 patients due t o total loss of convact with one andan absent EM G signal at 24 h in the other.

The EM G recordings were used as a qualitative indica-tor of diaphragmatic activity. There was no measurableEMG,,i, activity seen in 4 of I 1 patients at 1 h and 1 of 11patients at 1 h and 6 h. They subsequently reappeared at6 h (4 patients) and 24 h (1 patient) postoperatively. Thefive patients with absent EMG,,, recordings at 1 h had asignificantly greater increase in their thoracic contribu-tion to total tidal volume (Vt,lc,ex,t 1 h - Vth,,rcM,ontrol)compared with the six patients who had recordableEMGr,i, at 1 h postoperatively. The mean VtllorGxn-crease 2 SD was 39.3 ? 14.0 (n =5) uersus 15.8 ? 10.8(n = 6; P


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Table 3. Gastric and Esophageal Pressure Indices (N = 13)Measurements Control 1 h Postoperation 6 h Postoperation 24 h Postoperation

2.29 ? 1.13-8.58 i 3.57 -7.22 2 2.93 -7.33 t 3.29 -8.57 Ir 3.960.36 % 0.77* 0.37 i 1.2W -0.34 ? 0.250.43 i 0.20

Pgas-,nsp (cmH20) 3.22 2 0.99 -1.48 i 3.95* -0.73 i 3.63'Pgas-,nsp/ A Peso-,nsp

11 Peso-lnsp (cmH2O)A P,,-,nsp (cmH*O) 11.79 t 3.95 5.74 t 5.73* 6.60 +5.13* 10.86 i r 3.73Positive A P,,,f A P Of13 10113 8/13 Of13Values are mean 2 SD.Pgas=gastric pressure; P =esophageal pressure; PgaS-,nSp difference in Pgasbetween the start and end of inspiration; P =difference inP,,, betweenthe start and end of inspiration; Pd,-,nsp= changes in transdiaphragrnatic pressure during inspiration.' P


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350 -- 300 -E5 250 --mw2 200 -39 50

100 -

+Control - hpostop. p- 6 h postop. 0- 4 h postop40050 i A

50 i

/ I

O L - 7-5 -4 -3 -2 -1 0 1 2 3 4 5

delta PRESSURE gastric (cm H,O)Fig. 5. Tracing of changes in abdominal volume and gastricpressure in one patient with left shift (at 1 h and 6 h) recordedpreoperatively and 1 h, 6 h, and 24 h postoperativly. The arrowsindicate the direction of inspiration.phragm,15,17.1" Installation of sensors or electrodes inboth these methods is difficult to perform and no pre-operative control value is available. The placement ofthe sensor device itself can induce a local or a generalchange in the function of the diaphragm. It is difficult todistinguish between an active contraction and a passivemovement of the diaphragm with the sonomicrometrytechnique . We therefore chose direct EMG,,, recordingand combined it with a number of indirect measure-ments.

The EMG,,, activity that wa s absent in 4 of 11 patientsat 1 h and 1 of 1 1 patients at 1 h and 6 h reappeared at6 h or 24 h, postoperatively further strengthening theview that there is a possible reduction of diaphragmaticactivity in the immediate postoperative period. We areunable to tell from t he EMG activity data alone if t herecovery was complete at 24 h because the experimentalmethod used to record the raw EMG data did not allowus to reliably quantify it, and this interpretation wasmade worse by the the fact that the patients left thehospital within 24 h of surgery, limiting our duration ofrecording.The mechanism for the postoperative inhibition of thediaphragm is unclear. Ford et al. suggested three poten-tial mechanisms; anesthesia, local trauma (irritation andinflammation), and local abdominal pain. Animal exper-iments on nonoperated but anesthetized controls havenot induced the type of abnormal breathing pattern thatis characteristic of operated animals, perhaps indicatingthat anesthesia has no role in this inhibition. l 9 Similarly,

Anesthesiology,V 91, N o 2, Aug 1999

anesthetized patients undergoing laparoscopic hernia re-pair showed no reduction in diaphragmatic activity6Pain as a cause of this inhibition seems unlikely due tothe fact that the abnormal breathing pattern could not bereversed despite adequate analgesia.20321esidual capnoperitoneum probably does not affect diaphragmatic ac-tivity because patients undergoing laparoscopic herniasurgery under capnoperitoneum have not been shownto develop a reduction in diaphragmatic activity6 and,furthermore, patients undergoing cardiac surgery with-out capnoper itoneum demonstrate a reduction in dia-phragmatic activity.'" Local trauma in the abdomen thatis associated with inhibitory phrenic nerve output hasbeen demonstrated in animal studies,22making this themost likely cause for t he inhibition. This inhibition of thediaphragm was considered due to a decrease in contrac-tility of the diaphragm or a decrease in phrenic nerveactivity.23 nhibition due to decreased contractility of thediaphragm was ruled out on the basis of restored transdiaphragmatic pressure swings during bilateral phrenicnerve stimulation following upper abdominal surgeryz4and also due to the ability of this group of patients tovoluntarily revert to predominantly abdominal breathingwhen asked to do so in the postoperative period.' Ericeet aL6 also demonstrated a normal diaphragmatic pressure during the sniff maneuver in their patients, suggest-ing that the voluntary diaphragmatic activity is intactpostoperatively. Reflex inhibition of the phrenic nerve

--c Control + hpostop. * hpostop. a 4hpostop.160

120

1 10 -2 -1 0 1 2 3 4 5 6 7 8deita PRESSURE gastric (cmHzO)Fig. 6 . Tracing of changes in abdominal volume and gastricpressure in one patient with persistent right shift at all mea-surement periods (ie.,preoperatively and l h, 6 h, and 24 hpostoperatively). The arrows indicate the direction of inspira-tion.


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output therefore seems to be the likely cause of thereduction in diaphragmatic activity. The present studymeasures the reduction in activity and does not distinguishbetween voluntary and reflex activity of the diaphragm.The results of our study differ from that of Coutureet aZ.,who showed that diaphragmatic activity was preservedafter laparoscopic cholecystectomy. This dissimilarity isdifficult to explain due to different time frames of datacollection and the different data presentation techniquesused, but it is worth noting that those authors patientsexhibited a positive gastric pressure in the immediate post-operative period while 10 of 13 of our patients showed anegative gastric pressure in the similar period.

Critique of the StudyDue to the limited duration (24 h) of recording in this

study, we are unable to say from our measurements if thediaphragmatic recovery was complete. N o comparisoncould be made with patients undergoing open cholecys-tectomy since this procedure is now rarely carried out inour hospital and if done is usually reserved for complicatedcases, which would introduce a bias in the study.Conclusion

The present study using both the direct and indirectindices of diaphragmatic activity shows that the dia-phragmatic activity is reduced during the immediatepostoperative period after laparoscopic cholecystec-tomy. These measurements also suggest that the recov-er y of diaphragm is already initiated during the firstpostoperative day.

The patien t clinical data were collected at the LJme:i UniversityHospital, Umei, Sweden.

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2. Lindberg P, Gunnarsson L, Tokigs L, Secher E, Lundquist H,Brismar B, Hedenstierna G: Atelectasis and lung function in the post-operative period. Acta Anaesthesiol Scand 1992; 3 6 5 4 6 -533. Steiner CA, Bass EB , Talamini MA , Pitt HA , Steinberg EP: Surgicalrates and operative mortality for open and laparoscopic cholecystec-tomy in Maryland. N Engl J Med 1994; 330:403-84. Putsen-Himmer G, Putensen C, Lammer H, Lingnau W, Aigner F,

Benzer H: Comparison of postoperative respimtory filnction after laparos-copy or open laparotomy for cholecytrctomy. ANESTHSIOLOGY992; 77:675- 805. Gunnarsson L, Lindberg P, Tokics L, Thorstensson 0,Thorne A:

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abdominal pressure after upper abdominal surgery. Anesth Analg 1989;9. Asher M I, Coates AL, Collinge JM, Millic-Emili J: Measurement of10. Dnimmond GH , Park GR: Changes in intragastric pressure on1 1. Chadha TS, Watson H, Birch S, enouri GA

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691598-603pleural pressure in neonates. J Appl Physiol 1982; 52(2):491- 4induction of anaesthesia. Br J Anaesth 1984; 56873 -9MA, Sackner MA : Validation of respiratory inductive plethysmographyusing different calibration procedures. Am Rev Respir Dis 1982; 125:644 9

12. Konno K, Mead J: Measurement of t he separate volume changesof rib cage and abdomen during breathing. J Appl Physiol 1967;22(3):407-22

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14 . Loring SH, DeTroyer A: Actions of respiratory muscles, TheThorax. Edited by R ~ L I S S ~ S, Macklem PT. New York, Marcel Dekker,1985, pp 327-50

15. Ford GT, Rosenal TW, Clergiie FC, Whitelaw WA: Respiratoryphysiology in upper abdominal surgery, Clinics in Chest Medicine.Edited by Olsen G N . Philadelphia, WB Saunders, 1993, pp 237-52

16. Clergue F, Whitelaw WA, Charles JC, Gandjbakhch I , PansardJL,Deren ne JP, Viars P: Inferences about respiratory muscle use aftercardiac surgery from compartmental volume and pressure measure-

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Zap01 WM: Diaphragmatic shortening after thoracic surgery in humans.ANESTifSiOI.O(;Y 1993; 79:654-65

19. Road JD , Burgess KR, Whitelaw WA, Ford GT: Diaphragm func-tion and respiratory response after upper abdominal surgery in dogs.J Appl Physiol 1984; 57(2):576-82

20. Simmoneau G , Vivien A, Sartene R, Kunstlinger F, Samii K ,Noviant Y, Duroux P: Diaphragm dysfunction induced by upper ab-dominal surgery: Role of postoperative pain. Am Rev Respir Dis 1983;

21. Clergue F, Montembault C, Despierre 0,Ghesquiere F, Harari A,Viars P: Respiratory effects of intrathecal morphine after upper ahdom-inal surgery. ANESTHSIOLOGY984; 61:677-8 5

22. Prabhakar N R, Marek W, Loeschcke HH: Altered brcdthing pat-tern elicited by stimulation of abdominal visceral afferents. J ApplPhysiol 1985; 58:1755-60

23. Mankikian 3, Cantincau JP, Bertrand M , Kieffer E, Sartene R,Viars P: Improvement of diaphragmatic fiinction by a thoracic extra-dural block after upper abdominal surgery. ANESTHSIOLOGY988; 68:

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ments. ANESTHSI OI . OGY 19%; 82:1318 -27

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