Ada Anaesthesiol &and 1988: 32: 585-589

The influence of position on ventilation-perfusion distribution after abdominal surgery F. BONNET, J. L. BOURGAIN, D. MATAMIS, B. TESSEIRE and P. VIARS Departnicnts of Anaesthesiology, HGpital Henri Mondor, CrCteil, Itistitut Custave Roussy, Villejuif and Groupe Hospitalier la Piti6 Salpbtrii:rc, Paris, France

l'hc effects of a change in position on gas exchange and ventilation perfusion (VA/Q distribution were studied in 12 patients, after ahdominal surgery. V& distribution was determined from retention and excretion curves of six inert gases of different solubilities, in supine and sitting patients, during spontaneous hreathing. Changing position from supine to sitting resulted in an increase in minute ventilation and a dccrcase in Pam? without any rhange in Pao?. With regard to V,& distribution, an estimated shunt of 5.2"1;~ 5 3.4 was documented in all the patients in the supine position, and was associated with a large perrcntage of low V,&regions (20.0y0 13.0) in six of them. Patients with associated estimated shunt and low Vh/Qrcgions were those with the greatest amount of venous admixture (respectively: 27.3:; t 7.2, and 14.9';(, ri- 3.0, for patients without low i.'/Q regions, P< 0.01). When patients were placed in the sitting position, the estimated shunt was not redured, but the percentage of low V,& regions decreased when it was documented. Despite the improvement of VAlQdistribution in the sitting position, the lack of significant change in Paoi may be explained by the simultaneous decrease in Pvo.~ caused by a decrease in cardiac output.

Received 18 Januay , accepted for publication 20 May 1988

liby ulords: Position: hemodynamic effects, ventilatory cfl'ects; pulmonary gas exchange; ventilation: gas exchange, perfusion (ventilation-perfusion ratio), shunting.

A decrease in arterial oxygen tension is common after abdominal surgery ( 1 , 2) and may be related to intra- pulmonary shunting and/or inequality between the distribution of ventilation and perfusion (3-5). Venti- lation-perfusion (Vh/Q mismatching may be due either to small airways closure, to a decrease in func- tional residual capacity (FRC) (6-8), or to decreased ventilation at the lung bases observed after abdominal surgery (8) , or to an alteration in hypoxic pulmonary vasoconstriction. In normal subjects, position affects FRC and both ventilation and perfusion distribution (9-14) Changing the position of the patient from supine to sitting results in an increase in FRC and a greater distribution of ventilation to the base of the lung (12). Therefore, one would expect that a change in posilion from supine to sitting would improve gas exchange and ventilation-perfusion (V&J distri- bution arter abdominal surgery.

To examine this hypothesis, consecutive abdominal surgery patients were alternately positioned sitting and supine, and V,& distribution was determined using the six-inert-gas method ( 15).

PA'T'TEN'I'S AND METHODS Twelve patients, 11 men and one woman who had undergone surgery of the abdominal aorta, were studied on the morning following the

operation. Their ages ranged from 36 to 78 years (mean 56 f 10 s.d.). I n all patients, preoperative standard spirometric rests, blood gases and chest radiograms were obtained. They agreed to participate in the study after a detailed explanation of the procedure (informed consent).

Anaesthesia was induced with flunitrazepam and fentanyl and maintained with nitrous oxide in oxygen, pancuronium and further analgetics as necessary. Orotracheal intubation was performed using an 8 or 8.5 tracheal tuhe. During the operation a radial artery cannula and a pulmonary artery catheter were inserted percutane-

After surgery, controlled ventilation was necessary for 8 to 12 h. Whcu haeniodynamic conditions were stable and central body temperature was higher than 37" C, the patients were allowed to breathe spontaneously while still intuhated. 'I'he study was begun between 16 and 20 h after the end of surgery.

Fresh gas was delivered to the patients using an on-demand valve (Mennely, Compagnie Franpise des Produits OxyginCs, France). The same Pio, was maintained throughout the study (0.3 in four patients and 0.21 in eight patients). T h e patients were assigned randomly to the supine or sitting positions.

The measurements described below were then performed in both positions. Thirty minutes of steady state werc observed between each change of position. A sitting position was arrariged by an elevation of the upper part of the bed to about 60", leading to a n elevation of the trunk while the legs were left horizontal.

~ 'l'idal volume, respiratory rate and minute ventilation were meas- ured with a calibrated Wright spirometer.

~ Poq, Pco? and oxygen saturation were measured in artcrial and mixed venous blood (ABL 30, Radiometer Copenhagen; OSM I I Radiometer).

- Venous admixture was calculatcd by the method of Berggren (16).

ously.

586 F. BONNET E?’ AI,

Alvcolii-arterial difIerence of oxygen P(A-ajo? was calculated as I’(A-~)O? = (Pro2 Paco2/0.8) Paoj, where 1’101 is the partial press- urr of oxygen i n thc fresh gas delivrred. Cardiac output was measured hy the thcrmodilution technique (CO compntrr 95 10-A, Edwards Laboratorirs, USA) and given iis the mean value of three consrrutivr measurements. I’ulmonary artrry prcssure (PAP), pulmonary artrry occlusion prcssurc (PAOP) and right atrial pressure (RAP) were measured via thc pulnionary artrry ra thr t r r (Statham I’ 23 DB transducer, Statliani Instruments, IJSA). V& distribution was measurrd by thr incrt gas techiiique de- scrihcd by Wagner s( Wrst [ 15, 17, 18). A mixture of‘ six inert gasr5 (sulphur hcxafluoridc (SF6), ethane, cyclopropane, enflu- ranc, dicchylcthcr, acctone) dissolved in an isotonic saline solution was inluscd at 3 ml/min. Alter 30 min of continuous infusion, niixcd wnous arid arterial samples were simultaneously collected, as well as mixed rxpired gas lkom a heated mixing box. This box was adaptrd to the rxpiratory limb d t h r tubing by a heatrd tube via a onr-way valve. ‘l’hr hlood samples were equilibrated with nitrogen and the expired gas samples were then analyzed Tor SF 6 hy ail clcc-iron capturc detector (Packard 429, Packard Instru- ment Co, Downcrs Grove, USA) and for thr other five gases by a 1l;imr ionization detector (I’ackard). ‘I’lic I)lood gas solubility coeflicirnts of t t i r six inert gases were

dctcrmincd lor cach patient. ‘ Ihe relative concentrations of the inert gasts iu arterial and mixed venous blood samples were derived from the cquilihratrd samples and the measured soluhilities. T h e error of nie;isurcment of SF 6 determined in our laboratory, that is the standard deviation ofthe mean value of ten measurements, was I .3:;, ; i d h r thr other five gases i t was less than 1.8 cxc.rctinti of tlic six gasrs of diflirrent solubil ‘l‘hcst. data p1ottc.d against the blood gas partition coefficients were ~ransliirmed into ii multicompartmental plot of‘hlood flow and venti- latiun VCTSIIS V \ / ( l (15, 18). ‘l‘he model includes 50 compartments, ril‘ which o11c i s the cstirnatcd shurit (V,/Q<0.005) and one is the dead space (V,\/Q> 100). Normal V,& ratios arc considered to hr lkom 0.1 to 10; low V&ratios cxtcnd from 0.005 to 0.1; and high %/Q !>om 10 I(I 100.

I h t a wcrc ;irialyzed using analysis of‘ variancc, two-sided &test, and linear regression. A I’-\,aluc oficss than <0.05 was considered to Iic aiqiificant. Values wcrc expressed as mcau i standard deviation.

KES ULI’S All the patients studied were smokers. Preoperatively, blood gas analysis documented a mean Pa02 of 10.80 f 0.13 kPa and a mean Paco2 of 5.07 & 0.05 kPa. Preoperative spirometry showed a 151 & 36 (% expect- ed) residual volume, a 99 & 8 (% expected) vital ca- pacity (VC) and a 81 2 18 ((;d, expected) forced expira- tory volume in 1 second (FEV 1) associated with a 83 f 14 ((yo expected) value of FEV 1 /CV). An increase in P ( A - ~ ) o ~ was documented in all the patients (mean value 5.1 f- 1.6 kPa).

A linear correlation was documented between pre- and postoperative ( P ( A - ~ ) o ~ ( r = 0.84, P<O.O5).

A change in position from supine to sitting resulted in a decrease in cardiac output and in an increase in spontaneous ventilation due to an increase in tidal volume (Table 1). Pacon and P+02 both decreased, but Paw and P ( ~ - a ) o ~ did not vary (Table 1). The result-

‘Iahle I Postoperative ventilatory and hcniodynamic ~)ar,uiic.tcrs (mean i s.d.).

Supine Sitting

Minute Ventilation (Lmin- ’ ) 9.3 2.5 ** 10.4 3.2

Pao? (kl’a) 10.6 f 2.8 10.7 f 2.9 Pacoz (kPaj 5 . 8 f I . I ** 5 . 5 k 0 . 4

Respiratory rate ( m i n - ’ ) 18.7 ? 6.2 19.1 f 6.2

P(A-ajo2 (kPaj 5.0 f 2.0 5.1 t 1.5 Vd/Vt ((2,j 46.5 2 2.8 46.5 f 3.3 Cardiac index ( I . min. m2) 4 .9f1 .2 ** 4.5f1 .1

ure (kI’aj 0.9 0.8 0.8 i 0.8 Pi.02 (kPa) 5.2 f 0.8 4.9+6.1 Venous admixture ( I : ( , ) 21.4 k 8.1 20.0 f 7.1)

Pulmonary artery occluded prcss-

Oxygen consumption (ml . min)

* * P < 0.01: comparison between supine and sitting position.

187 f 62 193 ? 56

ing qffect of changes in venous admixture and cardiac index induced by the sitting position was an increase in Paol in five patients and a decrease in seven patients (Table 2).

The fit of the inert gas data to the desired retention solubility and excretion solubility was tested by the least squares method. T h e mean value of the remain- ing sum of squares was 2.9 * 1.2 for all measurements, allowing a valuable analysis of the V& distribution. The postoperative impairment in gas exchange was related to an increase in venous admixture, ranging in the supine position from 8.0 to 41.3:L. Two types of Vii,/Q distribution could be identified. A definite estimated shunt associated with less than 3% of per- fusion in the regions of low $’,& was documented in six patients. The association of both estimated shunt and regions of low V A / a was observed in six other patients. The highest values of venous admixture were observed in patients showing this second type of V.& distribution (respectively, 27.30$ & 3.2 and 14.9% ? 3.0, P<O.Ol). The magnitude of low V.A/Q was neither related to the weight or the body inass index of the patients nor to preoperative spirometric data. Postoperatively, patients with documented low $‘.&had a minute ventilation, a cardiac output and a mean value of Pa02 comparable to those of patients without low VAiQ.

When the patients were moved from supine to sit- ting, the estimated shunt did not change (Fig. 1, 2, Table 3) . By contrast, the percentage of regions with low V,& ratios documented in the supine position was significantly decreased when the patients werr changed to the sitting position (Fig. 2, Table 3 ) . Thc mean VAiQwas increased in the sitting position, while the log standard deviations of ventilation and blood flow distributions in different V,& regions remained unchanged (Table 3).

V&/a DISTRIBUTION AND POSITION 587 'Table 2 Changes in Pa02 according to changes in venous admixture, cardiac output, Pvo2.

Patirnts APaos (kPa) A Venous admixture (yo) A GO (Yo) APVoZ (kPa) AEstimated shunt (yo) ALow V,/Q('X)

1 2 3 4 5 6 7 8 9

10 1 1 12

- 2.0 -0.93 - 1.47 + 0.40 - 1.60 + 1.87 - 0.27 + 2.00 -0.20 + 0.40 + 1.20 - 0.40

- 0.5 + 0.7 + 4.8 - 1.5 + 1.4 - 2.6 - 1 .7 - 9.4 + 2.2 - 6.0 - 5.9 - 0.9

- 9.8 - 16.2 + 1.0 - 2.2 - 5.7 - 15 - 6.0 - 4.4 - 18 - 2.7 - 5.0 - 2.2

-0.15 - 0.53 -0.40

0 -0.53 - 0.20 - 0.27

0 0

- 0.27 - 0.53 - 0.53

- 0.3 + 0.6 - 0.5

0 + I . ! + 0.2 +3.1 + 0.7 + 2.5

- 1.4 + 1.5

- 3.8

0 + 3 + 2.8 - 0.8

0 0

- 2.7 - 23

0 - 0.5 - 24.9

-4.1

Measured Pao? was correlated with Paoz calculated from the VA/a distribution data (Pao2 calc= 1.17 Pao2-19.08, r = 0.92, Pc0.02) . Venous admixture cal- culated by Berggren's equation was correlated with the sum of estimated shunt plus low VA/a (venous admixture= 1.13 (shunt+low fjA/Q) - 0.61, r=0.80, P< 0.05).

VDfVT 37.7%

SITTING :7 OSfOT , I

1 ,

VENT . 13.5

0 . 6

0 . 4 I

0 . 2 I

I

I 1

0.01 0.1 1 10 100 L0g.V L "

L/mn 1.4J SUPINE

1 . 2

1

0 . 8

0 . 6

0 . 4

0.2

0.01 0.1 1 10 100 LO9.V 0

) /

Fig. 1. Example of the distribution of blood flow ( and ventilation (-------------) in I.min-' with respect to V/Qrat io on a log scalc (abscissa) derived from the retention and excretion solubility data. V/Q distribution is not significantly affected by the change in position liom supine to sitting. A small estimated shunt is document- ed in the supine position, not significantly affected by the sitting position.

DISCUSSION In healthy subjects, changing the patient's position from supine to sitting, decreased cardiac output, in- creased minute ventilation and increased Pao2 (12, 19). In the present study, when patients were placed in the sitting position, minute ventilation increased and, as the Vd/Vt ratio did not change, alveolar venti- lation also increased while Paco? decreased. Further- more, cardiac output also decreased in the sitting posi- tion. As a consequence, a shift to higher values of the mean ventilation and perfusion on the V&scale was observed (Table 3). The resulting effect depended on the VA/a distribution when patients were supine. When the majority of ventilation and perfusion was distributed to regions with normal V,.& no improve- ment in VA/Q distribution was to be expected from the change in position (Fig. 1).

When there was a high percentage of low VA/Q regions while supine, changing position shifted both ventilation and perfusion from low vA/aratios to near normal V A / ~ ratios (Fig. 2).

Other mechanisms could interfere with the overall changes in ~ A / Q ratios. After abdominal surgery, the sitting position has been reported to increase FRC ( 1 0). If, in this case, FRC becomes greater than closing ca- pacity in patients in whom closing capacity had ex-

Table 3 Postoperative ventilation perfusion distribution.

Supine Sitting

5.2 k 3.4 9.5 2 13.4

84.9 i 13.4 46.5 f 2.7 0.98 0.32 0.78 0.23 0.48 k 0.20 0.91 k 0.37

3.9f 1.3 5 . 4 ~ 6.3

88.5 7.7 46.5 f 3.3 1.21 k0.38 0.77 k 0.24 0.56 f 0.24 0.92 f 0.3 1

588 F. BONNET El' AL.

SUPINE

VD/VT 5.0% 4 1 . 4 %

1

0 . 8 6.8 VENT.

0 .4

0 . 2

0.01 0.1 1 10 100 v /.

SITTING QS/QT 3.6%

VD/VT 45.9 %

VENT. 6 . 9

Pig. 2. Distribution of tilood flow ) and ventilation (----------) in 1.rnin-I with respect to V / Q ratio on a log scale (ab- scissa). In the sitting position, perfusion of blood flow in the low V/ Qra t in region is shown. Tho supine position worsens the V/Qrat io , ticwloping an iricrcase in perfusion to the low V / Q region without any important change in estimatrd shunt.

ceeded FRC, an improvement in arterial oxygen ten- sion could result (7) . In addition, diaphragmatic dys- function has been documented in the postoperative period (20, 21) and may alter the distribution ofventi- lation, decreasing the fraction of tidal volume distrib- utcd to the lung bases (9, 22). In patients in the sitting position the ventilation to the lung bases may in- crease (13) and improve o,& ratios in these regions (23, 24).

'I'he lack of decrease of the estimated shunt in the sitting position has to be considered. Definite atelecta- sis developing during and after anaesthesia might ex- plain the occurrence of this estimated shunt (25). The improvement in diaphragmatic activity in patients in the sitting position may induce an increase in transpul- monary pressure at the lung bases, but probably not enough to overcome opening pressure for the collapsed area responsible for the estimated shunt. Since esti- mated shunt did not improve when patients were moved into the sitting position, despite a decrease in cardiac output and Paoa, it is also suggested that some degrce of impairment in hypoxic vasoconstriction does cxist. An alternative explanation is that atelectasis is

predominant in postero-caudal lung regions which are dependent in both positions and thus might receive a relative equal amount of lung perfusion (25).

v.& mismatching explains postoperative hypoxae- mia in the present study; postoperative hypoxaemia in the supine position is related to an estimated shunt in some patients and to the sum of an estimated shunt and fi.&mismatching in others who have the largest values of P(A-a)o, in the postoperative period. Esti- mated shunt has been reported to be the main cause of postoperative hypoxaemia by Siler et al. and Dia- ment et al., but in these two studies the shunt was estimated from the difference in Pao:, breathing room air and 1000/, oxygen (26, 27). This methodology has recently been questioned for FioP lower than 0.3 (28). By contrast, in the study of Georg et al., uneven V,] Q distribution was the main cause of postoperative hypoxaemia because the increase in shunt estimated by the tritium isotope technique was not large enough to account for the observed hypoxaemia (5).

In the present study, measured PaoL was slightly greater than predicted from the V& distribution, suggesting a small overestimation of gas exchange im- pairment by the six-inert-gases technique. Since the P50 value was not measured in this study but only estimated, this could lead to an overestimation of Pa02 established from the inert gas data. Indeed, red cells 2-3 DPG levels are altered in several clinical con- ditions, including large blood transfusion (29). Fur- thermore, Dueck et al. suggested that some variability in the breathing pattern during spontaneous venti- lation could explain why measured Pa02 are slightly greater than predicted Pa02 in their study (30). In postoperative patients this variability in breathing pat- tern is common and could be an additional expla- nation for the high estimated Paon. By contrast, venous admixture was slightly greater than the sum of esti- mated shunt and low $'A/Q. This could be due to some contribution of regions of between 0.1 and 0.3 to venous admixture.

The importance oflow V&units noted in the pres- ent study was not linked to postoperative ventilatory pattern or haemodynamic parameters. Patients at risk to develop postoperative hypoxaemia have been dem- onstrated to be those with preoperative negative values ofFRC-CC ratio (31) . By contrast, no preoperative spi- rometric tests were shown to predict the extent of V,& mismatching in the study of Lundh & Hedenstierna, although elderly patients with pre-existing ventilation perfusion abnormalities were more at risk to develop postoperative impairment in gas exchange (32, 33). In this study pre- and postoperative values of P ( A - ~ ) o ? were positively correlated, suggesting that pre-existing disturbances in gas exchange, which could be caused by

Vq'Q DISIRIBU'IIC

negative FRC-CC differences, could be implicated in postoperative hypoxaemia (6, 7) .

Finally, our results show that Paoz decreased in sevcn patients in the sitting position and increased in the othrr five (Table 3 ) . This confirms previous results (34-36) and reflects the different changes in venous admixture. Patients with a significant improvement in venous admixture induced by the sitting position have an improvement in Paoz. When the changes in venous admixture are slight, the decrease in PVoL induced by the decrease in cardiac output is responsible for a decrcase in Pao2.

KEFEKENCES 1. M~rmhall B E, Wyche M Q. Hypoxemia during and after anes-

ihcsiii. Ane,thesioloQ 1972; 37: 178-208. 2. Craig D B. Postoperative recovery of pulmonary function. Anesth

A47/al,~ 1981: 60: 46-52. 3. I'aarwr W. Active lobar collapse of Lhc lung after abdominal

opcrations: a contribution to the study of postoperative lung complications. Lancet 1910: ii: 1080--1083.

4. Gcirdh T', Linderholm H, Norlandrr 0. Pulmonary function in rclation to anaesthesia and surgery evaluated by analysis of oxy- gcn Irmsion ofarterial blood. Acta Anaesthesiol Scand 1958: 2: 15-26.

5. G o i ~ J, Hornum I , Mellemgaard K. The mechanism of hy- poxaemia after laparotomy. Thorax 1967: 22: 382-386.

6. Alcxandcr J 1, Spence A A, I'arikh R K, Stuart B. The role of aiiway closure in postoperative hypoxaemix Br 3 Anaesth 1973: 45: 34-40.

7. Kchdcr K, Marsh M, RodarteJ K, Hyatt R E. Airwa.y closure. A w L ~ P . ~ ~ u ~ o ~ Y 1977: 47: 40- 52.

8. Anscombe A R , Buxton R S J. Effect of abdominal operations on total lung capacity and its subdivisions. Br Med 3 1958: ii: 84 86.

9. K(iusstis (1 S, Fixley M, Genest J et al. Voluntary factors influen- cing the distribution of inspired gas. An1 Rev Respir Dis 1977: 116: 357 467.

10 l i s u IJ 0, Hickcy R F. Effect of posture on functional residual (apacity postoperatively. Anesthesiolog, 1976: 44: 520-521.

1 I . E'oiirnier l', Mensch-Dechenne J, Ramon-Bilker B, Valladares W, 1.orkhat-t A. Eflect ofsitting up on pulmonary blood pressure, flow and volume in man.

12. Coonan ' I ,J, Hope C E. Cardiorespiratory effects of change of body position. Can Anaesth Soc 3 1983: 30: 424-437.

13. Kancko K, Milk-Emili J, Dolovich M B, Dawson A, Bates D V. KcKional distribution of ventilation and perfusion as a function of body position. 3 Appl Physiol 1966: 21: 767-777.

14. Gauer 0 H, 'lhron H L. Postural changes in the circulation. In Hamilton W F, Dow P, ed. Handbook of Physiology, sect 2, \'ol 3 . Washington DC: American Physiological Society, 1965:

15. Wagncr P D, Saltzman H A, West J B. Measuremrnt ofcontinu- ous distribution of ventilation-perfusion ratios: theory. 3 Appl &riol 1974: 36: 588-599.

16. M'crt J B. Ventilation-blood flow and gas exchange. 2nd edn. OxkJrd: Blackwell, 1970.

17. Wagiirr P D, Dantsker D R, Dueck R , Clausen J L, West J B. Veiltilation-perfusion inequality in chronic obstructive pulmon- ary disease. 3 Chi lnuest 1977: 59: 203-216.

18. Evans J W, Wagner P D. Limits on VA/Qdistributions from

Alp1 Physiol 1979: 46: 36-40.

2401-lb.2439.

>N AND POSI'I'ION 589 analysis of experimental inert gas elimination. J Appl Physiol

19. Anthonisen N R, Bartlett D, 'Ienney S M. Postural cflect on ventilatory control. J Appl f'h;ysiol 1965: 20: 191-196.

20. Simoneau G, Vivien A, Sartenc A et al. Diaphragm dysfunction induced by upper abdominal surgery - role of postoperative pain. Am Reu Respiv- Dis 1983: 128: 899-903.

21. Ford G T, Whitelaw MT L, Rosenal T W, Cruse P J , Guenter C A. Diaphragm funrtion after upper abdominal surgery in hu- mans. Am Reu Respir 52s 1983: 127: 4311136.

22. 'Iahir A H, George R B, Weill H, Adriani J. Effects ofabdominal surgery upon diaphragmatic function and regional ventilation. Intern Surg 1973: 58: 337-340.

23. Smith G, Cheney F W, Winter 1' M. The en'ect of changes in cardiac output on intrapulmonary shunting. B7 3 Anaesth 1974:

24. Paul D R, Hoyt J L, Boutros A K. Cardiovascular and rcspir- atory changes in responsc to change of posture in the very obesc. Anesthesiology 1976: 45: 73-78.

25. 'I'okics L, Hedenstierna G, Strandberg A, Brismar B, Lundquist H. Lung collapse and gas exchange during general ariesthcsia: effects of spontaneous breathing, muscle paralysis, and positivc end-expiratory pressure. Anesthesiolyey 1987: 66: 157-167.

26. SilerJ N, Rosenberg H, Pull T D, Kaplan J A, Bardin H, Marshall B E. Hypoxemia after upper abdominal surgery: comparison of venous admixture and ventilation/perfusion inequality com- ponents using a digital computer. Ann Surg 1974: 179: 149--155.

27. Diamcnt M L, Palmer K N V. Vcnous/arterial pulmonary shunt- ing as the principal cause of postoperative hypoxrmia. Lancd 1967: i: 15-17.

28. Lawler P G P, Nunn J F. A reassessment of the validity of the isoshunt graph. Br 3 Anaesth 1984: 56: 132551334,

29. Bordiuk J M, McKcnna P J, Giannelli S Jr, Ayrrs S M. Altcr- ations in 2-3 diphosphoglycerate and 0 2 hemoglobin aflinity in patients undergoing open heart surgery. Circulation 1971: 43:

30. Dueck R, Rathbun M, Greenhnrg A C . Lung volume and VA/ Q distribution response to intravenous versus inhalation anrs- thesia in sheep. Anesthesiology 1984: 61: 55-65.

31. Craig D B, Whaba W M, Don H F, Couture J G, Berklade M R. "Closing volume'' and its relationship to gas exchange in seated and supine positions. 3 Appl f'hysiol 1971: 31: 717-772.

32. Lundh R , Hedenstierna G. Ventilation-perfusion relationships during anaesthesia and abdominal surgery. Acta AnaPsthesiol Scand

33. Wiren J E, Lindell S E, Hellekant C. Pre- and postoperative lung function in sitting and supine position related to postopera- tive chest x-ray abnormalities and arterial hypoxaemia. C,"l:lin

34. Waughan R h', Wise L. Postoperative arterial blood gas measurements: effect of position on gas exchange. A m Sur,q 1975:

35. Russel W J. Position of patient and respiratory function i n immediate postoperative period. Rr Mad 3 1981: 283:

36. Vu-Dinh Minh Chun D, Fairshtcr R D, Vasquez P, Wilson A F, Dolan G F. Supine rhange in arterial oxygenation in patients with chronic obstructive pulmonary disease. Am Reu Respir Dic

1977: 42: 889-898.

46: 337-342.

SUPPI I : 141-146.

1983: 27: 167-173.

Physid 1983: 3: 257-266.

183: 705-709.

1079-1 080.

1986: 133: 820-824.

Address: I? Bonnet Departement d'Anesth6sie Reanimation N"II Hbpital Henri Mondor 51, av. du Markhal de Lattre de Tassigny 94010 Creteil Ccdex, France