doi:10.1152/japplphysiol.00552.2014 117:1074-1079, 2014. First published 11 September 2014;J Appl Physiol

Jones, Carl R. O'Donnell and Daniel S. TalmorStephen H. Loring, Negin Behazin, Aileen Novero, Victor Novack, Stephanie B.pneumoperitoneum in humansRespiratory mechanical effects of surgical

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Respiratory mechanical effects of surgical pneumoperitoneum in humans

X Stephen H. Loring,1 Negin Behazin,1 Aileen Novero,1 Victor Novack,2 Stephanie B. Jones,1

Carl R. O’Donnell,3 and Daniel S. Talmor1

1Department of Anesthesia, Critical Care, and Pain Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts;2Soroka University Medical Center, Beer Sheva, Israel; and 3Division of Pulmonary and Critical Care Medicine, Beth IsraelDeaconess Medical Center, Boston, Massachusetts

Submitted 23 June 2014; accepted in final form 10 September 2014

Loring SH, Behazin N, Novero A, Novack V, Jones SB, O’DonnellCR, Talmor DS. Respiratory mechanical effects of surgical pneumo-peritoneum in humans. J Appl Physiol 117: 1074–1079, 2014. Firstpublished September 11, 2014; doi:10.1152/japplphysiol.00552.2014.—Pneumoperitoneum for laparoscopic surgery is known to stiffen thechest wall and respiratory system, but its effects on resting pleuralpressure in humans are unknown. We hypothesized that pneumoperi-toneum would raise abdominal pressure, push the diaphragm into thethorax, raise pleural pressure, and squeeze the lung, which wouldbecome stiffer at low volumes as in severe obesity. Nineteen predom-inantly obese laparoscopic patients without pulmonary disease werestudied supine (level), under neuromuscular blockade, before andafter insufflation of CO2 to a gas pressure of 20 cmH2O. Esophagealpressure (Pes) and airway pressure (Pao) were measured to estimatepleural pressure and transpulmonary pressure (PL � Pao � Pes).Changes in relaxation volume (Vrel, at Pao � 0) were estimated fromchanges in expiratory reserve volume, the volume extracted betweenVrel, and the volume at Pao � �25 cmH2O. Inflation pressure-volume (Pao-VL) curves from Vrel were assessed for evidence of lungcompression due to high PL. Respiratory mechanics were measuredduring ventilation with a positive end-expiratory pressure of 0 and 7cmH2O. Pneumoperitoneum stiffened the chest wall and the respira-tory system (increased elastance), but did not stiffen the lung, andpositive end-expiratory pressure reduced Ecw during pneumoperito-neum. Contrary to our expectations, pneumoperitoneum at Vrel didnot significantly change Pes [8.7 (3.4) to 7.6 (3.2) cmH2O; means(SD)] or expiratory reserve volume [183 (142) to 155 (114) ml]. Theinflation Pao-VL curve above Vrel did not show evidence of increasedlung compression with pneumoperitoneum. These results in predom-inantly obese subjects can be explained by the inspiratory effects ofabdominal pressure on the rib cage.

laparoscopy; respiratory mechanics; esophageal pressure; esophagealballoon; diaphragm

PNEUMOPERITONEUM IS USUALLY induced before laparoscopic sur-gery by insufflating CO2 or air into the abdomen, and it isknown to increase respiratory system elastance (Ers) (i.e.,decrease respiratory system compliance) by stiffening the chestwall. Pneumoperitoneum has also been reported to stiffen thelung in some studies (3, 6, 16, 22), but not in others (4, 12), andit decreases the end-expiratory lung volume (EELV)(4, 8, 22).Ventilation strategies recommended to mitigate the respiratoryeffects of pneumoperitoneum include raising positive end-expiratory pressure (PEEP) and applying recruitment maneu-vers to reexpand collapsed air spaces (3, 8, 16, 29, 32).

The mechanisms whereby the chest wall and lung becomestiffer have not been fully described. Although increasing

intraperitoneal volume would logically raise abdominal pres-sure and expand the abdominal wall to a less compliant regionof its pressure-volume characteristic, this alone cannot explainchest wall stiffening, because application of PEEP after pneu-moperitoneum, which would only further expand the abdomi-nal wall volume, causes a decrease in chest wall (Ecw) andlung elastance (EL) (3, 4, 16). However, acute increases inabdominal volume also stretch the diaphragm and stiffen thechest wall, as demonstrated in studies in dogs and head-up pigs(13, 14, 22). Therefore, pneumoperitoneum could stiffen theabdominal wall and diaphragm while raising pleural pressureand compressing the lungs. The lungs, being exposed to asustained high pleural pressure, might become stiffer second-ary to airway closure, as in obesity (2, 23). Although pleuralpressure during pneumoperitoneum has been estimated in an-imals using pleural or esophageal balloons (4, 12, 22), esoph-ageal pressure (Pes) measurements have not been reported atresting lung volume (VL) during pneumoperitoneum in hu-mans. The present study was undertaken to test the hypothesisthat raising intra-abdominal pressure would raise pleural(esophageal) pressure, compress the lungs, and reduce VL atequilibrium, and thereby stiffen the lungs by mechanismssimilar to those described in obese subjects (2).

METHODS

Subjects. Twenty-nine subjects were recruited before elective lapa-roscopic surgery using a protocol approved by our research ethicscommittee. Operations included cholecystectomy (2), exploratorylaparoscopy, fundoplication, gastric banding (3), gastric bypass (7),gastric sleeve, herniorrhaphy, and hysterectomy (3). No subject had ahistory of lung or respiratory disease or any contraindication foresophageal manometry. Patients were anesthetized, pharmacologi-cally paralyzed, intubated, and mechanically ventilated while supineand level. Airflow was measured with a Fleisch pneumotachographand integrated later to obtain volume change. Airway pressure (Pao)was measured at the endotracheal tube, and Pes was measured usingan esophageal balloon catheter, filled with 0.5 ml air, and passed toposition the tip of the balloon 40–45 cm from the nares or incisors.Transpulmonary pressure (PL) was calculated as PL � Pao � Pes.Pressure and flow signals were digitized, recorded, and analyzed usingWinDaq hardware and software (Dataq Instruments, Akron, OH).

Protocol. Measurements were made before and after insufflation ofthe abdomen using a clinical CO2 insufflator to maintain a peritonealgas pressure of 15 mmHg (20 cmH2O). Respiratory mechanics weremeasured during volume-controlled mechanical ventilation with aPEEP of 0 and then 7 cmH2O (Fig. 1), with tidal volume (VT) andfrequency set by the anesthesiologist. To measure the minimum Pao[threshold pressure (Pao,thr)] required to initiate lung inflation fromrelaxation volume (Vrel), the ventilator was disconnected to let thesubject exhale to atmospheric pressure for 15 s. An Ambu bag wasconnected in place of the ventilator, and Pao was gradually raised overseveral seconds by squeezing the Ambu bag while watching the Pao

Address for reprint requests and other correspondence: S. H. Loring,Anesthesia, Dana 717, 330 Brookline Ave., Boston, MA 02215 (e-mail:sloring@bidmc.harvard.edu).

J Appl Physiol 117: 1074–1079, 2014.First published September 11, 2014; doi:10.1152/japplphysiol.00552.2014.

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trace to produce a ramp increase in Pao (Ambu in Fig. 1). Then thesubject was returned to mechanical ventilation.

To measure changes in Vrel caused by pneumoperitoneum, wemeasured the volume difference between Vrel and minimal gasvolume (here assumed to be residual volume). The subject wasallowed to exhale to atmospheric pressure for 15 s, after which Paowas reduced to �25 cmH2O for �5 s, and the expired volume wasmeasured by integrating flow during the period of negative Pao (Evacin Fig. 1). The exhaled volume determined in this way was termed theexpiratory reserve volume (ERV). Assuming that the minimal gasvolume did not change with pneumoperitoneum, the measured changein ERV was equal to the change in Vrel. After a period of mechanicalventilation with 7-cmH2O PEEP, the ERV was determined again (Fig.1). Then pneumoperitoneum was induced with insufflation of CO2,and the entire sequence of measurements was repeated.

Analysis. During tidal ventilation before each respiratory maneu-ver, pressures, flow, and volume were measured in a representativebreath at end expiration (ee) and during the 150 ms end-inspiratorypause (ei), and at the end of the exhalation to Vrel. Ers, Ecw, and EL

were calculated as follows: Ers � (Pao,ei � Pao,ee)/VT; Ecw �(Pes,ei � Pes,ee)/VT; EL � (PL,ei � PL,ee)/VT. The data from tidalbreathing during the two periods on 0-cmH2O PEEP were averaged.Pes values measured during relaxation after exhalations to Vrel(Pes,rel) were averaged before and again after pneumoperitoneum. Anincrease in Pes,rel or decrease in ERV during pneumoperitoneumwould indicate compression of the lungs at Vrel.

The possibility that pneumoperitoneum caused lung compressionand airway closure near Vrel was assessed in two ways that do notrequire Pes measurements. In the first method, we determined theminimum Pao required to initiate inflation. Volume-time data duringthe slow increase in Pao were fit to two straight lines: a line ofconstant volume before inflation, and a line fit to the initial linearportion of the inflation volume-time curve. The minimum Pao re-quired to initiate inflation, the Pao,thr, was estimated as the Paomeasured at the intersection of these two lines (Fig. 2). Significantcompression of the lungs by pneumoperitoneum would be expected toincrease Pao,thr.

In the second method, the Pao-VL curves from the slow inflationsof each subject were examined for a lower “knee” or region of

maximal curvature, indicating increasing compliance (decreasingelastance) with increasing VL, suggesting progressive recruitment oflung (Fig. 3). We compared Pao-VL curves before and during pneu-moperitoneum to see if they were displaced to higher inflation pres-sures by pneumoperitoneum, suggesting lung compression.

Statistics. Results are presented as means (SD) and as percentagesfor categorical data. We utilized paired t-test for the pre-pneumoperi-toneum vs. pneumoperitoneum and PEEP 0 vs. 7 cmH2O analyses.Significance was assumed for P � 0.05 (two-tailed).

RESULTS

Of the 29 patients recruited, 3 were excluded because of achange in experimental protocol, and 7 others were excludeddue to technical problems or major deviations from the proto-

Fig. 1. Continuous recording from subject P7illustrating the measurements before pneumo-peritoneum. See text for explanation. Esoph-ageal pressure (Pes) was not measured inperiods of esophageal contraction (EC) likethose after the negative pressure evacuations(Evac). (The small expiratory flow at Evac isnot apparent at this scale.) Pao, airway pres-sure; PEEP, positive end-expiratory pressure;Ambu, Ambu bag.

Fig. 2. Tracings of volume and Pao during slow inflation before pneumoperi-toneum in subject P5. Lines fit to the volume trace intersect at the time whenPao is 3.9 cmH2O (arrow), indicating the threshold Pao (Pao,thr) needed tostart inflating the lungs. This pressure was determined before and duringpneumoperitoneum in all subjects. Pred vol, predicted volume.

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col. The 19 subjects analyzed averaged 43 yr in age (range20–74 yr), and 4 of 19 were men. The body mass index (BMI)averaged 39.8 (9.8) [mean (SD)], reflecting the study popula-tion that included patients undergoing bariatric surgery; 14were obese (BMI � 30), 3 were overweight (BMI � 25–30),and 2 were of normal weight (BMI � 18.5–25).

At Vrel, pneumoperitoneum did not significantly affect ei-ther Pes or ERV (Fig. 4, A and B). There were small, incon-sistent changes in Pes,rel, which decreased on average from 8.7(3.4) to 7.6 (3.2) cmH2O (P � 0.26), and ERV, which de-creased from 183 (142) to 155 (114) ml (P � 0.089). Pneu-moperitoneum did not significantly change Pao,thr required toinitiate inflation, which changed from 1.1 (0.9) to 0.7 (1.4)cmH2O (P � 0.16). In addition, no subject whose inflationPao-VL curve from Vrel showed a pronounced upward curva-ture (knee), suggesting airway closure and recruitment, showedan increase in the transrespiratory pressure required to begininflation after pneumoperitoneum (Fig. 3). These findings sug-gest that at Vrel, pneumoperitoneum does not increase pleuralpressure or compress the lungs.

Pneumoperitoneum increased Ers and Ecw during tidal ven-tilation with 0- and 7-cmH2O PEEP (P � 0.0001). EL was notsignificantly affected (Table 1).

Increasing PEEP from 0 to 7 cmH2O affected elastancesdifferently before and during pneumoperitoneum (Table 1).Increasing PEEP reduced Ers with pneumoperitoneum (P �0.0001), but not before. Increasing PEEP reduced Ecw bothbefore (P � 0.011) and with pneumoperitoneum (P � 0.009).Increasing PEEP had no significant effect on EL, either beforeor during pneumoperitoneum.

DISCUSSION

Principal findings of this study are that, contrary to ourexpectations, pneumoperitoneum induced at Vrel did not sig-nificantly change Pes, ERV, or Pao,thr required to initiateinflation from Vrel. Pneumoperitoneum did not significantlyaffect EL, consistent with some studies in animals (4, 12) butnot others in which EL increased (3, 6, 16, 22). However,pneumoperitoneum did markedly increase Ecw and Ers, asexpected from previous studies (3, 4, 6, 8, 12, 16, 22, 25, 27,30). These findings suggest that pneumoperitoneum does notsubstantially increase pleural pressure or compress the lungs atVrel. The addition of 7-cmH2O PEEP caused a substantialdecrease in the Ers with pneumoperitoneum, but not before,and the EL was not affected by PEEP. In what follows, wediscuss previously described mechanisms to explain each ofthese findings.

Pneumoperitoneum increases the Ecw. Insufflating gas intothe abdomen necessarily stretches the abdominal wall andexpands the chest wall as a whole (i.e., the rib cage andabdomen). This cannot by itself account for an increase in Ecw,because raising PEEP, which further increases the abdominal

Fig. 3. Pressure-volume curve during the slow inflations before and duringpneumoperitoneum in subject P5. In this subject, there is no apparent shift inthe Pao,thr required to begin inflating the lungs.

A B

Fig. 4. Effects of pneumoperitoneum at relaxationvolume. A: Pes at relaxation volume. B: expiratoryreserve volume (ERV), the volume exhaled duringapplication of negative Pao. There was no signifi-cant effect of pneumoperitoneum. Each symbolrepresents a subject.

Table 1. Effects of pneumoperitoneum and PEEP onelastance

PEEP � 0 cmH2O

P Value

PEEP � 7 cmH2O

P ValuePre Pneumo Pre Pneumo

Ers 29.6 (11.2) 42.9 (11.9) �.0001 27.7 (14.7) 38.7 (12.9)‡ �0.0001EL 20.0 (12.2) 21.6 (10.1) 0.253 19.0 (15.2) 19.6 (11.9) 0.66Ecw 10.5 (3.8) 21.4 (4.6) �.0001 9.0 (3.7)* 18.2 (6.1)† �0.0001

Values are means (SD) in cmH2O/l. Ers, respiratory elastance; EL, lungelastance; Ecw, chest wall elastance; PEEP, positive end-expiratory pressure;Pneumo, pneumoperitoneum; Pre, pre-pneumoperitoneum. Elastance differ-ence at 7-cmH2O PEEP from that at 0-cmH2O PEEP: *P � 0.02, †P � 0.01,‡P � 0.0001.

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wall stretch and rib cage volume, causes a decrease in Ecw (3,4, 16, 28). Furthermore, the relaxed rib cage itself becomesmore compliant as its volume increases above FRC (26). Amore likely explanation for stiffening of the chest wall duringpneumoperitoneum is the diaphragm’s interactions with theabdomen and rib cage.

The influence of the diaphragm on the elastance of therelaxed chest wall is apparent when the chest wall pressure-volume curve is obtained in the usual way, by changing VL. AsVL in a passive subject is reduced below FRC, the chest wallbecomes progressively stiffer. This stiffening is usually attrib-uted to stretching and passive tension in the diaphragm, whichstiffens the diaphragm-abdomen pathway for volume displace-ment (1). In addition, movement of the diaphragm into thethorax reduces the surface area of the lungs apposed to the ribcage, reducing the lungs’ mechanical advantage in displacingthe rib cage, thus stiffening the rib cage pathway for VL

displacement (20). In a similar way, pneumoperitoneum wouldincrease intra-abdominal volume and stretch both the dia-phragm and the abdominal wall and reduce the area of lung-apposed rib cage, thus stiffening both the diaphragm-abdomenand rib cage pathways for volume displacement.

Pneumoperitoneum does not cause significant change in Pesor ERV at Vrel. Raising abdominal pressure might be expectedto push the diaphragm into the rib cage, raise pleural pressure,and cause a decrease in VL. This is the explanation for themajor expiratory action of abdominal muscles. It is, therefore,surprising that, in our subjects, pneumoperitoneum caused onlysmall, inconsistent changes in Pes at Vrel. Assuming thatpressure at the top of the peritoneal cavity was atmosphericbefore pneumoperitoneum, abdominal insufflation would haveraised intra-abdominal pressure by 20 cmH2O. Could a corre-spondingly large increase in pressure in the pleural space havebeen obscured by artifacts in the measurement of Pes? Severalobservations support the opposite conclusion: that pleural pres-sure changes were small and physiologically insignificant.First, we found only small and inconsistent changes in ERVwith pneumoperitoneum (Fig. 4B), leading to the conclusionthat Vrel is not changed with pneumoperitoneum. Second, inthe slow inflation of the respiratory system after pneumoperi-toneum, no subject exhibited a rightward shift of a knee in thepressure-volume curve that would have suggested pneumoperi-toneum-induced lung compression (Fig. 3). Similarly, Pao,thrmeasured at the inflection of the volume-time trace during slowinflations showed that the minimal pressure required to initiateinflation did not increase with pneumoperitoneum, evidenceagainst significant compression of the lungs by a high pleuralpressure.

Why does a substantial rise in abdominal pressure notincrease pleural pressure and decrease VL substantially? Wespeculate that the explanation involves the inspiratory effectthat increasing abdominal pressure has on the rib cage. Theo-retical analyses and experimental evidence suggest when thediaphragm contracts during inspiration, it pulls on its insertionson the lower rib cage, applying a cephalad “insertional” forcethat is inspiratory to the rib cage (15, 33). Furthermore,diaphragm contraction raises abdominal pressure, whichpushes outward on the area of diaphragm apposed to the ribcage (18), moving the lower ribs outward to expand the ribcage (5, 15).

When abdominal pressure increases without diaphragmaticcontraction, the diaphragm’s inspiratory action on the rib cageis normally insufficient to completely counteract the expiratoryeffect of diaphragmatic movement into the thorax. Thus a risein abdominal pressure is usually expiratory. However, whenthe diaphragm is relatively stiff, increasing abdominal pressurecan stretch and raise tension in the diaphragm, resulting in aninspiratory rib cage expansion. This apparently paradoxicaleffect was demonstrated in tetraplegic subjects, whose onlysignificant inspiratory muscle is the diaphragm. When thesesubjects made maximal inspirations to TLC, they achieved ahigher maximal VL when their abdominal pressure was in-creased by an elastic abdominal binder (17). In this situation,the diaphragm, contracted during maximal inspiratory efforts,was relatively stiff and, therefore, not easily pushed into thethorax by abdominal compression. The increased abdominalpressure caused increased tension in the diaphragm, whichbecame inspiratory to not only the rib cage, but the entirerespiratory system (17).

The inspiratory effects on the rib cage of increased abdom-inal pressure could also result from abdominal pressure in-creases in the absence of diaphragm contraction, if the dia-phragm is relatively stiff, for example at Vrel when the muscleis stretched enough to develop passive tension. As abdominalpressure increases, the stiffened diaphragm resists displace-ment into the rib cage, and increasing diaphragmatic tensioncauses an inspiratory insertional force, while increased abdom-inal pressure pushes outward to expand the rib cage. Theresulting inspiratory effects on the rib cage would be greatestat low VL values (15) and could counteract the expiratoryeffect of increased abdominal pressure in displacing the dia-phragm. Indeed, infusing fluid into the abdomen of dogsstretched the diaphragm and displaced the diaphragmatic domecephalad without reducing resting VL, as measured plethysmo-graphically (10). Thus increasing abdominal volume and pres-sure can result in negligible changes in pleural pressure andPes, as observed in upright pigs (22). Consistent with theseideas, Gilroy et al. (9) found that, when gastric volume wasacutely changed in seated subjects, increased abdominal vol-ume caused unexpectedly small decreases in VL and largeincreases in rib cage volume, suggesting an inspiratory effectof abdominal pressure on the rib cage.

It is worth distinguishing the effects of pneumoperitoneumduring laparoscopic surgery from those of a gradual increase inintra-abdominal volume caused by less acute conditions, suchas pregnancy, obesity, and ascites. Although conditions likeobesity are associated with increased abdominal pressure (2,28), they do not usually achieve levels seen with pneumoperi-toneum (�20 cmH2O). In chronic conditions, there is likelysufficient time for length-adaptation of skeletal muscle in theabdominal wall, and possibly the diaphragm, to accommodatethe additional intra-abdominal volume without causing a largerise in abdominal pressure. Length adaptation of diaphragmaticmuscle would reduce diaphragmatic tension and transdiaphrag-matic pressure, allowing the diaphragm to be displaced furtherinto the thorax, thus increasing pleural pressure at rest.

Increasing PEEP reduces the Ers with pneumoperitoneum,but not without. As noted above, when the pressure-volumecharacteristic of the relaxed chest wall is obtained in the usualway by changing pressure applied to the airway, chest wallstiffening at volumes below Vrel has been attributed to passive

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diaphragmatic tension. The passive tension stiffens the dia-phragm-abdomen pathway for volume displacement and re-duces the mechanical advantage of the lung in displacing therib cage. In this circumstance, raising VL by raising Paodecreases diaphragmatic tension, decreasing Ecw. As the lungsare inflated above Vrel, the passive chest wall pressure-volumecharacteristic is relatively linear, and, therefore, further in-creases in Pao (or PEEP) do not change Ecw. The samemechanisms would apply after pneumoperitoneum. At relax-ation in the supine position, pneumoperitoneum produces sub-stantial diaphragmatic tension that stiffens the chest wall.Raising VL decreases diaphragmatic tension and reduces Ecw.

Unlike Ers, Ecw was reduced in our subjects by increasingPEEP, both with and without pneumoperitoneum. The decreasein Ecw was not correlated with BMI, so this result was notlikely due to the preponderance of obese subjects in our study.Increases in PEEP did not affect the EL, either with or withoutpneumoperitoneum. This suggests that the lungs were on thelinear portion of their inflation pressure-volume curves aboveVrel, and that pneumoperitoneum does not cause substantialcompression of the lungs at Vrel.

Critique of method and comparison with previous results.Because most of our subjects were obese and only two were ofnormal weight, the possibility must be considered that theprincipal findings of our study depend on obesity and wouldnot have occurred in normal-weight subjects. The first princi-pal finding is that pneumoperitoneum did not affect Pes at Vrel.An increase in Pes due to obesity should not prevent a furtherincrease due to pneumoperitoneum, unless the obesity causedan increase in diaphragmatic tension and prevented the rise inabdominal pressure from being transmitted to the thorax.However, obesity does not appear to increase diaphragmatictension, as the resting Pes and gastric pressures in obesesubjects are increased to the same extent, with the result thatthe resting transdiaphragmatic pressure and presumably ten-sion are not greater than in normal subjects (28). Also, therewas no relation in our subjects between BMI and the change inPes with pneumoperitoneum.

The second principal finding is that pneumoperitoneum didnot change ERV at Vrel. This might be explained if obesityraised pleural pressure enough to compress the lungs, reduceERV, and thus prevent any further decrease in ERV caused bypneumoperitoneum. This also seems unlikely, as there was norelation between BMI and either ERV at baseline or the changein ERV with pneumoperitoneum. Thus the available datasuggest that our principal findings could apply to obese andnormal subjects, although we cannot exclude the alternative.

Previous studies found that EELV, measured by nitrogenwashout during mechanical ventilation, decreased with pneu-moperitoneum in swine (4, 24) and patients (8). Futier et al. (8)found that pneumoperitoneum reduced EELV 530 ml in nor-mal-weight patients and 136 ml in obese patients, whereas wefound a nonsignificant decrease in ERV of only 29 ml. Theprevious studies using gas dilution techniques to measure thevolume in the lungs during tidal ventilation above Vrel couldhave been sensitive to pneumoperitoneum-induced changes inthe distribution of tidal ventilation above Vrel, whereas ourmeasurements of ERV to determine changes in Vrel assumeda constant minimal gas volume of the lung at residual volume.To the extent that the pressure-volume characteristics of thelung and minimal gas volume can change gradually and pro-

gressively during ventilation with low PEEP (e.g., by gasabsorption), gas dilution techniques could have indicated adecreased gas volume in the absence of a significant increase inpleural pressure. As a result, these different methods of assess-ing VL need not necessarily agree.

Estimation of pleural pressure by Pes is subject to gravita-tional artifacts. In the supine position, Pes is apparently in-creased several centimeters of H2O by the weight of the heartand overlying mediastinal structures (7, 11, 19, 21, 31). Pneu-moperitoneum, by elevating the ventral rib cage, might lift theheart off the esophagus, causing an artifactual decrease in Peswhile the actual pleural pressure increased. Similarly, a changein the shape of the lung and chest wall brought about bypneumoperitoneum could cause interregional differences intidal pleural pressure changes. Such effects could cause smalldifferences between changes in Pes and pleural pressures. Forthese reasons, we measured Pao,thr at the onset of inflation andERV to assess the impact of pleural pressure change duringpneumoperitoneum, methods that do not depend on Pes mea-surement. On the other hand, our measurements based on Pesagree with other methods, suggesting negligible pleural pres-sure change with pneumoperitoneum, which supports the util-ity of Pes in estimating pleural pressure.

Conclusions. We found that, although pneumoperitoneummarkedly increases the Ecw and Ers, at Vrel pneumoperito-neum does not raise pleural pressure or compress the lungs inour predominantly obese subjects. This apparent incongruitycan be explained by the inspiratory action of diaphragmatictension on the rib cage, which counteracts the expiratory effectof increased abdominal pressure. With inflation above Vrel, thetransrespiratory (airway) pressure and pleural pressure arehigher with pneumoperitoneum due to increased Ecw.

Do the results of this study suggest a change in our approachto mechanical ventilation during pneumoperitoneum? Probablynot. The approach often recommended is to apply moderatelevels of PEEP and perhaps recruitment maneuvers (3, 29, 32),both of which have been shown to improve respiratory me-chanics and gas exchange to some degree, and neither of whichcarries appreciable risk for patients with healthy respiratorysystems. Added PEEP would increase Pes values, and Pesvalues are higher than normal in obese subjects (2, 28), butobesity of our subjects was not obviously responsible for ourfindings. High Pes values are also common in patients withacute lung injury, although this is likely due largely to intratho-racic and abdominal edema, whose effects may differ fromthose of acute abdominal volume expansion. The principalimplication of our results is that the passive respiratory systemhas a remarkable ability to accommodate acute increases inabdominal volume and pressure without squeezing the lungs.

GRANTS

This work was supported by National Heart, Lung, and Blood InstituteGrants, HL-52586 and HL-108724 and the Beth Israel Anesthesia Foundation.

DISCLOSURES

No conflicts of interest, financial or otherwise, are declared by the author(s).

AUTHOR CONTRIBUTIONS

Author contributions: S.H.L. and N.B. conception and design of research;S.H.L., N.B., A.N., and S.B.J. performed experiments; S.H.L., N.B., A.N.,V.N., and C.R.O. analyzed data; S.H.L., N.B., A.N., V.N., C.R.O., and D.S.T.interpreted results of experiments; S.H.L. and A.N. prepared figures; S.H.L.

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and N.B. drafted manuscript; S.H.L., N.B., A.N., V.N., S.B.J., C.R.O., andD.S.T. edited and revised manuscript; S.H.L., N.B., A.N., V.N., S.B.J., C.R.O.,and D.S.T. approved final version of manuscript.

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