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Respiratory mechanical effects of surgical

pneumoperitoneum in humans

Stephen H. Loring, Negin Behazin, Aileen Novero, Victor Novack, Stephanie B.


Jones, Carl R. O'Donnell and Daniel S. Talmor
J Appl Physiol 117:1074-1079, 2014. First published 11 September 2014;
doi:10.1152/japplphysiol.00552.2014
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J Appl Physiol 117: 10741079, 2014.


First published September 11, 2014; doi:10.1152/japplphysiol.00552.2014.

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. ODonnell,3 and Daniel S. Talmor1
1

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

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

laparoscopy; respiratory mechanics; esophageal pressure; esophageal


balloon; diaphragm

induced before laparoscopic surgery by insufflating CO2 or air into the abdomen, and it is
known to increase respiratory system elastance (Ers) (i.e.,
decrease respiratory system compliance) by stiffening the chest
wall. Pneumoperitoneum has also been reported to stiffen the
lung in some studies (3, 6, 16, 22), but not in others (4, 12), and
it decreases the end-expiratory lung volume (EELV)(4, 8, 22).
Ventilation strategies recommended to mitigate the respiratory
effects of pneumoperitoneum include raising positive endexpiratory pressure (PEEP) and applying recruitment maneuvers to reexpand collapsed air spaces (3, 8, 16, 29, 32).
The mechanisms whereby the chest wall and lung become
stiffer have not been fully described. Although increasing
PNEUMOPERITONEUM IS USUALLY

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).
1074

intraperitoneal volume would logically raise abdominal pressure and expand the abdominal wall to a less compliant region
of its pressure-volume characteristic, this alone cannot explain
chest wall stiffening, because application of PEEP after pneumoperitoneum, which would only further expand the abdominal wall volume, causes a decrease in chest wall (Ecw) and
lung elastance (EL) (3, 4, 16). However, acute increases in
abdominal volume also stretch the diaphragm and stiffen the
chest wall, as demonstrated in studies in dogs and head-up pigs
(13, 14, 22). Therefore, pneumoperitoneum could stiffen the
abdominal wall and diaphragm while raising pleural pressure
and compressing the lungs. The lungs, being exposed to a
sustained high pleural pressure, might become stiffer secondary to airway closure, as in obesity (2, 23). Although pleural
pressure during pneumoperitoneum has been estimated in animals using pleural or esophageal balloons (4, 12, 22), esophageal pressure (Pes) measurements have not been reported at
resting lung volume (VL) during pneumoperitoneum in humans. The present study was undertaken to test the hypothesis
that raising intra-abdominal pressure would raise pleural
(esophageal) pressure, compress the lungs, and reduce VL at
equilibrium, and thereby stiffen the lungs by mechanisms
similar to those described in obese subjects (2).
METHODS

Subjects. Twenty-nine subjects were recruited before elective laparoscopic surgery using a protocol approved by our research ethics
committee. Operations included cholecystectomy (2), exploratory
laparoscopy, fundoplication, gastric banding (3), gastric bypass (7),
gastric sleeve, herniorrhaphy, and hysterectomy (3). No subject had a
history of lung or respiratory disease or any contraindication for
esophageal manometry. Patients were anesthetized, pharmacologically paralyzed, intubated, and mechanically ventilated while supine
and level. Airflow was measured with a Fleisch pneumotachograph
and integrated later to obtain volume change. Airway pressure (Pao)
was measured at the endotracheal tube, and Pes was measured using
an esophageal balloon catheter, filled with 0.5 ml air, and passed to
position 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 using
WinDaq hardware and software (Dataq Instruments, Akron, OH).
Protocol. Measurements were made before and after insufflation of
the abdomen using a clinical CO2 insufflator to maintain a peritoneal
gas pressure of 15 mmHg (20 cmH2O). Respiratory mechanics were
measured during volume-controlled mechanical ventilation with a
PEEP of 0 and then 7 cmH2O (Fig. 1), with tidal volume (VT) and
frequency set by the anesthesiologist. To measure the minimum Pao
[threshold pressure (Pao,thr)] required to initiate lung inflation from
relaxation volume (Vrel), the ventilator was disconnected to let the
subject exhale to atmospheric pressure for 15 s. An Ambu bag was
connected in place of the ventilator, and Pao was gradually raised over
several seconds by squeezing the Ambu bag while watching the Pao

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Loring SH, Behazin N, Novero A, Novack V, Jones SB, ODonnell


CR, Talmor DS. Respiratory mechanical effects of surgical pneumoperitoneum in humans. J Appl Physiol 117: 1074 1079, 2014. First
published September 11, 2014; doi:10.1152/japplphysiol.00552.2014.
Pneumoperitoneum for laparoscopic surgery is known to stiffen the
chest wall and respiratory system, but its effects on resting pleural
pressure in humans are unknown. We hypothesized that pneumoperitoneum would raise abdominal pressure, push the diaphragm into the
thorax, raise pleural pressure, and squeeze the lung, which would
become stiffer at low volumes as in severe obesity. Nineteen predominantly obese laparoscopic patients without pulmonary disease were
studied supine (level), under neuromuscular blockade, before and
after insufflation of CO2 to a gas pressure of 20 cmH2O. Esophageal
pressure (Pes) and airway pressure (Pao) were measured to estimate
pleural pressure and transpulmonary pressure (PL Pao Pes).
Changes in relaxation volume (Vrel, at Pao 0) were estimated from
changes in expiratory reserve volume, the volume extracted between
Vrel, and the volume at Pao 25 cmH2O. Inflation pressurevolume (Pao-VL) curves from Vrel were assessed for evidence of lung
compression due to high PL. Respiratory mechanics were measured
during ventilation with a positive end-expiratory pressure of 0 and 7
cmH2O. Pneumoperitoneum stiffened the chest wall and the respiratory system (increased elastance), but did not stiffen the lung, and
positive end-expiratory pressure reduced Ecw during pneumoperitoneum. Contrary to our expectations, pneumoperitoneum at Vrel did
not 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]. The
inflation Pao-VL curve above Vrel did not show evidence of increased
lung compression with pneumoperitoneum. These results in predominantly obese subjects can be explained by the inspiratory effects of
abdominal pressure on the rib cage.

Respiratory Mechanics of Pneumoperitoneum in Humans

Loring SH et al.

1075

Fig. 1. Continuous recording from subject P7


illustrating the measurements before pneumoperitoneum. See text for explanation. Esophageal pressure (Pes) was not measured in
periods of esophageal contraction (EC) like
those after the negative pressure evacuations
(Evac). (The small expiratory flow at Evac is
not apparent at this scale.) Pao, airway pressure; PEEP, positive end-expiratory pressure;
Ambu, Ambu bag.

maximal curvature, indicating increasing compliance (decreasing


elastance) with increasing VL, suggesting progressive recruitment of
lung (Fig. 3). We compared Pao-VL curves before and during pneumoperitoneum to see if they were displaced to higher inflation pressures by pneumoperitoneum, suggesting lung compression.
Statistics. Results are presented as means (SD) and as percentages
for categorical data. We utilized paired t-test for the pre-pneumoperitoneum 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 a


change in experimental protocol, and 7 others were excluded
due to technical problems or major deviations from the proto-

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

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trace to produce a ramp increase in Pao (Ambu in Fig. 1). Then the
subject was returned to mechanical ventilation.
To measure changes in Vrel caused by pneumoperitoneum, we
measured the volume difference between Vrel and minimal gas
volume (here assumed to be residual volume). The subject was
allowed to exhale to atmospheric pressure for 15 s, after which Pao
was reduced to 25 cmH2O for 5 s, and the expired volume was
measured by integrating flow during the period of negative Pao (Evac
in Fig. 1). The exhaled volume determined in this way was termed the
expiratory reserve volume (ERV). Assuming that the minimal gas
volume did not change with pneumoperitoneum, the measured change
in ERV was equal to the change in Vrel. After a period of mechanical
ventilation 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 maneuver, pressures, flow, and volume were measured in a representative
breath at end expiration (ee) and during the 150 ms end-inspiratory
pause (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 tidal
breathing 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. An
increase in Pes,rel or decrease in ERV during pneumoperitoneum
would indicate compression of the lungs at Vrel.
The possibility that pneumoperitoneum caused lung compression
and airway closure near Vrel was assessed in two ways that do not
require Pes measurements. In the first method, we determined the
minimum Pao required to initiate inflation. Volume-time data during
the slow increase in Pao were fit to two straight lines: a line of
constant volume before inflation, and a line fit to the initial linear
portion of the inflation volume-time curve. The minimum Pao required to initiate inflation, the Pao,thr, was estimated as the Pao
measured at the intersection of these two lines (Fig. 2). Significant
compression of the lungs by pneumoperitoneum would be expected to
increase Pao,thr.
In the second method, the Pao-VL curves from the slow inflations
of each subject were examined for a lower knee or region of

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Respiratory Mechanics of Pneumoperitoneum in Humans

Loring SH et al.

Table 1. Effects of pneumoperitoneum and PEEP on


elastance
PEEP 0 cmH2O
Pre

PEEP 7 cmH2O

Pneumo

P Value

Pre

Pneumo

P Value

Ers 29.6 (11.2) 42.9 (11.9) .0001 27.7 (14.7) 38.7 (12.9) 0.0001
EL
20.0 (12.2) 21.6 (10.1) 0.253 19.0 (15.2) 19.6 (11.9)
0.66
Ecw 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, lung
elastance; Ecw, chest wall elastance; PEEP, positive end-expiratory pressure;
Pneumo, pneumoperitoneum; Pre, pre-pneumoperitoneum. Elastance difference at 7-cmH2O PEEP from that at 0-cmH2O PEEP: *P 0.02, P 0.01,
P 0.0001.

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

DISCUSSION

Principal findings of this study are that, contrary to our


expectations, pneumoperitoneum induced at Vrel did not significantly change Pes, ERV, or Pao,thr required to initiate
inflation from Vrel. Pneumoperitoneum did not significantly
affect EL, consistent with some studies in animals (4, 12) but
not others in which EL increased (3, 6, 16, 22). However,
pneumoperitoneum did markedly increase Ecw and Ers, as
expected from previous studies (3, 4, 6, 8, 12, 16, 22, 25, 27,
30). These findings suggest that pneumoperitoneum does not
substantially increase pleural pressure or compress the lungs at
Vrel. The addition of 7-cmH2O PEEP caused a substantial
decrease in the Ers with pneumoperitoneum, but not before,
and the EL was not affected by PEEP. In what follows, we
discuss previously described mechanisms to explain each of
these findings.
Pneumoperitoneum increases the Ecw. Insufflating gas into
the abdomen necessarily stretches the abdominal wall and
expands the chest wall as a whole (i.e., the rib cage and
abdomen). This cannot by itself account for an increase in Ecw,
because raising PEEP, which further increases the abdominal

Fig. 4. Effects of pneumoperitoneum at relaxation


volume. A: Pes at relaxation volume. B: expiratory
reserve volume (ERV), the volume exhaled during
application of negative Pao. There was no significant effect of pneumoperitoneum. Each symbol
represents a subject.

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col. The 19 subjects analyzed averaged 43 yr in age (range


20 74 yr), and 4 of 19 were men. The body mass index (BMI)
averaged 39.8 (9.8) [mean (SD)], reflecting the study population that included patients undergoing bariatric surgery; 14
were obese (BMI 30), 3 were overweight (BMI 2530),
and 2 were of normal weight (BMI 18.525).
At Vrel, pneumoperitoneum did not significantly affect either Pes or ERV (Fig. 4, A and B). There were small, inconsistent 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 decreased from 183 (142) to 155 (114) ml (P 0.089). Pneumoperitoneum did not significantly change Pao,thr required to
initiate inflation, which changed from 1.1 (0.9) to 0.7 (1.4)
cmH2O (P 0.16). In addition, no subject whose inflation
Pao-VL curve from Vrel showed a pronounced upward curvature (knee), suggesting airway closure and recruitment, showed
an increase in the transrespiratory pressure required to begin
inflation after pneumoperitoneum (Fig. 3). These findings suggest that at Vrel, pneumoperitoneum does not increase pleural
pressure or compress the lungs.
Pneumoperitoneum increased Ers and Ecw during tidal ventilation with 0- and 7-cmH2O PEEP (P 0.0001). EL was not
significantly affected (Table 1).

Increasing PEEP from 0 to 7 cmH2O affected elastances


differently before and during pneumoperitoneum (Table 1).
Increasing PEEP reduced Ers with pneumoperitoneum (P
0.0001), but not before. Increasing PEEP reduced Ecw both
before (P 0.011) and with pneumoperitoneum (P 0.009).
Increasing PEEP had no significant effect on EL, either before
or during pneumoperitoneum.

Respiratory Mechanics of Pneumoperitoneum in Humans

Loring SH et al.

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When abdominal pressure increases without diaphragmatic


contraction, the diaphragms inspiratory action on the rib cage
is normally insufficient to completely counteract the expiratory
effect of diaphragmatic movement into the thorax. Thus a rise
in abdominal pressure is usually expiratory. However, when
the diaphragm is relatively stiff, increasing abdominal pressure
can stretch and raise tension in the diaphragm, resulting in an
inspiratory rib cage expansion. This apparently paradoxical
effect was demonstrated in tetraplegic subjects, whose only
significant inspiratory muscle is the diaphragm. When these
subjects made maximal inspirations to TLC, they achieved a
higher maximal VL when their abdominal pressure was increased 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 the
thorax by abdominal compression. The increased abdominal
pressure caused increased tension in the diaphragm, which
became inspiratory to not only the rib cage, but the entire
respiratory system (17).
The inspiratory effects on the rib cage of increased abdominal pressure could also result from abdominal pressure increases in the absence of diaphragm contraction, if the diaphragm is relatively stiff, for example at Vrel when the muscle
is stretched enough to develop passive tension. As abdominal
pressure increases, the stiffened diaphragm resists displacement into the rib cage, and increasing diaphragmatic tension
causes an inspiratory insertional force, while increased abdominal pressure pushes outward to expand the rib cage. The
resulting inspiratory effects on the rib cage would be greatest
at low VL values (15) and could counteract the expiratory
effect of increased abdominal pressure in displacing the diaphragm. Indeed, infusing fluid into the abdomen of dogs
stretched the diaphragm and displaced the diaphragmatic dome
cephalad without reducing resting VL, as measured plethysmographically (10). Thus increasing abdominal volume and pressure can result in negligible changes in pleural pressure and
Pes, as observed in upright pigs (22). Consistent with these
ideas, Gilroy et al. (9) found that, when gastric volume was
acutely changed in seated subjects, increased abdominal volume caused unexpectedly small decreases in VL and large
increases in rib cage volume, suggesting an inspiratory effect
of abdominal pressure on the rib cage.
It is worth distinguishing the effects of pneumoperitoneum
during laparoscopic surgery from those of a gradual increase in
intra-abdominal volume caused by less acute conditions, such
as pregnancy, obesity, and ascites. Although conditions like
obesity are associated with increased abdominal pressure (2,
28), they do not usually achieve levels seen with pneumoperitoneum (20 cmH2O). In chronic conditions, there is likely
sufficient time for length-adaptation of skeletal muscle in the
abdominal wall, and possibly the diaphragm, to accommodate
the additional intra-abdominal volume without causing a large
rise in abdominal pressure. Length adaptation of diaphragmatic
muscle would reduce diaphragmatic tension and transdiaphragmatic pressure, allowing the diaphragm to be displaced further
into the thorax, thus increasing pleural pressure at rest.
Increasing PEEP reduces the Ers with pneumoperitoneum,
but not without. As noted above, when the pressure-volume
characteristic of the relaxed chest wall is obtained in the usual
way by changing pressure applied to the airway, chest wall
stiffening at volumes below Vrel has been attributed to passive

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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 becomes
more compliant as its volume increases above FRC (26). A
more likely explanation for stiffening of the chest wall during
pneumoperitoneum is the diaphragms interactions with the
abdomen and rib cage.
The influence of the diaphragm on the elastance of the
relaxed chest wall is apparent when the chest wall pressurevolume curve is obtained in the usual way, by changing VL. As
VL in a passive subject is reduced below FRC, the chest wall
becomes progressively stiffer. This stiffening is usually attributed to stretching and passive tension in the diaphragm, which
stiffens the diaphragm-abdomen pathway for volume displacement (1). In addition, movement of the diaphragm into the
thorax reduces the surface area of the lungs apposed to the rib
cage, reducing the lungs mechanical advantage in displacing
the rib cage, thus stiffening the rib cage pathway for VL
displacement (20). In a similar way, pneumoperitoneum would
increase intra-abdominal volume and stretch both the diaphragm and the abdominal wall and reduce the area of lungapposed rib cage, thus stiffening both the diaphragm-abdomen
and rib cage pathways for volume displacement.
Pneumoperitoneum does not cause significant change in Pes
or ERV at Vrel. Raising abdominal pressure might be expected
to push the diaphragm into the rib cage, raise pleural pressure,
and cause a decrease in VL. This is the explanation for the
major expiratory action of abdominal muscles. It is, therefore,
surprising that, in our subjects, pneumoperitoneum caused only
small, inconsistent changes in Pes at Vrel. Assuming that
pressure at the top of the peritoneal cavity was atmospheric
before pneumoperitoneum, abdominal insufflation would have
raised intra-abdominal pressure by 20 cmH2O. Could a correspondingly large increase in pressure in the pleural space have
been obscured by artifacts in the measurement of Pes? Several
observations support the opposite conclusion: that pleural pressure changes were small and physiologically insignificant.
First, we found only small and inconsistent changes in ERV
with pneumoperitoneum (Fig. 4B), leading to the conclusion
that Vrel is not changed with pneumoperitoneum. Second, in
the slow inflation of the respiratory system after pneumoperitoneum, no subject exhibited a rightward shift of a knee in the
pressure-volume curve that would have suggested pneumoperitoneum-induced lung compression (Fig. 3). Similarly, Pao,thr
measured at the inflection of the volume-time trace during slow
inflations showed that the minimal pressure required to initiate
inflation did not increase with pneumoperitoneum, evidence
against significant compression of the lungs by a high pleural
pressure.
Why does a substantial rise in abdominal pressure not
increase pleural pressure and decrease VL substantially? We
speculate that the explanation involves the inspiratory effect
that increasing abdominal pressure has on the rib cage. Theoretical analyses and experimental evidence suggest when the
diaphragm contracts during inspiration, it pulls on its insertions
on the lower rib cage, applying a cephalad insertional force
that is inspiratory to the rib cage (15, 33). Furthermore,
diaphragm contraction raises abdominal pressure, which
pushes outward on the area of diaphragm apposed to the rib
cage (18), moving the lower ribs outward to expand the rib
cage (5, 15).

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Loring SH et al.

gressively during ventilation with low PEEP (e.g., by gas


absorption), gas dilution techniques could have indicated a
decreased gas volume in the absence of a significant increase in
pleural pressure. As a result, these different methods of assessing VL need not necessarily agree.
Estimation of pleural pressure by Pes is subject to gravitational artifacts. In the supine position, Pes is apparently increased several centimeters of H2O by the weight of the heart
and overlying mediastinal structures (7, 11, 19, 21, 31). Pneumoperitoneum, by elevating the ventral rib cage, might lift the
heart off the esophagus, causing an artifactual decrease in Pes
while the actual pleural pressure increased. Similarly, a change
in the shape of the lung and chest wall brought about by
pneumoperitoneum could cause interregional differences in
tidal pleural pressure changes. Such effects could cause small
differences between changes in Pes and pleural pressures. For
these reasons, we measured Pao,thr at the onset of inflation and
ERV to assess the impact of pleural pressure change during
pneumoperitoneum, methods that do not depend on Pes measurement. On the other hand, our measurements based on Pes
agree with other methods, suggesting negligible pleural pressure change with pneumoperitoneum, which supports the utility of Pes in estimating pleural pressure.
Conclusions. We found that, although pneumoperitoneum
markedly increases the Ecw and Ers, at Vrel pneumoperitoneum does not raise pleural pressure or compress the lungs in
our predominantly obese subjects. This apparent incongruity
can be explained by the inspiratory action of diaphragmatic
tension on the rib cage, which counteracts the expiratory effect
of increased abdominal pressure. With inflation above Vrel, the
transrespiratory (airway) pressure and pleural pressure are
higher with pneumoperitoneum due to increased Ecw.
Do the results of this study suggest a change in our approach
to mechanical ventilation during pneumoperitoneum? Probably
not. The approach often recommended is to apply moderate
levels of PEEP and perhaps recruitment maneuvers (3, 29, 32),
both of which have been shown to improve respiratory mechanics and gas exchange to some degree, and neither of which
carries appreciable risk for patients with healthy respiratory
systems. Added PEEP would increase Pes values, and Pes
values are higher than normal in obese subjects (2, 28), but
obesity of our subjects was not obviously responsible for our
findings. High Pes values are also common in patients with
acute lung injury, although this is likely due largely to intrathoracic and abdominal edema, whose effects may differ from
those of acute abdominal volume expansion. The principal
implication of our results is that the passive respiratory system
has a remarkable ability to accommodate acute increases in
abdominal volume and pressure without squeezing the lungs.
GRANTS
This work was supported by National Heart, Lung, and Blood Institute
Grants, 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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diaphragmatic tension. The passive tension stiffens the diaphragm-abdomen pathway for volume displacement and reduces the mechanical advantage of the lung in displacing the
rib cage. In this circumstance, raising VL by raising Pao
decreases diaphragmatic tension, decreasing Ecw. As the lungs
are inflated above Vrel, the passive chest wall pressure-volume
characteristic is relatively linear, and, therefore, further increases in Pao (or PEEP) do not change Ecw. The same
mechanisms would apply after pneumoperitoneum. At relaxation in the supine position, pneumoperitoneum produces substantial diaphragmatic tension that stiffens the chest wall.
Raising VL decreases diaphragmatic tension and reduces Ecw.
Unlike Ers, Ecw was reduced in our subjects by increasing
PEEP, both with and without pneumoperitoneum. The decrease
in Ecw was not correlated with BMI, so this result was not
likely due to the preponderance of obese subjects in our study.
Increases in PEEP did not affect the EL, either with or without
pneumoperitoneum. This suggests that the lungs were on the
linear portion of their inflation pressure-volume curves above
Vrel, and that pneumoperitoneum does not cause substantial
compression of the lungs at Vrel.
Critique of method and comparison with previous results.
Because most of our subjects were obese and only two were of
normal weight, the possibility must be considered that the
principal findings of our study depend on obesity and would
not have occurred in normal-weight subjects. The first principal finding is that pneumoperitoneum did not affect Pes at Vrel.
An increase in Pes due to obesity should not prevent a further
increase due to pneumoperitoneum, unless the obesity caused
an increase in diaphragmatic tension and prevented the rise in
abdominal pressure from being transmitted to the thorax.
However, obesity does not appear to increase diaphragmatic
tension, as the resting Pes and gastric pressures in obese
subjects are increased to the same extent, with the result that
the resting transdiaphragmatic pressure and presumably tension are not greater than in normal subjects (28). Also, there
was no relation in our subjects between BMI and the change in
Pes with pneumoperitoneum.
The second principal finding is that pneumoperitoneum did
not change ERV at Vrel. This might be explained if obesity
raised pleural pressure enough to compress the lungs, reduce
ERV, and thus prevent any further decrease in ERV caused by
pneumoperitoneum. This also seems unlikely, as there was no
relation between BMI and either ERV at baseline or the change
in ERV with pneumoperitoneum. Thus the available data
suggest that our principal findings could apply to obese and
normal subjects, although we cannot exclude the alternative.
Previous studies found that EELV, measured by nitrogen
washout during mechanical ventilation, decreased with pneumoperitoneum in swine (4, 24) and patients (8). Futier et al. (8)
found that pneumoperitoneum reduced EELV 530 ml in normal-weight patients and 136 ml in obese patients, whereas we
found a nonsignificant decrease in ERV of only 29 ml. The
previous studies using gas dilution techniques to measure the
volume in the lungs during tidal ventilation above Vrel could
have been sensitive to pneumoperitoneum-induced changes in
the distribution of tidal ventilation above Vrel, whereas our
measurements of ERV to determine changes in Vrel assumed
a constant minimal gas volume of the lung at residual volume.
To the extent that the pressure-volume characteristics of the
lung and minimal gas volume can change gradually and pro-

Respiratory Mechanics of Pneumoperitoneum in Humans


and N.B. drafted manuscript; S.H.L., N.B., A.N., V.N., S.B.J., C.R.O., and
D.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.

17.

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