Reports of respiratory mechanics during laparoscopy are scarce. Drummond and Martin  found increases in the static elastance of the chest wall with abdominal insufflation during laparoscopy in the Trendelenburg (15 degrees head-down) posture, although they found no change in static lung elastance. They emphasized that the increased intrathoracic pressure will decrease cardiac output. Puri and Singh  found increases in total respiratory system elastance with insufflation in the Trendelenburg posture, but they did not separate lung from chest wall properties. Grissom et al.  also recently reported increases in static, total respiratory system elastance with insufflation. These increases were independent of whether the patient was placed in the Trendelenburg or reverse Trendelenburg (head-up) posture. Since static measurements may not reflect properties relevant to spontaneous or mechanical ventilation, especially at low lung volume , it is difficult to know how these results relate to the clinical condition. Sha et al.  suggest that lung resistance increases with increasing abdominal pressure during insufflation, although they did not include data of dynamic lung elastance.
Therefore, to understand the effects of increased abdominal pressure during insufflation of the pneumoperitoneum, we measured dynamic elastances and resistances of the total respiratory system, lungs, and chest wall in anesthetized/paralyzed patients undergoing laparoscopic surgery. Measurements were made, where possible, in the two postures in which laparoscopy is typically performed, Trendelenburg and reverse Trendelenburg. Since we have demonstrated that lung and chest wall properties are dependent on frequency and tidal volume in the physiologic range of breathing in awake [6-8] and anesthetized humans [9,10] and, furthermore, that these dependences may give useful information for understanding the mechanisms governing mechanical behavior in different conditions [10,11], we repeated measurements at tidal volumes ranging from 250 to 800 mL and frequencies ranging from 10 to 30/min. We tested the hypothesis that abdominal insufflation would result in increases in dynamic elastances and resistances of both the chest wall and lungs, and that the increases would be greater at higher insufflation pressure. We additionally hypothesized that these effects would be more pronounced in the Trendelenburg posture since gravitational effects should be larger. This information is important in deciding the potential effects of mechanical ventilation on lung injury and cardiovascular compromise.
After approval of the protocol from the University of Maryland Human Volunteers Research Committee, and after obtaining informed consent from the patients, 12 adults undergoing elective laparoscopic surgery were studied Table 1. No patient had any clinical history of pulmonary disease. Anesthesia was induced with propofol (1-2 mg/kg) or thiopental (4-5 mg/kg) intravenously. For most patients, paralysis for endotracheal intubation was achieved with a bolus of mivacurium (0.1-0.2 mg/kg) followed by a continuous infusion. However, the patients at risk for aspiration of gastric contents had paralysis for intubation achieved initially with succinylcholine (1.0-1.5 mg/kg) and continued paralysis with a mivacurium bolus and infusion as above. The trachea was intubated with either a 7.0- or 8.0-mm inner diameter endotracheal tube (NCC Hi-Lo Jet Trademark; Mallinckrodt, Glens Falls, NY). Routine clinical monitoring continued at all times. The patients were initially in a supine posture.
The patients were ventilated with 30% O2 and a mixture of 70% N (2) O and 0.4%-1.0% isoflurane delivered from a servoventilator (Siemens-Elema, 900B, Englewood, CO) in which the circuitry was adjusted to allow it to be driven by a computer. In this way, we produced a flow waveform with an inspiration:expiration ratio of 1:1 that was sinusoidal during inspiration while expiration was passive [10,12,13]. Positive end-expiratory pressure of 5 cm H2 O was applied to these patients at all times. When respiratory mechanics were not being measured, ventilation of the patient was set at 10 breaths/min with tidal volume (VT) adjusted to maintain arterial PCO2 between 30 and 40 mm Hg. To ensure that the lungs returned to the same volume at the end of each breath, the computer was programmed to delay the onset of inspiration until airway pressure (Paw) returned to 5 cm H2 O at the end of a breath at all times. Therefore, lung volume did not increase during measurements at the higher respiratory frequencies. However, the total number of breaths delivered in a minute was sometimes less than the "fundamental frequency," f, that was determined by the inspiratory flow wave . During measurements, adjustments in the level of anesthesia were generally made by changing the rate of the infused anesthetic, to avoid possible effects on bronchial musculature by variations in isoflurane level.
All measurement techniques have been previously verified . Differential pressure transducers (Celesco LCVR, Canoga Park, CA), with one port open to atmosphere, were used to measure Paw through a sampling port at the tip of the endotracheal tube, and esophageal pressure (Pes) via a polyethylene catheter attached to a latex balloon, inflated with 1 mL of air. For placement, the balloon/catheter was introduced through the lumen a 24-Fr esophageal stethoscope (Novasonics, Inc., Hauppaugh, NY) until the tip of the balloon was at nipple level. The stethoscope was removed, leaving the balloon in place. Placement of the balloon was checked with a method modified from Baydur et al. , as previously discussed . Airway flow was measured at the endotracheal tube connector using a pneumotachograph (Fleisch No. 2) and a differential pressure transducer (Celesco LCVR). A fourth Celesco LCVR transducer was used in differential mode to measure transpulmonary pressure, the difference between Paw and Pes. All signals were low-pass filtered at 5 Hz (Series 730, Frequency Devices Trademark; Haverhill, MA).
Measurements of respiratory mechanics were made immediately after the abdomen was instrumented for laparoscopy but before each specific surgical procedure was begun. All patients were studied in the Trendelenburg posture (15 degrees head-down tilt from horizontal), and eight were studied additionally in the reverse Trendelenburg posture (10 degrees head-up tilt from horizontal). In the Trendelenburg posture, measurements were before insufflation with CO2 (pneumoperitoneal pressure of the abdomen [Pab] = 0 mm Hg), and then during insufflation to Pab = 15 and 25 mm Hg. In the reverse Trendelenburg posture, measurements were made at Pab = 0 and 15 mm Hg. In the patients undergoing fundoplication, all measurements were made in the lithotomy posture, i.e., the posture used for the fundoplication procedure.
In each condition, eight combinations of f and VT were used, in the following sequence (except in a few instances when patient care dictated slight changes): 10/min = 800 mL, 250 mL, and 500 mL; 20/min = 500 mL, 800 mL, and 250 mL; 30/min = 250 mL and 500 mL. After at least three initial breaths at the given combination, we collected data from three consecutive breaths through the computer A/D interface. Then, f and VT were changed, and pressure/flow measurements were repeated. One entire set of measurements took less than 5 min.
Flow and pressure measurements from three successive breaths were digitized (sampling rate = 100/breath) and computer averaged. We used discrete Fourier transformation at the fundamental frequency (i.e., f) to fit the pressure and flow waveforms of the entire averaged breath into pure sine and cosine waves and find the complex ratios (i.e., ratios with real and imaginary parts) between each of the three measured pressures (Paw, Pes and Paw - Pes) and flow. From these, we calculated resistances and dynamic elastances of the total respiratory system (Rrs and Ers, respectively) chest wall (Rcw and Ecw), and lungs (RL and EL), assuming the resistance equaled the real part of each complex ratio and the elastance equaled the imaginary part times -pi f. We have previously verified this analysis method [12,13]. Note that elastance reflects the "stiffness" of respiratory system components whereas its reciprocal, compliance, reflects distensibility.
To test whether the resistances and elastances were affected by Pab or posture, and whether they were dependent on f and VT, we used a general linear model regression analysis, designed for repeated measurements . Values for elastance and for resistance were combined for two conditions at a time and, taking into account f and VT dependences, tested for a difference by assigning each condition a binary variable. Then values in each condition were tested separately for f and VT dependences. Regression coefficients, as listed in Table 2, are quantitative expressions of the dependence of the elastance on f (Coeff) or on VT (CoefVT) in the different conditions. We used analysis of variance and Student-Newman-Keuls testing to compare values for Coeff and for CoefVT in the different conditions. Significant differences are listed in Table 2 and Table 3, and indicate when the f or VT dependence of a given elastance and resistance was affected by posture or Pab.
We used the regression analysis  to determine whether changes in elastances and resistances at Pab = 0 mm Hg compared to Pab = 15 mm Hg were correlated to body weight or body mass index [BMI, i.e., weight in kg/(height in m)2]. The accepted level of significance for all analyses was P < 0.05.
In the 15 degrees head-down posture Figure 1, all elastances and resistances were greater at Pab = 15 and 25 mm Hg than at 0 mm Hg (P < 0.05). All elastances at Pab = 25 mm Hg were greater than at 15 mm Hg (P < 0.05), but changes in none of the resistances were significant. In all conditions, each elastance increased Table 2 and each resistance decreased Table 3 with increasing frequency (P < 0.05). The frequency dependences in Ers, Ecw, and Rcw were increased at the higher PabTable 2 and Table 3. At Pab = 0 and 15 mm Hg, Ers and EL decreased with increasing VT (P < 0.05), while Rcw showed an analogous decrease at Pab = 0 mm Hg only (P < 0.05).
The increases in Ers, Ecw, and Rcw between Pab = 0 mm Hg and Pab = 15 mm Hg were negatively correlated to body weight (P < 0.05); the increase in RL, on the other hand, displayed a positive correlation (P < 0.05). As BMI increased, the increase in EL between 0 and 15 mm Hg was more, while the increase in Ecw was less (P < 0.05).
In the 10 degrees head-up posture Figure 2, all elastances and resistances were greater at Pab = 15 mm Hg than at 0 mm Hg (P < 0.05). However, Ers, EL, Rrs, and RL were less head-up than at the same Pab while head-down (P < 0.05). Except for Ecw at Pab = 15 mm Hg, each elastance increased and each resistance decreased with increasing frequency while head-up (P < 0.05). Rcw decreased with increasing VT at either Pab while head-up (P < 0.05); at Pab = 15 mm Hg, Rrs also showed a negative dependence on VT (P < 0.05).
While head-up, the increases in Ers, EL, Rrs, and RL between Pab = 0 mm Hg and Pab = 15 mm Hg were positively correlated to BMI (P < 0.05); the increase in Ecw, on the other hand, displayed a negative correlation (P < 0.05). As body weight increased, the increases in Rrs and R (L) between 0 and 15 mm Hg were greater (P < 0.05).
We have shown that in seated, awake [6-8], or supine, anesthetized humans [9,10] and anesthetized dogs  that lung and chest wall resistances generally decrease as frequency increases, while the corresponding elastances tend to increase slightly with increases in frequency. Ecw and Rcw display negative dependences on VT, but lung properties have little VT dependence in healthy lungs. The results from the present study at Pab = 0 mm Hg in both postures generally agree with these previous results except that VT dependence of Ecw did not reach statistical significance in this group of patients, and EL decreased with increasing VT in the head-down posture. These differences may be due to the postures used or the application of positive end-expiratory pressure in the present study, and warrant further study.
As we have previously discussed , the chest wall is a complex system comprising the rib cage, diaphragm, abdominal contents, and abdominal wall, and the interaction among these compartments may vary in different conditions, especially if chest wall configuration changes. Thus it was difficult to predict the effect of increasing pneumoperitoneal pressure. For example, if the abdominal wall is immobilized (infinite elastance) by strapping while seated, overall chest wall elastance is not affected . This is because the elastance of the rib cage (rc) compartment (Erc) is in parallel with the elastance of the "diaphragm-abdomen (da)" compartment (Eda) with respect to pleural pressure. Because of this: Equation 1 Since Eda is much larger than Erc while seated , further increases in Eda do not have much effect on Ecw. In other words, with abdominal strapping, all the volume change during ventilation is "shunted" through the rib cage, whose elastance is nearly equal to Ecw while seated. However, while supine, head-down or head-up, Erc and Eda are more nearly equal and, as can be inferred from Equation 1, Erc is greater than Ecw. This is mostly because the gravitational effects of the abdominal contents on the abdominal wall are less than when seated, and the elastance of the abdominal wall is less if it a distended to a lesser degree [15,17]. Increasing Pab during laparoscopy while supine, head-up, or head-down should distend the abdominal wall, increase its elastance, and shunt more of the volume changes during ventilation through the rib cage. Ecw will then be nearly equal to Erc, which was greater than the original Ecw before insufflation.
An increased Pab should also move the diaphragm cranially and result in a decreased functional residual capacity (FRC). For example, FRC decreased 19% in patients in the Trendelenburg posture with insufflation with N2 O to keep Pab at approximately 8 mm Hg. We have shown that even small decreases in FRC will increase Ecw in anesthetized/paralyzed dogs , consistent with predictions from classical, static chest wall elastance curves . From the present results, we cannot decide how much influence decreases in FRC exerted. However, if FRC was an important mechanism, we would expect Ecw at Pab = 15 mm Hg to be greater in the head-down posture since FRC should be lower than when head-up , and increases in Ecw caused by insufflation to 15 mm Hg to be greater in patients with high BMI or body weight. In fact, no differences between in the postures were evident in Ecw at Pab = 15 mm Hg, and the increases in Ecw from 0 to 15 mm Hg Pab were generally less at high BMI or body weight.
Other possible mechanisms contributing to the increases in Ecw at increased Pab include: 1) changes in the interaction at the "zone of apposition"  at which the lungs are apposed to the lateral surface of the diaphragm; 2) changes in chest wall configuration; and 3) inhomogeneity in displacement among different parts of the chest wall. The latter, in particular, would be expected  to cause the increases in frequency dependence in EcwTable 2 and RcwTable 3 with increases Pab in the Trendelenburg posture. Further evaluation of these possible influences was beyond the scope of this study.
Changes in Rcw are seldom considered. However, we have suggested that increases in Rcw are generally linked to those in Ecw. This seemed to be the case during laparoscopy.
The presumed decreases in FRC caused by increased Pab would explain the observed increases in EL and RL. We found that even small decreases in FRC in awake volunteers  or in anesthetized/paralyzed dogs  were enough to cause large increases in EL and RL. In general, larger effects were found in patients with a high BMI or body weight, in whom we would expect larger decreases in FRC. In addition, EL and RL at Pab = 15 mm Hg were larger in the Trendelenburg posture, where FRC will be lower than in the reverse Trendelenburg posture .
Frequency dependences in EL and RL should become larger if regional inhomogeneities to flow develop . Although these frequency dependencies tended to increase at increased Pab in the Trendelenburg posture Table 2 and Table 3, no changes were significant. We infer that regional lung collapse with increased Pab due to the low FRC or deformation caused directly by the distended diaphragm did not occur to an appreciable extent.
We conclude that lung and chest wall impedances to inflation during mechanical ventilation increase with increasing pneumoperitoneal pressure during laparoscopic surgery. The effects depend on both positioning and body configuration. The increases in lung impedance will increase alveolar pressures, which increases the risk of lung injury , while the increase in chest wall impedance will increase intrathoracic pressure and its possible inhibitory effects on cardiac output. In many patients, however, these changes are not critical. They may become important to consider in obese patients, in whom lung effects should be exaggerated while chest wall effects may be less, and in patients with pulmonary disease, in whom impedances may already be high. Trendelenburg positioning should be avoided in such cases. We expect that increases in lung and chest wall impedances similar to those we found with increasing pneumoperitoneal pressures may occur in other conditions involving abdominal distention, such as ascites and pregnancy.
Surgical assistance for this study was provided by Dr. Scott Graham and the surgical house staff. Special thanks to the operating room nurses for all their support and cooperation during this study.
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