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Changes in Lung and Chest Wall Properties with Abdominal Insufflation of Carbon Dioxide Are Immediately Reversible

Fahy, Brenda G. MD; Barnas, George M. PhD; Nagle, Sheryl E. MD; Flowers, John L. MD; Njoku, Mary J. MD; Agarwal, Manish BS

General Article

Previously we have reported that large increases in lung and chest wall elastances as well as lung resistance occur with abdominal insufflation of carbon dioxide during laparoscopic surgery.To examine whether these effects were reversible with abdominal deflation, we calculated lung and chest wall elastances and resistances from measurement of airway flow and pressure and esophageal pressure in 17 anesthetized/paralyzed patients undergoing laparoscopic surgery. Measurements were made immediately prior to abdominal insufflation and after deflation. Lung and chest wall elastances and resistances were not changed from baseline (P > 0.05), although total respiratory elastance remained slightly increased compared to baseline (P < 0.05). The change in total respiratory elastance did not correlate with abdominal insufflation time, surgical site, smoking history, or physical characteristics of the patients. There were no differences in frequency and tidal volume dependences of the elastances and resistances before and after abdominal insufflation (P > 0.5). We conclude that residual changes in respiratory mechanics caused by carbon dioxide insufflation during laparoscopic surgery are minor, and that the reported compromise of respiratory function indicated by pulmonary function tests after laparoscopy does not appear to be due to changes in passive mechanical properties of the lungs or chest wall.

(Anesth Analg 1996;82:501-5)

Departments of Anesthesiology and Surgery, University of Maryland, Baltimore, Maryland.

This work was supported by Grant HL-44128 from the National Heart, Lung and Blood Institute.

Accepted for publication November 1, 1995.

Address correspondence and reprint requests to George M. Barnas, PhD, Anesthesiology Research Labs, University of Maryland, Room 534, MSTF Bldg., 10 S. Pine St., Baltimore, MD 21201.

During abdominal insufflation of carbon dioxide for laparoscopic surgery, we have previously shown large increases in lung and chest wall elastance as well as lung resistance [1]. We concluded the increase in lung impedance increased the risk of lung injury, while the increase in chest wall impedance will increase intrathoracic pressures, possibly decreasing cardiac output. Whether these changes were reversible after abdominal deflation was not evaluated. Residual effects, if present, could have postoperative respiratory implications. For example, changes in lung or chest wall properties may be correlated with some of the compromise of pulmonary function that is often reported after laparoscopic surgery [2,3].

In our current study, we examined residual effects on respiratory mechanics after abdominal deflation. Since frequency and tidal volume dependences of respiratory properties could contain information useful in understanding mechanical behavior in the normal range of breathing [4,5], we examined these effects as well.

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After approval from the University of Maryland Human Volunteers Research Committee and informed patient consent, 17 adult patients undergoing elective laparoscopic surgery were studied Table 1. Identical methods previously described were used [1] and 10 of the patients were used in both studies. To briefly summarize, after general anesthesia induction, 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). Paralysis was maintained with a mivacurium infusion.

Table 1

Table 1

Under general anesthesia, the patient was ventilated with 30% oxygen and a mixture of 70% N2 O and 0.4% to 1% isoflurane delivered from a servoventilator (Siemens-Elema, 900B, Englewood, CO) whose circuitry was adapted to be computer driven. In this way, a flow waveform was produced with an inspiration:expiration ratio of 1:1 that was sinusoidal during inspiration with passive expiration [6-8]. To ensure that the lungs returned to functional residual capacity (FRC) at the end of each breath, the computer delayed the start of inspiration until airway pressure (Paw) returned to 5 cm H2 O, the level that positive end-expiratory pressure was set at all times. Paw was measured at the tracheal tip of the endotracheal tube through a sampling port.

Differential pressure transducers (Celesco LCVR, Canosa Park, CA) measured Paw and esophageal pressure via a polyethylene catheter attached to a latex balloon inflated with 1 mL of air. Placement of the balloon was confirmed with a method modified by Baydur et al. [9] and previously described [1]. Airway flow was measured at the endotracheal tube connector using a pneumotachograph (Fleisch No. 2) and a differential pressure transducer. The adequacy of using this method for respiratory mechanics measurements has been demonstrated [6,10].

Measurements were made immediately after induction of anesthesia/paralysis with the subject supine prior to any surgical intervention and repeated prior to emergence from anesthesia/paralysis at the conclusion of surgery with the abdomen deflated. Each subject was ventilated with the following combinations of frequency and tidal volumes: 1) 10 breaths/min: 500 mL, 800 mL, and 250 mL; 2) 20 breaths/min: 500 mL, 800 mL, and 250 mL; 3) 30 breaths/min: 250 mL and 500 mL. After at least three or four initial breaths at the given combination of frequency and tidal volumes, we collected data from three consecutive breaths. We switched immediately to the next combination, and repeated the measurements. Thus, in a given condition, data collection lasted only about 5 min.

Flow and pressure measurements from three successive breaths (sampling rate = 100 breaths/mm) were digitized and computer averaged. At the fundamental frequency, discrete Fourier transformation was used to fit the flow and pressure waveforms of the entire averaged breath into pure sine and cosine waves to obtain the complex ratios between the measured pressures and flow. From these, resistances and dynamic elastances of the total respiratory system (Rrs, Ers), chest wall (Rcw, Ecw), and lungs (RL, EL) were calculated. This method has been discussed in detail and verified elsewhere [6-8]. Note that, since elastance is the mathematical inverse of compliance, an increase in elastance means a decrease in compliance.

Data were analyzed using a linear regression analysis with a regression program [11] to test for changes in elastances and resistances before abdominal insufflation and after abdominal deflation. Frequency and tidal volume dependences of each elastance and resistance before and after insufflation were also examined using this analysis. A similar type of regression [11] was also used to determine whether changes in elastance or resistances prior to abdominal insufflation and after deflation, where significant, were correlated to age, height, weight, body mass index (i.e., weight in kg/[height in m]2), end-tidal isoflurane, abdominal insufflation time, type of laparoscopic surgery, and smoking history. The accepted level of significance for all analyses was P < 0.05.

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After abdominal deflation EL and Ecw were slightly, but not significantly (P > 0.05), increased Figure 1. However, compared to baseline, E (rs) (the sum of EL and Ecw) was increased (P < 0.05). The increases in Ers were not correlated with any of the physical or clinical variables tested (P > 0.05); they were also not dependent on frequency or tidal volume (P > 0.05). Before insufflation, all elastances increased with increasing frequency (P < 0.05), and Ers and Ecw decreased with increasing VT (P < 0.05). No differences in frequency and tidal volume dependences occurred between preinsufflation and postinsufflation values (P > 0.5).

Figure 1

Figure 1

All resistances failed to change from preinsufflation values Figure 1 once the abdomen had been deflated (P > 0.05). Before insufflation, all resistances decreased with increasing frequency (P < 0.05), and Rrs and Rcw decreased with increasing tidal volume (P < 0.05), as has been previously observed [6]. No differences in frequency and tidal volume dependences occurred between preinsufflation and postinsufflation values (P > 0.5).

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Measurements of the effects on respiratory mechanics of laparoscopy are scarce. During abdominal insufflation of carbon dioxide, increases in static chest wall elastance [12] and static total respiratory system elastance [13] have been reported. An increase in elastance represents a decreased compliance. However, measurements were not reported after abdominal deflation. Only one study, involving laparoscopic tubal ligations, made such comparisons, and no significant change in total static respiratory elastance pre- and postabdominal insufflation was demonstrated [14]. However, separate lung or chest wall properties were not measured. Furthermore, static measurements may not reflect properties relevant to spontaneous or mechanical ventilation, especially at the low lung volumes occurring during anesthesia [15]. No studies involving laparoscopic upper abdominal surgery (laparoscopic fundoplication, laparoscopic cholecystectomy) have examined pre- and postabdominal insufflation residual effects on dynamic respiratory mechanics.

In the intial group of 12 patients studied during laparoscopic surgery [1], we noticed a trend for Rrs to decrease after surgery. Since comparisons among other conditions in the intial group were clear, we decided to report those clear results while continuing to measure more patients pre- and postoperatively. As seen by inspection in Figure 1, Rrs of the total of 17 patients studied exhibits a trend to decrease after surgery, but the relatively high variability in changes in Rrs makes this trend insignificant. The reason for such variability is yet unknown, but should be the topic of future studies.

The slight increase in Ers after deflation is possibly due to a slight decrease in FRC. Postoperative laparoscopic studies have shown a decrease in FRC [2,3], and a possible decrease in FRC could have caused the slight increases in ECW and EL[16] which each alone did not reach statistical significance. However, if FRC did decrease, an increase in RL would be expected [13,16], but was not observed. This indicates that other influences may affect RL, and apparently, changes in RL during laparoscopic surgery are governed by other factors in addition to FRC.

In addition to relatively minor changes in elastances and resistances, no differences in frequency or tidal volume dependences in EL and RL occurred, as would be expected if regional inhomogeneities to flow [17] or pulmonary edema [6] developed. It is therefore unlikely that significant regional lung collapse due to low FRC or deformation caused by the diaphragm distention or increased lung water were present by the end of surgery.

Several studies have examined the effects of laparoscopy on postoperative respiratory function [2,3,18]. However, these studies performed baseline measurements prior to anesthesia induction with subsequent values obtained several hours to days after emergence from anesthesia. In one study [2], decreases in FRC and forced vital capacity were evident six hours postoperatively. In the other study, forced vital capacity and forced expiratory volume in one second decreased 73% and 72%, respectively, on postoperative Day 1 compared to preoperative values; the FRC was not measured [3]. A third study found 50% decreases in maximum transdiaphragmatic pressure three hours after laparoscopic cholecystectomy [18]. The etiology of such postoperative dysfunction can involve multiple factors during the recovery period, including levels of patient effort and pain, loss of diaphragmatic contractility, and reflex inhibition of phrenic nerve activity because of irritation of splanchnic afferents. However, the results of the present study indicate that changes in the mechanical properties of the lungs and chest wall that could presumably contribute to such dysfunction do not consistently occur immediately after laparoscopic surgery. It is possible that there may be changes in these properties some time after recovery from laparoscopy, but we know of no studies concerning this. If these changes occur, however, they would be due to factors other than the direct effects of the surgery (in particular, abdominal insufflation), which are almost immediately reversible.

We conclude that although large increases in lung resistance and lung and chest wall elastances occur with abdominal carbon dioxide insufflation for laparoscopic surgery, these changes are largely reversible with abdominal deflation. It does not appear that decreases in pulmonary function reported postoperatively are due to alterations in respiratory mechanics.

Thanks to Myra Franklin for assisting with typing this document, and to all the anesthesiology staff and housestaff for all their support. Surgical assistance for this study was provided by the University of Maryland Surgical housestaff. Special appreciation is given to the operating room nurses for all their support and cooperation.

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