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Original Article

Changes in respiratory physiological dead space and compliance during non-abdominal, upper abdominal and lower abdominal surgery under general anaesthesia

Unoki, T.*; Mizutani, T.; Toyooka, H.*

Author Information
European Journal of Anaesthesiology: April 2004 - Volume 21 - Issue 4 - p 302-308

Abstract

Respiratory function changes during general anaesthesia with intermittent positive pressure ventilation (IPPV). Gas exchange is impaired due to development of shunt, atelectasis and ventilation-perfusion mismatching [1]. Previous investigations [2,3] have shown that pulmonary physiological dead space (VD phys) is increased during general anaesthesia with IPPV. Studies of the temporal changes in VD phys during the course of general anaesthesia indicate that the physiological dead space to tidal volume ratio (VD/VT) does not change in patients undergoing non-abdominal surgery [4,5]. However, to our knowledge the influence of site of surgery on changes in VD phys during general anaesthesia has not been studied. Therefore, in the present study we evaluated the changes in VD phys and dynamic compliance of the respiratory system (Crs) during general anaesthesia in non-abdominal, upper abdominal and lower abdominal surgery.

Methods

The study protocol was approved by the local Ethics Committee, which waived the need for informed consent because the study was purely observational. Inclusion criteria were adult patients scheduled to undergo general anaesthesia for elective surgeries in supine or lithotomy position (with 10-20° head down tilt) requiring a radial arterial cannula. Exclusion criteria were thoracic surgery, laparoscopic procedures, clinical evidence of cardiac or respiratory disease, application of positive end-expiratory pressure and emergence of spontaneous breathing during the surgery. The operations performed were classified as non-abdominal surgery (e.g. intercostal nerve transfer and maxillectomy), upper abdominal surgery (e.g. gastrectomy and duodenectomy) or lower abdominal surgery (e.g. cystectomy and hysterectomy).

The VD phys, Crs, respiratory rate (RR) and expiratory VT were measured using VenTrak 1550/ Capnogard 1265 (Novametrix medical systems, Wallingford, CT, USA). The system enabled online calculation of VD phys using the single breath carbon dioxide test (SBT-CO2) [6]. A schematic representation of the experimental setup is shown in Figure 1. The Capnogard 1265 is a barometric compensated mainstream, infrared capnometer that operates at a sampling rate of 87 Hz. It has a response time of <75 ms. The accuracy is 5% at PCO2 values between 5.5 and 13.3 kPa, and 0.27 kPa below 5.5 kPa. The VenTrak 1550 measures flow and volume using a miniaturized pneumotachograph. The CO2 and flow signals from these devices were fed into a computer and the SBT-CO2 was recorded using the computer software (Analysis Plus! Version 3.0; Novametrix medical systems, Wallingford, CT, USA). Arterial PCO2 was measured on a blood-gas analyser (860 Blood Gas System; Ciba Corning Diagnostics Corp, East Walpole, MA, USA). The PCO2 value was entered into the computer, which calculated physiological and alveolar dead space automatically. The combination CO2/flow sensor was placed between a heat and moisture exchanger (HME, Humid Vent Filter Compact-S; Hudson RCIAB, Upplands-Väsby, Sweden) and an elbow which was connected to the endotracheal tube (Fig. 1). All sensors and analysers were maintained and calibrated regularly according to the respective manufacturer's specifications. The VD/VT, Crs, expiratory VT and RR were measured 10 min after tracheal intubation, and 30, 60 and 120 min after the first measurement.

Figure 1
Figure 1:
A schematic representation of the experimental setup. HME: heat and moisture exchanger.

On arrival in the operating room, patients received standard anaesthetic monitoring, including ECG (lead II), non-invasive blood pressure and pulse oximetry (AS 3; Datex Instrumentarium, Helsinki, Finland). When an epidural block was indicated, an epidural catheter was inserted between the ninth thoracic and first lumbar interspace with the loss of resistance technique before induction of general anaesthesia. A test dose of lidocaine 1.5% 3 mL with epinephrine (5 μg mL−1) was given to exclude the possibility of intravascular or subarachnoid placement. Depending upon the type of surgery, patient's body size and age, epidural anaesthesia was initiated with a loading dose of lidocaine 1.5% 6-10 mL. Maintenance doses of lidocaine 1.5% 4-6 mL were given every 50-60 min. General anaesthesia was induced with intravenous (i.v.) injection of fentanyl 1-2 μg kg−1 and thiamylal 4-5 mg kg−1, followed by vecuronium 0.1-0.2 mg kg−1. The patients were orally intubated. Anaesthesia was maintained with sevoflurane 1-2% and nitrogen or nitrous oxide 50-66% in oxygen with or without epidural anaesthesia. Further doses of fentanyl and/or vecuronium were given as clinically indicated. The degree of muscle relaxation was not monitored. A radial artery cannula was inserted to allow continuous arterial pressure monitoring and arterial blood-gas sampling. Patients' lungs were mechanically ventilated throughout the study period using an anaesthesia ventilator (Narkomed® 2A; North American Drager, Telford, PA, USA, or Ohmeda 7810; Ohmeda, Madison, WI, USA, or Aestiva® 3000; Datex-Ohmeda, Madison, WI, USA). Initially, the ventilator was set in volume-controlled mode, 10-12 breaths min−1 and a VT of 8-10 mL kg−1 body weight. The VT and RR were adjusted to maintain normocapnia and were kept unchanged, unless clinically indicated, throughout the study. The anaesthetic gas composition, except sevoflurane, was kept constant during the study period.

All values are reported as mean ±SD, unless otherwise specified. Differences among the groups were determined with one-way analysis of variance (ANOVA). Statistical significance was followed by a post hoc analysis (Sheffe's multiple comparison test). Differences between the two groups (e.g. gender) were determined with non-paired t-test. The changes in physiological values were analysed by repeated measures of one-way ANOVA. Differences were considered significant at P < 0.05. All statistical analysis was performed on a personal computer with the statistical package (StatView® for Windows version 5.0; SAS Institute, NC, USA).

Results

Patient characteristics

Data were obtained from 34 patients. Patient characteristics and number of patients receiving epidural anaesthesia and/or positioned in lithotomy position during surgery are shown in Table 1. There were no significant differences in age (P = 0.20), body mass index (P = 0.69), height (P = 0.19) or weight (P = 0.92) among the three groups. Most patients in the upper abdominal and lower abdominal groups, but none in the non-abdominal group, received epidural anaesthesia. All patients in the lower abdominal group were in lithotomy position, whereas the patients in the other groups were supine during surgery.

Table 1
Table 1:
Patient characteristics, number of patients receiving epidural anaesthesia and number of patients in the lithotomy position.

Tidal volume and respiratory rate

The VT in the non-abdominal and lower abdominal groups changed significantly during the study period. In the non-abdominal group, VT increased gradually, whereas VT decreased in the lower abdominal group (Table 2). There were no significant changes in the RR during the study period in the three groups.

Table 2
Table 2:
RR and expiratoryVT.

Physiological dead space

Mean values of VD/VT at 0 min in the three groups were similar (P = 0.84) (Fig. 2, upper panel). Likewise, there were no significant differences in VD/VT among the three groups at 30 (P = 0.95), 60 (P = 0.71) or 120 min (P = 0.47). In the lower abdominal group, VD/VT increased significantly at 120 min compared with 0 (P = 0.005) and 30 min (P = 0.009). In the upper abdominal and non-abdominal groups, there were no significant changes in VD/VT over the study period.

Figure 2
Figure 2:
Upper panel: VD/VT and lower panel: Crs. Error bars indicate SD of means. *P < 0.05 compared with 0 min. **P < 0.01 compared with 0 min. ○: non-abdominal surgery; ▵: upper abdominal surgery; ▿: lower abdominal surgery.

Respiratory system compliance

Mean values of Crs at 0 min in the three groups were comparable (P = 0.79) (Fig. 2, lower panel). There were no significant differences in Crs among the three groups at 30 (P = 0.58), 60 (P = 0.15) or 120 min (P = 0.18). In the lower abdominal group, Crs had decreased significantly after 60 and 120 min, whereas it was decreased only at 120 min in the upper abdominal group. In the non-abdominal group, there were no significant changes in Crs during the study period.

PaO2/FiO2 ratio

There were no significant difference in PaO2/FiO2 ratio among the three surgery groups at 0 (P = 0.06), 30 (P = 0.99), 60 (P = 0.69) or 120 min (P = 0.52) (Fig. 3). There were no significant changes within any of the groups during the study period.

Figure 3
Figure 3:
PaO2/FiO2 ratio during non-abdominal surgery (○), upper abdominal surgery (▵) and lower abdominal surgery (▿). Error bars indicate standard deviations of means.

Discussion

The present study showed that the VD/VT increased over time in patients undergoing lower abdominal surgery under general anaesthesia. Concomitantly, Crs decreased over time in patients undergoing lower abdominal as well as upper abdominal surgery.

We used the VenTrak® 1550/Capnogard® 1265 for measuring VD/VT in the present study. Although, to our knowledge, the validity of this system for measuring VD/VT in adult human beings has not been investigated, several studies have validated the system for VD phys measurement in vitro and in animals [7,8]. In these studies, it was shown that VD phys derived from the VenTrak 1550/Capnogard 1265 system agreed well with values calculated with Bohr-Enghoff equations in small and large animals with surfactant depleted lungs [7,8]. Therefore, we find it likely that VD/VT can be measured accurately in adult human beings.

Several potential sources of error in online measurement dead space have been described [9]. These are rebreathing of gas in the tubing, variations in temperature and vapour content of expired gas, response delay of CO2, release of compressed gas during expiration and effects of other gases on flow measurement. Regarding rebreathing, although it was suggested that non-return valves in the Y-piece might decrease it [9], we could not incorporate valves in the breathing circuit, because this study was carried out in standard clinical settings. However, we believe that temporal changes in VD/VT were evaluated correctly in the present study since ventilatory settings were not changed basically throughout the study period. It appears that variations in temperature and vapour content of expired gas were negligible in the present study, since an HME was used in every patient.

Analyser delay in CO2 analysis can influence the estimation of airway dead space [9]. It is unlikely that this was significant in the present study, because flow and CO2 concentration were measured simultaneously at the same site. In addition, CO2 analysis was carried out by a mainstream capnometer that provided data at a sampling rate of 87 kHz. Similarly, the effect of compressed gas during expiration on the measurement of VD/VT seems to be negligible, since flow and CO2 concentration were measured between the endotracheal tube and the Y-piece.

It is known that flow measurement with the VenTrak® 1550 system is substantially affected by gas composition due to differences in gas viscosity [10]. Compensation can be made using a correction value according to the given gas fraction. In the present study, however, correction of flow measurement was not made, since our study focused on the time course of the respiratory mechanics, in particular VD/VT and Crs, in patients under general anaesthesia. In addition, the gas composition was kept constant during the investigation. Accordingly, it appears that these potential sources of error did not affect the main findings of our study.

Lumley and colleagues [4] found no change in VD/VT in patients undergoing femoropopliteal bypass operations during 150 min general anaesthesia. Similarly, Miyazaki [5] showed that VD/VT did not change in 36 patients undergoing minor surgery under general anaesthesia with a duration of 15-180 min and there were no differences between groups anaesthetized with air-oxygen-halothane, oxygen-halothane or nitrous oxide-oxygen-halothane. These findings are in accordance with our observation that VD/VT did not change over time in patients undergoing non-abdominal and upper abdominal surgery.

In the present study, VD/VT increased with time only in the lower abdominal group. All patients in that group underwent surgery in lithotomy position, whereas the patients in the other groups lay supine. In addition, the patients in the lower abdominal group were often placed in the head down position at the surgeon's request. To our knowledge, there are only few studies concerning the effects of lithotomy position on respiratory function during general anaesthesia. Fahy and colleagues [11] reported that the Trendelenburg position increased the impedance of the respiratory system in patients under general anaesthesia due to decreases in lung volume, especially in obese patients. General anaesthesia induces development of atelectasis in dependent lung regions during both spontaneous breathing and mechanical ventilation mainly due to relaxation of the diaphragm [12,13]. It is likely that the area of atelectasis in patients in head down position was larger than in supine patients, probably because the diaphragm was elevated. Fletcher and Larsson [14] reported an infant under general anaesthesia whose alveolar dead space increased to more than double the normal value. The authors speculated that development of atelectasis increased alveolar dead space because of over expansion of the remaining lung. Ryniak and colleagues [15] found that the exaggerated lithotomy position with head down tilt during perineal prostatectomy caused significant decreases in arterial oxygen tension and increases in CO2 tension and shunt. However, in the present study, the extent of head down tilt in the lower abdominal group was relatively mild and there was no significant change in PaO2/FiO2. Accordingly, we find it unlikely that the development of atelectasis was a major cause of the increase in VD/VT in the lower abdominal group.

Another possibility is the effect of variations in VT. We could not avoid changes in VT, because our study was purely observational. We found a decreasing VT over time in the lower abdominal group, whereas it increased in the non-abdominal group and was unchanged in the upper abdominal group. It is known that a decrease in VT results in a reduction of the anatomical dead space [16]. However, this phenomenon is observed only at a VT below 300 mL [16]. In our study, VT was kept well over 300 mL throughout the study period in all groups. Nunn and Hill [16] reported that VD/VT is unchanged in spite of an increase in VT with unchanged breathing rate, since alveolar dead space increases with VT. On the other hand, Fletcher and Jonson [17] showed that an increase in VT decreased VD/VT. They reported that median VD/VT was 0.44 and 0.31 at VT of 450 and 743 mL, respectively. In the present study, it is unlikely that the increase in VD/VT was attributable to the changes in VT, because the changes in VT were small compared with that in the study by Fletcher and Jonson [17].

In the present study, Crs did not change in the non-abdominal group, whereas it decreased in the groups undergoing abdominal surgery. Tanskanen and colleagues [18] reported that Crs was significantly lower 15 min after induction of general anaesthesia compared with immediately after induction in patients undergoing cerebral or cervical surgery in supine position. It remained unchanged 1 h after induction. In the present study, the first measurement of Crs was made at 10 min after the induction of anaesthesia. Therefore, it appears that immediate changes in Crs might already have taken place at the first measurement (10 min). The Crs is related to lung volume, i.e. compliance/functional residual capacity (FRC) is almost constant [1]. Accordingly, another possible mechanism for the decrease in Crs may be a reduction in FRC, since it is well known that general anaesthesia reduces FRC [19,20].

The decrease in Crs in the upper abdominal group might be related to insertion of retractors. Larsson and colleagues [21] reported that Crs was reduced without a decrease in FRC after retractor placement in patients undergoing upper abdominal surgery via a subcostal incision, whereas Crs did not change with an increase in FRC after retraction in a midline incision group. In the present study, all patients in the upper abdominal group, as well as in the lower abdominal group, underwent surgery via a midline incision. Thus, it is unlikely that the decrease in Crs in both these groups is attributable to retractor placement in our study.

It is known that postoperative pulmonary complications (PO-PC) occur more frequently after upper abdominal surgery compared with lower abdominal surgery [22]. It has been suggested that upper abdominal surgery induces diaphragmatic dysfunction, which might play an important role in causing PO-PC [23]. In the present study, we found an increase in VD/VT over time in patients undergoing lower abdominal surgery, but not in patients undergoing upper abdominal surgery. Moreover, the decrease in Crs tended to be larger in the lower abdominal group than in the upper abdominal group. It appears that changes in lung mechanics during surgery under general anaesthesia do not necessarily correlate with the POPC. However, postoperative respiratory complications were not recorded in our study.

We found a decrease in Crs particularly in patients subjected to lower abdominal surgery. Obeid and colleagues [24] showed that increased intra-abdominal pressure had a major influence on pulmonary compliance, i.e. a 50% decrease in Crs at 2.1 kPa in patients undergoing laparoscopic cholecystectomy. In the present study, it seems that a cranial shift of the diaphragm in the lithotomy position with head down tilt (lower abdominal group) might have caused an increase in upward pressure, thereby reducing the Crs.

Possible limitations of this study deserve to be mentioned. First, data were collected according to a fixed time schedule. Accordingly, we were unable to examine the effects of surgical procedure on VD/VT and/or Crs. Second, pulmonary circulation and smoking history, which are known to affect VD/VT[25], were not considered. Third, the effects of epidural anaesthesia on respiratory mechanics were not evaluated, since epidural anaesthesia was utilized in most of the patients who underwent abdominal surgery. However, it has been shown that thoracic epidural anaesthesia did not affect VD/VT and ventilation distribution after induction of general anaesthesia [26]. Fourth, in the present study, additional use of vecuronium after tracheal intubation was at the anaesthesiologist's discretion according to clinical conditions, and the degree of muscle blockade was not monitored. Hence, the influence of muscle blockade could not be evaluated.

In conclusion, we found that VD/VT increased over time in patients undergoing lower abdominal surgery in lithotomy and head down tilt under general anaesthesia. Additionally, Crs decreased over time both in patients undergoing upper abdominal and lower abdominal surgery.

Acknowledgments

The authors thank the staff of the Department of Anesthesiology, University of Tsukuba Hospital for their help.

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Keywords:

ANAESTHESIA; RESPIRATORY MECHANICS, respiratory dead space, lung compliance; SURGERY

© 2004 European Academy of Anaesthesiology