CJA
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Abstract Freely available
Right arrow Résumé de cet Article
Right arrow Full Text (PDF)
Right arrow Submit a scholarly reply
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Mäkinen, M.-T.
Right arrow Articles by Yli-Hankala, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Mäkinen, M.-T.
Right arrow Articles by Yli-Hankala, A.
Canadian Journal of Anesthesia 48:121-128 (2001)
© Canadian Anesthesiologists' Society, 2001

General Anesthesia

Gastric air tonometry during laparoscopic cholecystectomy: a comparison of two PaCO2 levels

Marja-Tellervo Mäkinen, MD*, Pertti O. Heinonen, MD*, Ulla-Maija Klemola, MD{dagger} and Arvi Yli-Hankala, MD PhD{ddagger}

* From the Department of Anaesthesia and Intensive Care Medicine, Meilahti Hospital,
{dagger} Eye-Ear Hospital,
{ddagger} and Women's Hospital, University of Helsinki, Helsinki, Finland.

Address correspondence to: Marja-Tellervo Mäkinen MD, Department of Anaesthesia and Intensive Care Medicine, University of Helsinki, Meilahti Hospital, Haartmaninkatu 4, P.O. Box 340 FIN-00029 HUCH, Finland. Phone: 358-9-47172458; Fax: 358-9-47174017; E-mail: marja-tellervo.makinen{at}hus.fi


    Abstract
 TOP
 Abstract
 Patients and methods
 Results
 Discussion
 References
 
Purpose: Pneumoperitoneum can cause disturbances in acid-base balance and splanchnic perfusion. We studied the effect of ventilation on acid-base balance and gastric mucosal tonometric values in patients undergoing laparoscopic cholecystectomy.

Methods: Twenty-four patients (ASA I-II) were randomly allocated into two groups. In the fixed ventilation group, ventilation was constant allowing free increase in PCO2, while in the constant CO2 group end-tidal PCO2 was fixed with ventilatory adjustment. Intraabdominal pressure was limited to 12 mmHg. Arterial acid-base balance, automated air tonometric variables and gastric mucosal to arterial PCO2 gap were determined frequently from anesthesia induction until three hours postoperatively.

Results: During pneumoperitoneum, in the fixed ventilation group arterial PCO2 changed from 5.0 ± 0.2 to 6.6 ± 0.4 kPa and pH from 7.43 ± 0.03 to 7.33 ± 0.04, tonometric PCO2 from 5.1 ± 0.5 to 6.9 ± 0.4 and pH from 7.44 ± 0.04 to 7.33 ± 0.04. In the constant CO2 group these variables remained at control levels (P < 0.01 between groups). The PCO2 gap remained unchanged without any differences between the groups. In the recovery room all measured variables were within normal range in both groups.

Conclusion: Despite inter-group differences in arterial and tonometric PCO2 and pH values during CO2 pneumoperitoneum, the patients did not develop splanchnic hypoperfusion detectable by air tonometric method, as indicated by normal PCO2 gap in both groups throughout the study.

INTRAPERITONEAL insufflation of carbon dioxide during laparoscopic surgery leads to possibly harmful physiologic alterations, such as increased airway pressures and hypercarbia. Disturbances in acid-base balance have been suggested to be caused by increased intraabdominal pressure or by absorption of CO2 from the abdominal cavity. Some of the observed acidotic changes might be of non-respiratory origin.1,2 Circulatory disturbances, such as increase in central venous pressure,3 development of venous stasis in lower limbs4 or reduced cardiac index5 might result in metabolic acidosis. Furthermore, pneumoperitoneum has been associated with disturbances in splanchnic micro-circulation depending on the level of intraabdominal pressure.6

Gastrointestinal saline tonometry was introduced in the late 1980s.7 The method has been improved to a clinically feasible on-line monitoring of splanchnic perfusion by new automated air tonometry.8 Results of tonometric measurements during laparoscopic cholecystectomy have been conflicting, varying from reports of splanchnic ischemia9 or deterioration10 to no detectable changes.11

We studied gastric air tonometry together with simultaneous measurement of arterial acid-base balance during laparoscopic cholecystectomy and immediate postoperative period. We compared the influence of two distinct PETCO2 levels, obtained by ventilatory arrangements, on acid-base balance and tonometric variables.


    Patients and methods
 TOP
 Abstract
 Patients and methods
 Results
 Discussion
 References
 
The protocol was approved by the IRB of the hospital, and written informed consent was obtained from 24 ASA I-II patients scheduled for elective laparoscopic cholecystectomy. They were randomly allocated using a sealed envelope method to one of the two study groups. Any respiratory disease or body mass index > 30 were taken as exclusion criteria.

Anesthesia
Patients were premedicated with 10 mg diazepam po one hour before surgery. Acetated Ringer's solution was given iv, 10 ml•kg–1 before surgery and 5 ml•kg–1•hr–1 throughout the operation. Following 0.2 mg glycopyrrolate, anesthesia was induced with 2 µg•kg–1 remifentanil and 2.5 mg•kg–1 propofol and maintained with 10 mg•kg–1•hr–1 propofol and initial 5 µg•kg–1•hr–1 remifentanil infusion. During surgery, the infusion rates were adjusted to maintain values of systolic arterial blood pressure and heart rate within ± 25 % from the control values.

Tracheal intubation was facilitated with 0.6 mg•kg–1 rocuronium. Neuromuscular block was maintained at 80-90 % level with 10 mg rocuronium increments, as evaluated using transcutaneous train-of-four stimulation of the ulnar nerve.

Ketorolac, 30 mg iv, was given during closure of trocar wounds. The patients were kept free of pain by giving meperidine, in increments of 10 mg, before transport to the recovery room. Postoperative pain was treated with oxycodone and nausea with droperidol given by recovery room nurses when needed.

Ventilation
The lungs were ventilated using a Sulla 909V® (Drëgerwerk AG, Lübeck, Germany) ventilator with a rebreathing circuit incorporating a CO2 absorber. A continuous fresh gas flow of 4 L•min–1 (1.5 L O2 and 2.5 L air), an inspiratory to expiratory ratio of 1:2 and zero end-expiratory pressure were applied. In both groups, respiratory frequency was set to 10 breaths•min–1 and inspiratory tidal volume adjusted to provide an end-tidal carbon dioxide tension (PETCO2) of 4.5 kPa before the start of surgery. Thereafter, in the FV (Fixed Ventilation) group, ventilation was left unaltered with fixed ventilatory settings. In the CC (Constant end-tidal Carbon dioxide) group, instead, a constant PET CO2 was maintained by adjusting the inspiratory tidal volume of ventilation until the end of anesthesia.

Surgery
Carbon dioxide pneumoperitoneum was introduced and maintained with a Laparoflator Electronic 3059® (F. M. Wiest Medizintechnik GmbH, Germany) device. Intraabdominal insufflation pressure was limited to 12 mmHg with computer control. After introducing trocars the patients were placed to a head up and right side up lateral tilt, 10° each. When the pneumoperitoneum was evacuated, the patients were returned to the horizontal position.

Measurements
After anesthetic induction a radial artery was cannulated, and a TRIP® Tonometry Catheter, 16F with stopcock (Datex-Ohmeda Div./Instrumentarium Corp., Helsinki, Finland), was introduced via the nasogastric route. Correct positioning of the catheter in the stomach was evaluated, first by estimating the distance from the nostril to the left upper abdominal quadrant, second by injecting air into the catheter while auscultating the abdomen, and third by aspiration of gastric contents. The catheter was connected to the TonocapTM Monitor for automated air tonometry through the TRIP® Catheter Sampling Line (Datex-Ohmeda).

Before surgery, gastric mucosal PCO2 (PgCO2) was determined three times at 10 min intervals, the last of which served as control value. Intraoperatively, the measurements were performed at 10 min intervals until 20 min after desufflation of pneumoperitoneum, and thereafter until three hours in the recovery room. The arterial blood samples, from which oxygen and carbon dioxide tensions (PaCO2), pH (pHa), bicarbonate and base excess were determined, were analyzed simultaneously with the tonometric measurements. The gastric mucosal to arterial PCO2 gradient, P(g-a)CO2, i.e. the PCO2 gap, was calculated as the difference between tonometric PCO2 (PgCO2) and arterial PCO2. Tonometric pH, i.e., gastric mucosal pH (pHg), was calculated using a modification of the Henderson-Hasselbalch equation.12

In addition, from anesthesia induction until tracheal extubation, the following measurements were continuously performed (Datex-Ohmeda AS/3TM Anesthesia Monitor): respiratory gas concentrations (inspiratory and expiratory CO2 and O2), respiratory rate, respiratory volumes (inspiratory and expiratory tidal and minute volume), airway pressures (peak inspiratory, end-inspiratory, end-expiratory), SpO2, ECG, HR, invasive arterial blood pressures, as well as core temperature from rectum and skin temperatures from big toe, upper third of ventral antebrachium and middle finger.

In the recovery room, besides the arterial samples and tonometry as described above, ECG, HR, SpO2, respiratory frequency and invasive arterial blood pressures were continuously recorded from 20 min to three hours following extubation.

Statistics
Statistical analyses were performed with Systat® statistical program and a freeware power calculation program. Patient group size calculations were based on an earlier study,10 according to which a minimum of nine patients in each group would be needed to detect a 1.0 kPa PCO2 gap difference with 95% sensitivity and 80% specificity. Thus, we decided to use a sample size of 12 patients in each group. Patient characteristics were compared with analysis of variance and Chi-square test. The effects of intervention (pneumoperitoneum) vs time and study group on repeated measurements were tested with multivariate repeated measures analysis. A posteriori analyses for repeated measurements within the groups vs between the groups were done using Tukey-type multiple comparisons test vs analysis of variance with Tukey's HSD (Honest Significant Difference) test. P < 0.05 was considered as statistical significance. Unless stated otherwise, all results are given as mean or mean ± SD.


    Results
 TOP
 Abstract
 Patients and methods
 Results
 Discussion
 References
 
There were no differences between the two groups with regard to demographic, operative, or anesthetic data (Table IGo).


View this table:
[in this window]
[in a new window]
 
TABLE I Demographic, operative, anesthetic and postoperative pain treatment data of the patients as total numbers or mean ± SD.
 
Ventilatory measurements during laparoscopic cholecystectomy are shown in Table IIGo. During pneumoperitoneum, PETCO2 increased in the FV group from 4.4 to 5.6 kPa (P < 0.01), while in the CC group it was maintained constant. In the FV group, expiratory tidal volume of ventilation remained unchanged. In the CC group maintenance of constant PETCO2, instead, required an increase of 47% in the tidal volume, that is, from 467 ± 119 to 685 ± 148 ml. Peak inspiratory airway pressure increased 20% in the FV and 50% in the CC group. The differences in ventilatory variables between the groups were significant during pneumoperitoneum (P < 0.01).


View this table:
[in this window]
[in a new window]
 
TABLE II Ventilatory variables of the study groups during laparoscopic cholecystectomy.
 
Arterial and tonometric PCO2 and pH values are shown in Table IIIGo. During pneumoperitoneum, PaCO2 increased in the FV group from 5.0 to 6.6 kPa (P < 0.01), while in the CC group it remained within 5.1-5.3 kPa. In the FV group, PgCO2 increased from 5.1 to 6.9 kPa (P < 0.01) and in the CC group from 5.2 to 5.8 kPa (P < 0.05). In the FV group, both pHa and pHg decreased (P < 0.01), whereas in the CC group the values remained at the control levels. Arterial and tonometric CO2 and pH values differed between the groups (P < 0.01). Before pneumoperitoneum, the mean P(g-a)CO2 gradient value in the FV or CC group was 0.0 and 0.1 kPa, respectively. At the end of pneumoperitoneum, the figures were 0.3 and 0.6 kPa, respectively (NS within and between groups)(FigureGo).


View this table:
[in this window]
[in a new window]
 
TABLE III Arterial and tonometric PCO2 and pH values during laparoscopic cholecystectomy.
 


View larger version (21K):
[in this window]
[in a new window]
 
FIGURE Tonometric to arterial PCO2 difference, the P(g-a)CO2 gap (kPa), before, during and after laparoscopic cholecystectomy.

Filled diamond = the FV group with fixed ventilation.

Open triangle = the CC group with constant end-tidal CO2.

C = control before pneumoperitoneum, X = exsufflation of pneumoperitoneum, R = arrival at recovery room.

The gap remained unchanged during surgery and in the immediate postoperative period, and there were no differences between the groups.

 
During cholecystectomy, arterial bicarbonate concentrations varied in the FV or CC group from 25.3 to 26.4 and from 25.1 to 25.6 mmol•l–1, and base excess from 1.6 to 0.7 and from 1.9 to 1.1 mmol•l–1, respectively (NS within and between groups).

Hemodynamic variables showed similar courses in both groups (NS between the groups). Heart rate increased to its maximum after creation of the pneumoperitoneum (in the FV group to 77 ± 14 and in the CC group to 65 ± 13 beats•min–1). The MAP increased in the FV group from the control 73 ± 12 to 96 ± 14 (P < 0.01) after creation of pneumoperitoneum, and in the CC group from 70 ± 6 to 90 ± 7 mmHg (P < 0.01). At the end of the pneumoperitoneum, the values of MAP were 87 ± 16 and 90 ± 11 mmHg in the FV and CC group.

The changes in body temperature were similar in the two groups. Rectal core temperature decreased, 0.7°C in the FV and 0.8°C in the CC group (P < 0.01 within groups). Skin temperatures increased after induction of anesthesia and remained at the elevated levels; arm by 2°C, finger and toe by 6°C (P < 0.01 within groups).

Postoperatively, during three hours in the recovery room, PETCO2 remained within 4.9-5.6 kPa in both groups. Respiratory frequency varied between 12.6-15.1 breaths•min–1 in both groups. As shown in Table IVGo, in the FV group, PaCO2 remained between 5.3-5.6, and in the CC group between 5.8-6.1 kPa. The corresponding values for PgCO2 were 6.0-6.6 and 6.2-6.7 kPa. In the FV group, P(g-a)CO2 varied between 0.5-1.1, and in the CC group between 0.3-0.8 kPa (FigureGo). Arterial pH remained between 7.36 and 7.41 and pHg between 7.34 and 7.37 in both groups (Table IVGo). The variations in PETCO2, respiratory frequency, PaCO2, PgCO2, P(g-a)CO2 (FigureGo), pHa or pHg were not significant within or between groups. Arterial bicarbonate levels remained in the FV and CC groups between 25.2-26.1 and between 25.8-26.2 mmol•l–1, and base excess levels between 1.1-1.3 and 0.9-1.0 mmol•l–1, respectively, NS. Heart rate varied between 64-80 beats•min–1, and MAP between 80–112 mmHg (NS within and between groups).


View this table:
[in this window]
[in a new window]
 
TABLE IV Arterial and tonometric PCO2 and pH values in the recovery room after cholecystectomy.
 
Postoperative nausea occurred in three patients in the FV group and in one patient in the CC group.


    Discussion
 TOP
 Abstract
 Patients and methods
 Results
 Discussion
 References
 
In this study, fixed ventilation during intraabdominal insufflation of CO2 resulted in slight, clinically acceptable hypercarbia and decrease in pH. The changes were reflected in corresponding tonometric values. Both acid-base balance and tonometric values remained unchanged, when minute volume of ventilation was increased to maintain constant end-tidal PCO2. Postoperatively, there were no differences between the groups in acid-base balance or gastric tonometric variables, the values of which showed normal physiological variation. This implicated rapid recovery of the intraoperative changes observed in the FV group. Despite these inter-group differences during pneumoperitoneum, the gastric mucosal to arterial PCO2 gradient was similar in both groups. Nor did the gradient change in either group during the study period.

Splanchnic ischemia is defined as critical hypoperfusion of splanchnic organs causing anerobic metabolism. A decrease in tissue oxygen consumption, tension and development of anerobic metabolism was suggested to occur at a critical gastric mucosal to arterial PCO2 gradient of 3.3 kPa.13 In studies focused on examination of normal values for gastric tonometry, PCO2 was considered normal up to 6.6 kPa and the PCO2 gap up to 1.1 kPa.14 Further, the lower limit of normal gastric mucosal pH was 7.32.7,15 Thus, the PCO2 gap and gastric mucosal pH values of our patients remained within these normal ranges. Furthermore, the gap between regional and arterial PCO2 did not change, strongly suggesting the unharmful nature of the surgical procedure.

During pneumoperitoneum, in the FV group, where CO2 was allowed to accumulate in the tissues, the increase in PaCO2 was 1.6 kPa. At the end of the pneumoperitoneum, the patients were slightly hypercarbic with the maximum PaCO2 of 6.6 kPa. Correspondingly, arterial pH decreased from 7.43 to 7.33. The decrease in arterial pH was of respiratory origin. Through a 47% increase in minute ventilation the values of PaCO2 and acid-base balance were maintained at the control level. Previously, during laparoscopic chlocystectomy, a 66% increase in minute ventilation was needed to keep PETCO2 at preoperative control,16 or a 48% increase to maintain PaCO2 at the control.17 There are also reports, where smaller increases were sufficient.18 The need of ventilatory change might depend on many factors, such as the preoperative CO2 balance of the patient, hemodynamic alterations and the exact aim of the adjustment.

In the recovery room, PaCO2 and pHa levels of our patients remained within the normal range of 5.3-6.1 kPa and 7.36-7.41, respectively, and respiratory frequency between 12-15 breaths•min–1. Despite differences during pneumoperitoneum the values of PaCO2 in both groups were similar in the recovery room. Thus, the findings of our study do not support claims of excessive accumulation of CO2 in the tissues during pneumoperitoneum followed by gradual postoperative elimination and delayed disturbances in acid-base balance.1,19 Rather, our results are in agreement with those of Kazama et al.20 demonstrating that excess CO2 output evoked by pneumoperitoneum decreased steeply already during the first 30 min after evacuation of intraabdominal CO2. However, we do not recommend unadjusted ventilation during laparoscopic surgery. In clinical practice, we strictly maintain normocarbia using either PETCO2 or PaCO2 as reference. The observed increase in airway pressure may be reduced by increasing frequency of ventilation instead of tidal volume.

During pneumoperitoneum, the occurrence and extent of metabolic acidosis might depend on the level and duration of intraabdominal pressure. In contrast to the present study with a pressure of 12 mmHg, metabolic acidosis was reported during laparoscopic cholecystectomy with the pressure maintained between 13-15 mmHg.2 During prolonged laparoscopic surgery, the extent of metabolic acidosis seemed to be influenced both by the level and duration of intra-abdominal pressure. Accordingly, at 10 mmHg pressure, only slight metabolic acidosis of short duration was observed, whereas at 15 mmHg profound acidosis of long duration and increased level of plasma lactate became evident after 90 min.21

In the previous reports of tonometry during laparoscopic cholecystectomy intraabdominal pressure was 12 mmHg,9 12-13 mmHg10 or 15 mmHg.11 Surprisingly, with saline tonometry, very low gastric intramucosal pH (7.15)9 was seen during 12 mmHg and normal pH during 15 mmHg intraabdominal pressure.11 In the third paper, where air tonometry was applied, the lowest gastric mucosal pH, 7.24, occurred at 60 min during recovery.10 Direct comparison with the values of our study is difficult as the PCO2 gap was not included in these reports. Controversial results may have several reasons, such as various details of patients, anesthetic, surgical and measurement techniques. On the other hand, the PCO2 gap of our patients was similar to that of patients undergoing open colon resection, where gastric mucosal to arterial PCO2 gap remained < 1 kPa during the first hour of surgery. However, during succeeding hours the gap increased significantly. Exposure to ambient air might have contributed to the development of impaired intestinal perfusion.22 Splanchnic blood flow, as assessed by estimated hepatic blood flow, was not affected in healthy patients during laparoscopic cholecystectomy with an intraabdominal pressure of 11-13 mmHg.23

Splanchnic perfusion is influenced by several local and systemic factors related to the patient and anesthetic and surgical techniques. Intraabdominal pressure might affect splanchnic perfusion directly or via hemodynamic changes, such as decreased cardiac output. Creation of pneumoperitoneum for laparoscopic cholecystectomy resulted in variable hemodynamic changes: cardiac index decreased more during 15 mmHg than 7.5 mmHg intraabdominal pressure.24 A small increase was reported at 12 mmHg,25 a substantial decrease5 at 14 mmHg. Furthermore, the change for a particular patient seems to be unpredictable.26 On the other hand, the PCO2 gap of intensive care patients was not affected by variations of alveolar ventilation unless cardiac output changes were associated.27 Recently, the Haldane effect was suggested as an alternative explanation for increase in P(g-a)CO2 gradient in various circumstances. Changes of mucosal oxygen saturation influence the relationship between carbon dioxide content and PCO2: at a given carbon dioxide content, mucosal PCO2 increases with increasing mucosal oxygen saturation.28 While gastrointestinal mucosal pH was originally suggested to constitute an index of the adequacy of splanchnic mucosal perfusion, the regional PCO2 measured by tonometry may simply reflect the balance between the metabolic production of CO2 in the tissue and the transport of CO2 away from the tissue by the circulation.29,30 Moreover, the regional PCO2 will inevitably be influenced by arterial PCO2. Thus, evaluation of tonometrically measured PCO2 should always be performed against PCO2 in the arterial blood.27,31

Two distinct ventilatory arrangements allowed us to compare the effects of two different levels of systemic PCO2 on tonometric values. The results obtained from frequent, simultaneous tonometric and arterial measurements showed the importance of relating the values of gastric mucosal PCO2 to those of arterial blood. In the presence of constant gap, the higher PgCO2 in the FV group compared with that in the CC group obviously reflected the level of arterial PCO2 instead of implicating inadequate gastric perfusion. Indeed, mere statistical significance between some few sets of tonometric measurements do not justify any kind of straightforward conclusions about splanchnic circulation. Owing to the complex variety of systemic and local physiological changes occurring in the splanchnic circulation during anesthesia and surgery, a cautious attitude is needed when making observation statements based on tonometric data.32

Our study was carried out in healthy patients undergoing uneventful laparoscopic cholecystectomy. During prolonged and more complex laparoscopic surgery, however, especially patients with impaired cardiovascular or pulmonary function may well be in danger of disturbances in acid-base balance and regional circulation. Therefore, before judging the critical usability of online air tonometry, further investigations are required to clarify the potential of the device for early warning of decrease in gastric mucosal perfusion.

Our patients, undergoing elective laparoscopic cholecystectomy, did not show any detectable disturbances in splanchnic perfusion, as evidenced by the constant PCO2 gap in normal range throughout the study in both groups. In the fixed ventilation group, which developed respiratory acidosis during pneumoperitoneum, tonometric evaluation of splanchnic perfusion entirely from the gastric mucosal PCO2 and pH, without calculation of the PCO2 gap, might have led to a false assumption of declining gastric intramucosal blood flow.

Accepted for publication October 8, 2000.


    References
 TOP
 Abstract
 Patients and methods
 Results
 Discussion
 References
 
1 Desmond J, Gordon RA. Ventilation in patients anaesthetized for laparoscopy. Can J Anaesth 1970; 17: 378–87.[Abstract/Free Full Text]

2 Gándara V, de Vega DS, Escriú N, Zorrilla IG. Acid-base balance alterations in laparoscopic cholecystectomy. Surg Endosc 1997; 11: 707–10.[Medline]

3 Hodgson C, McClelland RMA, Newton JR. Some effects of the peritoneal insufflation of carbon dioxide at laparoscopy. Anaesthesia 1970; 25: 382–90.[Medline]

4 Beebe DS, McNevin MP, Crain JM, et al. Evidence of venous stasis after abdominal insufflation for laparoscopic cholecystectomy. Surg Gynecol Obstet 1993; 176: 443–7.[Medline]

5 Joris JL, Noirot DP, Legrand MJ, Jacquet NJ, Lamy ML. Hemodynamic changes during laparoscopic cholecystectomy. Anesth Analg 1993; 76: 1067–71.[Abstract/Free Full Text]

6 Schilling MK, Redaelli C, Krähenbühl L, Signer C, Büchler MW. Splanchnic microcirculatory changes during CO2 laparoscopy. J Am Coll Surg 1997; 184: 378–82.[Medline]

7 Fiddian-Green RG, Baker S. Predictive value of the stomach wall pH for complications after cardiac operations: comparison with other monitoring. Crit Care Med 1987; 15: 153–6.[Medline]

8 Heinonen PO, Jousela IT, Blomqvist KA, Olkkkola KT, Takkunen OS. Validation of air tonometric measurement of gastric regional concentrations of CO2 in critically ill septic patients. Intensive Care Med 1997; 23: 524–9.[Medline]

9 Eleftheriadis E, Kotzampassi K, Botsios D, Tzartinoglou E, Farmakis H, Dadoukis J. Splanhnic ischemia during laparoscopic cholecystectomy. Surg Endosc 1996; 10: 324–6.[Medline]

10 Koivusalo A-M, Kellokumpu I, Ristkari S, Lindgren L. Splanchnic and renal deterioration during and after laparoscopic cholecystectomy: a comparison of the carbon dioxide pneumoperitoneum and the abdominal wall lift method. Anesth Analg 1997; 85: 886–91.[Abstract]

11 Thaler W, Frey L, Marzoli GP, Messmer K. Assessment of splanchnic tissue oxygenation by gastric tonometry in patients undergoing laparoscopic and open cholecystectomy. Br J Surg 1996; 83: 620–4.[Medline]

12 Takala J. Appliquide, Gastrointestinal Tonometry, 894796/PG5/0997© Datex-Engström Division, Instrumentarium Corp., Finland, 1997.

13 Kolkmann JJ, Otte JA, Groeneveld ABJ. Gastrointestinal luminal PCO2 tonometry: an update on physiology, methodology and clinical applications. Br J Anaesth 2000; 84:74–86.[Free Full Text]

14 Kolkman JJ, Steverink PJGM, Groeneveld ABJ, Meuwissen SGM. Characteristics of time-dependent PCO2 tonometry in the normal human stomach. Br J Anaesth 1998; 81: 669–75.[Abstract/Free Full Text]

15 Heard SO, Helsmoortel CM, Kent JC, Shahnarian A, Fink MP. Gastric tonometry in healthy volunteers: effect of ranitidine on calculated intramural pH. Crit Care Med 1991; 19: 271–4.[Medline]

16 Mäkinen M-T. Comparison of body temperature changes during laparoscopic and open cholecystectomy. Acta Anaesthesiol Scand 1997; 41: 736–40.[Medline]

17 Wurst H, Schulte-Steinberg H, Finsterer U. Zur Frage der CO2-Speicherung bei laparoskopischer Cholezystektomie mit CO2-Pneumoperitoneum. Anaesthesist 1995; 44: 147–53.[Medline]

18 Wahba RWM, Mamazza J. Ventilatory requirements during laparoscopic cholecystectomy. Can J Anaesth 1993; 40: 206–10.[Abstract]

19 Koivusalo A-M, Kellokumpu I, Lindgren L. Gasless laparoscopic cholecystectomy: comparison of postoperative recovery with conventional technique. Br J Anaesth 1996; 77: 576–80.[Abstract/Free Full Text]

20 Kazama T, Ikeda K, Kato T, Kikura M. Carbon dioxide output in laparoscopic surgery. Br J Anaesth 1996; 76: 530–5.[Abstract/Free Full Text]

21 Taura P, Lopez A, Lacy AM, et al. Prolonged pneumoperitoneum at 15 mmHg causes lactic acidosis. Surg Endosc 1998; 12: 198–201.[Medline]

22 Von Montigny S, Laterre P-F, Vanderelst P, De Kock M. The effects of intraoperative intravenous clonidine on gastric intramucosal PCO2. Anesth Analg 1998; 87: 686–90.[Abstract/Free Full Text]

23 Odeberg S, Ljungqvist O, Sollevi A. Pneumoperitoneum for laparoscopic cholecystectomy is not associated with compromised splanchnic circulation. Eur J Surg 1998; 164: 843–8.[Medline]

24 Wallace DH, Serpell MG, Baxter JN, O'Dwyer PJ. Randomized trial of different insufflation pressures for laparoscopic chplecystectomy. Br J Surg 1997: 84: 455–8.[Medline]

25 Hashimoto S, Hashikura Y, Munakata Y, et al. Changes in the cardiovascular and respiratory systems during laparoscopic cholecystectomy. J Laparoendosc Surg 1993: 3: 535–9.[Medline]

26 Elliott S, Savill P, Eckersall S. Cardiovascular changes during laparoscopic cholecystectomy: a study using transesophageal Doppler monitoring. Eur J Anaesth 1998; 15: 50–5.[Medline]

27 Bernardin G, Lucas P, Hyvernat H, Deloffre P, Mattei M. Influence of alveolar ventilation changes on calculated gastric intramucosal pH and gastric-arterial PCO2 difference. Intensive Care Med 1999; 25: 269–73.[Medline]

28 Jakob SM, Kosonen P, Ruokonen E, Parviainen I, Takala J. The Haldane effect - an alternative explanation for increasing gastric mucosal PCO2 gradients? Br J Anaesth 1999; 83: 740–6.[Abstract/Free Full Text]

29 Tang W, Weil MH, Sun S, Noc M, Gazmuri RJ, Bisera J. Gastric intramural PCO2 as monitor of perfusion failure during hemorrhagic and anaphylactic schock. J Appl Physiol 1994; 76: 572–7.[Abstract/Free Full Text]

30 Schlichtig R, Bowles SA. Distinguishing between aerobic and anaerobic appearance of dissolved CO2 in intestine during low flow. J Appl Physiol 1994; 76: 2443–51.[Abstract/Free Full Text]

31 Russell JA. Gastric tonometry: does it work? Intensive Care Med 1997; 23: 3–6.[Medline]

32 Takala J. Determinants of splanchnic blood flow. Br J Anaesth 1996; 77: 50–8.[Free Full Text]




This article has been cited by other articles:


Home page
Canadian J. AnesthesiaHome page
M. Weiss, A. Gerber, and A. Dullenkopf
Nitrous oxide does not affect automated air tonometry in children: [Le protoxyde d'azote n'agit pas sur la tonometrie a l'air, automatisee, chez les enfants]
Can J Anesth, November 1, 2003; 50(9): 930 - 932.
[Abstract] [Full Text] [PDF]


This Article
Right arrow Abstract Freely available
Right arrow Résumé de cet Article
Right arrow Full Text (PDF)
Right arrow Submit a scholarly reply
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Mäkinen, M.-T.
Right arrow Articles by Yli-Hankala, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Mäkinen, M.-T.
Right arrow Articles by Yli-Hankala, A.


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS