Critical Care Research Program, Department of Anesthesiology and Intensive Care, Division of Critical Care, Kuopio University Hospital, Kuopio, Finland 1Present address: Department of Intensive Care Medicine, University Hospital of Bern (Inselspital), Bern, Switzerland
Accepted for publication: May 20, 2000
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Abstract |
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Br J Anaesth 2000; 85: 5639
Keywords: gastrointestinal tract, mucosal perfusion; monitoring, splanchnic perfusion
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Introduction |
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The measurement of gastric mucosal PCO2 has become more popular in experimental and clinical studies and avoids the potential problems of pHi. An automated gas tonometer was developed to measure gastric mucosal PCO2, so that repeated analysis of saline samples for PCO2 and the potential errors of analysis are eliminated and the measurements are now easier.10 12 13 Clinical and experimental studies have validated gas tonometry using conventional saline tonometry as a reference.1416 However, the gradient between systemic PCO2 and gastric mucosal PCO2 is the variable of interest that reflects mucosal perfusion.4 17 Repeated arterial blood samples are needed to measure blood PCO2 which may not be feasible in clinical practice and may make clinicians unwilling to use gastric tonometry. On the other hand, without continuous or semi-continuous measurements important episodes of splanchnic hypoperfusion may not be noticed.
The partial pressure of carbon dioxide (CO2) of end expiratory gas (end tidal CO2, PE'CO2) can be used to estimate arterial PCO2.18 PE'CO2 is routinely monitored in intubated patients although PE'CO2 does not necessarily accurately represent arterial CO2 if the proportion of dead space ventilation is increased as in patients with lung injury.19 However, the difference between PE'CO2 and gastric mucosal CO2 (measured by gas tonometry) could reflect gastric mucosal perfusion continuously or semi-continuously without a need for laboratory testing. We hypothesized that this would be the case even in patients with increased physiologic dead space, providing that the dead space remains relatively constant. To our knowledge this possibility has not been tested. We designed our study to investigate if the gradient between gastric mucosal PCO2 and end-tidal CO2 can be used to monitor gastric mucosal perfusion.
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Patients and methods |
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Two gastric tonometers, a gas and a saline tonometer, were inserted in each patient via mouth. The correct positions of the tips of the tonometers were confirmed by x-ray. We used continuous gastric suctioning but H2-blockers were not given to any patient.20 21 Gas tonometer (Tonocap®, Datex/Instrumentarium, Helsinki, Finland) was used to measure gastric mucosal partial pressure of carbon dioxide (PrCO2) in 15 min intervals during the 8 h study period. In Tonocap® the device fills the tonometer TRIP-catheter (Tonometrics, Datex/Instrumentarium, Finland) with 5 ml gas (air) and a sample of this gas is drawn after an equilibration period. The PCO2 of this sample is measured by Tonocap® using the same standard infra-red method that is used to measure the partial pressure of end-tidal CO2 (PE'CO2). A time dependent correction factor of 1.12 (for incomplete equilibration time of 15 min) for the mucosal PCO2 (PrCO2) was used. The Tonocap® was calibrated before the measurements according to the manufacturers recommendation using calibration gas (5±0.03% CO2 in 95% oxygen, Datex/Instrumentarium, Helsinki, Finland). The mean value of PrCO2 was calculated each hour to allow comparison between gas and saline tonometers. End-tidal CO2 was measured from the expired air immediately distal to the intubation tube using an AS3 monitor (Datex/Instrumentarium, Helsinki, Finland). The gastric-mucosal end-tidal PCO2 difference (DPCO2gas) was calculated by subtracting end tidal PCO2 from gastric mucosal PCO2 (as measured by Tonocap®).
We measured PrCO2 using conventional saline tonometry and arterial PCO2 each hour throughout the study. With the saline tonometry PrCO2 was measured using 2.5 ml of sodium chloride in the tonometer balloon. Both the saline and arterial blood samples were analysed within 2 min of withdrawal using a bloodgas analyser (ABL-520, Radiometer, Copenhagen, Denmark). We did not take into account the potential bias related to blood gas analyser.10 A time dependent correction factor of 1.13 (for incomplete equilibration time of 60 min) for the PrCO2 was used with saline tonometry and the measurements were carried out according to the manufacturers recommendations. Gastric-mucosal arterial PCO2 difference (DPCO2sal) was calculated by subtracting arterial PCO2 from gastric mucosal PCO2 (as measured by saline tonometry). We regarded this difference (DPCO2sal) as the reference to represent true systemic-gastric mucosal PCO2. In addition to the comparison between DPCO2sal and DPCO2gas, we also compared the differences between gastric mucosal PCO2 (measured using gas tonometry) and arterial blood PCO2 or end-tidal PCO2. This was done to eliminate potential errors in the saline technique, such as those related to bloodgas analyser bias, inappropriate equilibration factors and tonometer catheter dead space effects.
Arterial end-tidal PCO2 difference was calculated by subtracting end-tidal PCO2 from arterial blood PCO2. This gradient was calculated to indirectly estimate dead space ventilation of the lung. The higher the gradient between arterial (PaCO2) end-tidal PCO2 (PE'CO2), the higher is the dead space ventilation of the lung. The fraction (%) of dead space ventilation (VD/VT) was estimated using the following equation: VD/VT = (PaCO2 PE'CO2)/PaCO2.
Statistical analysis
Our main interest in the analysis was to study the agreement between DPCO2gas and DPCO2sal. We studied this agreement using the method described by Bland and Altman.22 In addition to graphical display we also calculated bias (the mean difference between the two measurements) and precision (SD of the bias) for this comparison. Because we repeated measurements, the effect of time, and particularly time by group (DPCO2gas or DPCO2sal) interaction, was analysed using general linear model with repeated measures option (statistical package SPSS for Windows, version 7.5). This analysis was carried out to test whether changes in gastric-mucosal systemic PCO2 difference during the study were similar for DPCO2gas and DPCO2sal. We used regression analysis to study the correlation between two variables and t-test when appropriate. A P-value of <0.05 was considered statistically significant. Results are given as mean (SD).
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Results |
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Discussion |
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The advantage of DPCO2gas is that it reflects the adequacy of gastric mucosal perfusion continuously. A monitor is a warning device that reveals progressive change, e.g. perfusion abnormalities, promptly, and continuous monitoring is the best option in clinical practice. The gastric mucosal systemic PCO2 (arterial blood) gradient best reflects mucosal perfusion. Also, gut perfusion decreases early in shock, often when systemic haemodynamics are stable.23 Saline tonometry, and gas tonometry, both need repeated samples for arterial blood or saline PCO2. It is not feasible in clinical practice to draw and analyse arterial blood and gastric tonometer saline samples at frequent, e.g. 1015 min intervals, if patients are clinically stable. However, because splanchnic perfusion deteriorates early in shock, this clinically stable phase of critical illness would be ideal to monitor gastrointestinal perfusion. The measurement of gastric mucosal-end-tidal CO2 is a convenient method to continuously monitor gastric mucosal perfusion without a need to repeatedly analyse saline or arterial blood samples. Because no laboratory work is needed, several potential errors and problems related with sample handling and analysis are avoided. We used a separate monitor to analyse end-tidal CO2 but a newer version of Tonocap® automatically analyses and displays both gastric mucosal and end-tidal PCO2. Tonocap® (both mucosal PCO2 and end-tidal PCO2) has to be calibrated once every 2 months with a gas of known PCO2. There is no need for recalibration after ventilatory adjustments and also temperature has no effect on the measurements. The potential problem of water evaporation in the tubing of capnograph is avoided because Tonocap® includes a water separation system which is based on a hydrophilic membrane.
We are not aware of any studies that have evaluated the gastric-mucosal end-tidal PCO2 difference to assess splanchnic perfusion. There are several studies that examined the agreement between gastric mucosal PCO2 measured by saline and gas tonometry.1416 In our study the correlation between gastric mucosal PCO2 measured by saline and gas tonometry was not as good as has been reported elsewhere. We do not have a clear explanation for this discrepancy. Also, we do not know why gas tonometry systematically gave higher values than saline tonometry (Figs 6 and 8). We did not use H2-blockers in our patients but this should not affect the agreement between the two methods. It is not clear if H2-blockers are needed in critically ill patients to improve the performance of gastric tonometry.20 21 24 25 In patients with cardiogenic shock, a systematic disagreement between saline and gas tonometry was found.26 Under-correction of saline samples may be responsible although correction was done according to manufacturers recommendations. We regarded saline technique as a gold standard but this may not necessarily be true.27 28 In vivo, gas tonometry gave a closer agreement with the PCO2 of the test solution.27 Also, the bias between gas and saline tonometry was reduced by replacing saline by buffered electrolyte solutions.27 We used saline with our conventional tonometry and this may have contributed to the differences in our study. The degree of clinically important disagreement between different methods to estimate mucosal perfusion is more important than the disagreement per se.
The normal gastric mucosal systemic PCO2 difference is not known and more importantly we do not know how large a difference is clinically important in critically ill patients. In our previous study with healthy volunteers, the gastric mucosal arterial PCO2 gap varied between 1.4 and 3 kPa depending on whether nasogastric suction or H2-blockers were used.20 A more recent study in healthy volunteers suggested a normal threshold value of <1.1 kPa for a gastric mucosal arterial PCO2 difference.29 Gastric mucosal PCO2 depends on several factors such as aerobic and anaerobic production of CO2 and also on perfusion of the gastric mucosa,17 and it is not clear to what extent increased gastric mucosal PCO2 indicates tissue hypoxia or decreased mucosal perfusion. A recent experimental study suggested that gastric mucosal PCO2 has to increase to >13 kPa to indicate tissue hypoxia.30 In our study the bias and the precision of the agreement between DPCO2gas and DPCO2sal were 0.85 and 1.25 kPa, respectively. Therefore, we propose, that the small disagreement between these methods may not be clinically important.
One obvious problem with the use of the gastric mucosal end-tidal PCO2 difference is that in patients with impaired gas exchange, end-tidal CO2 does not represent arterial (and hence systemic) PCO2.19 In patients who do not have ALI this is not a large problem but in patients who have lung injury, end-tidal CO2 may underestimate systemic PCO2. We found that in patients who have ALI, DPCO2gas overestimated DPCO2sal more than in patients who do not have ALI. Figure 3 also shows that the disagreement between DPCO2gas and DPCO2sal increases as the arterial end-tidal PCO2 difference increases (indicating increased dead space ventilation). However, for at least two reasons the potential overestimation of the gastric mucosal systemic PCO2 difference is not a major clinical problem. First, it is physiologically obvious and easily recognizable. A significant difference between arterial blood PCO2 and end-tidal CO2, can be easily measured and used to interpret DPCO2gas. Secondly, an overestimate of the gastric mucosal systemic PCO2 difference using DPCO2gas means that truly increased PCO2 differences will not be left undetected. We found that changes in DPCO2gas reflected changes in DPCO2sal during our study period, but the time period for our study was relatively short and probably was during steady state CO2 production, lung function and dead space ventilation. Therefore, we cannot address the potential impact of changes in these variables during the progression of critical illness.
The difference between gastric mucosal end tidal PCO2 is a potentially useful method for continuous monitoring of splanchnic perfusion. It is easy to use and it does not require much additional work from staff, and the limits of the method are easy to assess and they do not jeopardize patient care. Studies of clinical outcome, based on interventions using this information are needed.
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Footnotes |
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References |
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