FESC, Medical Clinic I, University of Aachen, Pauwelsstraße 30, D-52057 Aachen, Germany*Corresponding author
Accepted for publication: March 7, 2002
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Abstract |
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Methods. We studied 20 consecutive patients (mean age 68 (SD 9) [range 4981] yr, 18 males, SAPS II score 55 (SD 18), ICU mortality 55%) with circulatory disorders during mechanical ventilation in the intensive care unit. Tonometer probes were placed via the nose, one into the stomach and the other in the oesophagus. PCO2 was measured with two automated gas analysers, at admission and 30 min, 1, 2, 3, 32, 40, and 48 h thereafter.
Results. One hundred and forty-eight paired measurements were obtained. Gastric PCO2 was greater than oesophageal PCO2 on admission (7.19 (1.43) vs 5.89 (0.73) kPa, P<0.01) and subsequently. Differences between the measures correlated (r=0.67) with the mean absolute value, indicating that overestimation increased as gastric PCO2 increased.
Conclusions. Oesophageal PCO2 is less than gastric PCO2, and the difference is greater when gastric PCO2 levels are greater. Air tonometry may not measure regional PCO2 levels in the oesophagus satisfactorily. Other methods and sites for carbon dioxide tonometry should be examined.
Br J Anaesth 2002; 89: 23741
Keywords: carbon dioxide, measurement; carbon dioxide, partial pressure; ventilation, mechanical
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Introduction |
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These problems may be avoided by capnometry in other parts of the body. Weil and co-workers found that oesophageal tonometry and more recently sublingual capnometry are practical alternatives to gastric tonometry.1217 Oesophageal luminal PCO215 and sublingual PCO212 could be correlated with gastric PCO2 in animals with haemorrhagic shock and in severely ill patients.17
We therefore tested the hypothesis that regional oesophageal air tonometry oesophageal PCO2 provides results similar to gastric tonometry, in patients with circulatory disturbances.
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Materials and methods |
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A tonometer probe (Trip catheter 14 F, Datex-Ohmeda, Finland) was placed via the nose into the stomach. The position was verified by aspiration of gastric juice followed by air insufflation and auscultation. A second probe was inserted into the stomach and correct placement confirmed clinically too. Then this probe was drawn back to lie with the tip 3035 cm from the nasal opening. Air was insufflated and the upper abdomen auscultated to check that the probe was not in the stomach. Finally, correct placement of both probes was verified radiologically. A gas analyser (Tonocap TC 200, Datex-Ohmeda) was connected to each tonometer catheter. With each measurement cycle, 6 ml of air is pumped into the balloon. A sample is then automatically drawn. The first 1.2 ml are from the dead space of the system and are discarded. The PCO2 is measured in the remainder with an infrared sensor.
Arterial blood gas analysis was done using a standard blood gas analyser (ABL 505 blood gas analyser, Radiometer, Copenhagen, Denmark). Samples were analysed by the blood gas analyser at 37°C and corrected for the patients actual body temperature using internal software according to the manufacturers handbook
(PCO2[temp]=PCO2[37°C]x100.021x[temp37°C])
The gastric or oesophageal PCO2 arterial PCO2 (PaCO2) difference (CO2 Gap[G,O]) was determined according to the formula:
CO2 Gap[G,O]=PCO2 [G,O]PaCO2
where the carbon dioxide Gap[G,O] is in kPa.
All patients had a radial arterial cannula (Leadercath 11509, 20 gauge 8 cm, Vygon, Aachen, Germany) and a pulmonary artery catheter (Continuous Cardiac Output Combo Catheter®, Baxter Edwards Critical Care, Irvine, CA), which was connected to a computer system (VigilanceTM, Baxter Edwards Critical-Care). Vascular pressures (central venous pressure (CVP); mean pulmonary artery pressure (MPAP); pulmonary artery occlusion pressure (PAOP); systemic mean arterial pressure (MAP), mm Hg) and cardiac output were measured at the given time points. Cardiac index (CI) in litre min1 m2, oxygen delivery index (DO2I) in ml O2 min1 m2 and oxygen consumption index (VO2I) in ml O2 min1 m2 were calculated from standard formulae.
Statistical analysis on a microcomputer was with the Statistical Package for the Social Sciences (SPSS 10.0, SPSS Inc., Chicago, IL). All continuous data were tested for normal distribution by the KolomogorovSmirnov test. Normally distributed data are presented as mean and standard deviation (SD), non-normally distributed data as median and interquartile range. Survivors and non-survivors were compared at study entry using an unpaired Students t-test if data were normally distributed and the Mann Whitney U-test if non-normally distributed. A chi-squared test was used for nominal data. To compare changes with time, repeated measures analysis of variance was used. Values at any time point were compared between survivors and non-survivors by unpaired Students t-test or Mann Whitney U-test, respectively. Furthermore, mean gastric PCO2 and oesophageal PCO2 values at each of the eight time points were correlated with each other and the corresponding mean values of haemodynamic variables (CI, MAP, MPAP, PAOP, SVRI, PVRI, DO2I, VO2I) and arterial blood gases. Simple linear regression analysis was performed on the differences of both methods against the means. Moreover, we calculated the mean bias and the average mean of both methods for any patient and performed simple linear regression analysis. Correlations were calculated using Pearsons correlation coefficient. Significance was assumed at P<0.05 unless otherwise stated.
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Results |
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Table 2 gives haemodynamic and blood gas values throughout the study. One hundred and forty-eight paired measurements of gastric PCO2 and oesophageal PCO2 were obtained. Gastric PCO2 was significantly greater than oesophageal PCO2 at admission (7.19 (1.43) vs 5.89 (0.73) kPa, P<0.01), and gastric carbon dioxide gap was greater than oesophageal carbon dioxide gap (1.73 (1.09) vs 0.45 (0.87) kPa, P<0.01). The differences persisted for the duration of the study (Fig. 1).
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Discussion |
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We found that oesophageal PCO2 was different from gastric PCO2 in critically ill patients with circulatory disturbances. The difference increased as gastric PCO2 increased. Differences of arterial blood supply in the oesophagus and other regions of the gastrointestinal tract, compared with the gastric mucosa, may limit the sensitivity of tonometry for early detection of general hypoperfusion,5 as selective vasoconstriction may occur in the stomach or small bowel.26 In contrast, Weil and co-workers found that increases in gastric PCO2 in rats with a haemorrhagic shock were highly correlated with increases in oesophageal PCO2,15 and that oesophageal blood flow and gastric blood flow decreased proportionally. Likewise, in dogs with septic shock, oesophageal PCO2 and gastric PCO2 measured with CRGT showed a similar trend.25 However, after endotoxin treatment, gastric PCO2 increased more rapidly than oesophageal PCO2. Sublingual tissue PCO2 measured with a miniature carbon dioxide electrode in rats with haemorrhage showed a highly significant linear correlation with gastric PCO2.13 Increased sublingual PCO2 correlated well (r2=0.84, P<0.001) with increased lactate concentrations in 46 patients with life-threatening illnesses.17 Unfortunately, gastric PCO2 levels were not assessed in this convincing study.
Our findings do not support these results. The methods for regional PCO2 measurement in the above experiments were quite different from our study except for the CRGT used by Guzman and co-workers,25 which is similar to the automated gas analyser of our study. In contrast to the air tonometry the ISFET method measures regional PCO2 directly in the gastric wall.15 The ISFET technology and CRGT allow continuous measurement and display, giving rapid easy measurements.15 25 In addition, the speed of onset and severity of haemorrhagic shock were profound in the animal study of Sato and co-workers. The close relationship they found between gastric PCO2 and oesophageal PCO2 may not apply under conditions of lesser severity in other settings such as septic shock.15
Secondly, we studied patients with acute circulatory disorders. Although overall mortality was high, patients were not profoundly shocked. Such patients may differ considerably from the haemorrhagic or septic shock studied in the animal experiments.
Finally, poor correlation of oesophageal PCO2 and arterial PCO2 compared with the close correlation of gastric PCO2 and arterial PCO2 suggests a methodological bias. The oesophagus is not a closed system and carbon dioxide may partly diffuse to the rhinopharynx or be diluted with ambient air. Gas diffusion is proportional to the difference in partial pressure between two phases and the area of the exchange surface, so that diffusion will increase with an increased gradient. This may have contributed to the observed disparity between oesophageal PCO2 and gastric PCO2 and explain the greater bias with greater regional PCO2 levels. In addition, the equilibration period will cause carbon dioxide loss near the balloon. This effect could be circumvented by shorter equilibration times or measurements using systems such as the COMOCADOF (fibre-optical catheter equipped with a carbon dioxide sensor capable of continuous carbon dioxide assessment).27
There are differences between the stomach and the oesophagus. Buffering of acid reflux into the oesophageal lumen from the stomach is by bicarbonate ions entering the oesophageal lumen, from swallowed saliva, and from the oesophageal wall.28 29 The epithelium of the oesophagus contains carbonic anhydrases (CA) II,30 which catalyse the interconversion of carbon dioxide and H2CO3.29 Oeso phageal luminal carbon dioxide may not come just from oesophageal tissues but also from fluid, which contains H2CO3, CA, and gastric acid. These possibilities do not explain our findings but suggest that oesophageal PCO2 measurements have the same uncertainties as gastric PCO2.
Although our patients received i.v. histamine receptor block we did not control the intragastric or intraoesophageal pH, and we cannot rule out possible interference of H+ with HCO3 in the oesophageal lumen. Routine use of H2 blockers to reduce the error of gastric PCO2 measurements has been questioned.31 The recommendations are based mainly on studies in human volunteers. H2 blockers in the critically ill patients may not affect the assessment of gastric PCO2.32 Discrepancies between healthy volunteers and critically ill patients may be related to reduced gastric acid secretion in the latter who have reduced visceral perfusion.33
Despite extensive study there are no accepted normal values for gastric PCO2, so critical appraisal of oesophageal PCO2 alone will be difficult.
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Conclusions |
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References |
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