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Departments of
*Anesthesiology 3 and
Anesthesiology 4, University Hospital, Bordeaux, France
Address correspondence and reprint requests to B. Grenier, DAR 3, Hôpital Pellegrin, 33076 Bordeaux Cedex, France. Address e-mail to bruno.grenier{at}chu-aquitaine.fr
| Abstract |
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Implications: This study, which aimed to reevaluate the ability of PETCO2 to estimate PaCO2 during neurosurgical procedures according to surgical position, indicates that PETCO2 cannot replace PaCO2 for the following reasons: scattering of individual values; occurrence of negative arterial to end-tidal CO2 gradient (P[a-ET]CO2; PaCO2 and PETCO2 variations in opposite directions; large changes in P(a-ET)CO2 between two samples; and instability of P(a-ET)CO2 over time.
| Introduction |
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The aim of this study was to reevaluate the accuracy of PETCO2 in estimating PaCO2 during neurosurgical procedures of >3 h and to measure the effect of surgical positioning on P(a-ET)CO2 over time.
| Methods |
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The choice of drugs used (total IV anesthesia) was made by the anesthetist. After orotracheal intubation, the lungs were ventilated with a ventilator with a tidal volume of 7.5 mL/kg, a respiratory rate of 16 breaths/min, an inspiratory to expiratory ratio of 0.33, and 50% air in oxygen. In all cases, these ventilatory variables led to an initial PETCO2 <35 mm Hg and a normal shape on the capnograph tracing. After hemodynamic stability was achieved, arterial blood was sampled from a radial catheter. At the same time, PETCO2 was measured (T0, patient SP) at the proximal end of the tracheal tube using a CO2 mainstream capnometer. For each patient, the capnometer was calibrated before use according to manufacturer's specifications. PaCO2 values were analyzed at 37°C and corrected for rectal temperature. Thus, P(a-ET)CO2 was calculated at T0 as the difference between temperature-corrected PaCO2 and PETCO2. Similarly, the following measurements of PaCO2 and PETCO2 were performed after positioning (T1), each subsequent hour (T2, T3, T4), and at the end of the procedure after the patient was returned to the SP position (T5). Patients in the ST position were managed with inflatable leg splints and a positive end-expiratory pressure (PEEP) of 10 cm H2O. In this group, arterial blood gases at T5 were sampled after splint and PEEP withdrawal.
Results are presented as mean ± SD. The normal distribution of values was checked by using a Kolmogorov-Smirnov test. A P value <0.05 was considered significant. The relationship between PaCO2 and PETCO2 was determined using a linear regression and the Bland-Altman method (4), which is becoming the standard when two measurement techniques must be compared. It allows a direct and visual analysis of the results, providing a bias (mean of differences) and limits of agreement (bias ± 2 SD). The precision of the bias was defined as 95% confidence intervals. One-way analysis of variance (ANOVA) was used to compare the SP, LT, PR, and ST groups for the following variables: PaCO2, PETCO2, and P(a-ET)CO2. P(a-ET)CO2 variations over time were analyzed by using ANOVA for repeated measurements. When indicated (P < 0.05), comparison between groups was performed using a projected least significant difference Fisher's test.
| Results |
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| Discussion |
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taken into account. As reported by these authors, large individual variations were observed (-14 to 19 mm Hg). However, most studies dealing with P(a-ET)CO2 have been performed in SP patients (2,711). To our knowledge, Pansard et al. (3) are the only investigators to have studied P(-ET)CO2 in patients in the LT position and to take account of it.
Mean P(a-ET)CO2 in the SP group was 6 ± 3 mm Hg. This value is similar to those reported by Askrog (7) in healthy subjects under general anesthesia (5 ± 2 mm Hg) and Kerr et al. (8) in severely head-injured patients (6 ± 6 mm Hg). However, our values are slightly lower than those reported by Russell and Graybeal (2,10) in neurosurgical patients in the operating room (7 ± 3 mm Hg), as well as in the intensive care unit (7 ± 4 mm Hg). Large individual variations were present in our study (P[a-ET]CO2 values of 019 mm Hg) and were comparable to those reported by Russell and Graybeal (2) during neurosurgical procedures (P[a-ET]CO2 values of -1 to 17 mm Hg). In the LT group, the mean P(a-ET)CO2 (7 ± 3 mm Hg) was significantly higher than that in other groups but was comparable to the P(a-ET)CO2 measured by Pansard et al. (3) (8 ± 3 mm Hg) in 35 patients undergoing renal surgery. These results could be explained by alterations in ventilation-perfusion ratios leading to an increase in alveolar dead space and increased P(a-ET)CO2. This hypothesis is enforced by the fact that, in the LT group, increased P(a-ET)CO2 resulted from a low PETCO2, whereas PaCO2 was the same in the four groups.
No data were found in the literature to compare results obtained in the PR and ST groups. Mean P(a-ET)CO2 in ST patients was only 5 ± 5 mm Hg, similar to that measured in the PR group (5 ± 5 mm Hg), although the physiological mechanisms are probably different. Indeed, P(a-ET)CO2 in the ST position was expected to be large (i.e., increase in ventilation-perfusion ratio) because of higher hemodynamic instability related to position and PEEP leading to a decrease in the perfusion component (8). Moreover, the ST position contributes to blood flow redistribution to pulmonary bases and create West's zone I (12) (collapsed pulmonary capillaries with high ventilation-perfusion ratios). However, our ST group included the more scattered values (-14 to 19 mm Hg) and 13 of the 22 negative P(a-ET)CO2 values. This may explain a lower than expected mean P(a-ET)CO2. In the PR position, functional residual capacity, already reduced by general anesthesia (13), further decreases because of increased abdominal pressure and impaired diaphragmatic excursion. This results in ventilation-perfusion heterogeneity with shunt effect (low (P[a-ET]CO2). In our study, other mechanisms were probably involved because the mean P(a-ET)CO2 was larger than expected. Consequently, further study that includes more patients should be conducted in the PR and ST groups. Direct measurements of alveolar dead space, cardiac output, pulmonary flow and ventilation distribution, and CO2 production (and, thus, depth of anesthesia) would be especially relevant.
The mean P(a-ET)CO2 in patients placed in the LT and PR positions did not change during the procedure. In SP patients, P(a-ET)CO2 was lower during surgery than after induction of anesthesia. Intraoperative hypothermia could have played a role by causing a decrease in PaCO2. However, blood gas measurements were corrected for body temperature, which excludes this hypothesis. A decrease in functional residual capacity (and then in P[a-ET]CO2) is present during general anesthesia. It occurs from the start of anesthesia, is immediately maximal, and does not depend on the anesthetic used (13). Why this mechanism may not be involved with the LT, PR, and ST groups is unknown. In ST patients, the mean P(a-ET)CO2 was significantly larger at the end of the operation, when patients were placed back into the SP position. This suggests an increase in alveolar dead space, which could be due to blood volume redistribution to the legs when the inflatable leg splints were removed at the time of the measurement. Despite apparent hemodynamic stability, no definitive conclusion can be made because cardiac output (and, thus, pulmonary blood flow) was not measured.
Several studies have focused on the relationship between PaCO2 and PETCO2, but the duration of the procedure has not been considered in the context of surgical position. Sharma et al. (6) did not report any change in P(a-ET)CO2 in 21 patients undergoing aneurysm or brain tumor surgery of >4 h. Fifteen patients were examined SP, three PR, and three LT. Unfortunately, the authors did not specify patient position in their results, preventing any comparison with our study. Pansard et al. (3) included patients in the LT position (n = 35) undergoing renal surgery (mean duration 102 ± 41 min). After positioning and hemodynamic stability, they reported a significant increase in P(a-ET)CO2 over time, which they explained by ventilation-perfusion heterogeneity with increased alveolar dead space. Large inter- and intraindividual variations were noted, as in our study.
PETCO2 values greater than PaCO2 were observed 22 times (4% of the measurements), and only in the PR and ST groups. This can be compared with results provided by Russell and Graybeal (2), who found only one negative P(a-ET)CO2 value in 35 SP neurosurgical patients. Isert (1) identified negative P(a-ET)CO2 values in 13% of patients undergoing brain surgery, with no mention of intraoperative position.
Unexplained negative P(a-ET)CO2 was first reported by Nunn and Hill in 1960 (5). It was later demonstrated that negative P(a-ET)CO2 is more frequent (
12% of cases) in patients ventilated with high tidal volumes and low respiratory rates (14,15). Indeed, with such ventilation settings, there is a slow emptying of alveoli with a long time constant. However, this mechanism cannot be accepted. Ventilatory variables were the same in all of our patients. However, PEEP in the ST group could favor the emptying of alveoli with low ventilation-perfusion ratios (16). This assumption is valid only if the pulmonary blood flow remains constant. Negative P(a-ET)CO2 has also been reported in children, during cesarean section and laparoscopies, or after cardiac surgery (11,1720). In pregnant patients, a decrease in functional residual capacity and an increase in cardiac output are responsible for a high frequency of negative P(a-ET)CO2 values (up to 50%). In addition to slow emptying of alveoli with a long time constant, a decrease in functional residual capacity, as well as an increase in CO2 production, have been held responsible for negative P(a-ET)CO2 values in children (18). Finally, during laparoscopic procedures, a further decrease in functional residual capacity is induced by the Trendelenburg position.
Linear regression is the method most frequently used to compare PETCO2 and PaCO2. In our study, poor correlation coefficients were obtained for all the patients and for each of the position groups. This correlation seemed too weak to reliably estimate PaCO2 from PETCO2. The same results are reported by several authors. For example, Russell and Graybeal (2) noted a correlation coefficient of 0.63 in 35 neurosurgical patients. In an intensive care unit values reported by the same team (9) were only slightly better (r2 = 0.71) and were comparable to those observed by Christensen et al. (21). According to Isert (1), PETCO2 can provide a correct estimation of hyper-, normo-, or hypocapnia in only 82% of cases. Because of poor statistical validity of linear regression, the Bland-Altman method is more appropriate when two measurement techniques must be compared. However, the superior (1315 mm Hg) and inferior (-5 to 0 mm Hg) limits of agreement in our study were too large to expect PaCO2 and PETCO2 to be interchangeable for clinical purposes.
We also looked for large variations of P(a-ET)CO2 between two successive samples11% varied by >5 mm Hg, especially in the PR and ST groups. Similarly, Isert (1) showed that 18% of the variations were above the threshold of 4 mm Hg. Finally, >25% of all changes in PaCO2 and PETCO2 between two successive samples varied in opposite directions. Similarly, in neurosurgical patients, Russell and Graybeal (2) reported the same pattern in 18.4% of the cases.
Although the mean P(a-ET)CO2 value in our study is similar to values reported in the literature, a reliable estimation of PaCO2 from PETCO2 cannot be made for the following reasons: scattering of individual values as demonstrated by using the Bland-Altman method; occurrence of negative P(a-ET)CO2; PaCO2 and PETCO2 variations in opposite directions; large changes in P(a-ET)CO2 between two samples; and instability of P(a-ET)CO2 over time according to position. As a result, in neurosurgical procedures of >3 h, capnography monitoring should be performed with regular analy- sis of arterial blood gases for ventilator optimal adjustment.
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