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* From Saint Vincents Hospital and Medical Center, New York, NY.
Correspondence to: Mark E. Astiz, MD, FCCP, Department of Medicine, Saint Vincents Hospital and Medical Center, 153 W 11th St, New York, NY 10011; e-mail: meastiz{at}aol.com
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Abstract |
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Design: Prospective observational study.
Setting: Medical and coronary ICUs in a tertiary-care teaching hospital.
Subjects: Twenty-five patients with circulatory failure, 19 patients with sepsis, and 6 patients with cardiac failure.
Measurements and main results: PslCO2, gastric intramucosal PCO2 (PiCO2), arterial lactate concentration, systemic oxygen delivery, and systemic oxygen consumption were measured at baseline and at 1, 3, 6, 12, and 24 h after the beginning of the study. PslCO2 and the PslCO2-PaCO2 gradient were increased but not significantly different in nonsurvivors compared to survivors at baseline. At 24 h, the mean (± SE) PslCO2 was 45 ± 4 mm Hg in survivors and 61 ± 4 mm Hg in nonsurvivors (p = 0.06), while the PslCO2-PaCO2 gradient was 14 ± 3 mm Hg in survivors and 29 ± 4 mm Hg in nonsurvivors (p < 0.05). No other significant differences in survivors and nonsurvivors were observed in any other index of perfusion. For all patients, the correlations between PslCO2 and PiCO2 (r = 0.459; p < 0.05) and cardiac index (r = 0.285; p < 0.05) were observed. The PslCO2-PaCO2 gradient also was correlated with the PiCO2-PaCO2 gradient (r = 0.323; p < 0.05). When patients were placed into subsets of sepsis and cardiac failure, the strength of the correlations increased in the patients with cardiac failure (PslCO2 vs lactate, r = 0.611 and p < 0.05; PslCO2 vs PiCO2, r = 0.613 and p < 0.05; PslCO2 vs PiCO2-PaCO2 gradient, r = 0.648 and p < 0.05).
Conclusion: PslCO2 correlated best with PiCO2 and arterial lactate concentration in patients with cardiac failure. PslCO2 and the PslCO2-PaCO2 gradient may be useful as indexes of the severity of perfusion failure.
Key Words: carbon dioxide • circulatory shock • gastric tonometry • lactate • sublingual capnometry
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Introduction |
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TOPAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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Materials and Methods |
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TOPAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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Heart rate was monitored continuously. Arterial pressure was monitored
via an arterial catheter in either the radial or the femoral artery.
All patients were catheterized with a pulmonary artery catheter. Serial
measurements of heart rate, MAP, pulmonary capillary wedge pressure,
and central venous pressure were made. Transducers were referenced to
the midaxillary line, and all pressures were measured at
end-expiration. Cardiac index (Ci) was measured by thermodilution using
measurements that varied by < 10%. Oxyghemoglobin saturation and
content were measured with a cooximeter. Arterial, mixed venous, and
tonometrically measured carbon dioxide tension were determined by a
blood gas analyzer (Stat Profile 5; Nova Biomedical; Waltham, MA).
Arterial lactate levels were determined by the enzymatic method (Vitros
950 lactate analyzer; Johnson and Johnson; Rochester, NY). Derived
hemodynamic variables were calculated from the following standard
formulas: systemic vascular resistance = (MAP - CVP/Ci) x 80
(where CVP is central venous pressure); systemic oxygen delivery
(DO2) = arterial oxygen
content x Ci; and oxygen consumption
(
O2) = arteriovenous oxygen
content difference x Ci.
A tonometric nasogastric tube (TRIP NGS catheter; Tonometrics; Worcester, MA) was inserted, after which radiographic confirmation of the catheter position was obtained. All patients were placed on a regimen of IV famotidine. Phosphate-buffered solution was used to improved the accuracy of the measurements.9 The intraluminal PCO2 was measured from 1.5-mL samples that were aspirated from the catheter balloon anaerobically after discarding the first 1 mL. The PiCO2 measurement was multiplied by the appropriate equilibration factor provided by the manufacturer.
PslCO2 was measured using a disposable CO2 sensor (Optical Sensors; Minneapolis, MN). It incorporates a CO2-specific fluorescent dye in a buffer solution encased in a silicone capsule that is permeable to CO2 gas. The sensor is attached to an instrument that measures the amount of CO2 present by projecting light onto the sensor with an optical fiber. Changes in the projected light are used to calculate the amount of CO2 present. For clinical measurements, the sensor is placed under the tongue with the sensor element facing the sublingual mucosa. Prior to each measurement, the sensor is calibrated against a known standard.
Measurements were taken on entry to the study and at 1, 3, 6, 12, and 24 h after the beginning of the study. Differences between survivors and nonsurvivors were compared by the Mann Whitney U test. Overall correlations between variables for all patients at all times, as well as correlations for individual patients, were analyzed by linear regression. In analyzing the data from individual patients, correlation coefficients were determined only when three or more data points were available for analysis. A p value < 0.05 was considered to be significant. Data are expressed as the mean ± SE.
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Results |
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The perfusion parameters at study entry are presented in Table 1 . One of 10 patients with gastric tonometric measurements survived. PslCO2 levels appeared to be lower in survivors than those in nonsurvivors, as did the PslCO2-PaCO2 gradient. Although not significantly different on entry into the study, these values were significantly different at the 3-h and 6-h data points (data not presented). The same parameters at 24 h are presented in Table 2 . Gastric tonometric values were available in only one survivor. PslCO2 levels were lower in survivors than in nonsurvivors (p = 0.06). The PslCO2-PaCO2 gradient was significantly lower in survivors than in nonsurvivors (p < 0.05). No other significant differences were found between survivors and nonsurvivors in any of the measured variables at any of the data points.
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Discussion |
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TOPAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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Our study examined the relationship of PslCO2 to a number of clinical indexes of tissue perfusion in patients with circulatory failure. Although we observed significant correlations with a number of variables, these correlations were not as strong as previously described in both clinical and experimental studies.6 7 8 Specifically, only a weak correlation was observed between PslCO2 and PiCO2, and no correlation was found between PslCO2 and lactate concentration. Of interest was the observation that the best overall correlation we observed was between PslCO2 and PvCO2.
Tissue hypoperfusion also can be monitored by examining the gradient between tissue PCO2 and PaCO2.12 13 This gradient has the advantage of incorporating the influence of the level of ventilation on tissue PCO2.13 14 Widening of the gradient is expected as the severity of perfusion failure increases. In our study, the PslCO2-PaCO2 gradient demonstrated generally better, but still relatively weak, correlations with a number of indexes of perfusion, including arterial lactate concentration.
The reason for the differences between our study and the previous clinical report in which strong correlations between arterial lactate concentration and PslCO2 were described is unclear. One factor that may contribute to the contrasting observations is differences in patient population. Whereas the report by Weil et al8 involved a large percentage of patients with traumatic injuries, most of our patients had sepsis. As our data suggest, the relationship between PslCO2 and other indexes of perfusion may vary depending on the subset of patients being studied. Patients with cardiac failure demonstrated much stronger correlations between PslCO2 and arterial lactate concentration, PiCO2, and PiCO2-PaCO2 gradient than did patients with sepsis. Of note, is the fact that the experimental studies5 6 7 validating sublingual capnometry have involved global hypoperfusion in the form of hemorrhagic shock or a hypodynamic model of septic shock. The pathophysiologic changes associated with hyperdynamic sepsis, especially abnormalities of microcirculatory blood flow, may dissociate indexes of systemic perfusion from indexes of regional perfusion. In addition, the direct inhibition of mitochondrial respiration by inflammatory mediators during septic shock also may contribute to the poor correlation between lactate levels and PslCO2.14 15 Indeed, in prior studies12 13 involving primarily patients with sepsis, either a weak relationship or no significant relationship has been reported between gastric tonometric measurements and arterial lactate concentrations.
Under experimental conditions, changes in PslCO2 correlate with measurements of splanchnic tissue blood flow.5 6 7 In addition, PslCO2 and gastric PCO2 correlate relatively well, with reported correlation coefficients of 0.71 and 0.89, respectively.4 5 6 7 These studies have involved a different methodology for measuring gastric PCO2 than that used in this study and have involved primarily patients experiencing hemorrhagic shock. We were not able to duplicate this close relationship clinically, particularly in patients with sepsis in whom significant but weak correlations between PslCO2 and PiCO2 were present. Whether this discrepancy is related to our measuring techniques or to the influence of alterations in regional blood flow during sepsis requires additional study.
Our study was not designed to examine the use of PslCO2 as a prognostic indicator of survival. Too few patients were studied, and our patient selection did not incorporate an adequate mix of survivors and nonsurvivors. Nevertheless, at 24 h differences in PslCO2 levels between survivors and nonsurvivors approached statistical significance, and a significantly greater PslCO2-PaCO2 gradient gap was evident in nonsurvivors compared to survivors. These differences were also present at the 3-h and 6-h data points. No significant differences between survivors and nonsurvivors were observed when other indexes of perfusion were examined. Accordingly, although it was not the focus of this study, our data are consistent with the report of Weil et al,8 suggesting a possible role for PslCO2 as an index of the severity of perfusion failure.
In conclusion, PslCO2 can be measured in critically ill patients with circulatory failure who require mechanical ventilation. PslCO2 correlated best with PiCO2 and arterial lactate concentration in patients with cardiac failure and may have a role as an index of the severity of perfusion failure.
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Footnotes |
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O2 = oxygen consumption Received for publication January 2, 2001. Accepted for publication May 11, 2001.
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References |
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This article has been cited by other articles:
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  E. J. Bridges and S. Dukes Cardiovascular Aspects of Septic Shock: Pathophysiology, Monitoring, and Treatment Crit. Care Nurse, April 1, 2005; 25(2): 14 - 40. [Full Text] [PDF]
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 J. A. Guzman, M. S. Dikin, and J. A. Kruse Lingual, splanchnic, and systemic hemodynamic and carbon dioxide tension changes during endotoxic shock and resuscitation J Appl Physiol, January 1, 2005; 98(1): 108 - 113. [Abstract] [Full Text] [PDF]
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