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J Appl Physiol 87: 933-937, 1999;
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Vol. 87, Issue 3, 933-937, September 1999

Effects of hyper- and hypoventilation on gastric and sublingual PCO2

Andrej Pernat1, Max Harry Weil1,2, Wanchun Tang1,2, Hitoshi Yamaguchi1, Andreja Marn Pernat1, Shijie Sun1,2, and Joe Bisera1,2

1 Institute of Critical Care Medicine, Palm Springs 92262; and 2 University of Southern California School of Medicine, Los Angeles, California 90033


    ABSTRACT
TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES

We investigated the effects of hyper- and hypoventilation on gastric (PgCO2) and sublingual (PslCO2) tissue PCO2 before, during, and after reversal of hemorrhagic shock. PgCO2 was measured with ion-sensitive field-effect transistor sensor and PslCO2 with a CO2 microelectrode. Under physiological conditions and during hemorrhagic shock, decreases in arterial (PaCO2) and end-tidal (PETCO2) PCO2 induced by hyperventilation produced corresponding decreases in PgCO2 and PslCO2. Hypoventilation produced corresponding increases in PaCO2, PETCO2, PgCO2, and PslCO2. Accordingly, acute decreases and increases in PaCO2 and PETCO2 produced statistically similar decreases and increases in PgCO2 and PslCO2. No significant changes in the tissue PCO2-PaCO2 gradients were observed during hemorrhagic shock in the absence or in the presence of hyper- or hypoventilation. Acute changes in PgCO2 and PslCO2 should, therefore, be interpreted in relationship with concurrent changes in PaCO2 and/or PETCO2.

tissue carbon dioxide tension; hyperventilation; hemorrhagic shock


    INTRODUCTION
TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES

HYPERCARBIA OF MIXED VENOUS blood (1, 11, 27) and of tissues, and especially the gastric wall (2, 9, 10, 12, 24), are now well recognized as indicators of reduced tissue perfusion accompanying low cardiac output circulatory shock states. Tissue hypercarbia and acidosis may also follow dysoxia caused by altered cellular metabolism or perfusion in settings of normal cardiac output as observed during septic shock (6, 21, 26). The clinical application of this concept prompted gastric tonometry (7-9), in which increases in gastric wall PCO2 (PgCO2) were quantitated as the pH equivalent. The measurement was initially regarded as predictive of visceral ischemia, especially in settings of traumatic injuries and surgical operations after blood and fluid losses and in critically ill patients presenting with cardiogenic and septic shock (4, 13, 17, 20). More recently, esophageal PCO2 and sublingual PCO2 (PslCO2) emerged as less invasive and attractively simple alternatives (18, 19, 23).

Recent reports indicated that, under physiological conditions, increases in arterial PCO2 (PaCO2) are associated with increases in PgCO2 and intestinal tissue PCO2 (3, 22, 26). The effects of decreases in PaCO2 under physiological conditions are as yet less well identified (22). Moreover, it is not as yet apparent how acute changes in PaCO2 affect PgCO2 and PslCO2 as quantitative indicators of organ perfusion during the low-flow states of circulatory shock. In the present study, our intent was to extend earlier observations under physiological conditions to those under conditions of hemorrhagic shock. Our hypothesis was that, during hemorrhagic shock, acute increases or decreases in PaCO2 induced by changes in the frequency of mechanical ventilation in anesthetized animals would alter the PgCO2 and PslCO2 measurements and thereby moderate the quantitative interpretation of these measurements as indicators of impaired tissue perfusion.


    MATERIALS AND METHODS
TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES

The study was approved by the Institute's Animal Care Committee. All animals received humane care in compliance with the Principles of Laboratory Animal Care formulated by the National Society for Medical Research, and the Guide for the Care and Use of Laboratory Animals prepared by the Institute of Laboratory Animal Resources and published by the National Institutes of Health.

Animal preparation. Sprague-Dawley rats were fasted overnight, except for free access to water. Anesthesia was initiated by an intraperitoneal injection of 45 mg/kg pentobarbital sodium and supplemented with additional doses of 10 mg/kg at hourly intervals. Animals were positioned on a surgical board in a supine position with extremities immobilized in full abduction. The trachea was surgically exposed, and a 14-gauge cannula (Abbocath-T, Abbott Hospital, North Chicago, IL) was advanced into the trachea for a distance of 2 cm. End-tidal PCO2 (PETCO2) was measured with a side-stream infrared CO2 analyzer (End-Tid IL 200, Instrumentation Laboratory, Lexington, MA) adapted to the tracheal tube. The tracheal tube was connected to a volume-controlled mechanical ventilator (model 683, Harvard Apparatus, South Natick, MA). The inspired O2 concentration was maintained at 60%. Neuromuscular blockade was induced with a bolus of 0.1 mg/kg vecuronium bromide injected intravenously followed by a continuous intravenous infusion of 1 µg · kg-1 · min-1. Frequency of ventilation was initially established at 80 breaths/min and tidal volume at 0.65 ml/100 g body wt. Tidal volume was then adjusted to maintain PETCO2 between 35 and 40 Torr.

From the surgically exposed right carotid artery, an 18-gauge polyethylene catheter (Intramedic PE50, Becton-Dickinson, Sparks, MD) was advanced into the thoracic aorta for aortic blood pressure measurements and blood sampling. Through the left jugular vein, another 18-gauge polyethylene catheter was advanced into the right atrium. This catheter allowed for injection of chilled saline at 10°C as a thermal tracer for cardiac output measurements. Through the surgically exposed left femoral artery and vein, 18-gauge catheters were advanced into the abdominal aorta and into the inferior vena cava. These catheters allowed for arterial blood shedding and for reinfusion of shed blood into the vena cava. Through the surgically exposed right femoral artery, a thermocouple microprobe (model 9030-12-34, Columbus Instruments, Columbus, OH) was advanced into the thoracic aorta for measurements of cardiac output. The dead space of the catheters was filled with normal saline containing 5 IU/ml bovine heparin. The aortic catheter was connected to the barrel of a 20-ml plastic syringe, which served as a reservoir for shed blood.

PslCO2 was measured with a CO2 microelectrode (MI-720 CO2 electrode, Microelectrodes, Londonderry, NH). The sensor was lodged between the tongue and sublingual mucosa and secured against the closed mouth with adhesive tape.

For placement of the PgCO2 sensor, the stomach was exposed with a midline epigastric incision. An ion-sensitive field-effect transistor sensor (CO-1035, Nihon Kohden, Tokyo, Japan) was embedded into the submucosa of the anterior wall of the stomach to a depth of 1 mm and secured by a ligature. The abdomen was then closed in one layer.

Experimental procedures. After anesthesia, instrumentation, neuromuscular blockade, and mechanical ventilation had been established, baseline measurements were recorded. Rats weighing between 450 and 550 g were investigated. Under physiological conditions, PaCO2 and PETCO2 in five animals were decreased during hyperventilation for an interval of 30 min. They were then restored to baseline levels of ventilation for a subsequent interval of 30 min. PaCO2 and PETCO2 were then increased during hypoventilation, also for an interval of 30 min, and then returned to baseline levels of ventilation for a final interval of 60 min. The protocol is summarized in Fig. 1.


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  		Fig. 1.   Effects of hyperventilation and hypoventilation (stippled areas) on arterial (PaCO2), gastric (PgCO2), and sublingual (PslCO2) PCO2 under physiological conditions. Means ± SD are represented; n = 5 animals.

Ten animals were subjected to bleeding over an interval of 60 min and then randomized to a protocol of either hyperventilation in five animals or hypoventilation in five animals, as shown in Figs. 2 and 3, respectively. Bleeding was commenced 15 min after the baseline measurements had been completed. Blood was allowed to flow from the aortic catheter into the reservoir filled with 1 ml of saline containing 5 IU of porcine heparin/ml to prevent clotting of shed blood. As previously described (28), the rate of bleeding was regulated by fine adjustments of pressure within the reservoir utilizing a pressure regulator (model 10, Fairchild, Winston-Salem, NC) and a mercury manometer. The barrel was initially pressurized at 100 mmHg for 10 min, and thereafter decreased to 80 mmHg for 20 min and to 70 mmHg for another 20 min. Aortic pressure was then reduced to values ranging from 55 to 60 mmHg, and it was maintained at this level for an additional 50 min. After 60 min, the animals were randomized to either hypocapnia or hypercapnia by the sealed-envelope method. Hypocapnia or hypercapnia was induced by increasing ventilatory frequency to 140 breaths/min or decreasing it to 40 breaths/min, respectively. After 20 min, ventilatory frequency was restored to the baseline level of 80 breaths/min and maintained at that level until blood was reinfused, as shown in Figs. 2 and 3. Measurements were obtained for an additional interval of 30 min after completion of reinfusion.


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  		Fig. 2.   Mean ± SD values of PgCO2, PslCO2, PaCO2, and end-tidal PCO2 (PETCO2) during hyperventilation (stippled area) superimposed on hemorrhagic shock in 5 animals. Hemodynamic data include mean arterial pressure (MAP), cardiac index, arterial blood lactic acid (lactate), and volume of blood removed before reinfusion (shed blood; shaded area). BL, baseline.



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  		Fig. 3.   Mean ± SD values of PgCO2, PslCO2, PaCO2, and PETCO2 during hypoventilation (stippled area) superimposed on hemorrhagic shock in 5 animals. Abbreviations for hemodynamic data are defined in Fig. 2 legend.

At the end of the experiment, animals were euthanized by an intravenous injection of 100 mg/kg pentobarbital sodium. An autopsy was performed with gross inspection of thoracic and abdominal organs to identify potential adverse effects of the surgical interventions.

Measurements. A two-point calibration of electrodes for measurements of PslCO2 and PgCO2 preceded and followed each experiment, with tonometers maintained at 37°C and with gas mixtures of nitrogen and either 5% or 15% CO2.

Blood pH, PCO2, PO2, and lactate were measured on 0.5-ml blood samples utilizing an automated blood-gas and electrolyte analyzer (Stat Profile Ultra, Nova Biomedical, Waltham, MA). Cardiac output was measured by an adaptation of the thermodilution technique in which a bolus of 200 µl of saline was injected into the right atrium, and blood temperatures were measured in the thoracic aorta. Cardiac index was computed with an adaptation of commercially available data-acquisition system and software (National Instruments, Austin, TX). All electronic outputs were recorded on a PC-based data-acquisition system utilizing CODAS software (DATAQ Instruments, Akron, OH) at a sampling rate of 300/s.

Data analyses. Means ± SD are reported. Time-based values within groups were analyzed by repeated-measures ANOVA. Differences in time-based values were analyzed by Tukey's procedures for post hoc tests. Relationships among PgCO2, PslCO2, and PaCO2 were analyzed with time series cross-correlation techniques. Proportional changes in PaCO2 and tissue PCO2 parameters after hypo- and hypercapnia were compared by Friedman's ANOVA and the Wilcoxon signed-rank pairs test. A P value of <0.05 was regarded as significant.


    RESULTS
TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES

No abnormalities were observed on gross examination at autopsy, and no animals were excluded from data analyses.

When the frequency of ventilation was increased under physiological conditions in anesthetized animals, PaCO2 decreased from a baseline value of 36 ± 2 to 23 ± 2 Torr (P < 0.01). PETCO2 decreased correspondingly (Table 1). These changes were accompanied by simultaneous decreases in both PgCO2 and PslCO2 by quantitatively similar amounts (Table 2, Fig. 1). When the frequency of ventilation was returned to baseline values, PaCO2, PETCO2, and tissue PCO2 values were restored to approximately baseline values. Changes in tissue PCO2 corresponded closely to those of PaCO2.

                              
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  		Table 1.   Hemodynamic parameters, PETCO2, and tissue PCO2-to-PaCO2 gradients during hyperand hypoventilation under physiological conditions


                              
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  		Table 2.   Absolute increases and decreases in PaCO2 and tissue PCO2 after increases or decreases in ventilation under physiological conditions

When the frequency of ventilation was decreased, PaCO2 increased from 34 ± 4 to 62 ± 10 Torr (P < 0.01), and there were comparable increases in PETCO2. Increases in tissue PCO2 exceeded those of PaCO2 by ~20%, but these differences were not statistically significant (Table 2).

The time series cross correlation between PaCO2 and PslCO2 was 0.93, and between PaCO2 and PgCO2 it was 0.91. The hemodynamic data, together with numerical gradients between PgCO2 and PaCO2 and the gradients between PslCO2 and PaCO2, are shown in Table 1. Except for decreases in mean arterial pressure during hypoventilation, there were no significant hemodynamic changes or differences in the PCO2 gradients.

After onset of bleeding, arterial pressure, PaCO2, and PETCO2 declined, and arterial blood lactate increased as expected (19). The PgCO2 increased from 50 ± 3 to 69 ± 11 Torr (P < 0.01), and PslCO2 increased from 47 ± 5 to 71 ± 8 Torr (P < 0.01) (Fig. 2). When the frequency of ventilation was increased after maximal decline in arterial pressure and cardiac index, PaCO2 decreased further from 26 ± 4 to 16 ± 2 Torr (P < 0.05), and PETCO2 decreased from 25 ± 5 to 14 ± 3 Torr (P < 0.05). PgCO2 decreased from 69 ± 11 to 52 ± 10 Torr (P < 0.05), and PslCO2 decreased from 71 ± 8 to 50 ± 5 Torr (P < 0.01). Accordingly, we observed directionally concordant reductions in PaCO2, PETCO2, PgCO2, and PslCO2 during hemorrhagic shock. All PCO2 values returned to those before hypocapnia after ventilation was restored to baseline levels. Decreases in tissue PCO2 and especially PslCO2 induced by hyperventilation during hemorrhagic shock were numerically larger, but numerical differences were not statistically different from those of PaCO2 (Table 3).

                              
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  		Table 3.   Absolute increases and decreases in PaCO2 and tissue PCO2 after increases or decreases in ventilation during hemorrhagic shock

When the frequency of ventilation was decreased during hemorrhagic shock, PaCO2 increased from 25 ± 3 to 49 ± 5 Torr (P < 0.01), and PETCO2 increased from 24 ± 4 to 54 ± 5 Torr (P < 0.01). These increases were associated with a time-coincident increase in PgCO2 from 77 ± 11 to 106 ± 13 Torr (P < 0.05) and in PslCO2 from 65 ± 6 to 87 ± 8 Torr (P < 0.01). After the frequency of ventilation was returned to baseline levels, these effects were reversed (Fig. 3). As in the instance of hyperventilation, there were no significant differences in the magnitude of individual changes in PaCO2, PgCO2, and PslCO2 or in the numerical gradients between PgCO2 and PaCO2 or PslCO2 and PaCO2 (Tables 3 and 4).

                              
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  		Table 4.   Tissue PCO2-to-PaCO2 gradients during hyperventilation and hypoventilation superimposed on hemorrhagic shock


    DISCUSSION
TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES

These experiments confirmed that acute increases or decreases in PaCO2 produced comparable changes in tissue PCO2 under physiological conditions in murine models as they did in pigs and in one reported human patient (3, 22, 26). During hemorrhagic shock, acute increases and decreases in PaCO2 induced directional and quantitatively proportional changes in tissue PCO2.

PgCO2 and, more recently, PslCO2 serve as early indicators of the presence of perfusion failure and, therefore, circulatory shock and as quantitators of its severity (14, 16, 18, 19, 25). As in the present experiments, the onset of shock is associated with increases in PgCO2 and PslCO2 of between 15 and 25 Torr. However, increases in PaCO2 of 24 Torr produced by hypoventilation would also account for these numerical increases in PgCO2 and PslCO2 under physiological conditions. The converse is also true. Increases in tissue PCO2 due to shock would be neutralized by hyperventilation in which the PaCO2 is decreased to 16 Torr, PgCO2 from 69 to 52 Torr, and PslCO2 from 71 to 50 Torr. Accordingly, we are alerted to the importance of taking acute changes of PaCO2 into account under conditions when abnormal values of PaCO2 accompany increases (or decreases) in PgCO2 and PslCO2.

For practical purposes in clinical practice, acute increases or decreases in PgCO2 or PslCO2 may be adjusted by amounts that correspond to respective increases or decreases in PaCO2 when these measurements are utilized for diagnosis and quantification of the severity of circulatory shock. As further demonstrated in our study, PETCO2 of itself is a close correlate of PaCO2, and it may, therefore, serve as a noninvasive alternative for PaCO2 for making such corrections. This is in accord with earlier proposals that differences between tissue PCO2 and PaCO2, the so-called tissue PCO2-to-PaCO2 gap, may be a more appropriate measurement than tissue PCO2 alone (3, 5). The PCO2 gap between tissues and arterial blood typically increases during shock. This reflects the effect of metabolic acidosis and especially lactic acidosis coincident with perfusion failure. Although the tissue PCO2-to-PaCO2 gap was not significantly different after the frequency of ventilation was increased or decreased in the present experiments, earlier studies provided evidence that the computation of such gradients increases precision. PgCO2 and PslCO2 were previously measured during hemorrhagic shock when mechanical ventilation remained constant (19). The PgCO2-to-PaCO2 gap increased from 43 ± 12 to 56 ± 8 Torr, and the PslCO2-to-PaCO2 gap increased from 52 ± 9 to 64 ± 6 Torr. Accordingly, measurement of the gap numerically amplified the changes. Yet, if hyperventilation is superimposed as in the present study, there would be an apparent decrease in the PCO2 gap and a potential underestimate of the severity of perfusion failure. Guzman et al. (15) have pointed to this dilemma. We also recognize the need for additional studies for the present experiments to pinpoint only acute changes in ventilation. Chronic effects of altered ventilation, the resulting respiratory acid-base changes, and how these may be related to measurements of PgCO2 and PslCO2 deserve additional studies. Such would best distinguish between compensated and decompensated states of acidosis (acidemia) and alkalosis (alkalemia).

We further acknowledge that the present study is based on an experimental design that may not fully expose correction factors with which interpretation of tissue PCO2 during circulatory shock states may be improved. In selecting mechanical hypoventilation in anesthetized animals for inducing hypercarbia, rather than increases in inspired CO2, we minimized hemodynamic effects. However, increases and decreases in ventilation were induced with mechanical ventilators in anesthetized animals. We, therefore, also recognize that both tissue measurements and gradients may be different during spontaneous hyper- or hypoventilation or in settings in which there are changes in the work of breathing.

In conclusion, quantitative values of tissue PCO2 are moderated by acute changes in PaCO2, both during normal circulation and in settings of hemorrhagic shock. Tissue PCO2 as a marker of the severity of hypoperfusion must, therefore, be interpreted in relation to concurrent abnormalities in PaCO2 and potentially in relationship to its noninvasive surrogate PETCO2.


    ACKNOWLEDGEMENTS

This study was supported in part by National Heart, Lung, and Blood Institute Grant R01-HL-54322, the Rosse Family Foundation, and Mr. and Mrs. Jack Samuelson of La Canada, CA.


    FOOTNOTES

The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.

Address for reprint requests and other correspondence: M. H. Weil, Institute of Critical Care Medicine, 1695 North Sunrise Way, Bldg. #3, Palm Springs, CA 92262-5309 (E-mail: Weilm{at}aol.com).

Received 9 November 1998; accepted in final form 17 May 1999.


    REFERENCES
TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES

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2.   Brantigan, J. W., E. C. Ziegler, K. M. Hynes, T. Y. Miyazawa, and A. M. Smith. Tissue gases during hypovolemic shock. J. Appl. Physiol. 37: 117-122, 1974[Free Full Text].

3.   Creteur, J., D. De Backer, and J. L. Vincent. Monitoring gastric mucosal carbon dioxide pressure using gas tonometry. In vitro and in vivo validation studies. Anesthesiology 87: 504-510, 1997[Medline].

4.   Doglio, G. R., J. F. Pusajo, M. A. Egurrola, G. C. Bonfigli, C. Parra, L. Vetere, M. S. Hernandez, S. Fernandez, F. Palizas, and G. Gutierrez. Gastric mucosal pH as a prognostic index of mortality in critically ill patients. Crit. Care Med. 19: 1037-1040, 1991[Medline].

5.   Duke, T., W. Butt, M. South, and F. Shann. The DCO2 measured by gastric tonometry predicts survival in children receiving extracorporeal life support. Comparison with other hemodynamic and biochemical information. Chest 111: 174-179, 1997[Abstract/Free Full Text].

6.   Fiddian-Green, R. G. Gastric intramucosal pH, tissue oxygenation and acid-base balance. Br. J. Anaesth. 74: 591-606, 1995[Free Full Text].

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J APPL PHYSIOL 87(3):933-937
8570-7587/99 $5.00 Copyright © 1999 the American Physiological Society


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Chest, September 1, 2001; 120(3): 923 - 927.
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