["Utilitarian system" : Heine's legacy poem "legs, to each man two were given" with his lyrical comments on the field of urology]. / "Nützlichkeitssystem" : Heines Nachlassgedicht "Beine hat uns zwey gegeben" mit seinen lyrischen Bemerkungen zum urologischen Bereich.

The chequered biography as well as the enormous and controversial impact history of the poet Heinrich Heine form the notably changing sum of, in his time but also with a view to the future, the more than difficult and manifold relationships from political, social, religious, cultural and economic as well as industrial historical conditions and problems. The works and personality of the poet can rightly be characterized by the subtitle as a current biography laced with innuendo as "the discovery of the European intellectual".

Dopamine-1 receptor stimulation attenuates the vasoconstrictive response to gut ischemia.

The effects of fenoldopam, a dopamine-1 (DA-1) receptor agonist, were studied in two groups of anesthetized dogs before and after induction of splanchnic ischemia by way of hemorrhage. During the first portion of the experiment, both groups received fenoldopam (1.5 microg x kg(-1) x min(-1)) for 45 min followed by a 45-min washout. During the second portion, hemorrhage (10 ml/kg) was induced, followed by no intervention in group I (controls) and restarting of the fenoldopam infusion in group II. Prehemorrhage, fenoldopam increased composite portal blood flow by 33% (P < 0.01). After hemorrhage-induced splanchnic ischemia, fenoldopam restored portal vein blood flow to near baseline, maintained the splanchnic fraction of cardiac output, and attenuated the rise in gut mucosal PCO(2). DA-1 receptor stimulation increased portal blood flow and redistributed blood flow away from the serosal layer in favor of the mucosa during basal conditions and after hemorrhage, suggesting a more concentrated distribution of splanchnic DA-1 receptors within the mucosal layer vasculature. Fenoldopam maintained splanchnic blood flow during hypoperfusion and attenuated the splanchnic vasoconstrictive response to hemorrhage.

Metformin-associated lactic acidosis.

In 1995, the oral antihyperglycemic agent, metformin, was introduced in the United States for treating diabetes mellitus. Rare cases of metformin-associated lactic acidosis caused by the accumulation of the drug in patients with renal dysfunction have been described, although a detailed time course of the resulting metabolic derangements has not been reported. A case of metformin-associated lactic acidosis is presented along with key serial laboratory abnormalities observed during the treatment phase. The patient made a complete recovery following therapy with hemodialysis and supportive care.

E5 murine monoclonal antiendotoxin antibody in gram-negative sepsis: a randomized controlled trial. E5 Study Investigators.

CONTEXT: Knowledge and understanding of gram-negative sepsis have grown over the past 20 years, but the ability to treat severe sepsis successfully has not. OBJECTIVE: To assess the efficacy and safety of E5 in the treatment of patients with severe gram-negative sepsis. DESIGN: A multicenter, double-blind, randomized, placebo-controlled trial conducted at 136 US medical centers from April 1993 to April 1997, designed with 90% power to detect a 25% relative risk reduction, incorporating 2 planned interim analyses. SETTING: Intensive care units at university medical centers, Veterans Affairs medical centers, and community hospitals. PATIENTS: Adults aged 18 years or older, with signs and symptoms consistent with severe sepsis and documented or probable gram-negative infection. INTERVENTION: Patients were assigned to receive 2 doses of either E5, a murine monoclonal antibody directed against endotoxin (n = 550; 2 mg/kg per day by intravenous infusion 24 hours apart) or placebo (n = 552). MAIN OUTCOME MEASURES: The primary end point was mortality at day 14; secondary end points were mortality at day 28, adverse event rates, and 14-day and 28-day mortality in the subgroup without shock at presentation. RESULTS: The trial was stopped after the second interim analysis. A total of 1090 patients received study medication and 915 had gram-negative infection confirmed by culture. There were no statistically significant differences in mortality between the E5 and placebo groups at either day 14 (29.7% vs 31.1%; P = .67) or day 28 (38.5% vs 40.3%; P = .56). Patients presenting without shock had a slightly lower mortality when treated with E5 but the difference was not significant (28.9% vs 33.0% for the E5 and placebo groups, respectively, at day 28; P = .32). There was a similar profile of adverse event rates between E5 and placebo. CONCLUSIONS: Despite adequate sample size and high enrollment of patients with confirmed gram-negative sepsis, E5 did not improve short-term survival. Current study rationale and designs should be carefully reviewed before further large-scale studies of patients with sepsis are conducted.

Splanchnic hemodynamics and gut mucosal-arterial PCO(2) gradient during systemic hypocapnia.

The effects of hypocapnia [arterial PCO(2) (Pa(CO(2))) 15 Torr] on splanchnic hemodynamics and gut mucosal-arterial P(CO(2)) were studied in seven anesthetized ventilated dogs. Ileal mucosal and serosal blood flow were estimated by using laser Doppler flowmetry, mucosal PCO(2) was measured continuously by using capnometric recirculating gas tonometry, and serosal surface PO(2) was assessed by using a polarographic electrode. Hypocapnia was induced by removal of dead space and was maintained for 45 min, followed by 45 min of eucapnia. Mean Pa(CO(2)) at baseline was 38.1 +/- 1.1 (SE) Torr and decreased to 13.8 +/- 1.3 Torr after removal of dead space. Cardiac output and portal blood flow decreased significantly with hypocapnia. Similarly, mucosal and serosal blood flow decreased by 15 +/- 4 and by 34 +/- 7%, respectively. Also, an increase in the mucosal-arterial PCO(2) gradient of 10.7 Torr and a reduction in serosal PO(2) of 30 Torr were observed with hypocapnia (P < 0.01 for both). Hypocapnia caused ileal mucosal and serosal hypoperfusion, with redistribution of flow favoring the mucosa, accompanied by increased PCO(2) gradient and diminished serosal PO(2).

Gut mucosal-arterial Pco2 gradient as an indicator of splanchnic perfusion during systemic hypo- and hypercapnia.

OBJECTIVES: By accounting for influences of systemic acid-base disturbances, gut mucosal-arterial Pco2 gradient (Pico2 - Paco2) has been increasingly advocated as a more specific marker of splanchnic perfusion than Pico2 alone. We examined the stability of the Pico2 - Paco2 gradient compared with raw Pico2 measurements during induced systemic hypo- and hypercapnia. DESIGN: A prospective animal study. SETTINGS: A university research laboratory. SUBJECTS: Twenty anesthetized, paralyzed, and mechanically ventilated mongrel dogs. INTERVENTIONS: After a baseline period during which Paco2 was maintained near 40 torr, the animals were divided into four groups. Minute ventilation was then altered by adjusting tidal volume, frequency, or both to achieve group Paco2 values of 15, 20, 60, and 80 torr for groups 1 through 4, respectively. Portal blood flow was monitored and maintained near baseline levels by infusion of intravenous fluids. Intestinal Pico2 was measured continuously by using capnometric recirculating gas tonometry. MEASUREMENTS AND MAIN RESULTS: Mean (+/- SE) aggregate baseline Pico2 - Paco2 was 16.9+/-3.3 torr. After 60 mins of hypoventilation, Pico2 - Paco2 decreased to 14.2+/-1.1 and to 13.7+/-2.7 torr in groups 3 and 4, respectively (p = NS, compared with baseline for both). On the other hand, after 60 mins of hyperventilation, Pico2 - Paco2 increased to 37.9+/-3.6 and 28.0+/-6.3 torr in groups 1 and 2, respectively (p < .0001, compared with baseline for both). CONCLUSIONS: In this model of maintained portal blood flow, Pico2 - Paco2 remained essentially stable after hypoventilation but increased significantly after inducing hyperventilation. Our findings warrant cautious interpretation of Pico2 - Paco2 as an indicator of splanchnic perfusion during systemic hypocapnia.

Methemoglobinemia induced by topical anesthesia: a case report and review.

Topical anesthetic drugs are widely used by clinicians during hospital and outpatient procedures and are also available to the public in a variety of over-the-counter preparations. Although generally safe, they may cause potentially life-threatening methemoglobinemia. We describe a patient who developed repeated episodes of severe methemoglobinemia after administration of topical Cetacaine spray (a proprietary mixture of benzocaine, tetracaine, and butamben) employed for pharyngeal anesthesia before endotracheal intubation, and briefly review the etiology and pathophysiology of this disorder. Cautious interpretation of oxyhemoglobin saturation values obtained by pulse oximetry or estimated from arterial blood gas analysis is crucial lest the diagnosis of severe methemoglobinemia and the resulting hypoxemia are overlooked. If necessary, the condition is usually readily corrected by intravenous administration of methylene blue.

Gastric intramucosal PCO2 as a quantitative indicator of the degree of acute hemorrhage.

PURPOSE: Gastric intramucosal PCO2 (PiCO2) is a marker of splanchnic dysoxia and hypoperfusion that is increasingly used in intensive care medicine. We assessed two methods, saline-balloon tonometry versus continuous capnometric recirculating gas tonometry (CRGT), for detecting changes in PiCO2 in animals subjected to various degrees of hemorrhage and examined whether changes in PiCO2 would correlate with the degree of hemorrhage as assessed by blood loss volume. MATERIALS AND METHODS: Following a baseline equilibration period, 20 anesthetized dogs were subjected to bleeding of 0, 23, 35, 41, or 47 mL/kg. After 30 minutes, the shed blood was reinfused and the experiments continued for an additional 120 minutes. RESULTS: Aggregate baseline PiCO2 was 43 mm Hg by both methods. PiCO2 did not change significantly over time in the control animals by either method. PiCO2 by CRGT rose significantly in each of the other groups at the end of the hemorrhage period and after resuscitation. Similar trends were observed in PiCO2 measured by saline tonometry but were significant only with the most severe hemorrhage. Strong correlation was observed between the degree of hemorrhage and change in PiCO2 by both methods. CONCLUSION: PiCO2 serves as a quantitative indicator of the severity of hypovolemic perfusion failure associated with hemorrhage. Compared with standard saline tonometry, CRGT may be a more sensitive method of monitoring the severity of hemorrhage.

Therapeutic use of antithrombin concentrate in sepsis.

Sepsis and its associated complications of disseminated intravascular coagulation (DIC) and multiple organ dysfunction syndrome (MODS) continue to be a major cause of morbidity and mortality. Improved detection of all forms of DIC is essential to assure earlier diagnosis. Studies already indicate that the therapeutic use of antithrombin (AT) concentrate may produce a more positive outcome for sepsis-associated DIC. If DIC could be identified earlier and AT concentrate could then be given earlier in the sepsis continuum, study results for the use of AT concentrate in humans might reveal a statistically significant difference versus placebo, and the efficacy of AT concentrate for this syndrome is more likely to be proved. Fixed-bolus doses of AT concentrate based on body weight are currently preferred, but improved, user-friendly assays for plasma AT levels would permit more rapid turnaround time for AT results and could help fine-tune the use of AT concentrate to the specific needs of each patient. Clinical trials involving the therapeutic use of AT concentrate in sepsis should continue, and it can be hoped that their design will reflect the concepts and conclusions offered by this panel of investigators.

Gastric and esophageal intramucosal PCO2 (PiCO2) during endotoxemia: assessment of raw PiCO2 and PCO2 gradients as indicators of hypoperfusion in a canine model of septic shock.

STUDY OBJECTIVES: To validate capnometric recirculating gas tonometry (CRGT) for continuously monitoring gut intramucosal PCO2 (PiCO2) in a septic shock model, and to compare gastric vs esophageal PCO2 vs intramucosal-arterial PCO2 gradients. INTERVENTIONS: CRTG catheters were placed in the stomach and esophagus of six anesthetized dogs. A saline solution filled balloon tonometry (ST) catheter was also placed in the stomach. After equilibration, 3 mg/kg Escherichia coli lipopolysaccharide (LPS) was administered IV. PiCO2 measurements were made at 0, 45, and 90 min post-LPS by ST and continuously by CRGT. RESULTS: Baseline PiCO2 was 41.5+/-1.9 (+/-SE) in the stomach by CRGT, 38.0+/-1.0 by ST, and 43.0+/-4.4 mm Hg in the esophagus (p=not significant). Gastric PiCO2 by CRGT increased to 47.0+/-2.4 mm Hg by 25 min post-LPS (p<0.05), whereas gastric (ST) and esophageal PiCO2 increased significantly by 45 min post-LPS. Good agreement was observed between gastric CRGT and ST measurements (mean bias, 1.3 mm Hg). The PiCO2-PaCO2 gradient increased post-LPS, but was significant only for gastric CRGT measurements 90 min post-LPS infusion. CONCLUSION: CRGT provided continuous gastric PiCO2 measurements that were in close agreement with ST but detected changes earlier than the conventional technique. Continuous esophageal PiCO2 represents a valid alternative for assessing gastric PiCO2.

Relationship between systemic oxygen supply dependency and gastric intramucosal PCO2 during progressive hemorrhage.

BACKGROUND: As systemic oxygen delivery (DO2) is reduced, oxygen consumption (VO2) is maintained until a critical level is reached (DO2crit) below which VO2 becomes supply-dependent and anaerobic metabolism ensues. We examined the relationship between gastric intramucosal PCO2 (PiCO2) and the onset of systemic supply dependency. We also compared PiCO2 to mixed venous and portal venous blood PCO2 (PmvCO2 and PpvCO2) to assess their utility as premonitory indicators of supply dependency. METHODS: Six dogs were subjected to stepwise hemorrhage to effect a progressive decrease in DO2. Inflection points for changes in VO2, PiCO2, PmvCO2, and PpvCO2 versus DO2 were determined. RESULTS: Mean DO2crit was 6.0 +/- 0.7 mL x kg(-1) x min(-1), whereas the DO2 at which inflection points occurred for PiCO2 and PpvCO2 were 13.2 +/- 1.4 and 11.2 +/- 1.5 mL x kg(-1) x min(-1), respectively (p < 0.05 for both). CONCLUSION: Continuous monitoring of PiCO2 using capnometric recirculating gas tonometry can serve as an early indicator of systemic hypoperfusion before the onset of systemic supply dependency.

Failure of three decision rules to predict the outcome of in-hospital cardiopulmonary resuscitation.

The objective of this study was to evaluate three decision-support tools (the Pre-Arrest Morbidity or PAM score, the Prognosis After Resuscitation or PAR score, and the Acute Physiology and Chronic Health Evaluation or APACHE III score) for their abilities to predict the outcomes of in-hospital cardiopulmonary resuscitation (CPR). The medical records of all 656 adult inpatients undergoing CPR during a two-to-three-year period in three large hospitals were retrospectively reviewed, and demographic and clinical variables were abstracted. Of 656 patients undergoing resuscitation, 248 (37.8%) survived the resuscitation attempt long enough to be stabilized (immediate survival), but only 35 (5.3%) survived to discharge. Only 11 patients had PAM scores higher than 8, none of whom survived to discharge; 131 patients had PAR scores above 8, of whom six survived to discharge. The PAR score and the APACHE III score had the greatest areas under the receiver operating characteristic curves (when predicting the outcome of survival to discharge), although no individual area for either outcome was greater than 0.6. None of the decision-support tools studied was able to effectively discriminate between survivors and non-survivors for the outcomes of immediate survival and survival to discharge following in-hospital CPR. This is consistent with previous work utilizing the APACHE II score, which did not identify a threshold above which patients did not benefit from CPR. The findings for the PAR score and the PAM score stand in contrast to previous studies that found them to be potentially useful decision rules. Further work is needed to develop a decision-support tool that better discriminates between survivors and non-survivors of in-hospital CPR.

Continuous assessment of gastric intramucosal PCO2 and pH in hemorrhagic shock using capnometric recirculating gas tonometry.

OBJECTIVES: To test a novel device for continuous monitoring of gut intramucosal PCO2 and pH and to compare its use with conventional intermittent saline balloon-tonometry in a model of hemorrhagic shock. DESIGN: A prospective animal study. SETTINGS: A university research laboratory. SUBJECTS: Eight anesthetized, mechanically ventilated mongrel dogs. INTERVENTIONS: Two balloon-tip tonometry catheters, one conventional and one modified for continuous recirculating gas tonometry, were inserted into each animal's stomach by the oral route. Gastric intramucosal PCO2 was recorded continuously by capnometric recirculating gas tonometry throughout the experiment. After a baseline period of 90 mins, vital signs, arterial and mixed venous blood gases, and intramucosal PCO2 values were obtained by recirculating gas tonometry and by the conventional method. Using a modified Wiggers' model, the animals were then subjected to hemorrhage of up to 45 mL/kg, or the volume required to effect a decrease in mean arterial pressure to < 30 mm Hg. After 30 mins, the shed blood was reinfused and the experiment continued for an additional 30 mins. Vital signs, arterial and mixed venous blood samples, saline tonometry samples, and recirculating gas tonometry readings were obtained immediately before and 30 mins after reinfusion of blood. MEASUREMENTS AND MAIN RESULTS: Mean +/- SD baseline intramucosal PCO2 was 47.6 +/- 9.5 torr (6.3 +/- 1.3 kPa) by capnometric recirculating gas tonometry and 45.8 +/- 3.4 torr (6.1 +/- 0.5 kPa) by conventional saline tonometry (p = NS). By 5 mins after inducing hemorrhage, intramucosal PCO2 by recirculating gas tonometry had increased significantly (49.3 +/- 9.7 torr [6.6 +/- 1.3 kPa]; p < .05), and by 30 mins, it had increased to 59.7 +/- 11.3 torr (8.0 +/- 1.5 kPa; p < .001 compared with baseline). After 30 mins of hemorrhage, the conventional method showed an increase in intramucosal PCO2 to 63.0 +/- 20.9 torr (8.4 kPa +/- 2.8 kPa; p = NS vs. baseline by conventional method; p = NS vs. corresponding recirculating gas tonometry values). Gastric intramucosal pH, as determined by recirculating gas tonometry, decreased significantly at 5 mins after starting hemorrhage (7.13 +/- 0.10 to 7.10 +/- 0.10, p < .02). After 30 mins of hemorrhage, intramucosal pH decreased to 6.88 +/- 0.14 (from 7.10 +/- 0.10) by the conventional saline tonometry technique (p < .01) and to 6.89 +/- 0.10 by recirculating gas tonometry (p < .001 vs. baseline). Intramucosal PCO2 by both techniques remained significantly increased above baseline values 30 mins after reinfusion of the shed blood. CONCLUSIONS: Capnometric recirculating gas tonometry allows continuous and automated assessment of gastrointestinal tract perfusion by providing on-line measurements of intramucosal PCO2, which can also be used to derive intramucosal pH. The technique is able to detect changes in intramucosal PCO2 in response to an induced insult over intervals as short as 5 mins.

End-tidal partial pressure of carbon dioxide as a noninvasive indicator of systemic oxygen supply dependency during hemorrhagic shock and resuscitation.

When oxygen delivery (DO2) critically decreases, oxygen consumption (VO2) becomes supply dependent. We examined whether end-tidal PCO2 (PetCO2) would identify supply dependency during shock. Five dogs (Group I) underwent progressive hemorrhage to decrease DO2 until they could no longer maintain a stable blood pressure. Five additional animals (Group II) were bled until VO2 decreased to 70% of baseline, followed by resuscitation. The PetCO2 versus time inflection point was compared with the DO2 at onset of supply dependency (DO2crit). DO2crit for Groups I and II were 6.9 +/- .4 and 8.1 +/- 1.3, respectively (p = NS), and not statistically different from the DO2 values at which PetCO2 decreased (6.6 +/- .7 and 6.3 +/- .7 mL/kg per min, respectively). AT constant minute volume, PetCO2 effectively indicated the onset of supply dependency and rapidly increased during resuscitation, paralleling the changes in VO2 in this model of hemorrhagic shock.

Poor in vivo reproducibility of gastric intramucosal pH determined by saline-filled balloon tonometry.

PURPOSE: The reproducibility of gastric intramucosal pH (pHi) determinations by saline-filled balloon tonometry has not been assessed adequately. We examined the agreement of pHi obtained using pairs of tonometry catheters under various conditions in a canine model of global hypoxia. METHODS: Two gastric balloon tonometry catheters were inserted into each of 16 anesthetized dogs. Cimetidine was administered to six of the animals (group 1). Hypoxia was induced for 30 minutes by reducing the F1O2 to 0.08. pHi was determined under basal conditions, at completion of hypoxia, and during the posthypoxic period. RESULTS: The mean bias of the paired pHi determinations was 0.03 for group 1 and 0.00 for group 2 (P = NS). The corresponding 95% limits of agreement spanned 0.24 and 0.28 pH units, respectively. Agreement of pHi determinations between tonometry catheters was not significantly affected by varying of the equilibration period, by administration of cimetidine, or by the presence of posthypoxic conditions. CONCLUSIONS: Clinically important disagreement was observed in simultaneous pHi determinations obtained using separate gastric balloon tonometry catheters exposed to identical in vivo conditions. Poor reproducibility of individual pHi determinations may limit the accuracy of pHi obtained by gastric balloon tonometry in the clinical setting.

Progressive gastric intramucosal acidosis follows resuscitation from hemorrhagic shock.

The time course of gastric intramucosal pH (pHi) during the early phase of resuscitation of hemorrhagic shock has not been adequately characterized. We examined pHi using gastric tonometry catheters in an anesthetized dog model of hemorrhagic shock. Shock was induced in 10 animals to maintain mean arterial blood pressure (MAP) at 40-45 mmHg for 30 min, followed by transfusion of shed blood plus additional saline as needed to maintain MAP at pre-shock values. Five animals served as controls. Baseline pHi values were nearly identical in both groups. Resuscitation promptly restored MAP. Following a precipitous drop of pHi during shock, there was only partial recovery 60 min post-shock, followed by progressive worsening of intramucosal acidosis (7.02 +/- .10 vs. 6.82 +/- .24 at 60 and 210 min post-shock, respectively; p < .002). MAP, heart rate, and pHi did not change significantly during the experiment in the control group. These results indicate that prompt and adequate MAP response to resuscitation failed to prevent significant decreases of pHi in the first few hours post-resuscitation. This finding may be related to persistent splanchnic hypoperfusion or reperfusion injury.

Continuous infusion versus intermittent administration of ceftazidime in critically ill patients with suspected gram-negative infections.

The pharmacodynamics and pharmacokinetics of ceftazidime administered by continuous infusion and intermittent bolus over a 4-day period were compared. We conducted a prospective, randomized, crossover study of 12 critically ill patients with suspected gram-negative infections. The patients were randomized to receive ceftazidime either as a 2-g intravenous (i.v.) loading dose followed by a 3-g continuous infusion (CI) over 24 h or as 2 g i.v. every 8 h (q8h), each for 2 days. After 2 days, the patients were crossed over and received the opposite regimen. Each regimen also included tobramycin (4 to 7 mg/kg of body weight, given i.v. q24h). Eighteen blood samples were drawn on study days 2 and 4 to evaluate the pharmacokinetics of ceftazidime and its pharmacodynamics against a clinical isolate of Pseudomonas aeruginosa (R288). The patient demographics (means +/- standard deviations) were as follows: age, 57 +/- 12 years; sex, nine males and three females; APACHE II score, 15 +/- 3; diagnosis, 9 of 12 patients with pneumonia. The mean pharmacokinetic parameters for ceftazidime given as an intermittent bolus (IB) (means +/- standard deviations) were as follows: maximum concentration of drug in serum, 124.4 +/- 52.6 micrograms/ml; minimum concentration in serum, 25.0 +/- 17.5 micrograms/ml; elimination constant, 0.268 +/- 0.205 h-1; half-life, 3.48 +/- 1.61 h; and volume of distribution, 18.9 +/- 9.0 liters. The steady-state ceftazidime concentration for CI was 29.7 +/- 17.4 micrograms/ml, which was not significantly different from the targeted concentrations. The range of mean steady-state ceftazidime concentrations for the 12 patients was 10.6 to 62.4 micrograms/ml. Tobramycin peak concentrations ranged between 7 and 20 micrograms/ml. As expected, the area under the curve for the 2-g q8h regimen was larger than that for CI (P = 0.003). For IB and CI, the times that the serum drug concentration was greater than the MIC were 92 and 100%, respectively, for each regimen against the P. aeruginosa clinical isolate. The 24-h bactericidal titers in serum, at which the tobramycin concentrations were < 1.0 microgram/ml in all patients, were the same for CI and IB (1:4). In the presence of tobramycin, the area under the bactericidal titer-time curve (AUBC) was significantly greater for IB than CI (P = 0.001). After tobramycin was removed from the serum, no significant difference existed between the AUBCs for CI and IB. We conclude that CI of ceftazidime utilizing one-half the IB daily dose was equivalent to the IB treatment as judged by pharmacodynamic analysis of critically ill patients with suspected gram-negative infections. No evaluation comparing the clinical efficacies of these two dosage regimens was performed.

Development and validation of a technique for continuous monitoring of gastric intramucosal pH.

A novel method for continuously monitoring gastric intramucosal PCO2 and pH was developed and tested. Gas was continuously circulated through a modified balloon-tipped catheter connected to an external closed system fitted with an infrared CO2 sensor to monitor PCO2. Performance of the capnometric recirculating gas tonometry (CRGT) system was tested in vitro using an equilibration chamber and in vivo in six anesthetized dogs. Serial PCO2 measurements were made using CRGT and compared with intermittent PCO2 values obtained by conventional tonometry catheters. In the animal experiments, gastric intramucosal PCO2 and pH were determined before and after inducing hypoxia by decreasing the Flo2 to 0.08. After initial placement, PCO2 determined by the CRGT reached a near plateau within 45 min, and at that time point values were comparable to those obtained by conventional intermittent tonometry. Significant increases in gastric intramucosal PCO2 were detectable by CRGT within 5 min of inducing systemic hypoxia, and there was a concomitant significant decrease in intramucosal pH. Continuous monitoring of gastric intramucosal PCO2 and pH is feasible, has potential advantages over conventional methods, and can provide significant trending information over intervals as short as 5 min.