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Anesth Analg 1999;89:1084
© 1999 International Anesthesia Research Society

CARDIOVASCULAR ANESTHESIA

Regional Capnometry with Air-Automated Tonometry Detects Circulatory Failure Earlier Than Conventional Hemodynamics After Cardiac Surgery

Gilles Lebuffe, MD*, Christophe Decoene, MD{dagger}, Annie Pol, MD{dagger}, Alain Prat, MD{dagger}, and Benoit Vallet, MD, PhD*

*Département d’anesthésie-réanimation II, Hôpital Claude Huriez and {dagger}Clinique de Chirurgie Cardio-vasculaire, Centre Hospitalier Universitaire, Lille, France

Address correspondence and reprint requests to Benoit Vallet, MD, PhD, Département d’anesthésie-réanimation II, Hôpital Claude Huriez CHU Lille, Place de Verdun, 59037 Lille Cedex, France. Address e-mail to bvallet{at}chru-lille.fr


   Abstract
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 Abstract
Introduction
 Methods
 Results
 Discussion
 References
 
Gastrointestinal automated online air tonometry has been proposed for monitoring gastric perfusion in patients at risk of circulatory failure (CF) after cardiopulmonary bypass. In this study, CF was prospectively defined as the requirement for vasoactive support to maintain mean arterial pressure >= 70 mm Hg after optimization of preload. Hemodynamic variables—oxygen (O2) delivery (DO2), O2 uptake (VO2), venous-to-arterial [P(v-a)CO2], gastric-to-arterial [P(r-a)CO2], and gastric-to-end-tidal [P(r-et)CO2]PCO2 gap—were retrospectively compared in 14 patients with or without CF during a 12-hr postbypass period (H0–H12). In contrast to patients without CF (n = 7), in patients with CF (n = 7) increased VO2 was not associated with an increase in DO2. P(r-a)CO2 was larger at H0 in CF patients and was the only variable that differed between the two groups. P(v-a)CO2 did not vary significantly in both groups, whereas P(r-a)CO2 increased to a larger extent from H0 to H12 in patients with CF, suggesting selective gastrointestinal hypoperfusion in this group. P(r-et)CO2 provided comparable information to P(r-a)CO2. Hospital length of stay was 4 days longer (P < 0.05) in patients with CF. Increased P(r-a)CO2 and P(r-et)CO2, as monitored with automated air tonometry, were associated with rapid occurrence of CF and prolonged hospital stay after cardiac surgery.

Implications: Regional and automated capnometry may be used noninvasively to identify patients at risk of circulatory failure after cardiopulmonary bypass earlier than with conventional variables.


   Introduction
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 Abstract
 Introduction
Methods
 Results
 Discussion
 References
 
Systemic cardiovascular and oxygen (O2) variables are not reliable predictors of regional hypoperfusion and associated hypoxia. Gastric tonometry has been proposed to detect regional hypoperfusion by measurement of gastric mucosal carbon dioxide (CO2) partial pressure (PrCO2). When related to arterial PCO2 (PaCO2), gastric-to-arterial CO2 gap [P(r-a)CO2] appears as a meaningful marker of regional hypoperfusion (1). An automated technique using air tonometry to measure PrCO2 semicontinuously and to relate it to end-tidal PCO2 [P(r-et)CO2] was recently proposed as a routine tool (2).

Patients are at risk of circulatory failure after cardiopulmonary-bypass (CPB) (3). The increasing metabolic demand during this postoperative period requires an increase in O2 delivery to tissues. Absence of such an increase induces a redistribution of flow from nonvital to vital areas with a risk of gastrointestinal hypoperfusion. Persistent regional tissue hypoperfusion results in inadequate O2 delivery (DO2), leading to gut barrier dysfunction. This has been hypothesized to provoke distant organ injury. Detection and reversal of gut ischemia have been proposed as a means to limit the development of multiple organ dysfunction syndrome (MODS) and its associated increased morbidity and mortality (4–7). In several studies, gastric mucosal acidosis has been shown to frequently develop after cardiac surgery (approximately 50% of patients) and is associated with greater morbidity and a trend for longer hospital stay (8,9). However, in these studies, early detection of enlarged P(r-a)CO2 was not readily available because of limitations associated with saline tonometry that preclude easy online PrCO2 measurement (10). Such limitations are now resolved by using air tonometry (2), which allows for rapid, reliable semicontinuous PrCO2 measurement. Moreover, this device is considered noninvasive and features P(r-et)CO2 as a way to assess P(r-a)CO2. It remains unknown whether automated gastric tonometry can identify patients at risk of cardiac failure earlier than other variables after CPB. The purpose of this study was therefore to determine 1) whether the P(r-a)CO2 gradient is increased before observing abnormalities of any other monitoring variable in patients with circulatory failure (CF) and 2) whether end-tidal PCO2 can be used to replace PaCO2 in the setting of cardiac surgery.


   Methods
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 Methods
Results
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We studied 14 consecutive patients scheduled for elective cardiac surgery requiring CPB. Patients with any history of hepatic disease (alanine aminotransferase [ALT] above 50 units/L), gastritis, gastric and duodenal ulcers, or congestive heart failure (ejection fraction below 50%) were excluded. A standardized anesthetic technique was used. General anesthesia was induced with sufentanil (1 µg/kg IV) and midazolam (0.1 mg/kg IV), followed by pancuronium (0.1 mg/kg IV). Patients were mechanically ventilated with an inspiratory O2 concentration of 50% supplemented with air. Each patient received 150 mg of ranitidine IV after induction of anesthesia. Anesthesia was maintained with sufentanil, midazolam, and pancuronium. A membrane oxygenator with continuous flow was used for CPB. The pump flow rate was set at 2.20 L · min-1 · m-2 at moderate hypothermia (28°–32°C).

After anesthesia induction, a radial artery catheter and a thermodilution pulmonary artery catheter (Swan-Ganz catheter, 7.5F; Baxter Edwards Critical, Irvine, CA) were inserted. Heart rate, mean arterial pressure (MAP), mean right arterial pressure (mm Hg), mean pulmonary artery pressure (mm Hg), and pulmonary artery occlusion pressure were monitored. Cardiac output (CO, L/min) was measured in triplicate by thermodilution using 10 mL of room temperature saline, the mean value being used for derived variable calculation. Arterial and mixed-venous O2 tension were measured by a blood-gas analyzer (Ciba Corning, Halsted, Essex, UK), and the results were corrected to body temperature. O2 content was calculated by multiplying 1.34 by hemoglobin concentration and O2 saturation plus dissolved O2. DO2 (mL · min-1 · kg-1) was calculated as the product of thermodilution CO and arterial O2 content, and O2 uptake (VO2, mL · min-1 · kg-1) as the product of CO and arterial-to-venous O2 content difference. O2 extraction (ERO2, %) was calculated as the ratio of VO2 over DO2 (O2ER = VO2/DO2). Arteriovenous CO2 gradient [P(v-a)CO2, mm Hg] was calculated as the pulmonary artery-to-arterial PCO2 difference. Lactate was measured by an enzymatic colorimetric method (Wako Analyzer, Biochem Systems, Rungis, France), with normal value being <=2.2 mmol/L.

The tonometer (catheter TRIP®NGS, Tonometrics, Charlottenlund, Denmark) was inserted nasally and its position confirmed by auscultation over the epigastrium after injection of 50 mL of air into its lumen. The tonometer and the airway sampling line attached to the patient’s airway adapter were connected to an automated gas analyzer (TonocapTM, Datex, Helsinki, Finland). After the tonometer balloon was filled with air and allowed to equilibrate for 15 min, the gas was automatically sampled and measured by infrared spectroscopy. The monitoring of end-tidal CO2 (PetCO2) was interrupted every 15 min to allow for the determination of PrCO2 from the tonometer. The TonocapTM trend screen allowed monitoring of regional-to-end-tidal PCO2 gradient [P(r-et)CO2]. Arterial blood samples were taken simultaneously with measurement of PrCO2 to calculate the regional-to-arterial PCO2 difference [P(r-a)CO2]. Blood-gas values were entered via the TonocapTM keyboard for the calculation of gastric intramucosal pH (pHi), with pHi = pHa - log(PrCO2/PaCO2).

Immediately after arrival in the intensive care unit (ICU), all patients were ventilated and treated by an intensivist independent from the investigator. All previously defined variables were measured upon arrival in the ICU and subsequently every 2 h within the first 12 h after cardiac surgery. Lactate concentration was measured every 4 h. Catecholamine infusion requirement, length of intubation, ICU, and hospital stay were recorded. Twenty-four hours after admission, serum levels of creatinine, ALT, and neurologic function were recorded. Patients were then prospectively divided into two groups according to whether they required catecholamine infusion to maintain MAP >=70 mm Hg after optimal cardiac filling had been guided by pulmonary artery occlusion pressure >=12 mm Hg. Patients who required catecholamines to maintain MAP >=70 mm Hg constituted the CF group (Group 1). Information obtained from conventional monitoring, automated tonometry, and calculated gastric and venous-to-arterial PCO2 gap were then retrospectively compared between patients with (Group 1) or without CF (Group 2).

Data are expressed as mean ± SD. The matched-pair rank test (Friedman and subsequent Wilcoxon tests) was applied to compare values of different observation time points with initial values. The difference between the groups was assessed by the Mann-Whitney U-test. Statistical significance was accepted at P < 0.05.


   Results
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Discussion
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Patient status (including ejection fraction, mean duration of surgery, and cross-clamp) is presented in Table 1. Duration of CPB was longer in Group 1 than in Group 2 (Table 1). The mean peak perioperative P(r-a)CO2 was observed during the rewarming phase and was not significantly different between the two groups (10.7 ± 1.8 in Group 1, 8.0 ± 2.8 in Group 2).


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  		Table 1. Demographics
 
Vasoactive requirement occurred at 184.2 ± 107.0 min in Group 1 (at H0, no patient received any catecholamine; at H2, 3 patients were treated; at H4, 1 patient; at H6, 3 patients). Four patients received a mean dose of epinephrine of 1.51 µg · kg-1 · min-1 (range 1.25–1.80 µg · kg-1 · min-1), 2 patients received dopamine at 7.86 µg · kg-1 · min-1 (range 7.14–8.58 µg · kg-1 · min-1, and 1 patient received dobutamine at 6 µg · kg-1 · min-1.

Hemodynamic variables are given in Table 2. DO2 was significantly lower in Group 1, whereas VO2 increased to the same extent in both groups and, consequently, was counterbalanced by a progressive increase in ERO2 (Fig. 1). Lactate tended to be higher in Group 1, but was not statistically different from lactate in Group 2 (Table 3). P(v-a)CO2 did not change significantly in either group (Table 4).


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  		Table 2. Systemic and Pulmonary Hemodynamics, Systemic Oxygen Delivery, and Consumption in Patients With (Group 1, n = 7) or Without Circulatory Failure (Group 2, n = 7)
 


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  		Figure 1. Relation between O2 extraction (ERO2) and O2 delivery (DO2) during the postoperative period in patients with (Group 1) or without circulatory failure (Group 2). Each set of data points represents mean ± SD of 7 patients in each group. Gr = group.

 

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  		Table 3. Metabolic and Tonometric Variables Observed in Patients With (Group 1, n = 7) or Without Circulatory Failure (Group 2, n = 7)
 

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  		Table 4. Systemic and Regional PCO2 Gradients Observed in Patients With (Group 1, n = 7) or Without Circulatory Failure (Group 2, n = 7)
 
At admission in the ICU, PrCO2 was already significantly higher in Group 1 (Table 3). It increased significantly in both groups during the first 10 h of the study and began to decrease at H12 (Fig. 2). Since PaCO2 remained stable, P(r-a)CO2 significantly widened after ICU admission and continued to worsen in Group 1 during the study, with the highest values being observed at H8 (Table 4). P(r-et)CO2 also increased significantly in Group 1, with the highest value being observed at H8 (Table 4). Arterial-to-end-tidal PCO2 [P(a-et)CO2 remained stable in both groups (Fig. 2, Table 4)]. At H24, serum creatinine was significantly higher in Group 1 (126.7 ± 51.9 µmol/L) than in Group 2 (80.9 ± 17.6 µmol/L; P = 0.03), whereas ALT was not different in both groups (Group 1: 19.8 ± 12.2 units/L; Group 2: 18.5 ± 5.2 units/L; P = not significant [NS]). Neurologic deficit was not observed in any patient.



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  		Figure 2. Time course of gastric mucosal PCO2 (PrCO2), arterial PCO2 (PaCO2), and end-tidal PCO2 (PetCO2) in patients with (Group 1) or without circulatory failure (Group 2). Time points statistically different from admission in the intensive care unit (H0) are marked with an asterisk (Friedman test and Wilcoxon test). Each data point represents mean ± SD of 7 patients in each group. Gr = group.

 
In Group 1, 2 patients developed congestive cardiac failure, 3 patients developed pneumonia, 1 patient developed cholecystis, and 1 patient developed MODS and was transferred to another ICU for renal hemodiafiltration. All patients survived. In Group 2, there were no complications. Duration of intubation (Group 1: 2.5 ± 2.4 days; Group 2: 0.9 ± 0.5 days; P = NS) and ICU length of stay (Group 1: 3.8 ± 2.4 days; Group 2: 2.0 ± 0.3 days; P = NS) were not significantly different between the two groups. Hospital length of stay was longer in Group 1 (17.0 ± 4.9 days) than in Group 2 (11.3 ± 3.2 days; P = 0.01).


   Discussion
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 Abstract
 Introduction
 Methods
 Results
 Discussion
References
 
The recovery period in patients undergoing cardiac surgery is associated with an increased metabolic demand due to thermoregulatory responses, return of pain sensitivity, and possible O2 debt reimbursement (11,12). Therefore, during the postoperative period the risk of hemodynamic instability and tissue hypoxia may be increased. This study shows that patients with spontaneously adapted CO (Group 2), who do not receive inotropes, satisfy the demand of systemic O2 increase by an increase in systemic DO2. Their O2 uptake increased from 3.4 to 4.4 mL · kg-1 · min-1 from H0 to H12, with P(v-a)CO2 and blood lactate remaining within normal range and stable, suggesting that DO2 was above its critical value. In contrast, the limited systemic DO2 in patients with a nonadapted CO (Group 1) is associated with a necessary increase in systemic ERO2 to meet the O2 demand. O2 uptake was lower, significantly different from its value in Group 2 at H4 and H6, and did not increase before H8. This was associated with a transient widening in P(v-a)CO2 and an increased lactate concentration. It is now well established in experimental and clinical studies that reduction in DO2 below its critical value is associated with an abrupt increase of blood lactate levels and a significant widening in P(v-a)CO2 (13–15). Critical DO2 in anesthesized patients has been determined to be about 8 mL · kg-1 · min-1 for a similar level of O2 uptake than that observed in our patients (16). Several patients in Group 1 had DO2 that was less than this critical value, and this may explain the lower O2 uptake and increased lactate level in these particular patients. As PaCO2 remained stable, the widening in P(v-a)CO2 reflected a slight systemic venous hypercarbia due, at least in part, to an increased addition of CO2 to each unit of blood that traverses hypoperfused tissues (17).

A significant widening of P(r-a)CO2 was observed immediately after ICU admission in patients who would require inotropes only 2–6 h after their admission. This increased CO2 gap occurred at a period at which none of our patients received inotropes, and at a time where standard hemodynamics and O2 variables were not particularly helpful in anticipating any risk of CF. P(r-a)CO2 was therefore the only variable to help in discriminating patients that would encounter postoperative hemodynamic instability.

Several investigators, using pHi as a marker of gastrointestinal blood flow, have also reported impairment of gastrointestinal perfusion and permeability after cardiac surgery (8,18). In the study of Ohri et al. (18), gastrointestinal hypoperfusion was maximal between 3 and 5 h after CPB and coincided with the maximum of total body VO2 and ERO2. Landow et al. (8) found a decrease in pHi at ICU admission in patients with low systemic DO2. Furthermore, a strong association was noted between pHi and hepatic venous lactate concentrations and hepatic venous hemoglobin saturation, suggesting a splanchnic mismatch between O2 delivery and O2 demand. P(r-a)CO2 was not provided in these studies. In our own study, in patients exhibiting inotropic support requirement, P(r-a)CO2 increased during the first 8 h after ICU admission with a maximum mean value around 20 mm Hg, whereas P(r-a)CO2 was only 11 mm Hg in patients without CF.

The normal value for difference between gastric and arterial PCO2 has been established in normal volunteers to be around 7 mm Hg (19). Increased P(r-a)CO2 during a decrease in O2 delivery can be explained by several mechanisms (1). When DO2 is above its critical value, ensuring a constant CO2 production by oxidative phosphorylation, increased PrCO2 reflects a decreased CO2 washout secondary to decreased gastric blood flow. When DO2 is below its critical value, cell dysoxia occurs and PrCO2 results from an imbalance between decreased aerobic CO2 production and increased anaerobic CO2 production due to H+ buffering by bicarbonates. This is obviously associated with an even larger impaired CO2 washout (1,20). A value of 11 mm Hg, such as observed in Group 2 patients, is compatible with a certain degree of hypoperfusion, but does not correspond to occurrence of dysoxia at the level of the gastric mucosa. Indeed, Schlichtig and Bowles (21) and Guzman et al. (22) demonstrated in a low-flow state dog model that intestinal anaerobiosis began when P(r-a)CO2 was between 25–35 mm Hg. This value is very close to the mean value we observed in Group 1 patients, suggesting that these patients were at risk of cell dysoxia at the level of the gastrointestinal tract. The highest regional to arterial CO2 gap values we observed were around 40 mm Hg, and were associated with increased lactate level and the largest P(v-a)CO2 gap (around 16 mm Hg). The advantage of P(r-a)CO2 for detecting a cell dysoxia gradient when compared with lactate and P(v-a)CO2 gap is derived from its immediate availability and minimally invasive character.

The regional capnometry monitor (TonocapTM) uses P(r-et)CO2 and has been proposed as a routine monitor, with end-tidal CO2 used as a noninvasive index of PaCO2. However, P(r-et)CO2 gap depends on P(r-a)CO2 and on the P(a-et)CO2 gradient. These two gradients can be influenced by hemodynamic instability. Indeed, the measurement of PetCO2 appears to correlate with reductions in CO (23). When alveolar ventilation remains constant, the reduction in PetCO2 reflects a reduction in pulmonary blood flow or a reduction in CO2 production, and the two occur together during systemic hypoperfusion (23). In the present study, the significant widening of P(r-et)CO2 observed in patients with CF can be attributed mainly to a P(r-a)CO2 increase, since P(a-et)CO2 remained almost stable in all patients when PrCO2 increased significantly. This finding suggests that P(r-et)CO2 may be used, with some basic precautions such as a periodic assessment of PaCO2, as a noninvasive index of gastrointestinal perfusion.

Several studies, in cardiac surgery, have reported that gastrointestinal hypoperfusion assessed by pHi or P(r-a)CO2 predicted postsurgical problems. Mythen and Webb (24) have observed a longer length of stay in the ICU, a greater incidence of complications, and a greater mortality in patients with pHi below 7.32. In contrast, the use of volume expansion to maintain pHi above 7.32 during cardiac surgery was associated with fewer complications and a lower hospital length of stay (25). In a postcardiac surgery study, P(r-a)CO2 displayed good specificity and sensitivity in predicting prolonged ICU length of stay (26). In our study, hospital length of stay was significantly increased (5 days) in patients with P(r-a)CO2 between 12 and 21 mm Hg. This was observed despite the fact that group sample sizes were not very large (n = 7 in each group). Organ failure and increased morbidity associated with the occurrence of high P(r-a)CO2 can be explained by the putative consequences of gastrointestinal hypoperfusion. The reduction of gastrointestinal blood flow associated with gastric mucosal dysoxia can promote increased gut permeability and activation of inflammatory pathways leading to distant organ injury and MODS (27).

In summary, increased P(r-a)CO2 and P(r-et)CO2 represent early indicators of CF and are prognostic of increased morbidity in patients after cardiac surgery with CPB. Gastrointestinal tonometry, in particular with the now commercially available automated online capnometer, seems a promising clinically applicable approach to gut perfusion monitoring and might be helpful in optimizing treatment in patients at risk of CF. Other studies will be necessary to determine whether P(r-a)CO2 normalization will modify morbidity and hospital length of stay in ICU patients.


   References
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 

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Accepted for publication June 22, 1999.




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Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press