Gastric Mucosal End-Tidal Carbon Dioxide Partial Pressure Difference as a Continuous Indicator of Splanchnic Perfusion During Prolonged Anesthesia

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1 Med. J. Cairo Univ., Vol. 81, No. 1, June: , Gastric Mucosal End-Tidal Carbon Dioxide Partial Pressure Difference as a Continuous Indicator of Splanchnic Perfusion During Prolonged Anesthesia RAGAA A.A.M. HERDAN, M.D.*; ABDELRADY S. IBRAHIM, M.D.*; SAHAR A.M. EL-GAMMAL, M.D.**; MOHAMED ABDEL-MONEIM BAKR, M.D.*; MOHAMED MOHAMED ABDEL LATIF, M.D.* and HANY AHMED IBRAHEEM, M.D.* The Departments of Anesthesiology & Intensive Care* and Clinical Pathology**, Faculty of Medicine, Assiut University Abstract Aim of the Study: This study was designed to investigate the influence of prolonged anesthesia on gastric mucosal tonometric values compared to commonly measure global indices of splanchnic hypoperfusion. Patients and Methods: 36 adult patients scheduled for elective prolonged microvascular surgeries with duration more than 5 hours under general anesthesia were allocated into three groups according to the duration of the prolonged surgery (12 in each): Group I: With duration of about 6 hr, group II: With duration of about 10 hr and group III: With duration of about 12 hr. Measurement: Heart rate, mean arterial blood pressure, central venous pressure, end tidal carbon dioxide tension, ABG (ph, PaCO2 and pao2) and tonometric parameters including; gastric intra-luminal PCO2, the difference between gastric intra-luminal PCO2 (PgCO2) and end-tidal PCO2 (PgCO2-PetCO2) and gastric intra-mucosal ph (phi) and Serum Lactate concentration. Measurements done after induction of anesthesia (baseline) and every two hours from start of mechanical ventilation till the end of surgery. Results: There were gradual significant increases (p<0.01) in the mean values of PgCO2 and gastric mucosal end tidal CO2 partial pressure difference through all subsequent readings in the three groups compared with the baseline value. There were gradual decrease in the mean values of gastric intramucosal ph over time and this decrease reaches its maximum value at 12 hours after induction of anesthesia in group III. The arterial lactate concentration mean values showed significant increases (p<0.000) in group I, group II and group III at different study periods when compared to baseline value. Conclusion: Prolonged general anesthesia produced GI hypoperfusion manifested by increased PgCO2, PgCO2- PetCO2 gap and decreased phi despite maintaining 02 delivery. Key Words: Gastric mucosal Splanchnic hypoperfusion Prolonged anesthesia. Correspondence to: Dr. Abdelrady S. Ibrahim, The Department of Anesthesiology & Intensive Care, Faculty of Medicine, Assiut University Introduction THE splanchnic circulation contributes to the regulation of volume and blood pressure in humans Hi, as well as less well-defined effects on acidbase regulation [2] Gut mucosal hypoperfusion is an early consequence of hypovolemia and inadequate cardiac output (CO), and is demonstrable long before arterial blood pressure decreases [3]. Different authors consider gastrointestinal (GI) tonometry to be a noninvasive, organ-specific, metabolically oriented method for monitoring the adequacy of gut perfusion, oxygenation and cellular energy balance [4]. Compared to global indices, i.e. blood pressure, cardiac output, arterial ph (pha) or lactate concentrations, gastric intramucosal ph (phi) is an early and better indicator of the adequacy of tissue perfusion [5]. Gastric tonometry is used as an additional valuable end point for resuscitation [6]. Determining PgCO 2 is made easier today by air-automated tonometry, a technique that allows a short equilibration time (10 min), when compared with the previously used saline tonometry [7]. This study was designed to investigate the influence of prolonged anesthesia on gastric mucosal tonometric values compared to commonly measure global indices of splanchnic hypoperfusion (blood pressure, arterial ph and lactate concentration). Patients and Methods This study was carried out in Assiut University Hospital, Faculty of Medicine from April 2010 Oct After approval from our local ethics committee and obtaining an informed written consent from each patient. 36 adult patients (ASA I 359

2 360 Gastric Mucosal End-Tidal Carbon Dioxide and II), scheduled for elective prolonged microvascular surgeries with duration more than 5 hours under general anesthesia, were enrolled in the study. Patients with cardiovascular or respiratory dysfunction, liver or renal failure were excluded from the study. The patients were allocated into three groups according to the duration of the prolonged surgery: Group I: With duration of about 6 hr, group II: With duration of about 10 hr and group III: With duration of about 12 hr. Anesthesia: The patients were premedicated with midazolam 0.1mg/kg (I.M.), atropine 0.5mg (I.M.) and omeprazole, 40mg (I.V.) given one hour before anesthesia to reduce the impact of gastric secretion on the intramucosal (phi). An intravenous cannula was inserted and fluids administration was initiated in the form of lactate free crystalloid solutions 6-8 ml/kg/hr. After pre-oxygenation with 100% oxygen for 3min. Anesthesia was induced with i.v. Thiopental Na 5mg/kg, fentanyl lgg/kg and atracurium besilate 0.5mg/kg to facilitate endotracheal intubation. Anesthesia was maintained with isoflurane % with oxygen (100%), and i.v. Infusion of fentanyl gg/kg/h and atracurium besilate mg/kg/hour. The patient's lungs were ventilated mechanically using respiratory rate of breaths/min, a tidal volume of approximately 10mL/kg and I:E ratio of 1:2, to maintain an end tidal CO mmHg and PEEP of SmmHg was established. Central venous catheter (subclavian vein or internal jugular vein) and arterial line following Allen's test (radial artery or dorsalis pedis artery)-according to the site of operation were inserted under local anesthesia and complete aseptic technique. Patients who showed persistent fall in mean arterial blood pressure and/or heart rate more than 20% of the baseline values were treated with rapid I.V. Infusion of lactate free crystalloid solutions and/or atropine injection. Blood transfusion for blood loss replacement was done when needed. The patients were continuously monitored for electrocardiogram (ECG), heart rate (HR), arterial oxygen saturation (Sp0 2 ), end tidal carbon dioxide tension (ETCO 2 ), non invasive arterial blood pressure (NIBP) and temperature (nasopharyngeal probe). CVP in all patients during the study period was maintained between 6-10 mmhg by adjusting the infusion rate and temperature was maintained within C by using warmed blanket. At the end of the surgical procedure, the residual muscle relaxant effect was reversed and the patients were extubated and send to recovery room. Postoperative pain relieve was provided after return of consciousness using fentanyl I.V. Infusion in a dose of 0.5 to lgg/kg/hr for at least 24 hr according to patients' needs. Gas tonometer (Tonocap; Datex / Instrumentarium, Helsinki, Finland) The tonometry module contains an infrared CO 2 gas concentration sensor and a gas sampling system to move gas between the patient's stomach and the sensor. The patient was connected to the module with a tonometric catheter (Tonometrics Catheter, TONO-16F), which was introduced transnasally into the patient's stomach after induction of anesthesia. Correct positioning of the tonometer was confirmed by aspiration of gastric contents and injection of air down the nasogastric tube while auscultating over the epigastric region. In addition to the tonometry lumen, the catheter incorporates a lumen for feeding, decompression, or aspiration. This unique radiopaque multiple lumen catheter includes a semipermeable silicone balloon at the distal end of the catheter, which is positioned in the stomach. CO 2 freely equilibrates between the gastric mucosa, the gastric lumen and the balloon. In Tonocap, the device fills the tonometer catheter with 5m1 gas (air) and a sample of this gas is drawn after an equilibration period. The PCO 2 of this sample is measured by Tonocap using the same standard infrared method that is used to measure the partial pressure of end-tidal CO 2. Measurement parameters: Hemodynamic data: Heart rate (11R), mean arterial blood pressure (MAP), and central venous pressure (CVP). Respiratory data: End tidal carbon dioxide tension (ETCO 2 ), and ABG (ph, PaCO 2 and pao 2 ). Tonometric parameters: Gastric intra-luminal PCO 2 and calculating the difference between gastric intra-luminal PCO 2 (PgCO 2 ) and endtidal PCO 2 (PgCO 2 -PetCO 2 ) and calculating gastric intra-mucosal ph using Henderson- Hasselbalch equation: PHi=6.1+log (arterial [HCO3-]/PCO 2 (tonometer) x K). Arterial Lactate concentration (mg/dl). Measurement times: Measurements done after induction of anesthesia (baseline) and every two hours from start of mechanical ventilation till the end of surgery. Statistical analysis: It was performed by using SPSS for windows (Version 16). The present data are expressed as mean±standard deviation (SD). Paired t-test was applied to compare between the basal (control) reading and the subsequent readings inside the same group. ANOVA (one way analysis of variance) test was applied to compare the data among the three studied groups. Student's t-test (Unpaired t-

3 Ragaa A.A.M. Herdan, et al. 361 test) was applied to compare the data in-between each two studied groups according to the statistically significant difference results of ANOVA test. Associations were performed by Pearson's correlation test to detect the degree of relationship between different variables inside the same group. Statistically significant difference was considered when p-value was <0.05. Results There were insignificant differences between the three groups as regard to the demographic data and clinical characteristics (Table 1). The mean duration of surgery was 5.02±0.43 hours in group I, 9.24±0.51 hours in group II and 12.25±0.49 hours in group III. Table (1): Demographic data (Mean±SD). Parameters GI G II G III Age (year) 31.33± ± ±8.75 Sex (M:F) 8 (66.7%): 7 (58.3%): 7 (58.3%): 4 (33.3%) 5 (41.7%) 5 (41.7%) Height (cm) ± ± ±4.60 Weight (kg) 75.16± ± ±6.86 Changes in cardio-respiratory parameters: There were statistically insignificant changes (p<0.05); in HR, MABP and CVP mean values at different times of the study inside each group and between the groups when compared to baseline value. Compared with the mean baseline value measured after induction of anesthesia, there were insignificant differences (p>0.05) in the mean value of end tidal carbon dioxide at different times of the study in the three groups. There was statistically insignificant difference between group I and group II at all time intervals after induction of anesthesia and also between group I and group III except at 6 hours, while comparison between group II and group III showed statistically significant differences at 6, 8 and 10 hr after induction (p<0.05). Changes in gastric intra-luminal partial pressure of CO 2 (Table 2): Compared with the mean baseline value measured after induction of anesthesia, there were gradual significant increases (p<0.01) in the mean value of PgCO2 through all subsequent readings in the three groups. However, the changes in mean value of PgCO2 were found to be statistically insignificant among the three investigated groups (p>0.05). Changes in gastric mucosal end tidal CO2 partial pressure difference (Table 2, Fig. 1): There were statistically significant increases (p<0.001) in the mean values of gastric mucosal end tidal CO2 partial pressure difference at different study periods compared with the baseline value. They were still within the normal values, but approached the maximal level of normality especially at 10 and 12 hours after induction of anesthesia in groups II and III. There were statistically significant differences between group I and group III and between group II and III but not between group I and II. Changes in gastric intra-mucosal ph (Table 3): There were insignificant differences (p>0.05) in the mean value of gastric intra-mucosal ph at different times of the study period compared with the mean baseline value in the three groups. There were gradual decrease in the mean values of gastric intra-mucosal ph over time and this decrease reaches its maximum value at 12 hours after induction of anesthesia in group III. The changes in mean value of phi were found to be statistically insignificant among the three investigated groups (p>0.05). Changes in arterial lactate concentration (Table 3): The arterial lactate concentration mean values showed significant increases (p<0.000) in group I, group II and group III at different study periods when compared to baseline value. They increase gradually over time but they are still within their normal limits. However there was statistically insignificant difference (p>0.05) among the three groups at all time intervals. Changes in arterial ph: In the baseline period the ph mean value was found to lie within its normal range in the three groups. The subsequent values showed insignificant changes (p<0.05) when compared to baseline value in the three studied groups. Changes in Pao 2 : Following institution of mechanical ventilation with FIO2 0.1, the base line mean value of Pao2 was 220±22 4mmHg in group I, 210±23.6mmHg in group II and mmHg in group III. There was statistically significant increase (p<0.000) in the mean values of Pao2 at different times of the study period in the three groups and no significant differences were found among the three groups at all investigated times (p>0.05). Changes in PaCO 2 : The baseline value of PaCO 2 was 35.5±3.6mmHg in group I, mmHg in group II and 35.40±3.80mmHg in group III. These values showed a slight insignificant decrease in the three investigated groups during all study periods.

4 362 Gastric Mucosal End-Tidal Carbon Dioxide Statistical (Pearson's) correlation: There was positive statistical correlation between gastric mucosal end tidal CO 2 partial pressure difference (r=0.632 andp=0.000) versus duration of surgery in all studied patients at the end of surgeries in the three investigated groups. There was positive statistical correlation between the arterial lactate concentration (r=0.937 and p=0.000) versus duration of surgery in all studied patients at the end of surgeries in the three investigated groups. In all studied patients, there was a statistically significant positive correlation between the arterial lactate concentration (mg/dl) versus gastric mucosal end tidal CO 2 partial pressure difference (mmhg) at the end of surgery (r=0.538 and p=0.001). The relationship between the gastric intra-mucosal ph (phi) and duration of surgery showed negative correlation in all studied patients at the end of surgeries but this correlation was statistically insignificant (r=0.009 and p= ). Table (2): Changes in gastric intra-luminal partial pressure of CO2 (mmhg) and gastric mucosal end tidal CO2 partial pressure difference (mmhg) with time in the three investigated groups. Parameters GI G H G In Gastric intra-luminal partial Baseline 45.24± ± ±0.41 pressure of CO2 (mmhg) 2h after induction 45.65±0.48** 45.67E1.44** 45.41E1.47** 4h after induction 46.10±0.45** 46.10±0.43** 45.85±0.55** 6h after induction 46.57±0.44** ±0.43** 46.29±0.51** 8h after induction 46.97±0.44* * 46.73±0.52** 10h after induction 47.36±0.48** 47.13±0.50** 12h after induction 47.52±0.46* * Gastric mucosal end tidal CO2 partial Baseline 9.49± ± ±0.44 pressure difference (mmhg) 2h after induction 11.06±0.68*** 11.25±0.46*** 10.33±0.77*** 4h after induction 12.01±0.52*** 11.85±0.55*** 11.26±0.53*** 6h after induction 13.15±0.63*** 13.06±0.59* ** 11.95±0.78*** 8h after induction 13.55±0.59*** 12.81±0.77*** 10h after induction 14.20E1.41*** 13.46±0.72*** 12h after induction 14.19±0.52*** *p<0.05 **p<0.01 ***p<0.001 Table (3): Changes in gastric intra-mucosal ph and arterial lactate concentration (mg/dl) with time in the three investigated groups. Parameters GI G H G In Gastric intra-mucosal ph Baseline 7.43± ± ±0.03 2h after induction 7. 41±0.04* 7.43±0.02* 7.41±0.05* 4h after induction 7. 40±0.03* 7.40±0.03* 7.39±0.04* 6h after induction 7.38±0.02* 7.39±0.02* 7.40±0.03* 8h after induction 7.37±0.01 * 7.38±0.03 * 10h after induction 7.36±0.02* 7.37±0.02* 12h after induction 7.35±0.03 * Arterial lactate concentration (mg/dl) Baseline 4.63± ± ±0.11 2h after induction 5.67±0.25*** 5.64±0.26*** 5.67±0.25*** 4h after induction 6.92±0.31*** 6.98±0.22*** 6.82±0.40*** 6h after induction 8.12E1.24*** 8.21E1.24*** 8.04±0.44*** 8h after induction 9.48±0.25*** 9.21±0.25*** 10h after induction 10.50±0.26*** 10.36±0.24*** 12h after induction 11.70±0.27*** *p<0.05 **p<0.01 ***p<0.001

5 Ragaa A.A.M. Herdan, et al. 363 Group 1 Group 11 ['Group III Baseline 2 hr after 4 hr after 6 hr after 8 hr after 10 hr after 12 hr after induction induction induction induction induction induction Fig. (1): Changes in gastric mucosal end-tidal CO2 partial pressur difference with time in the three groups (PgCO2-PetCo2). Discussion The present study investigated the effects of prolonged anesthesia on gastric mucosal tonometric values compared to commonly measure global indices of splanchnic hypoperfusion. The results demonstrated that prolonged anesthesia decreased insignificantly the HR and MAP in the three investigated groups during all periods of the study as compared with the baseline values measured directly after induction of anesthesia. The decrease was found to be mostly progressive with time as the patients were subjected to more myocardial depression due to prolonged use of anesthetics (isoflurane and fentanyl). However, mean values of HR and MAP were satisfactory and lie within its normal range. Patients who showed persistent fall in MAP and/or HR more than 20% of the baseline values were treated with rapid I.V. Infusion of lactate free crystalloid solutions and/or atropine injection. The decrease in HR might result in decrease in cardiac output and visceral perfusion. It is possible that cardio-respiratory variables greater than normal levels are necessary for perfusion of gastric mucosa during surgery. This is in accordance with Stephen's et al., study (2003) which considered the traditional methods of monitoring as HR and MAP are inadequate. They added that measurement of CVP, CI, oxygen transport variables; arterial blood gases and serum lactate assess global perfusion and would not identify localized peripheral organ hypoperfusion [8]. Tissue oxygenation in our study was assessed indirectly by measuring tonometric parameters including gastric intramucosal CO2 tension which was elevated in the three groups throughout the intraoperative period. We explained that as the regional PCO2 measured by tonometry simply reflect the balance between the metabolic production of CO2 in the tissue and the transport of CO2 away from the tissue by circulation, and it is affected inevitably by arterial CO2 tension. Because mucosal PCO2 gradually accumulates due to a stagnant blood flow or increased anaerobic metabolism, an increase in luminal PCO2 can be observed. Thus, the increase of the PgCO2 can be related to decrease gastric blood flow with normal aerobic metabolism or to beginning of anaerobic production of CO2 [9]. In our study, the mean value of P02 was significantly increased with time in the three groups. This means that global oxygen delivery increased all over the time of the operations. Thus, the increase in PgCO2 was most probably related to the decreased gastric blood flow and not to the beginning of anaerobic metabolism. Because the PgCO2 is influenced directly by abnormalities of systemic arterial PCO2, other factors, such as hypoventilation or disturbance in the systemic acid-base balance, must be considered in the interpretation of high PaCO2. In our study, we fixed the ventilation parameters to exclude the effects of hypoventilation on arterial PCO2. Also, we maintained standard intravascular volume to maintain the systemic acid-base balance. Therefore, calculation of P (g-a) CO2 is considered the most specific variable for detection of gastric mucosal hypoperfusion and ischemia. A CO2 gap between 8mmHg (normal) and 18mmHg therefore suggests a redistribution of flow, calling for therapeutic intervention [1 0]. In the present study, we found that PetCO2 accurately represented arterial PCO2 and can be used instead of it. So, an alternative to the mucosal-to-arterial CO2 difference (PgCO2-PaCO2) is to relate PgCO2 to end-tidal PCO2 (PgCO2-PetCO2). This difference may be used as a useful index of GI perfusion in critically ill patients 1111 or in high-risk surgery [121. A gap of 21 to 25mmHg is associated with organ failure together with a prolonged need for critical care

6 364 Gastric Mucosal End-Tidal Carbon Dioxide and hospital stay [13 ]. As end-tidal PCO2 is a function of arterial PCO2, the gradient between PetCO2 and PgCO2 may reflect mucosal perfusion. In the present study, we found a significant difference in the PgCO2-PetCO2 gap mean values inside each of the three studied groups as compared with the baseline values. These values tended to increase gradually with time and approach the maximum level of normality especially at 10 and 12 hr in group II and III. Our patients' lungs were ventilated mechanically using an unchanged ventilatory settings to keep PetCO2 of 35-40mmHg to exclude the effects of hypoventilation on the arterial PCO2. So we considered the increase in PgCO2 was the cause of increasing the PgCO2-PetCO2 difference. Gilles Lebuffe and colleagues (2004) used the gastric tonometry in their study on 290 patients to assess the value of PgCO2-PetCO2 gap in predicting postoperative complications in surgery of more than 2 hr duration. They concluded that PgCO2- PetCO2 gap is the best predictor of increasing probability of postoperative functional recovery delay and they suggested the use of gastric tonometry as a monitor of GI perfusion in high risk surgical patients and an intraoperative predictor for poor outcome [14]. Another study by Uusaro et al., demonstrated that PgCO2-PetCO2 gap was an early indicator of splanchnic hypoperfusion [15]. The CO2 gap is a better marker than phi for the adequacy of GI mucosal perfusion, as it is independent of systemic, metabolic and respiratory alterations in acid base balance [16]. In our study, calculation of the gastric phi using Henderson- Hasselbalch equation showed a statistically significant gradual decrease in the mean values of the gastric phi over time. The decrease reached its maximum values at 12 hr in group III. PHi parallels the changes in the gastric and end tidal CO2 difference. So, gastric phi may be used as a marker of the adequacy of GI mucosal perfusion as CO2 gap. Satoshi et al., (2000) hypothesized that reduced blood volume is a major contributor to the postoperative decrease in phi in patients of coronary artery bypass grafting (CABG) [17]. Robert and co-workers (2002) demonstrated that low phi (phi-7.3) and increased PgCO2-PaCO2 difference (>10mmHg) as significant markers of tissue hypoperfusion in patients after cardiac surgery [18]. Dugas and colleagues' (2000); found a good correlation between regional markers of tissue hypoperfusion (phi and PCO2 gap) and metabolic markers (lactate and L/P ratio) [19]. Those results are in agreement with the present study results. Duke and co-workers' study (1997) concluded that (phi and PCO2 gap) can predict survival better than (pha, blood lactate level and base deficit) [20]. In our study, arterial lactate concentration increased significantly with time inside each group. We attributed the hyperlactatemia not only due to increased tissue production of lactate related to dysoxia; but also due to impaired utilization and excretion of lactate caused by liver and renal tissues under perfusion. Heitor et al., (2000) demonstrated concurrent increase of arterial blood lactate with increased gastric PCO2 during hemorrhagic shock [21]. General recommendations for the use of lactate is to follow trends rather than a single measurement as time is a factor when considering lactate level and for prolonged anesthesia patients, the longer the lactate is elevated, the more incidence of MODS and mortality. Also to first rule out causes of tissue hypoxia before assuming that other factors are contributing to the increased lactate levels is essential [22]. In conclusion: Prolonged general anesthesia produced GI hypoperfusion manifested by increased PgCO2, PgCO2-PetCO2 gap and decreased phi despite maintaining 02 delivery which was manifested by increased Pa02. 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