ASSESSMENT OF SPLANCHNIC PERFUSION DURING CARDIOPULMONARY BYPASS BY CONTINUOUS GASTRIC TONOMETRY AND TRANSESOPHAGEAL ECHOCARDIOGRAPHY

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1 ASSESSMENT OF SPLANCHNIC PERFUSION DURING CARDIOPULMONARY BYPASS BY CONTINUOUS GASTRIC TONOMETRY AND TRANSESOPHAGEAL ECHOCARDIOGRAPHY Fawzia A. Fetouh, MD. Osama M. Asaad, MD. Ahmed E. El-Agaty, MD. Wael H. El-Siory, MD. From departments of anesthesia, Faculty of Medicine, Cairo University, Egypt Address of correspondence: Fawzia A. Fetouh, MD, Tel.: , address: Backgroumd: Abdominal complications after cardiac surgery while relatively uncommon are associated with a significant mortality. Perioperative splanchnic ischemia appears to be an important cause of these complications. The aim of this study was to evaluate the effects of normothermic cardiopulmonary bypass (CPB) on splanchnic blood flow using Transesophageal echocardiography (TEE) Doppler-measured superior mesenteric artery blood flow and continuous gastric tonometry during coronary artery bypass graft surgery (CABG). Methods: Twenty patients undergoing elective on-pump CABG were included in that Single-arm prospective observational study. Superior mesenteric artery blood flow (SMA-BF) was measured with duplex ultrasound using TEE probe, while gastric mucosal perfusion was assessed using continuous gastric tonometry during CABG surgery under normothermic (>35 C) CPB. Measurements were made six times: T1 (after induction of anesthesia), T2 (after initiation of CPB), T3 (30 min on bypass), T4 (60 min on bypass), T5 (5 min after weaning from CPB), T6 (end of surgery). Also blood samples were collected for arterial blood lactate levels. Results: SMA-BF showed a highly significant decrease from baseline value (p value < 0.01) after initiation of CPB (T2) till its end (T4) and increased shortly after bypass then decreased again significantly below baseline at the end of surgery (T6). While gastric mucosal CO 2 gap (Pg-aCO 2 gap) showed a highly significant increase from baseline value (p value < 0.01) 30 minutes after CPB initiation (T3) then 5 minutes after weaning from CPB (T5) and at the end of surgery (T6), however no correlation was found between both variables. Conclusion: This study showed that normothermic CPB is associated with a significant reduction of both SMA-BF and gastric mucosal blood flow, however the splanchnic blood flow reduction alone cannot account for mucosal ischemia which may even become worse when blood flow is restored. Transesophageal echo-doppler allows the intraoperative measurement of blood flow distribution to splanchnic viscera and may be considered a reliable tool specially when coupled with arterial lactate measurement and gastric tonometry to expect which patients well develop splanchnic ischemia during CPB. KEY WORDS: gastric tonometry, transesophageal echocardiography, cardiac surgery, splanchnic perfusion

2 Introduction: Splanchnic hypoperfusion is a common finding in patients undergoing cardiopulmonary bypass (CPB). Although overt injury of the intra-abdominal organs after cardiac surgery is relatively uncommon, they are associated with a high mortality. Splanchnic ischemia perioperatively appears to be an important cause of these complications. In addition, splanchnic ischemia is hypothesized to be one cause of the systemic inflammatory response syndrome and multiorgan failure that may follow cardiac surgery through damage of the mucosal barrier, allowing gut translocation of endotoxin stimulating the inflammatory response to cardiac surgery. 1, 2 Several methods can be used to measure splanchnic blood flow (SBF), but not all are applicable for human studies. The indicator dilution technique using constant-rate infusion of the dye indocyanine green (ICG) has evolved as a gold standard, but it requires hepatic vein catheterization for the determination of hepatic ICG extraction. 3 Gastric tonometry determines the perfusion status of the gastric mucosa by measuring local carbon dioxide tension (PgCO 2 ). The monitor automatically fills the catheter with 4 ml of room air, CO 2 diffuses from the mucosa into the lumen of the stomach and then into the silicone balloon of the tonometer. The balloon gas is drawn after equilibration with gastric mucosa and measured with an infrared sensor. The measured PCO 2 reflects gastric intramucosal CO 2. Gastric mucosal CO 2 and the CO 2 gap (difference between gastric mucosal CO 2 and arterial CO 2 ) have been shown to reflect gastric mucosal perfusion. 4 Visualization of major abdominal arteries and main hepatic veins by transesophageal echocardiography (TEE) has been reported, allowing intraoperative assessment of splanchnic hemodynamics. However, the impact of TEEmeasured superior mesenteric artery blood flow (SMA-BF), on mucosal perfusion is still ill-defined and under investigated. 5, 6 The aim of this study was to measure splanchnic blood flow during CPB employing TEE-Doppler measured SMA-BF, and to study gastric tonometry data simultaneously in the same patients; to assess the impact of splanchnic as well as systemic hemodynamic changes on gastric mucosal perfusion during on-pump coronary artery bypass graft (CABG) procedure. Methods: After obtaining ethics Committee approval and written informed consent from each patient, 20 patients underwent elective on-pump CABG surgery and completed the study after they satisfied inclusion and exclusion criteria. The study was conducted in cardiac surgical unite in Kasr El- Aini hospital. Exclusion criteria included Gastrointestinal (GIT) diseases contraindicated for placement of TEE probe (i.e. Esophageal avarices and upper gastrointestinal bleeding), use of corticosteroids, evolving myocardial infarction (< 7days), preoperative hemodynamic instability, perioperative intraaortic balloon pump use, and failure to visualize properly the SMA by TEE. All preoperative medications were continued preoperatively including the morning of the day of surgery. Ranitidine 50mg/ 8 hours IV was started at the night before surgery and continued for 2 weeks ( switched to 150 mg/ 12 hours oral tablets after discharge from intensive care unit), and 0.1 mg/ kg morphine sulphate was given intramuscularly one hour preoperatively. After reaching the operating theater, the standard monitors were attached to the patients. The Monitor used was (Datex ohmeda D-LCC manufactured by Planar system INC. USA). Induction of anesthesia was performed by using midazolam (0.1 mg/kg), fentanyl (5-10 µg/kg) and pancuronium (0.1 mg/ Kg) to facilitate tracheal intubation. Maintenance of anesthesia was achieved by isoflurane 0.6 to 1.5%. Ventilatory parameters were adjusted to keep PaCO2 between 35 and 44 mmhg. FiO2 was readjusted to maintain PaO2 between 200 and 300 mmhg. Increments boulses of pancuronium (I mg / hour) as well as of fentanyl (2µg/kg) were used to control adequate level of anesthesia and to maintain hemodynamic stability. Following intubation, central venous catheter was inserted, nasopharngyeal temperature and end tidal CO 2 were continuously measured. A nasogastric tonometer catheter (Tonometrics TM - catheter, Tono-16F, Datex-Ohmeda, Instrumentarium corp, Helsinki, Finland) was inserted to measure gastric mucosal partial pressure of carbon dioxide (PgCO 2 ) using continuous gas tonometry (Tonocap, Datex- Ohmeda, Instrumentarium corp, Helsinki, Finland). Correct positioning was assessed by measuring distance to epigastrium before insertion, aspiration of gastric contents and by auscultation

3 Omniplanar TEE-probe (ATL ultrasound Bothell WA, , USA) (connected to General Electric, Vivid 3 echo machine) was prepared and inserted. Heparin sulphate 4 mg/kg was administered prior to CPB and supplemented as needed to maintain an activated clotting time (ACT) of at least 400 sec. CPB was instituted by a roller pump (STOCKERT S3, SORIN GROUP, DEUTSCHLAND, München, Germany) using a membrane oxygenator (MEDTRONIC, USA) and 40-µ arterial line filter with non-pulsatile perfusion (at a flow rate of 2.4 L/min/m 2 ). Antegrade intermittent warm blood cardioplegia was used for myocardial protection. Systemic temperature was allowed to drift to 35 C. Mean arterial pressure was kept at 60 to 80 mmhg with the aid of nitroglycrine or noradrenaline and manipulating pump flow. Anesthesia during cardiopulmonary bypass was maintained using propofol infusion at a rate of 3 mg/ kg/ hr. Heparin sulphate was reversed with a corresponding dose of protamine sulphate at the end of proximal anastomosis. Interventions: 1- Gastric mucosal partial pressure of carbon dioxide (PgCO 2 ) was measured using continuous gas tonometry. Pg-aCO 2 gap was calculated after correcting PaCO 2 to the patient s temperature. 2- SMA-BF was measured by TEE where the probe was advanced into the stomach, with an appropriate rotation and upward flexion applied to keep the image of the aorta on the screen. The superior mesenteric artery (SMA) was then visualized (figure 1, 2 and 3) in two scanning planes. (1) Transversal plane: transducer at 0 degrees; the first tract of the SMA appears at the 1 to 3 o clock position of the aorta. (2) Longitudinal plane: transducer at about 110 degrees to 140 degrees; SMA appears in long axis, with both the first tract, directed anteriorly, and the second tract, directed caudally. The SMA-BF was calculated from the time averaged mean velocity (TAMV, which is the midpoint of the area under the Doppler curve) and vessel diameter (d), according to the formula: SMA-BF (ml/minute) = л (½ d) 2 TAMV 60 Where л = 3.14, d = diameter of the artery. The inner diameter of the SMA (SMA-d) was determined on the real-time B-mode image at the same point of Doppler sampling, with the calipers positioned at the internal surfaces of the vessel wall. 5 Figure (1): SMA in transverse plane. The plus signs show the site of diameter estimation Figure (2): Blood flow estimation in SMA using pulsed wave Doppler after induction of anesthesia. Figure (3): Blood flow estimation in SMA using pulsed wave Doppler during CPB

4 3- Cardiac output (CO) was measured by TEE (before and after CPB) by placing pulsed wave Doppler across the left ventricle outflow tract (LVOT) in a deep transgastric view, to obtain the time velocity integral (VTI). After obtaining the LVOT diameter (d) the cardiac output is calculated by multiplying the VTI times the cross sectional area of the LVOT (assuming a circular shape) times the HR according to the following formula: CO (L/minute) = л (½ d) 2 VTI 60. Where CO = Cardiac output, л = 3.14, d = Diameter of the artery and VTI = Velocity time integral. During CPB, pump flow was considered the CO. 7 Data collection; The hemodynamics; [ Heart rate (HR), mean arterial pressure (MAP), central venous pressure (CVP), cardiac output (CO), systemic vascular resistance (SVR) (calculated using standard formula 8 )], Tonometry data; [PgCO 2 and Pg-aCO 2 gap] and TEE data; [SMA-d, TAMV, SMABF & SMA- BF percentage of CO ], were assessed at: (T1) following induction of anesthesia, (T2) 5 min after initiation of CPB, (T3) 30 minutes during CPB, (T4) 60 minutes during CPB, (T5) Five minutes after weaning from CPB, (T6) at the end of operation. At the previously mentioned time periods, blood samples were also collected for arterial blood lactate levels. Postoperative data; GIT complications, ICU stay and mortality among the study patients were documented. Statistical analysis: Data are expressed as mean ± SD, numbers and ratios as appropriate. Chi-squared (χ ² ) test was used for categorical variables. Intragroup comparison of measured variables was performed using repeated measures analysis of variance (ANOVA) with post hoc Dunnett's test for multiple comparisons against baseline value to further investigate any statistically significant findings. Correlation analysis between various variables in the study was done using Pearson product moment correlation coefficient (r). Statistical analysis was done using computer program SPSS 16.0 for Microsoft Windows (SPSS Inc., Chicago, IL, USA). P value < 0.05 was considered statistically significant. Results: Twenty patients completed the study protocol. Patient s demographic data, risk factors and operative data are summarized in table-1. No patient needed intraoperative inotropic or vasoconstrictor drugs to support hemodynamics. Hemodynamic data changes are shown in table (2). As regard CO, there was a significant decrease from baseline value (p < 0.05) during CPB (T2 till T4 where pump flow was considered the cardiac output) followed by a significant increase from the baseline value only 5 minutes after weaning from CPB (T5) followed by a non significant increase from baseline value at the end of surgery. The sequential changes of serum lactate are shown also in table -2. There was a significant increase in the serum lactate over time (p < 0.01) started 30 min after CPB till end of surgery. Table 1: Demographic data, risk factors and Operative data Parameter Mean ± SD (n=20) Age (years) 57.7±5.17 Sex (Male/Female) 16/4 Height (cm) 172.1±6.2 Weight (Kg) 80.45±13.9 BSA (m2) Ejection fraction 61.65±4.4 Risk factors (no of patients) Hypertension 20 Diabetes mellitus 7 Operative data CPB time (min) 98.1±14.3 Aortic crossclamp time (min) 74.2±11.8 Number of anastomoses 3.15±0.67 Note: Values are presented as mean ± SD and ratio for sex Abbreviations: BSA, body surface area; CPB, cardiopulmonary bypass

5 Table 2: Intra operative hemodynamic data Parameter (n=20) T1 T2 T3 T4 T5 T6 HR (beat/min) 85 ± ±14.5* 94 ± 8 * MAP (mmhg) 85 ± ± 8** 63 ± 7** 61 ± 7 ** 72 ± 5 ** 78 ± 4 * CVP (mmhg) 2.9 ± ± ± 1.5 * CO (L/min) 5.8 ± ± 0.4 * 3.8 ± 0.5 * 3.9 ± 0.6 * 7.1 ± 1.1 * 6.5 ± 1.2 SVR(dyne.sec. cm -5 ) 1160 ± ± ±282* 1280 ± ±137** 936 ±195* Arterial lactate (mmol/l) 0.73 ± ± ± 0.15* 2.6 ± 0.2* 3.2 ± 0.3* 4.1 ± 0.11* Note: Values are presented as mean ± SD, *p < 0.05 vs. baseline, **p < 0.01 vs. baseline Abbreviations: T1, after induction; T2, CPB time = 5 min; T3, CPB time = 30 minutes; T4, CPB time = 60 minutes; T5, 5 minutes after weaning from CPB; T6, end of surgery. HR, Heart rate; MAP, Mean arterial pressure; CVP, Central venous pressure; CO, Cardiac output; SVR, Systemic vascular resistance. SMA-d reduced significantly from baseline 0.75±0.07 cm after induction of anesthesia, to be 0.71±0.09 cm at 60 minutes CPB time (T4) (p < 0.05) and another significant reduction at the end of surgery (T6) to be 0.7±0.08 cm (p < 0.01) (Figure 4). *p < 0.05 vs. baseline, **p < 0.01 vs. baseline Baseline SMA-BF was 637±141 ml/min after induction of anesthesia and showed a highly significant decrease in comparison to baseline to be 437±153 ml/min after initiation of CPB (T2) till its end (T4) (p < 0.01). A moderate increase occurred shortly after bypass (T5) (581±150 ml/min) but still below base line followed by significant decrease below baseline at the end of surgery (T6) (526±97 ml/min) (p < 0.05) (Figure 6). Figure (4): Changes in superior mesenteric artery diameter in the study patients. *p < 0.05 vs. Baseline, **p < 0.01 vs. to baseline TAMV was 24±2.1 cm/sec after induction of anesthesia then decreased significantly to be 16.7±2.7 cm/sec (p < 0.01) after CPB was established (T2) and another significant decrease to be 19.9±7.7 cm/sec (p < 0.05) at 60 minutes CPB time (T4) (Figure 5). Figure (6): Changes in superior mesenteric artery blood flow in the study patients. *p < 0.05 vs. baseline, **p < 0.01 vs. baseline SMA-BF percentage of CO (SMABF/CO) was 11.2±3.2 % after induction of anesthesia and showed significant decreased to reach 8.3±1.9 % after weaning from CPB (T5) and 8.5±2.4 % at the end of surgery (T6) (P value < 0.01) (Figure 7). Figure (5): Changes in time averaged mean velocity in the study patients

6 Pg-aCO2 gap was 7.3±3.2 mmhg after induction of anesthesia, later on, Pg-aCO2 gap showed a significant increase compared to baseline 30 minutes after CPB initiation (T3) then at 5 minutes after weaning from CPB (T5) and finally at the end of surgery (T6) (11.6±1.9, 12±4.7 and 13±5.1 mmhg respectively) (p < 0.01) (Figure 8). Figure (7): Changes in superior mesenteric artery blood flow percentage from cardiac output (SMABF/CO) in the study patients. *p < 0.01 vs. baseline PaCO 2 was 31.6±4.8 mmhg after induction of anesthesia, followed by a significant decrease compared to baseline with initiation of CPB (T2) and at 30 minutes of CPB time (T3) (27.3±6.3 and 26.1±7.8 mmhg, respectively) (p < 0.01). Then it showed a significant increase 5 minutes after weaning from CPB (T5), and at the end of surgery (T6) (36.8±5.5 and 35.5±5.5 mmhg, respectively) (p < 0.01) (Figure 8). Figure (8): Changes in PaCO 2, PgCO2 and Pg-aCO2 in the study patients. *p < 0.01 vs. baseline PgCO 2 was 38.8±3.8 mmhg after induction of anesthesia, then showed a significant decrease compared to baseline with initiation of CPB (T2) (35.3±4.3 mmhg) (p < 0.01), to be followed by a significant increase from baseline, 5 minutes after weaning from CPB (T5) and at the end of surgery (T6) (48.8±3.9 and 48.4±5.3 mmhg, respectively) (p < 0.01) (Figure 8). Correlation analysis showed no significant correlation between Pg-aCO 2 gap and SMA-BF (r = , p = 0.99), but there was positive correlation between CO & SMA-BF (r = 0.794, p = 0.058). There was highly positive correlation between serum lactate and PgCO2 and Pg-aCO2 gap (r = 0.894, p value < 0.01). There were neither postoperative gastrointestinal complications nor postoperative mortality among the study patients. The mean postoperative ICU stay was 2 ± 0.67 days. Discussion: This study examined the adequacy of gut blood flow and oxygenation during normothermic CPB by measuring the SMA-BF and its relationship to gastric mucosal CO 2 gap intraoperatively using TEE and continuous gastric tonometry. The results of the current study demonstrated that; SMA-BF exhibited a statistically significant decrease from baseline value during the whole CPB period and at the end of surgery and gastric mucosal CO 2 gap showed a statistically significant increase from baseline value during CPB that continued thereafter till the end of surgery. Although abdominal complications are relatively rare after cardiac surgery (2.5% of patients undergoing cardiac surgery), they are associated with a high mortality (about 33% of affected patients), and account directly for nearly 15% of deaths in those patients. Ischemia/reperfusion of the splanchnic organs in the perioperative period appears to be the most important cause of these complications. 1,9,10 Several methods have been advocated for assessment of splanchnic blood flow through measurement of total hepato-splanchnic blood flow by Fick s principle, laser Doppler flowmetry (LDF), and hepatic venous oxygen saturation. Other methods are used for detection of splanchnic ischemia include gastric tonometry, splanchnic lactate extraction, and D-dimer. Of the above methods only few are suitable for routine intra operative use

7 The changes in SMA-BF, in our study, were associated with the changes in systemic hemodynamic variables mainly CO. There was positive correlation between CO & SMA-BF (r=0.794, P=0.058). CO vs SMA-BF reductions were -33%,-37% & -35% vs -32%, -22% & -30% at T3, T4 & T5 respectively. Post bypass, the CO increased by +22% & +20% at T5 & T6 respectively, where the SMA-BF reduction improved to be -9% & -18% at T5 & T6 respectively. Therefore the ratio of SMABF/CO was 11.2±3.2 % after induction of anesthesia and showed highly significant decreased to reach 8.3±1.9 % after weaning from CPB (T5) and 8.5±2.4 % at the end of surgery (T6) (Figure 7). The findings in our study are supported by the work of Tao and his colleagues, 11 who demonstrated that normothermic CPB is associated with decreased gastric mucosal ph despite adequate global perfusion during CPB in pigs. Croughwell and his colleagues, 12 found similarly that CPB regardless of its temperature is associated with a decrease in gastric mucosal ph denoting gastric mucosal ischemia. Similar findings were observed in the study of Okano and 13 colleagues, which documented that hepatosplanchnic oxygenation was better preserved during mild hypothermic than normothermic CPB using hepatic venous oxygen desaturation as a marker of splanchnic ischemia. Also, hepatosplanchnic blood flow was better preserved during mild hypothermic CPB than during normothermic CPB when hepatic venous oxygen saturation was used to monitor hepatosplanchnic blood flow. 14 Velissaris and colleagues, found similarly a significant perioperative gastric intramucosal acidosis after mild hypothermic CPB (35 C). In the study by Braun and his colleagues, 15 his results also agreed that normothermic CPB is associated with significant splanchnic ischemia when splanchnic oxygen consumption and arterial lactate concentrations used to assess splanchnic perfusion. But in contrary to our study, their results showed that splanchnic blood flow measured by ICG constant infusion technique is preserved during normothermic CPB and they concluded that splanchnic blood flow measured by ICG constant infusion technique doesn t correlate with changes in liver functions examined by calculation of lactate uptake, and ICG extraction during normothermic CPB. Abu EL-Fetouh and her colleagues, 16 noted that hepatic blood flow is not reduced significantly during normothermic CPB when TEE of the middle hepatic vein was used in assessment. Visualization of the major branches of the abdominal aorta as well as the hepatic veins by TEE has been reported by many investigators, although technically difficult; the use of TEE to measure flow in the splanchnic vessels is the least invasive method to do so. 17, 18 In some patients, the SMA cannot be visualized by the transesophageal approach, and in others the angle of insonation may be inadequate. In the present study only patients with satisfactory SMA visualization were included. To our knowledge, among previous studies describing splanchnic blood flow during cardiac surgery only one study utilized TEE to measure blood flow in SMA in off-pump CABG by Fiore et al 5 and no previous studies described the use of TEE measured SMA-BF coupled with gastric tonometry and arterial lactate in the same study. The reports of preserved splanchnic blood flow during normothermic CPB in the some studies do not actually contradict with the measured reduction in SMA-BF in the current study as the measured blood flow in the former is the total hepatosplanchnic blood flow where the more developed hepatic autoregulation can mask the final effect of decreased portal vein flow secondary to decreased SMA-BF. An elevated CO 2 gap is considered indicative of an imbalance between gastric perfusion, metabolism, and alveolar ventilation and is believed to be the most accurate reflection of splanchnic ischemia, with a gap of more than 8 mm Hg considered 19, 20 abnormal. The finding of no correlation between gastric mucosal CO 2 gap and SMA-BF changes in our study can be explained by 2 possible causes; (1) Mucosal hypoperfusion is due to blood flow redistribution away from the mucosa as a part of the inflammatory response to CPB, (2) Worsening of mucosal perfusion despite increased SMA-BF can be attributed to a reperfusion injury. 21 However, during CPB (T2, T3 and T4) the relation between both variables was in same direction as splanchnic hypoperfusion. In addition, we think it is important that this might simply be the difference between macrovascular blood flow that is being measured by the TEE assessments of SMA blood flow as opposed to microvascular assessments that are difficult to be assessed. It may simply be that

8 although we have adequate blood flow in the main superior mesenteric artery, at the level of the capillaries, the blood flow can be significantly impaired. Again, there is large heterogeneity exists in blood flow distribution inside the mesenteric vascular bed due to an uneven distribution across the different intestinal wall layers. Accordingly, after cardiac surgery, blood flow in large conductance vessels has been reported to behave differently to microcirculation, so that gastric mucosal ph does not always reflect changes in splanchnic blood flow in cardiac surgical patients 23. In the present study, although, the systemic hemodynamics improved in relation to baseline values at end of surgery (T6) and SMA-BF showed moderate increase occurred shortly after bypass (T5), Pg-aCO2 gap showed a highly significant increase compared to baseline value (7.3±3.2 mmhg) at 5 minutes after weaning from CPB (T5) and finally at the end of surgery (T6) (12±4.7 and 13±5.1 mmhg respectively). Experimentally, a pronounced reactive hyperemia was regularly seen after a sustained reduction of mesenteric arterial flow due to a mechanical occlusion of the SMA. 22. This results agree with our results which showed a remarkable increase of blood flow to the gastrointestinal tract after a hypoperfusion during CPB. At least one study reports a progressive worsening of gastric mucosal acidosis in the immediate postoperative period in patients undergoing OPCAB. 18 Thoren and colleagues, 24 demonstrated that local mucosal perfusion (assessed by laser Doppler flowmetry) did not reflect total splanchnic blood flow in postcardiac surgical patients. Again, Gårdeba and colleagues, 3 documented similar findings, that neither gastric mucosal ph nor CO 2 gap correlated to splanchnic blood flow when measured by both ICG constant infusion technique and TEE of the right hepatic vein. The highly positive correlation between serum lactate and PgCO2 and Pg-aCO2 gap (r = 0.894, P value < 0.01) indicated poor splanchnic perfusion during CPB. Manthous et al, 25 stated that the increased serum lactate concentrations may be a reflection of pyruvate accumulations, this may be secondary to reduced hepatic clearance during or after CPB. However other authors, 26 have found increased intestinal production of lactate during CPB, which may reflect transient intestinal ischemia. The presence of gastric mucosal acidosis (indicated by high PgCO2), coupled with lactic acidemia, suggest that delivery of oxygen to the abdominal organs at the conclusion of cardiopulmonary bypass is insufficient to meet demand. Also, it could be explained on the basis of impaired hepatic lactate metabolism. We suggest that this is more likely the response to a systemic inflammatory process, which is often seen in patients after CPB. A growing proportion of cardiac surgery patients are older and many have concomitant medical problems that can impair their recovery. Useful strategies are needed to reduce the occurrence of splanchnic ischemia in those and other high-risk populations if surgical outcome is to improve in the future. One limitation does exist in this study, is that a post operative follow up in ICU by gastric tonometry wasn t done to detect the postoperative trend of splanchnic perfusion and correlate detected splanchnic ischemia with postoperative abdominal complications.. A challenge is raised to find out the predictive value of these monitors for postoperative abdominal complications after cardiac surgery. In conclusion, this study demonstrated.that normothermic CPB is associated with a significant reduction of both SMA-BF (measured by TEE) and gastric mucosal blood flow (measured by gastric tonometry), however the splanchnic blood flow reduction alone cannot account for mucosal ischemia which may even worse when blood flow is restored. Transesophageal echo-doppler allows the intraoperative detection of relative changes in SBF and may prove to be a useful tool specially when coupled with arterial lactate measurement and gastric tonometry to expect which patients will develop splanchnic ischemia during CPB. Future studies are needed to understand better if any therapeutic intervention could attenuate mesenteric hypoperfusion References: 1. Hessel E. Abdominal organ injury after cardiac surgery. Seminars in Cardiothoracic and Vascular Anesthesia 2004; 8(3): Warltier D. The Systemic Inflammatory Response to Cardiac Surgery: Implications for the Anesthesiologist. Anesthesiology 2002; 97(1): Gårdeba M, Settergren G, Brodin L. Splanchnic blood flow and oxygen uptake during

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