Secondary Logo

Journal Logo

Clinical Cardiovascular

Gastric Intramucosal Perfusion during Descending Aortic Repair under Femoro-Femoral Bypass

Tachibana, Kaori; Hisano, Kenjiro; Sakuraya, Fumika; Tang, Sijian; Shiiya, Norihiko; Hashimoto, Toshikazu; Takita, Koichi; Morimoto, Yuji

Author Information
doi: 10.1097/01.mat.0000195284.91336.ff
  • Free


Surgery for descending aortic aneurysms involves a high risk of postoperative complications such as spinal injury and visceral organ injury.1,2 The simple clamping of the aorta during repair of descending aneurysms leads to profound homeostatic disturbances in nearly all organ systems in the body.2 Extracorporeal distal aortic perfusion during aortic cross-clamping provides perfusion to the renal, mesenteric, and spinal cord regions, which serves to minimize ischemic complications compared with simple cross-clamping.3

Options for distal aortic perfusion techniques include left atrial-femoral bypass, prior axillo-femoral bypass and femoro-femoral cardiopulmonary bypass (F-F bypass).3 F-F bypass is one of the most commonly used techniques because it provides several advantages over other bypass techniques, i.e., improved exposure of operative fields, easy insertion of the cannula, improved myocardial protection, and versatility to allow conversion to total cardiopulmonary bypass (CPB).3,4

Although distal aortic perfusion with F-F bypass provides perfusion to visceral vessels during aortic cross-clamping and reduces the postoperative visceral dysfunction,1 its impact on visceral mucosal perfusion has been unclear. Generally, CPB with nonpulsatile pump flow can result in the reduction of gastric mucosal perfusion and oxygenation during and/or after CPB.5,6 The partial CPB flow by F-F bypass might have disadvantages in gastric mucosal perfusion.

Gastric tonometry, which directly reflects the gastric intramucosal PCO2 (PgCO2) and pH (pHi), has been regarded as a minimally invasive modality to estimate the visceral mucosal perfusion or, more precisely, mucosal oxygenation.7–9 Recently, air-automated tonometry (Tonocap, Datex, Helsinki, Finland) was proven to be a useful adjunct for evaluation of gastric mucosal perfusion during CPB.10 In this study, we evaluated gastric mucosal perfusion during F-F bypass by using air-automated tonometry.

Materials and Methods

After obtaining institutional review board approval and informed consent, six patients undergoing repair for descending aortic aneurysm under F-F bypass were enrolled in a prospective study. Patient characteristics are listed in Table 1.

Table 1
Table 1:
Patient Demographics (n = 6)

Patients received no premedication. Anesthesia was induced with 100–200 μg fentanyl and 100–200 mg propofol followed by 0.1 mg/kg vecuronium. During the surgery, anesthesia was maintained with a combination of fentanyl and sevoflurane. Patients were intubated using a double-lumen endotracheal tube and mechanically ventilated to maintain PaCO2 at 40 to 45 mm Hg throughout the surgery. Operations were performed with right lung ventilation and left lung collapse.

All patients received proximal aortic cross-clamps placed just distal to the left subclavian artery and distal to the mid-descending aorta above the celiac axis. The catheters for distal aortic perfusion were placed in the left common femoral artery and vein. After a left groin incision, a femoral arterial cannula was placed and directed proximally into the iliac artery. A femoral venous cannula was passed under echocardiographic guidance over the guidewire into the right atrium. F-F bypass was conducted using a membrane oxygenator and a centrifugal pump. Pump flow was maintained between 1.6 and 3.0 l/min/m2, and mean arterial pressure was adjusted to between 60 and 90 mm Hg. Body temperature was assessed by urinary bladder temperature and kept at 34°C during aortic cross-clamping. Femoral arterial blood gas was regulated by alpha-stat methods and PaCO2 was adjusted to 40 mm Hg using a membrane oxygenator. The fraction of inspired oxygen of the membrane oxygenator was 0.8 during F-F bypass. In all patients, visceral and lower extremity vessels were perfused with F-F bypass.

Gastric mucosal PCO2 (PgCO2) was measured using a standard tonometry oro-gastric tube (TRIP, NGS catheter, Tonometrics, Helsinki, Finland) connected to an automated gas analyzer (Tonocap, Datex, Helsinki, Finland). The correct position of the tonometer was confirmed by chest x-ray. Gastric air and juice were completely aspirated to ensure good mucosal/balloon equilibration. The air, which is inflated by the Tonocap into the balloon on the tip of the tonometer, calibrates within 15 minutes through the semipermeable silicone.

The value of pHi was calculated by inserting the PgCO2 and arterial carbonate concentration into a modified Henderson Hasselbalch equation: pHi = 6.1 + log10 (arterial [HCO3]/PgCO2).11 PCO2 gap was obtained as follows: PgCO2 – PaCO2. Data were recorded at the following five points: just before initiating F-F bypass (pre F-F), 30 minutes after starting F-F bypass (F-F 30 min), just before the end of F-F bypass (end of F-F), 30 minutes after the end of F-F bypass (post F-F 30 min), and at the end of surgery (surgery end). Arterial pH (pHa), base excess, and serum lactate were also recorded to evaluate the status of systemic metabolic acidosis.

The perioperative hepatorenal functions were also analyzed to estimate the postoperative impact of distal aortic perfusion on visceral function. Aspartate aminotransferase, alanine aminotransferase, serum total bilirubin, blood urea nitrogen, and serum creatinine at the baseline (presurgery), first postoperative day (1 POD), 3rd postoperative day (3 POD) and 1 week after surgery (7 POD) were measured.


Data are presented as means and standard deviations and were analyzed by using one-way analysis of variance followed by Scheffe test. Differences were considered statistically significant at p < 0.05.


The average period of F-F bypass was 104.3 ± 58.5 minutes. Pump flow was 2.2 ± 0.6 l/min/m2 and 2.2 ± 0.9 l/min/m2 at F-F 30 min and at end of F-F, respectively. Mean arterial pressures at the femoral artery were 82.3 ± 13.7 mm Hg at F-F 30 min and 69.5 ± 15.0 mm Hg at end of F-F.

The PCO2 gap significantly increased during F-F bypass (3.0 ± 2.1 mm Hg at pre F-F, 14.2 ± 5.5 mm Hg at F-F 30 min, and 8.0 ± 1.41 at end of F-F; p = 0.004 and 0.007 vs. pre F-F, respectively; see Figure 1). The pHi did not alter during F-F bypass but was significantly low after the weaning from F-F bypass (7.35 ± 0.05 at pre F-F and 7.21 ± 0.10 at post F-F 30 min; p = 0.009) (Figure 2). The PCO2 gap recovered to the presurgical level at the end of surgery (5.8 ± 2.7 mm Hg at surgery end), although pHi remained acidotic (7.31 ± 0.03 at surgery end). Systemic metabolic acidosis progressed after F-F bypass (at post F-F 30 min; p = 0.012, Table 2.). The hospital stay of patients was 40 ± 12 days. No remarkable postoperative hepatorenal impairment was observed in any patient (1, 3 and 7 PODs; Table 3).

Figure 1.
Figure 1.:
Changes in PCO2 gap during F-F bypass. Pre F-F, just before initiating F-F bypass; F-F 30 min, 30 min after establishing F-F bypass; end of F-F, just before the end of F-F bypass; post F-F 10 min, 10 min after F-F bypass weaning; post F-F 30 min, 30 min after F-F bypass weaning; surgery end, end of surgery. *p < 0.05 vs. pre F-F bypass.
Figure 2.
Figure 2.:
Changes in gastric intramucosal pH (pHi) during F-F bypass. *p < 0.05 vs. pre F-F bypass.
Table 2
Table 2:
Perioperative Hemodynamic Changes
Table 3
Table 3:
Perioperative Hepatorenal Function Variables


In this study, a high PCO2 gap was detected during F-F bypass. The PCO2 gap has been considered to be a good marker of mucosal perfusion that can exclude the effect of the systemic metabolic acidosis or ventilation like the value of pHi.9,12 Thus, a high PCO2 gap during F-F bypass could suggest low gastric tissue perfusion and oxygenation.

Absence of pulsatile flow can influence the mucosal perfusion during CPB.5 Nonpulsatile flow with CPB can decrease the energy delivery into the vascular systems, impairing the capillary patency. Thus, gut mucosal permeability increases under CPB,13–15 resulting in the distribution of blood flow away from the mucosa. Indeed, gut mucosal hypoperfusion has been observed during and after CPB despite adequate blood flow to the visceral vessels.13,16,17 In addition, increased oxygen consumption and excessive demand of the body for oxygen have also been detected during and after CPB,13 reflecting the inflammatory reaction due to the CPB in the visceral area.18 Tao et al. report that the decrease in gut mucosal perfusion under CPB results from a combination of redistribution of blood flow away from the mucosa and increased oxygen demand.16 Hypothermia is also recognized as a cause of increased vascular resistance and reduced mucosal perfusion during CPB.14 Accordingly, these factors might have caused the high PCO2 gap and, in turn, low gastric mucosal oxygenation during F-F bypass.

The pHi value did not change during CPB, but decreased after CPB. The pHi variables have been reported to correlate with systemic factors such as metabolic acidosis and ventilation.12 The pHi value, therefore, has been used extensively to assess the patients’ outcomes after surgery.9,19,20 In this study, a significant increase in plasma lactate and decline in base excess proceeded at weaning from F-F bypass, presumably due to the increased oxygen consumption and excessive demands of body on oxygen after CPB.13 These results suggest the progression of systemic metabolic acidosis at the weaning from F-F bypass, which may be associated with the low pHi after F-F bypass.

Gut mucosal hypoperfusion during surgery can induce multiple organ dysfunction syndrome.19 Miller et al. reported that the PCO2 gap for retaining 18 mm Hg was found to be prognostic of multiple organ dysfunction syndrome and death.21 It has also been reported that abnormal low pHi (below 7.25 or 7.35) is associated with increased morbidity and mortality in patients after surgery and in intensive care unit patients.21,22 In this study, the Pco2 gap increased but did not reach the intramucosal acidotic level during F-F bypass, and it was restored to the presurgical level at the end of surgery. The fall in pHi after F-F bypass showed a tendency to recover toward the end of surgery. No significant postoperative hepatorenal dysfunction was found in laboratory data of 7 POD in this study.

Accordingly, F-F bypass could impair gastric mucosal perfusion, but may have little effect on postoperative visceral function. Monitoring of the PCO2 gap by gastric tonometry may be useful for the evaluation of gut mucosal perfusion during F-F bypass for descending aortic repair.


1. Safi HJ, Miller CC, 3rd, Yawn DH, et al: Impact of distal aortic and visceral perfusion on liver function during thoracoabdominal and descending thoracic aortic repair. J Vasc Surg 27: 145–152, 1998.
2. Cooley DA, Golino A, Frazier OH, et al: Single-clamp technique for aneurysms of the descending thoracic aorta: Report of 132 consecutive cases. Eur J Cardiothorac Surg 18: 162–167, 2000.
3. Coady MA, Mitchell RS: Femoro-femoral partial bypass in the treatment of thoracoabdominal aneurysms. Semin Thorac Cardiovasc Surg 15: 340–344, 2003.
4. Hilgenberg AD, Rainer WG, Sadler TR, Jr: Aneurysm of the descending thoracic aorta: replacement with the use of a shunt or bypass. J Thorac Cardiovasc Surg 81: 818–824, 1981.
5. Hamulu A, Atay Y, Yagdi T, et al: Effects of flow types in cardiopulmonary bypass on gastric intramucosal pH. Perfusion 13: 129–135, 1998.
6. Ohri SK, Bowles CT, Siddiqui A, et al: The effect of cardiopulmonary bypass on gastric and colonic mucosal perfusion: A tonometric assessment. Perfusion 9: 101–108, 1994.
7. Cerny V, Cvachovec K: Gastric tonometry and intramucosal pH–theoretical principles and clinical application. Physiol Res 49: 289–297, 2000.
8. Gutierrez G, Palizas F, Doglio G, et al: Gastric intramucosal pH as a therapeutic index of tissue oxygenation in critically ill patients. Lancet 339: 195–199, 1992.
9. Kolkman JJ, Otte JA, Groeneveld AB: Gastrointestinal luminal PCO2 tonometry: An update on physiology, methodology and clinical applications. Br J Anaesth 84: 74–86, 2000.
10. Masai T, Taniguchi K, Kuki S, et al: Usefulness of continuous air tonometry for evaluation of splanchnic perfusion during cardiopulmonary bypass. ASAIO J 49: 108–111, 2003.
11. Maynard N, Bihari D, Beale R, et al: Assessment of splanchnic oxygenation by gastric tonometry in patients with acute circulatory failure. JAMA 270: 1203–1210, 1993.
12. Uusaro A, Russell JA, Walley KR, Takala J: Gastric-arterial PCO2 gradient does not reflect systemic and splanchnic hemodynamics or oxygen transport after cardiac surgery. Shock 14: 13–17, 2000.
13. Braun JP, Schroeder T, Buehner S, et al: Splanchnic oxygen transport, hepatic function and gastrointestinal barrier after normothermic cardiopulmonary bypass. Acta Anaesthesiol Scand 48: 697–703, 2004.
14. Ohri SK, Bjarnason I, Pathi V, et al: Cardiopulmonary bypass impairs small intestinal transport and increases gut permeability. Ann Thorac Surg 55: 1080–1086, 1993.
15. Sinclair DG, Haslam PL, Quinlan GJ, et al: The effect of cardiopulmonary bypass on intestinal and pulmonary endothelial permeability. Chest 108: 718–724, 1995.
16. Tao W, Zwischenberger JB, Nguyen TT, et al: Gut mucosal ischemia during normothermic cardiopulmonary bypass results from blood flow redistribution and increased oxygen demand. J Thorac Cardiovasc Surg 110: 819–828, 1995.
17. Sicsic JC, Duranteau J, Corbineau H, et al: Gastric mucosal oxygen delivery decreases during cardiopulmonary bypass despite constant systemic oxygen delivery. Anesth Analg 86: 455–460, 1998.
18. Doguet F, Litzler PY, Tamion F, et al: Changes in mesenteric vascular reactivity and inflammatory response after cardiopulmonary bypass in a rat model. Ann Thorac Surg 77: 2130–2137, 2004.
19. Mythen MG, Purdy G, Mackie IJ, et al: Postoperative multiple organ dysfunction syndrome associated with gut mucosal hypoperfusion, increased neutrophil degranulation and C1-esterase inhibitor depletion. Br J Anaesth 71: 858–863, 1993.
20. Theodoropoulos G, Lloyd LR, Cousins G, Pieper D: Intraoperative and early postoperative gastric intramucosal pH predicts morbidity and mortality after major abdominal surgery. Am Surg 67: 303–308, 2001.
21. Miller PR, Kincaid EH, Meredith JW, Chang MC: Threshold values of intramucosal pH and mucosal-arterial CO2 gap during shock resuscitation. J Trauma 45: 868–872, 1998.
22. Perez A, Schnitzler EJ, Minces PJ: The value of gastric intramucosal pH in the postoperative period of cardiac surgery in pediatric patients. Crit Care Med 28: 1585–1589, 2000.
Copyright © 2006 by the American Society for Artificial Internal Organs