OBJECTIVE: Demonstrate the effect that increased intra-abdominal pressure (IAP) has on visceral oxygen delivery and bowel tissue oxygenation (TPO2). METHODS: Six Duroch swine underwent abdominal insufflation with helium to pressures of 15 and 25 mm Hg for 1 hour. Animals were instrumented with a pulmonary artery flotation catheter to measure cardiac output and calculate systemic oxygen delivery. Fluorescence quenching optodes were implanted in the terminal ileum and the subcutaneous tissue of an axillary fold to measure bowel and systemic (control) tissue oxygen levels, respectively. RESULTS: Bowel tissue oxygen fell from 43 +/- 12 mm Hg at baseline to 31 +/- 12 mm Hg, with 15 mm Hg of abdominal pressure at 60 minutes. With 25 mm Hg IAP, bowel TPO2 fell from 24 +/- 12 to 12 +/- 8 mm Hg (p < 0.02). No change in axillary TPO2 was observed during either period of increased IAP. Cardiac output (CO), systemic oxygen delivery, and mixed-venous oxygen saturation (Svo2) also declined, although blood pressure and oxygen consumption remained constant. CONCLUSIONS: Increased IAP produces significant decreases in bowel submucosal TPO2 without similar changes in extra-abdominal (subcutaneous) TPO2. This decline is dependent on the extent and duration of the elevation in IAP. Readily accessible parameters, such as CO and Svo2, also decline with increased IAP and may be useful variables to monitor as relative indicators of bowel hypoperfusion and TPO2.
OBJECTIVE: Demonstrate the effect that increased intra-abdominal pressure (IAP) has on visceral oxygen delivery and bowel tissue oxygenation (TPO2). METHODS: Six Duroch swine underwent abdominal insufflation with helium to pressures of 15 and 25 mm Hg for 1 hour. Animals were instrumented with a pulmonary artery flotation catheter to measure cardiac output and calculate systemic oxygen delivery. Fluorescence quenching optodes were implanted in the terminal ileum and the subcutaneous tissue of an axillary fold to measure bowel and systemic (control) tissue oxygen levels, respectively. RESULTS: Bowel tissue oxygen fell from 43 +/- 12 mm Hg at baseline to 31 +/- 12 mm Hg, with 15 mm Hg of abdominal pressure at 60 minutes. With 25 mm Hg IAP, bowel TPO2 fell from 24 +/- 12 to 12 +/- 8 mm Hg (p < 0.02). No change in axillary TPO2 was observed during either period of increased IAP. Cardiac output (CO), systemic oxygen delivery, and mixed-venous oxygen saturation (Svo2) also declined, although blood pressure and oxygen consumption remained constant. CONCLUSIONS: Increased IAP produces significant decreases in bowel submucosalTPO2 without similar changes in extra-abdominal (subcutaneous) TPO2. This decline is dependent on the extent and duration of the elevation in IAP. Readily accessible parameters, such as CO and Svo2, also decline with increased IAP and may be useful variables to monitor as relative indicators of bowel hypoperfusion and TPO2.
Authors: Philippe Esquis; David Consolo; Guy Magnin; Philippe Pointaire; Philippe Moretto; Maria Dolores Ynsa; Jean-Luc Beltramo; Carole Drogoul; Michel Simonet; Laurent Benoit; Patrick Rat; Bruno Chauffert Journal: Ann Surg Date: 2006-07 Impact factor: 12.969
Authors: Adrian B Cresswell; Wayel Jassem; Parthi Srinivasan; Andreas A Prachalias; Elizabeth Sizer; William Burnal; Georg Auzinger; Paolo Muiesan; Mohammed Rela; Nigel D Heaton; Matthew J Bowles; Julia A Wendon Journal: Ann Intensive Care Date: 2012-07-05 Impact factor: 6.925