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Updated: Aug 14, 2026

Expired CO2 Measurement in Intubated or Spontaneously Breathing Patients from the Emergency Department
Published on: January 29, 2011
Abdominal insufflation with CO2 causes peritoneal acidosis independent of systemic pH
Eric J Hanly1, Alexander R Aurora, Joseph M Fuentes
1Department of Surgery, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Abstract:
We have shown that the inflammation-attenuating effects of CO(2) pneumoperitoneum during laparoscopy are not due to changes in systemic pH. However, acidification of peritoneal macrophages in an in vitro CO(2) environment has been shown to reduce LPS-mediated cytokine release. We tested the hypothesis that the peritoneum is locally acidotic during abdominal insufflation with CO(2)--even when systemic pH is corrected. Rats (n = 20) were anesthetized and randomized into two groups: continued spontaneous ventilation (SV) or intubation and mechanical ventilation (MV). All animals were then subjected to abdominal insufflation with CO(2). Mean arterial pH among SV rats decreased significantly from baseline after 15 and 30 minutes of CO(2) pneumoperitoneum (7.329 --> 7.210 --> 7.191, P < 0.05), while arterial pH among MV rats remained relatively constant (7.388 --> 7.245 --> 7.316, P = NS). In contrast, peritoneal pH dropped significantly from baseline and remained low for both groups during CO(2) abdominal insufflation (SV 6.74 --> 6.41 --> 6.40, P < 0.05; MV 6.94 --> 6.45 --> 6.45, P < 0.05). In a second experiment, rats (n = 10) were randomized to receive abdominal insufflation with either CO(2) or helium. Abdominal insufflation with helium did not significantly affect peritoneal pH (7.10 --> 7.02 --> 6.95, P = NS), and the decrease in pH among CO(2)-insufflated animals was significant compared with helium-insufflated animals (P < 0.05). Peritoneal pH returned to baseline levels in all groups within 15 minutes of desufflation in both experiments. A significant local peritoneal acidosis occurs during laparoscopy which is specifically attributable to the use of CO(2) and which is independent of systemic pH. These data provide additional evidence that localized peritoneal acidosis is central to the mechanism of CO(2)-mediated attenuation of the inflammatory response following laparoscopic surgery.
Insights
Carbon dioxide (CO(2)) insufflation during laparoscopy causes local peritoneal acidosis, independent of systemic pH changes. This localized acidosis is key to CO(2)
Area of Science:
- Physiology
- Surgical Innovation
- Inflammation Research
Background:
- Laparoscopic surgery utilizes carbon dioxide (CO(2)) insufflation, leading to observed anti-inflammatory effects.
- Previous research suggested systemic pH changes were responsible for these effects, but this has been disputed.
- In vitro studies indicated that localized acidification might reduce inflammatory responses.
Purpose of the Study:
- To investigate whether peritoneal acidosis occurs during CO(2) pneumoperitoneum in vivo, independent of systemic pH.
- To determine if CO(2) is the specific cause of peritoneal acidosis during laparoscopy.
Main Methods:
- Rats underwent CO(2) abdominal insufflation under either spontaneous ventilation (SV) or mechanical ventilation (MV) to assess systemic and peritoneal pH.
- A second experiment compared peritoneal pH changes during CO(2) versus helium insufflation.
- Peritoneal and arterial pH were measured at baseline and during insufflation.
Main Results:
- CO(2) insufflation caused a significant drop in peritoneal pH in both SV and MV groups, while arterial pH decreased significantly only in the SV group.
- Mechanical ventilation helped maintain stable arterial pH but did not prevent peritoneal acidosis.
- Helium insufflation did not induce significant peritoneal acidosis, unlike CO(2).
Conclusions:
- A localized peritoneal acidosis occurs during CO(2) pneumoperitoneum in laparoscopy.
- This acidosis is specifically caused by CO(2) and is independent of systemic pH.
- Localized peritoneal acidosis is a critical factor in the anti-inflammatory mechanisms of CO(2) during laparoscopic surgery.
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