Gastric intramural PCO2 during peritonitis and shock

Area of Science:

• Critical care medicine
• Gastroenterology
• Physiology

Background:

• Peritonitis with circulatory shock presents a complex physiological challenge.
• Understanding gastric intramural acid-base balance is crucial for monitoring shock.
• Previous studies linked hemorrhagic shock to early gastric CO2 and H+ increases.

Purpose of the Study:

• To investigate gastric intramural CO2 and H+ changes in experimentally induced peritonitis with circulatory shock.
• To compare these changes with those observed in hemorrhagic shock and cardiac arrest.

Main Methods:

• Peritonitis was induced in Sprague-Dawley rats via cecal ligation and fecal spillage.
• Hemodynamic parameters (mean aortic pressure, cardiac index) were monitored.
• Gastric intramural [H+], PCO2, arterial blood lactate, and central venous oxygen saturation were measured.

Main Results:

• A significant increase in gastric intramural [H+] (from 34 to 217 mmol/L) and arterial lactate (from 0.9 to 4.6 mmol/L) was observed.
• A delayed increase in gastric intramural PCO2 (from 45 to 128 mm Hg) occurred.
• Hemodynamic parameters showed a progressive reduction in mean aortic pressure and cardiac index.

Conclusions:

• Gastric intramural [H+] increased prominently, but PCO2 rose only late in peritonitis-induced shock, differing from hemorrhagic shock.
• Arterial blood lactate and central venous oxygen saturation were earlier indicators of perfusion failure.
• Gastric wall bicarbonate concentration differs from arterial blood, impacting gastric tonometry clinical methods.