Does enteral feeding potentially alter the PCO₂ gap and pHi?

Introduction

Measurement of pHi or the mucosal-arterial PCO₂ gap is advocated to detect splanchnic ischaemia and covert shock. Nasogastric feeding may significantly affect these measurements. We used a previously described animal model [1] to evaluate the effect of enteral feeds on the luminal PCO₂ response to intermittent splanchnic ischaemia.

Methods

Adult male Wistar rats (285-425 g) were anaesthetised with sodium pentobarbitone 60 mg/kg i.p. and ventilated with 100% oxygen and isoflurane via tracheostomy to a PaCO₂ of 30-40 torr. Distal aortic pressure was monitored continuously. A sensor (Paratrend 7, Diametrix Medical Inc., Bucks, UK) was inserted into the ileal lumen to record PCO₂ measurements every 2 s, Four rats received no feeds (controls) whilst in another four rats an ileal cannula was inserted and feed (Nutrison, Nutricia, Zoetermeer, Holland) infused at 3 ml/h. In each rat, five two-minute episodes of aortic hypotension were induced to a mean pressure of 30 mmHg by intermittent elevation of a silk sling placed around the proximal aorta.

Results

See Table. Feeds significantly elevated the mean baseline luminal PCO₂ and delayed and blunted the PCO₂ increases (∆PCO₂) in response to transient ischaemia.

Conclusion

Assuming no differences in PaCO₂ in both groups, the data suggest that enteral feeding increases the baseline mucosal-arterial PCO₂ gap and reduces baseline pHi. It may also impair the detection of splanchnic ischaemia by delaying and blunting the responses of these indices to reduced mucosal perfusion.

Table Table