Research

Urinary bladder partial carbon dioxide tension during hemorrhagic shock and reperfusion: an observational study

Arnaldo Dubin¹ , Mario O Pozo² , Vanina S Kanoore Edul³ , Gastón Murias⁴ , Héctor S Canales⁵ , Marcelo Barán⁶ , Bernardo Maskin⁷ , Gonzalo Ferrara⁸, Mercedes Laporte⁹ and Elisa Estenssoro¹⁰

¹  Medical Director, Intensive Care Unit, Sanatorio Otamendi y Miroli, Buenos Aires, Argentina

²  Staff physician, Intensive Care Unit, Clínicas Bazterrica y Santa Isabel, Buenos Aires, Argentina

³  Research Fellow, Cátedra de Farmacología, Facultad de Ciencias Médicas, Universidad Nacional de La Plata, La Plata, Argentina

⁴  Staff physician, Intensive Care Unit, Clínicas Bazterrica y Santa Isabel, Buenos Aires, Argentina

⁵  Staff physician, Intensive Care Unit, Hospital San Martín de La Plata, Argentina

⁶  Medical Director, Renal Transplantation Unit, CRAI Sur, CUCAIBA, Argentina

⁷  Medical Director, Intensive Care Unit, Hospital Posadas, Buenos Aires, Argentina

⁸  Resident, Intensive Care Unit, Hospital San Martín de La Plata, Argentina

⁹  Medical Director, Clinical Chemistry Laboratory, Hospital San Martín de La Plata, Argentina

¹⁰  Medical Director, Intensive Care Unit, Hospital San Martín de La Plata, Argentina

author email corresponding author email

Critical Care 2005, 9:R556-R561doi:10.1186/cc3797

Published:	17 August 2005

Abstract

Introduction

Continuous monitoring of bladder partial carbon dioxide tension (PCO₂) using fibreoptic sensor technology may represent a useful means by which tissue perfusion may be monitored. In addition, its changes might parallel tonometric gut PCO₂. Our hypothesis was that bladder PCO₂, measured using saline tonometry, will be similar to ileal PCO₂ during ischaemia and reperfusion.

Method

Six anaesthetized and mechanically ventilated sheep were bled to a mean arterial blood pressure of 40 mmHg for 30 min (ischaemia). Then, blood was reinfused and measurements were repeated at 30 and 60 min (reperfusion). We measured systemic and gut oxygen delivery and consumption, lactate and various PCO₂ gradients (urinary bladder–arterial, ileal–arterial, mixed venous–arterial and mesenteric venous–arterial). Both bladder and ileal PCO₂ were measured using saline tonometry.

Results

After bleeding systemic and intestinal oxygen supply dependency and lactic acidosis ensued, along with elevations in PCO₂ gradients when compared with baseline values (all values in mmHg; bladder ΔPCO₂ 3 ± 3 versus 12 ± 5, ileal ΔPCO₂ 9 ± 5 versus 29 ± 16, mixed venous–arterial PCO₂ 5 ± 1 versus 13 ± 4, and mesenteric venous–arterial PCO₂ 4 ± 2 versus 14 ± 4; P < 0.05 versus basal for all). After blood reinfusion, PCO₂ gradients returned to basal values except for bladder ΔPCO₂, which remained at ischaemic levels (13 ± 7 mmHg).

Conclusion

Tissue and venous hypercapnia are ubiquitous events during low flow states. Tonometric bladder PCO₂ might be a useful indicator of tissue hypoperfusion. In addition, the observed persistence of bladder hypercapnia after blood reinfusion may identify a territory that is more susceptible to reperfusion injury. The greatest increase in PCO₂ gradients occurred in gut mucosa. Moreover, the fact that ileal ΔPCO₂ was greater than the mesenteric venous–arterial PCO₂ suggests that tonometrically measured PCO₂ reflects mucosal rather than transmural PCO₂. Ileal ΔPCO₂ appears to be the more sensitive marker of ischaemia.