Research
Urinary bladder partial carbon dioxide tension during hemorrhagic shock and reperfusion: an observational study
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* Corresponding author: Arnaldo Dubin arnaldodubin@speedy.com.ar
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
Critical Care 2005, 9:R556-R561 doi:10.1186/cc3797
Published: 17 August 2005Abstract
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.