Dubin Arnaldo, Pozo Mario O, Edul Vanina S Kanoore, Murias Gastón, Canales Héctor S, Barán Marcelo, Maskin Bernardo, Ferrara Gonzalo, Laporte Mercedes, Estenssoro Elisa
Intensive Care Unit, Sanatorio Otamendi y Miroli, Buenos Aires, Argentina.
Crit Care. 2005 Oct 5;9(5):R556-61. doi: 10.1186/cc3797. Epub 2005 Aug 17.
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.
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.
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 DeltaPCO2 3 +/- 3 versus 12 +/- 5, ileal DeltaPCO2 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 DeltaPCO2, which remained at ischaemic levels (13 +/- 7 mmHg).
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 DeltaPCO2 was greater than the mesenteric venous-arterial PCO2 suggests that tonometrically measured PCO2 reflects mucosal rather than transmural PCO2. Ileal DeltaPCO2 appears to be the more sensitive marker of ischaemia.
使用光纤传感器技术持续监测膀胱局部二氧化碳分压(PCO2)可能是一种监测组织灌注的有用方法。此外,其变化可能与张力测定法测得的肠道PCO2变化相似。我们的假设是,在缺血和再灌注期间,使用盐水张力测定法测得的膀胱PCO2将与回肠PCO2相似。
对六只麻醉并机械通气的绵羊进行放血,使平均动脉血压降至40 mmHg并持续30分钟(缺血)。然后,重新输血,并在30分钟和60分钟时(再灌注)重复测量。我们测量了全身和肠道的氧输送与消耗、乳酸以及各种PCO2梯度(膀胱-动脉、回肠-动脉、混合静脉-动脉和肠系膜静脉-动脉)。膀胱和回肠的PCO2均使用盐水张力测定法进行测量。
放血后,全身和肠道出现氧供应依赖及乳酸酸中毒,与基线值相比,PCO2梯度升高(所有值以mmHg为单位;膀胱ΔPCO2为3±3,而基线为12±5;回肠ΔPCO2为9±5,而基线为29±16;混合静脉-动脉PCO2为5±1,而基线为13±4;肠系膜静脉-动脉PCO2为4±2,而基线为14±4;与基础值相比,所有P<0.05)。重新输血后,除膀胱ΔPCO2仍维持在缺血水平(13±7 mmHg)外,PCO2梯度恢复到基础值。
在低流量状态下,组织和静脉高碳酸血症是普遍存在的现象。张力测定法测得的膀胱PCO2可能是组织灌注不足的有用指标。此外,重新输血后观察到的膀胱高碳酸血症持续存在,可能表明该区域更容易受到再灌注损伤。PCO2梯度升高最大的部位是肠道黏膜。此外,回肠ΔPCO2大于肠系膜静脉-动脉PCO2这一事实表明,张力测定法测得的PCO2反映的是黏膜而非跨壁PCO2。回肠ΔPCO2似乎是更敏感的缺血标志物。