Objectives: Clinically applicable methods for continuous monitoring of visceral perfusion/metabolism do not exist. Gastric mucosal end-tidal partial pressure of carbon dioxide (PCO(2)) gradient has been used, but it has limitations, especially in patients with lung injury and increased dead space ventilation. We studied the agreement between gastric mucosal end-tidal (DPCO(2gas)) and gastric mucosal arterial PCO(2) (D((t-a))PCO(2)) gradients, and especially the effect of dead space ventilation (V(d)/V(t) ratio) on the agreement. We hypothesized that DPCO(2gas) can be used as a semi-continuous indicator of mucosal arterial PCO(2) gradient in sepsis.
Design: A randomized, controlled animal experiment.
Setting: National laboratory animal center.
Interventions: Twelvehour infusion of endotoxin in landrace pigs.
Measurements and results: We measured end-tidal PCO(2) continuously, gastric mucosal PCO(2) every 10 min (gas tonometry) and arterial PCO(2) every 120 min. Carbon dioxide production and the V(d)/V(t) ratio were determined by indirect calorimetry. In the endotoxin group ( n=7) cardiac index increased and systemic vascular resistance decreased. Endotoxemia increased dead space ventilation by 27% ( p=0.001). Both DPCO(2gas) and D((t-a))PCO(2)increased significantly in the endotoxin group ( p<0.0001 and p=0.049, respectively). Control animals remained stable throughout the experiment. When we compared DPCO(2gas) and D((t-a))PCO(2)(Bland-Altman analysis), the bias and precision were 0.9 and 0.9 kPa in the control group and 2.0 and 2.2 kPa in the endotoxin group, respectively. The disagreement between DPCO(2gas) and D((t-a))PCO(2) increased as the V(d)/V(t) ratio increased.
Conclusions: DPCO(2gas) is a clinically applicable method for continuous monitoring of visceral perfusion/metabolism. Septic lung injury and increased dead space ventilation decrease the accuracy of the method, but this may not be clinically important.