The aim of this study was to evaluate how tissue gas tensions and tissue metabolites measured in situ can detect hypoperfusion and differentiate between aerobic and anaerobic conditions during hemorrhagic shock. We hypothesized that tissue PCO2 (PtCO2) would detect hypoperfusion also under aerobic conditions and detect anaerobic metabolism concomitantly with or earlier than other markers.


Prospective experimental animal study with eight anesthetized pigs subjected to a continuous blood loss ∼ 8% of total blood volume per hour until death. We measured cardiac index, organ blood flows, and tissue levels of PO2, PCO2, glucose, pyruvate, lactate, and glycerol in intestine, liver, kidney, and skeletal muscle.


With reduction in blood flow to the organs under aerobic conditions, PtCO2 increased ∼ 1–4 kPa from baseline. With the onset of tissue hypoxia there was a pronounced increase of PtCO2, lactate, lactate-pyruvate (LP) ratio, and glycerol. Tissue pH and bicarbonate decreased significantly, indicating that metabolic acid was buffered by bicarbonate to generate CO2.


Moderate tissue hypoperfusion under aerobic conditions is associated with increased PtCO2, in contrast to metabolic parameters of ischemia (lactate, LP ratio, and glycerol) which remain low. From the onset of ischemia there is a much more rapid and pronounced increase in PtCO2, lactate, and LP ratio. PtCO2 can be used as a marker of hypoperfusion under both aerobic and anaerobic conditions; it gives an earlier warning of hypoperfusion than metabolic markers and increases concomitantly with or earlier than other markers at the onset of tissue anaerobiosis.