| Summary: | Tissue oxygen tension (tPO2) reflects the balance between local oxygen supply and demand and could thus be a useful monitoring modality. However, both the consistency and amplitude of the tPO2 response in different organs during varied cardiorespiratory insults is unknown. Using an anaesthetised rat model I investigated the effects of endotoxaemia, progressive haemorrhage and acute hypoxaemia on tPO2 measured in deep (liver and renal cortex) and peripheral (skeletal muscle and bladder) organ beds. Different patterns were seen in each of the shock states with conditionspecific variations in the degree of acidaemia, lactataemia, and tissue oxygen responses between organs. Endotoxaemia resulted in a rise in bladder tPO2, an early fall in muscle and liver tPO2 but no significant change in renal cortical tPO2. In a more severe model of endotoxaemic sepsis, different patterns were seen between cortical and outer medullary oxygenation, and the intra/extravascular compartments of the kidney. Progressive haemorrhage however produced proportional falls in liver, muscle and bladder tPO2 but renal cortical tPO2 was maintained until profound blood loss had occurred. Administration of high inspired oxygen concentrations initially increased tissue PO2 although this fell with continued blood loss. By contrast, acute hypoxaemia and hyperoxaemia induced proportional changes in tPO2 in all organ beds. Tissue PO2 monitoring in a long-term sepsis model revealed a fall in global oxygen delivery during early sepsis (6h) with concurrent decreases in muscle, liver and renal cortical tissue PO2. Myocardial function was severely compromised at this timepoint, due largely to hypovolaemia despite concurrent background fluid resuscitation. Furthermore, fluid loading and an oxygen challenge test revealed discordance between the macro- and microcirculation, likely contributing to the oxygen supply-demand imbalance. By contrast, during established sepsis (24h), tissue oxygen tensions normalised with an improvement in myocardial and circulatory function. However, at this timepoint there was evidence of ill health, continued hyperlactataemia and organ failure, thus highlighting the complexity of this particular disease state. Taken together, these studies highlight the heterogeneity of responses in different organ beds during varied shock states. This likely relates to local changes in oxygen supply and utilisation. They also challenge the traditional paradigm that a fall in global oxygen delivery by whatever means has a similar response at the organ level. Furthermore, it highlights the particular sensitivity and/or adaptation of some organs to specific insults. Consequently, the baseline tissue oxygen tension in peripheral organ beds does not necessarily mimic that observed in deeper, vital organs. However, if combined with a dynamic challenge (e.g. an oxygen challenge test), these differences can be unmasked, thus highlighting the potential utility of this monitoring device in clinical practice.
|
|---|
