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. We therefore investigated the effects of endotoxemia, hemorrhage and hypoxemia on tPO₂ measured in deep and peripheral organ beds. Using an anesthetised Wistar rat model, we monitored arterial pressure (MAP), blood gas and lactate levels, descending aortic and renal blood flow, and tPO₂ in skeletal muscle, bladder epithelium, liver and renal cortex during (i) a 10 mg/kg lipopolysaccharide infusion, (ii) sequential removal of 10% of circulating blood volume and (iii) reductions in inspired oxygen concentration. Comparison was made against sham-operated animals. Different patterns were seen in each of the shock states with condition-specific variations in the degree of acidemia, lactatemia, and tissue oxygen responses between organs. Endotoxemia resulted in a rise in bladder tPO₂, an early fall in liver tPO2 but no significant change in muscle and renal cortical tPO₂. Progressive hemorrhage however produced proportional falls in liver, muscle and bladder tPO₂ but renal cortical tPO₂ was maintained until profound blood loss had occurred. By contrast, progressive hypoxemia showed proportional falls in tPO₂ in all organ beds. This study highlights the heterogeneity of responses in different organ beds during varied shock states that are likely related to local changes in oxygen supply and utilization. Whole body monitoring is not generally reflective of these changes.