Tissue oxygenation in hypovolaemic shock

Abstract

Tissue hypoxia is an essential feature in the pathophysiology of hypovolaemic shock. In traumatized patients gross injury and haemorrhage may induce both general and local oxygen deficiency. Prolonged hypoxia can induce irreversible changes in tissues, inhibit wound healing, and increase susceptibility to infection. Correction of cardiac index and arterial PO2 does not necessarily ensure a normal tissue PO2, and therefore, arterial oxygen tension provides an inadequate index of peripheral tissue oxygenation. There are two methods currently available for clinical measurements of tissue gases: 1) mass spectrometry, and 2) tonometry with an implanted silicone rubber tube. These methods have shown that the tissue PO2 levels provide an excellent index of peripheral perfusion. During periods of experimentally induced low cardiac output, tissue PO2 decreases almost proportionally to decreases in cardiac output, whereas tissue PCO2 increases slightly. In experimental animals correction of short-term hypovolaemia restores tissue oxygen tensions to normal. However, in patients with multiple injury and hypovolaemic shock the tissue PO2 remains depressed for several days, despite the elevation of cardiac index above normal levels after extensive resuscitation. The poor tissue PO2 response, despite increased arterial PO2, clearly places the majority of the obstacle to oxygen delivery at the microcirculatory-cellular level.