[Tissue oxygenation: physiological and pathophysiologic aspects in intensive care]

Continuous oxygen supply to the tissues is one of the many important factors in intensive care. However, as a basic requirement for the structure and function of higher developed organisms energy production by oxydative metabolism is of outstanding importance, because there is no significant storage of energy and anaerobic metabolism is insufficient. The determinants of oxygen supply--blood flow and oxygen content--are well known. The system stands out for its extensive ability to compensate imbalances. Nevertheless one has to bear in mind also rather trivial disturbances like insufficient respiration and hypovolemia. Absolute values of global parameters, however, provide no information on the oxygen supply of individual organs that are variably susceptible to hypoxia. Regional perfusion and tissue respiration are influenced by various factors. Together with systemic components the physiologic oxygen transport along the oxygen cascade follows demand. Regardless of their position on the oxygen cascade malfunctions of oxygenation impair first the function and eventually the structure of the tissues. An utilisation block on the cellular level can prevent sufficient energy production despite optimized oxygen supply, the damage of reperfusion can intensify the effects of hypoxia. Typical haemodynamic patterns follow the tissue hypoxia. For maintaining an equilibrium between oxygen demand and supply it is important that oxygen consumption is also influenced by numerous factors. Only when an imbalance between oxygen supply and demand--an oxygen debt--is realized at an early stage, the critically ill patient can be saved from irreversible damage. In the field of intensive care the frequently latent tissue hypoxia is often a result of the chronic oxygen debt of individual, particularly vulnerable organs. Considering those aspects the intestinal mucosa is particularly suited for the monitoring of tissue oxygenation in the critically ill patient.