The task of the cardiorespiratory system is to deliver enough oxygen to meet the metabolic requirements of the body. Of all metabolic substrates, oxygen has the highest percentage of extraction and oxygen reserves are exhausted within a few minutes. Arterial oxygen content and cardiac output are the determinants of oxygen delivery (DO2). O2-delivery in intensive care patients can be compromised by many factors, especially diminished O2-uptake in the lung, reduced hemoglobin content, and/or altered cardiac performance. To calculate DO2, determination of cardiac output (CO), O2-tension, O2-saturation, and hemoglobin is necessary. O2-consumption (VO2), the best mirror of the actual global metabolic activities of the tissues, can be measured invasively using arterial-venous O2-content difference (avDO2) and cardiac output, which requires pulmonary artery catheterization. The body has two basic mechanisms to meet increased VO2 or to compensate for a decrease in DO2: an increase in CO and a rise in O2-extraction ratio. The avDO2 and O2-extraction ratio are known to be very good indicators for the adaptation of the cardiorespiratory system to the actual metabolic requirements of the body. The oxygen supply-to-demand ratio (DO2/VO2) yields information on the extent to which these compensatory mechanisms either function or fail. It was demonstrated that changes of the avDO2 and changes of the DO2/VO2 are always paralleled unidirectionally by changes of mixed venous O2-saturation (SvO2). Therefore these parameters can easily be replaced by SvO2 for clinical purposes. Continuous real time in-vivo control of SvO2 has now become possible using commercially available devices with fiberoptic catheters. Pathophysiological changes in the O2-supply-to-demand-ratio as well as effects of ongoing therapy can be determined at the bedside.