The fundamental purpose of the cardiovascular and respiratory systems is to supply oxygen to the tissues. In the vast majority of cases of physiological decompensation leading to critical illness it is a reduction of oxygen availability to the tissues, on a regional or global scale, that is the vital defect. Only rarely is a deficit in the supply of other metabolites (e.g. glucose) or a failure of removal of metabolic waste products (e.g. carbon dioxide, lactate) significant at a cellular level in the presence of an adequate oxygen supply. The other situation in which anaerobic metabolism can predominate, in the presence of an adequate oxygen supply, is metabolic poisoning which interferes with the cellular utilization of oxygen (e.g. cyanide, carbon monoxide, or, debatably, sepsis).
The ideal variable to monitor in patients would be oxygen tension at a mitochondrial level; however, this remains impossible in the clinical setting. The closest clinical approach to this ideal is the measurement of interstitial or tissue oxygen tension, which is used clinically in some centers for the early detection of ischemia in free flaps.
It is known that oxygen diffusion occurs in pre- and postcapillary vessels, and that free exchange of oxygen occurs between precapillary arteriole, capillary, postcapillary venule, and tissue. Thus the tissues and the microvasculature have a relatively uniform oxygen tension throughout. Therefore measurement of tissue oxygen tension indicates the oxygen availability at the outer surface of the cells of the tissue studied, which is influenced by the local balance between supply and demand. Thus the technique has the potential to be a very useful indicator of the adequacy of perfusion, but is still limited by the lack of a reliable user-friendly monitoring system. The other major problem with this type of monitoring concept is that it can only look at a small area of tissue which may not be representative of regions that are susceptible to hypoxic injury such as the renal medulla and the liver.
The alternative way of gaining an insight into the balance between oxygen supply and demand is the measurement of venous oxygen content, which is conveniently done by optical measurement of venous hemoglobin oxygen saturation. Unlike arterial saturation, which can be measured transcutaneously by analyzing only that part of the signal which is pulsatile, it is not possible to measure venous saturation non-invasively. In the same way as tissue oxygen tension indicates the balance between supply and demand, a rise in venous saturation indicates a rise in supply relative to demand and a fall in venous saturation indicates the opposite. Venous oxygen saturation can be used to monitor individual organs (e.g. the brain in head injury or during cardiopulmonary bypass), but is most commonly used to monitor mixed venous oxygen saturation (SvO2) in the pulmonary artery. This global assessment of the adequacy of oxygen delivery to the body is very valuable; however, it does not necessarily reflect the status of individual tissues ( D§h.0,,eL§( 1988).
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