الفهرس 
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Abstract
Improvements in surgical techniques and perioperative anesthetic management have led to enhancement of surgery and intensive care therapy for patients who would never before have been acceptable candidates. Ongoing developments in monitoring techniques have shed new light on our knowledge of pathophysiological processes associated with critical illness (Boldt, 2002).
Since the first public demonstration of modern anesthesia in Boston in 1846 there has been a tremendous increase in monitoring devices, especially in the past 30 years. Modern technology has provided a large number of sophisticated monitors. Most of these newly developed techniques have enhanced our understanding of the mechanism of patient decompensation and have helped to guide appropriate therapeutic interventions. Aggressive marketing strategies have been promoted to monitor a variety of functions. However, it still remains unclear whether they are able to enhance patient safety or even improve patient outcome (Boldt 2002).
All cells require oxygen for aerobic metabolism to maintain normal cellular function. Because oxygen cannot be stored in the cells, a constant supply that matches the metabolic needs of each cell is required. Failure to deliver sufficient oxygen to the tissues may result in organ dysfunction, as seen in many forms of underresuscitated shock. Therefore, early detection and correction of tissue hypoxia is essential in the management of critically ill patients (Yuh-Chin, 2005).
Inadequate tissue perfusion and oxygenation are likely to contribute to the development of organ failures and increased mortality in critically ill patients (pittard, et al., 1994). For this reason, assessment of the adequacy of oxygen supply to organs and tissues is essential. Monitoring of tissue oxygenation and organ function in the clinical setting is largely based on measuring traditional variables of resuscitation, such as global hemodynamics, pulse oximetry, capillary refill, urine output, or indirect biochemical markers. These parameters remain insensitive indicators of dysoxia and are considered to be poor surrogates for the oxygen availability at tissue levels, since tissue oxygenation is determined by the net balance between cellular oxygen supply and oxygen demand.
Methods to detect tissue dysoxia and oxygen debt can grossly be subdivided into two groups; namely, techniques directed at the assessment of oxygenation at the systemic level, and monitoring techniques for measurements at the organ level (siegemund, et al., 1999). Clinical assessment of tissue hypoxia is indirect and largely based on measuring aspects of whole body oxygen transport and uptake, or indirect biochemical markers. Assessing oxygen transport may involve
• Clinical examination of the patient
• Oxygen delivery from the inspiratory gases to the alveoli
• Oxygenation of arterial blood
• Delivery of oxygen to the tissues
• Oxygen uptake
• Oxygen content of the mixed venous blood
• Interaction of arterial oxygenation and mixed venous oxygenation
• Lactate and assessment of regional PCO2 or pH
These measures allow indirect assessment of tissue oxygenation and potential hypoxia. The more complex the clinical disorder, the more carefully should the oxygen transport system be assessed, so that impairment of any part of the process can be promptly detected and treated before definite tissue (siegemund ,et al., 1999).