8 The protocols adopted by various studies are similar but with some variations. For NIRS-measured SctO 2, intervention protocols aiming to increase SctO 2 when it is decreased (also known as cerebral desaturation) have been adopted in cardiac 6,7 and non-cardiac surgeries. The universal feature among the standard monitors such as blood pressure and pulse oximetry used in anesthetized patients is that something can be done based on the monitoring. Monitoring is clinically meaningless if nothing can be done about the physiology it monitors. Question-2: Can cerebral oximetry optimize the essential physiology? Therefore, it can be stated that NIRS-based cerebral oximetry monitors essential and important physiology – the perfusion and oxygenation of cerebral tissue as long as all components of SctO 2-determing physiological processes are known or at a minimum considered. Cerebral oximetry is viewed as such a technology because (1) if the same brain region is monitored continuously in the same patient, the trend of change in SctO 2 reflects the balance between cerebral oxygen supply and consumption, and (2) if cerebral metabolic rate is relatively constant, SctO 2 is determined by oxygen delivery to the brain. Therefore, any device that can monitor indices of tissue perfusion and oxygenation may be useful. However, they are not routinely monitored. Tissue perfusion and oxygenation are arguably the end point of all physiological management in the operating room and intensive care unit. Tissue perfusion and oxygenation are essential physiological components because ischemia and hypoxia are (rapidly) harmful. When cerebral metabolic rate of oxygen, arterial blood oxygen content, and the volume percentage of different blood compartments are all relatively stable, SctO 2 can be regarded as a surrogate of cerebral perfusion. Therefore, it can be challenging to decipher the exact cause of a change in SctO 2 when the needed supplementary information is not available. These physiological processes alter SctO 2 reading. If cerebral oxygen supply is stable, an increase in cerebral metabolic rate of oxygen will expand venous blood volume and shift the volume ratio toward more venous blood. Cerebral oxygen demand is determined by cerebral metabolic rate of oxygen. If arterial blood oxygen content is stable, an increase in CBF will expand arterial blood volume and shift the volume ratio toward more arterial blood. Cerebral oxygen supply is determined by cerebral blood flow (CBF) and arterial blood oxygen content. 5 The second consideration is the balance between cerebral oxygen supply and demand. 2 Moreover, it was suggested that it may change during hypoxia, 2 hypercapnia/hypocapnia, 3 neural excitation, 4 and phenylephrine administration. It varies inter-individually and possibly between different brain regions in the same individual. The volume percentage of different cerebral blood compartment is not fixed. SctO 2 is higher if the saturated arterial blood is more and/or the desaturated venous blood is less, and vice versa. The first is the proportional volumes of the arterial, venous and capillary blood in the brain region illuminated by cerebral oximetry. As a result, SctO 2 is determined by two physiological considerations. Different to pulse oximetry which monitors arterial blood hemoglobin saturation (SpO 2), cerebral oximetry monitors hemoglobin saturation in mixed arterial, venous, and capillary blood in cerebral tissue (SctO 2). The first question asks if what cerebral oximetry monitors qualifies as essential physiology. Question 1: Does cerebral oximetry monitor essential and important physiology?
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