![]() ![]() ![]() Determinants of cerebral oxygenation are multifactorial, and a personalized clinical approach depends on the individual pathophysiological causes. A recent study suggests that only 8.6% of centers use routinely PtiO 2, 1.3% use venous saturation of the jugular bulb (SvjO 2) and 1.7% near infrared spectroscopy (NIRS). Even in developed countries, O 2 tissue pressure (PtiO 2) monitoring rates do not exceed 19% of centers. However, monitoring of cerebral oxygenation in traumatic brain injured patients is not routinely applied, it has some limitations, and the evidence-based support is not so solid. ![]() The etiologies of CTH are multiple (Table 1), and can be pathophysiologically approached and investigated following the oxygen route (Fig. CTH is common and prevalent in neurocritical ill patients, and in most cases, it is due to changes in basic physiological parameters. DO 2 is the result of CBF x CaO 2, which does not allow the detection of local tissue or microcirculatory abnormalities that limit the local supply of O 2 at the tissue level (Fig. When DO 2 is inadequate or the mitochondria cannot use the supplied O 2, ‘‘cerebral tissue hypoxia’’ (CTH) occurs, which constitutes a secondary insult that magnifies the primary brain injury and worsens clinical outcomes, especially in severe traumatic brain injured patients. This requires a good functioning of the respiratory, cardiovascular (including microcirculation) and hematological systems, all regulated by the state of the internal steady. The achievement of oxygen final metabolism, in the mitochondria, starts from ambient air or a gaseous mixture provided by non-invasive O 2 supplemental techniques or mechanical ventilator. Under physiological conditions, the brain utilizes only 33% of the O 2 received, being able to increase extraction when DO 2 is compromised in any of its determinants. Two requirements are essential to ensure the availability of O 2 to the brain (DO 2): sufficient cerebral blood flow (CBF) and adequate arterial oxygen content (CaO 2). Since the brain cannot store O 2, it needs its constant supply to maintain its main energy source, which is adenosine triphosphate. Oxygen (O 2) is vital for neuronal survival. For this purpose, we developed the acronym “THE MANTLE,” a bundle of therapeutical interventions, which covers and protects the brain, optimizing the components of the oxygen transport system from ambient air to the mitochondria. The causes of hypoxia are variable and can be analyzed pathophysiologically following “the oxygen route.” The current trend is precision medicine, individualized and therapeutically directed to the pathophysiology of specific brain damage however, this requires the availability of multimodal monitoring. Brain tissue hypoxia occurs when the supply of oxygen is not adequate or when for some reasons it cannot be used at the cellular level. Multiple physiological parameters determine the oxygen delivered to the brain, including blood pressure, hemoglobin level, systemic oxygenation, microcirculation and many factors are involved in the delivery of oxygen to its final recipient, through the respiratory chain. Cerebral tissue oxygenation represents the balance between oxygen supply and consumption, largely reflecting the adequacy of cerebral perfusion. To ensure neuronal survival after severe traumatic brain injury, oxygen supply is essential. ![]()
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