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Fig. 4 | Journal of Intensive Care

Fig. 4

From: Traumatic brain injury: pathophysiology for neurocritical care

Fig. 4

Brain ischemia after hyperventilation. A female in her 40s with traumatic brain injury was transferred to the hospital by ambulance. Brain CT scan revealed acute subdural hematoma. Surgical interventions were performed, and the patient’s ICP and SjO2 were monitored. The SjO2 value drops after hyperventilation. This phenomenon can be explained by the vasoconstriction effect from reduced PaCO2. Cerebral perfusion pressure changes might not have any remarkable effect because SAP and ICP values have been constant. Clinically, physicians would not be able to detect brain ischemia only from vital signs in this case without monitoring for brain oxygenation, such as SjO2 monitoring. The ICP will stay constant even if there are changes in the intracranial volume (e.g., the change in the volume of the vascular bed during the space compensatory phase). While the ICP will spread to the CSF space or any similar space until the compensatory effect is lost, no remarkable changes in the ICP are seen during the space compensatory phase. As a consequence, hyperventilation therapy for ICP control will not be effective in this phase. It may even cause harm via the decrease in CBF induced by excess vasoconstriction. Resp. respiration, SAP systemic arterial pressure, ICP intracranial pressure, SjO 2 jugular bulb oxygen saturation, HV hyperventilation. Data were obtained from brain injury patient monitored at our hospital in the 1990s

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