Controlled hyperventilation in patients with intracranial hypertension. Application and management.
When elevated intracranial pressure (ICP) complicates the course of various forms of cerebral edema, the likelihood of survival with full recovery is greatly diminished. Controlled mechanical hyperventilation effectively lowers ICP in some patients by causing cerebral vasoconstriction. Improved survival occurs in patients with elevated ICP from head trauma and intracranial infection treated with hyperventilation; however, no benefit has been demonstrated in patients with increased ICP from strokes or hypoxic brain damage. Proper management of the hyperventilation requires knowledge of basic cerebral circulatory physiology. Arterial Paco2 tensions should be maintained between 25 and 30 mm Hg. Vasoconstrictive effects of hyperventilation diminish after 48 to 72 hours when renal mechanisms compensate for the respiratory alkalosis. When hyperventilation is discontinued, the Paco2 must be gradually returned to normal values, since sudden changes may cause a marked rise in ICP.
D001921:Brain / Q000098:blood supply; D001929:Brain Edema / Q000401:mortality / Q000628:therapy*; D002245:Carbon Dioxide / Q000172:deficiency; D002561:Cerebrovascular Disorders / Q000628:therapy; D006259:Craniocerebral Trauma / Q000628:therapy; D004562:Electrocardiography; D004660:Encephalitis / Q000628:therapy; D006801:Humans; D002534:Hypoxia, Brain / Q000628:therapy; D007427:Intracranial Pressure; D008581:Meningitis / Q000628:therapy; D012121:Respiration, Artificial / Q000379:methods*; D013997:Time Factors
D002245:Carbon Dioxide