Articles: brain-injuries.
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Acta Anaesthesiol Belg · Jan 1980
Effect of 1% enflurane (Ethrane) anesthesia on cerebral blood flow and metabolism in neurosurgical patients during normo- and hyperventilation.
We have measured the CBF in ten neurosurgical patients. A first measurment was made during anesthesia with nitrous oxide 70% and a second with nitrous oxide 70% + 1% enflurane, both at a PaCO2 of 40 Torr. A third measurement was performed also with nitrous oxide + 1% enflurane, but at a PaCO2 of 30 Torr. ⋯ There were little differences in lactate and pyruvate cerebral metabolic rates, all values remaining within normal ranges. In conclusion, we believe that enflurane is a favorable anesthetic agent for neurosurgical operations at the concentration of 1%, CMRO2 is reduced, there is no significant effect on cerebral blood vessels, CBF and CVR do not change. However, a complementary use of hypocapnia may reduce CBF to dangerously low levels, if at the start, it shows already a pathological decrease and if hyperventilation is applied at a marked degree.
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Our first care when anesthetizing a child having a head injury treated by neurosurgery is to preserve a correct blood perfusion pressure, by using anesthetic agents without vasodilator potency and to control cerebral oedema. The most suitable anesthetic agents are thiopentone, dextromoramide or fentanyl, diazepam and pancuronium. Artificial ventilation is used nearly systematically trying to obtain mild hypocapnia (PaCO2:30-35 Hg pH 7.45) inducing a benefic cerebral vasoconstriction. About the antiedematous agents, mannitol gives best results in case of emergency.
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Review Case Reports
Mechanisms of hyperventilation in head injury: case report and review.
We report the case of a head-injured patient with spontaneous hyperventilation who had recurrent episodes of relative hypoventilation associated with increases in intracranial pressure. Detailed ventilatory studies were performed during the 2nd week after injury. Our findings in this patient prompted us to review the possible mechanisms underlying the observed changes. We suggest that spontaneous hyperventilation in head injury is secondary to a decrease in cortical inhibitory influences on respiratory control mechanisms and that the transient episodes of relative hypoventilation observed in our patient may reflect modified ventilatory responses dependent on the altered state of consciousness. (Neurosurgery, 5: 701--707, 1979).