الفهرس 
IntroductionOnly 14 pages are availabe for public view
 |  | from | 139 |  |  |
| | | from | 139 | | |
Abstract
we concluded that hyperventilation to an ETCO2 level of 30 ± 2 mmHg with hyperoxia of 200-250 mmHg was the best strategy for the early management of severe to moderate head injured patients, because these levels are associated with a significant decrease in the middle cerebral artery blood flow velocity in both the left and right side particularly if we knew that this level of hypocapnia and hyperoxia was not associated with significant decrease in the estimated cerebral perfusion pressure. So, we are away from the risk of excessive hypocapnia induced cerebral vasoconstriction with the risk of cerebral ischaemia. Moreover, this level of hyperoxia will guard against cerebral ischaemia even at lower levels of PaCO2.
Hypocapnia to a level of ETCO2 of 30 ± 2 mmHg and hyperoxia of 100-250 mmHg have no significant effect on the estimated cerebral perfusion pressure in the early hours after closed head injury and also on the estimated intracranial pressure particularly if the baseline intracranial pressure is within normal limits.
Indeed, there is no significant correlation between the mean velocity, the estimated cerebral perfusion pressure, and the estimated intracranial pressure in the early hours after head injury, with the outcome of the patients taken during the period of hospital stay.
Lastly, we can assure that TCD is a reliable noninvasive bedside technique for monitoring cerebral blood flow velocity in head injured patient, cerebral perfusion pressure, intracranial pressure and cerebral vasospasm.