This study attempted to determine whether hypoxia produces neuropathologic changes in human brain. Three previously healthy young adults (16-19 years) without known cerebral or cardiac disease developed acute respiratory hypoxia (PaOs < 45 mm Hg) of 1-8 days duration. Patients were monitored throughout their illness with continuous recording of mean intrn-arterial blood pressure (MAP) and frequent intermittent determination of cardiac output (CO), arterial (PaOz) and mixed venous (PvCfc) oxygen tensions. Each patient was found to be responsive and following commands until the day of death.
Duration of hypoxemia (hrs) | Terminal PaO« (mm Hg) | Terminal CO (L/min) | Terminal MAP (mm Hg) |
192 | 30 | 8.00 | 55 |
28 | 24 | 2.96 | 57 |
31 | 38 | * | 80 |
*CO = 10.44 L/min 4 hrs prior to death.
In all cases measures were taken to maintain systemic blood pressure and flow at supernormal levels. The mode of death in each case was sudden refractory bradycardia unresponsive to maximal respiratory, vagolytic and cardiotonic therapies. Detailed pathologic examination of each brain by two neuropathologists unfamiliar with the clinical histories failed to reveal any of the pathologic changes that are known to be associated with ischemic-anoxic brain injury.
- April 1980 Neurology 30 Page 443
- Clinical Problems Page 182
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