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We evaluated the systemic and cerebral effects induced by an increase to 100% of the inspired oxygen fraction (FiO2) on 20 comatose patients with head injury (9 patients) and SAH (11 patients). Brain tissue oxygen tension (PtiO2) was measured through a Clark electrode inserted in penumbra-like areas. We performed 55 hyperoxia tests by increasing FiO2 from 35 +/- 8% to 100% in one second and calculating the PtiO2 index as: PtiO2 variation from baseline at 1 minute/arterial oxygen tension (PaO2) variation from baseline at 1 minute x 100. One hundred percent FiO2 caused an increase of both arterial (from 139 +/- 28 to 396 +/- 77 mmHg) and cerebral (from 22.6 +/- 14 to 65.4 +/- 60 mmHg) oxygenation after 1 minute. The range of the PtiO2 response was not uniform and two groups were identified. The change was small, 0.8 mmHg/min/100 mmHg PaO2 (+/- 0.7; range 0-2) when mean PtiO2 was 19.7 +/- 13.1 mmHg, while a stronger response, 8 mmHg/min/100 mmHg PaO2 (+/- 5; range 3-18) (p0.01) was found when mean PtiO2 was 31.7 +/- 14.3 mmHg. Since O2 diffusion should follow the gas diffusion law, the increase in diffusion distance due to a reduction of capillary density in focal lesions may explain this relationship.

Interest in tissue oxygen (PtiO2) monitoring is increasing. However the exact interactions between ptiO2, systemic and cerebral variables are a matter of debate. Particularly, the relationship between ptiO2, cerebral oxygen supply and consumption needs to be clarified. We designed a model to achieve progressive Cerebral Blood Flow (CBF) reduction through 3 steps: 1. baseline, 2. CBF between 50-60% of the baseline, 3. CBF30% of the baseline. In 7 pigs, under general anaesthesia, Cerebral Perfusion Pressure (CPP) and CBF were reduced through the infusion of saline in a lateral ventricle. PtiO2 and CBF were monitored respectively through a Clark electrode (Licox, GMS) and laser doppler (Peri-Flux). Blood from superior sagittal sinus and from an arterial line was simultaneously drawn to calculate the artero-venous difference of oxygen (AVDO2). Brain oxygen supply was calculated by multiplying relative CBF change and arterial oxygen content. PtiO2 reflected CBF reductions, as it was 27.95 (+/- 10.15) mmHg during the first stage of intact CBF, declined to 14.77 (+/- 3.58) mmHg during the first CBF reduction, declined to 3.45 (+/- 2.89) mmHg during the second CBF reduction and finally fell to 0 mmHg when CBF was completely abolished. CBF changes were also followed by a decline in O2 supply and a parallel increase in AVDO2.This model allows stable and reproducible steps of progressive CBF reduction in which ptiO2 changes can be studied together with oxygen supply and consumption.