Effects of arterial hypoxaemia, hypercapnia, and changes in cerebral perfusion pressure on mean cerebrospinal fluid and sagittal sinus pressure.

Abstract

In 20 anaesthetised, artificially ventilated dogs the influence of arterial hypoxaemia, hypercapnia, and decreased systemic arterial blood pressure on mean cerebrospinal fluid pressure and on the pressure in the superior sagittal sinus was studied. Below a PaO2 of 40 Torr and above a PaCO2 of 70 Torr, CSFP was significantly increased. The pressure rise in the torcular, however, was only moderate. Simultaneous CBF measurements showed marked cerebral hyperaemia to be the essential cause of the increase in CSFP. In deep normovolaemic arterial hypotension (MABP below 50 mm Hg), CSFP and SSP were significantly decreased. CBF fell sharply by about 50% compared to the resting values. In arterial normotension and under normocapnic-normoxic conditions, a pressure difference of about 3 mm Hg existed between CSFP and SSP. This pressure difference increased in hypoxia and hypercapnia and fell in arterial hypotension below the “opening-pressure” of the arachnoid villi. An artificially induced rise of CSFP in another 5 experimental animals was reflected to a minor degree in the torcular pressure. However, during rapid reduction of raised intracranial pressure, a transient, but marked pressure rise occurred in the torcular, persisting as long as systemic arterial blood pressure was increased (Cushing response). This is explained by post-compression cerebral hyperaemia and by the undamped transmission of the hypertensive arterial pressure to the dilated cerebral vessels. The origin of the rapid CSF pulse waves was studied in simultaneous recordings of intracranial CSF, cerebral venous, systemic arterial and central venous pressure, and it was shown that the height of CSFP is dependent on MABP, whereas the contour of the CSF pulse waves is shaped by rapid changes of cerebral blood volume in the post-capillary cerebral vascular bed.