ACID-BASE CHANGES IN CEREBROSPINAL FLUID AND BLOOD, AND BLOOD VOLUME CHANGES FOLLOWING PROLONGED HYPERVENTILATION IN MAN

Fifty patients with cerebral apoplexy (stroke) were randomly allocated to treatment with prolonged artificial hyperventilation (3 days) instituted in the acute phase of the stroke. In 24 patients, artificial ventilation was maintained at hypocapnic levels (Paco2 25 mm Hg) while in the remainder (26 patients) normocapnia was obtained by adding CO2. A comparable group (21 patients) which was not treated by artificial ventilation served as controls. This control group showed a constant active hyperventilation during the first 12 days (Paco2 32–34 mm Hg). A constant decrease in c.s.f. bicarbonate was found associated with an almost normal calculated c.s.f. pH. Initially, hypocapnic hyperventilation caused a marked increase in c.s.f. pH which had returned to normal 30 hours later in consequence of a decrease in c.s.f. bicarbonate. The introduction of normocapnic hyperventilation in these spontaneously hyperventilating patients produced an immediate acid shift of c.s.f. pH. An increase in c.s.f. bicarbonate resulted in a stable and almost normal c.s.f. pH 30 hours later. There was no sign of metabolic compensation in the blood, the standard bicarbonate remaining essentially unaltered in all groups during the 12 days of observation. During and after artificial hyperventilation, a progressive decrease in haemoglobin and serum protein concentrations suggested a blood volume increase and an extravasation of protein. Transient hyponatraemia (4.1 m.mol/l.), hypokalaemia (0.32 m.mol/l.) and water retention were seen during artificial ventilation.