• R J Andrews, J R Bringas, and G Alonzo.
• Department of Neurosurgery, Stanford University Medical Center, California.
• Neurosurgery. 1994 Mar 1; 34 (3): 466-70; discussion 470.

AbstractChanges in ventilatory rate affect arterial blood pH and PCO2 within seconds to minutes, but the corresponding acute changes for cerebrospinal fluid (CSF) pH and PCO2 have been as well documented. Using our previously-described swine model of brain retraction ischemia, we examined changes in arterial and CSF pH and PCO2 with acute changes in ventilation in four animals. Newly developed fluorescent dye technology permitted near-instantaneous recording of CSF pH and PCO2 during acute hyperventilation (end-tidal PCO2 of 20 mm Hg) and acute hypoventilation (end-tidal PCO2 of 50 mm Hg). The Puritan-Bennett 3300 Intra-Arterial Blood Gas Monitor (PB3300) was used with the sensor placed in the CSF in the interhemispheric fissure posterior to the corpus callosum. The following data were gathered at 5, 15, 30, and 60 minutes after the ventilatory change: arterial pH and PCO2, end-tidal CO2, laser-Doppler cerebral blood flow, and CSF pH and PCO2. The baseline (normoventilation) values for arterial and CSF pH and PCO2 in swine were comparable to those in humans: arterial pH 7.44 and PCO2 43 mm Hg; CSF pH 7.31 and PCO2 55 mm Hg. Changes in pH and PCO2 with hyperventilation and hypoventilation occurred rapidly in both arterial blood and CSF. Steady-state values were reached within 15 minutes for hypoventilation, and 30 minutes for hyperventilation. The correlation between arterial and CSF values for both pH and PCO2 at 5, 15, 30, and 60 minutes were all very highly significant (P < 0.001) except for arterial and CSF PCO2 at 5 minutes (P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

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