Abstract
We measured brain surface pH and cisternal cerebrospinal fluid (CSF) acid-base variables in Na-pentobarbital anesthetized dogs during KCl induced cardiac arrest. Electrocardiographically, an agonal rhythm occurred within seconds, presumably resulting in rapid fall in cerebral blood flow. The mean arterial blood pressure fell from 125 +/- 22 (mean +/- 1 SD) to 35 +/- 28 mm Hg at 30 seconds and to 19 +/- 3 mm Hg at 60 seconds after KCl injection. The mean brain surface pH (n = 8) dropped abruptly from 7.30 to 6.80 within 3 minutes after induction of cardiac arrest. Changes in cisternal CSF pH, however, occurred slowly with the mean pH falling from 7.33 to 7.27 at 4 minutes and to 6.99 at 10 minutes after induction of cardiac arrest. The fall in cisternal CSF pH was due to a rise in CSF concentration of organic acids as well as a rise in CSF Pco2; the mean cisternal CSF [HCO3-] fell 3.6 mEq/l while the mean cisternal CSF lactate concentration and the mean CSF Pco2 rose, respectively, 2.1 mEq/l and 37.8 mm Hg 10 minutes after induction of cardiac arrest. We conclude that during acute ischemic anoxia gross pH disequilibria develop between brain extracellular fluid and cisternal CSF; analyses of the latter fluid provide unreliable information about brain metabolic status and its acid-base balance even up to ten minutes after induction of cardiac arrest.
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