• A B Sanders, C W Otto, K B Kern, J N Rogers, P Perrault, and G A Ewy.
• Department of Surgery, University of Arizona Health Sciences Center, Tucson 85724.
• Ann Emerg Med. 1988 Jul 1; 17 (7): 667-71.

AbstractOur study was performed to determine the pattern of arterial, venous, and cerebral spinal fluid (CSF) acidosis in a canine model of cardiac arrest and resuscitation; and the effect of bicarbonate treatment on arterial, venous, and CSF acidosis. Animals were instrumented to sample arterial blood, mixed venous blood, and CSF through a cisternal catheter. Following six minutes of ventricular fibrillation, manual CPR efforts were begun and continued for 30 minutes of cardiac arrest. Arterial, mixed venous, and CS fluids were sampled at baseline, six, 12, 18, 24, 27, and 30 minutes. Ten experimental dogs received sodium bicarbonate (2 mEq/kg) at 20 minutes of cardiac arrest, while ten animals in the control group received no alkali treatment. The experimental group showed a significantly higher arterial (7.79 +/- 0.20 vs 7.46 +/- 0.16 at 30 minutes) and venous pH (7.34 +/- 0.12 vs 7.19 +/- 0.10 at 24 minutes) following bicarbonate administration. This higher pH occurred despite a concomitant increase in arterial (31 +/- 10 vs 19 +/- 9 mm Hg at 27 minutes; 31 +/- 9 vs 10 +/- 8 at 30 minutes) and venous (104 +/- 30 vs 63 +/- 10 mm Hg at 24 minutes) pCO2. CSF analysis showed a gradually worsening acidosis. However, CSF pH (7.12 +/- 0.14 vs 7.16 +/- 0.23 at 30 minutes) and pCO2 were not significantly changed by the administration of bicarbonate.

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