EFFECT OF CEREBRAL BLOOD-FLOW GENERATED DURING CARDIOPULMONARY-RESUSCITATION IN DOGS ON MAINTENANCE VERSUS RECOVERY OF ATP AND PH

Background and Purpose: Cardiopulmonary resuscitation with external ch est compression generates low perfusion pressures that may be inadequa te for restoring cerebral metabolism and may worsen intracellular pH. We tested the hypothesis that cerebral reperfusion with a low perfusio n pressure after arrest restores brain adenosine triphosphate (ATP) an d pH to levels attained at the same perfusion pressure without precedi ng complete ischemia. Methods: Brain ATP and intracellular pH were mea sured by magnetic resonance spectroscopy, and cerebral blood flow was measured with microspheres in anesthetized dogs. External chest compre ssions were begun in group A (n=6) immediately after the onset of arre st (ie, arrest time zero) and in group B (n=10) after 6 minutes of arr est (ie, arrest time 6 minutes). In both groups, mean cerebral perfusi on pressure was regulated at 30 mm Hg for 70 minutes by adjustment of inflation pressure of a pneumatic thoracic vest. Results: At 12 minute s of resuscitation, cerebral blood flow was 27+/-4 mL/min per 100 g in group A and 21+/-4 mL/min per 100 g in group B, but ATP in group B (5 8+/-10% of prearrest) was less than in group A (105+/-6%). With prolon ged resuscitation, ATP deteriorated to near zero levels in dogs in gro up B, with blood flow less than 15 mL/min per 100 g. Dogs with greater blood flow never achieved complete metabolic recovery. In group B, in tracellular pH was unchanged from the 6.3 value at the start of resusc itation, even in those dogs with extremely low blood flows. Conclusion s: Levels of cerebral perfusion pressure sufficient to maintain cerebr al oxidative metabolism without complete ischemia during cardiopulmona ry resuscitation are not sufficient to restore metabolism after comple te ischemia during cardiopulmonary resuscitation. However, low ''trick le'' blood flow did not worsen intracellular acidosis.