Acidemia and brain ph during prolonged cardiopulmonary resuscitation in dogs

Scott M. Eleff, Hideyoshi Sugimoto, D. Hal Shaffner, Richard J. Traystman, Raymond C. Koehler

Research output: Contribution to journalArticlepeer-review

Abstract

Cardiopulmonary resuscitation (CPR) generating low perfusion pressures and beginning immediately after cardiac arrest maintains cerebral ATP but not cerebral pH or arterial pH. We tested the hypothesis that preventing severe arterial acidemia prevents cerebral acidosis, whereas augmenting arterial acidemia augments cerebral acidosis. Methods In dogs anesthetized with pentobarbital and fentanyl, cerebral pH and ATP were measured with31 P MR spectroscopy and blood flow was measured with radiolabeled microspheres. A pneumatically controlled vest was placed around the thorax, and chest compressions were begun immediately after electrically induced cardiac arrest. Cerebral perfusion pressure was maintained with epinephrine at 30 mm Hg for 90 minutes. The arterial acidemia observed during CPR was untreated in a control group, corrected to a pH of 7.3 with the use of sodium bicarbonate, or maintained below pH 6.5 with intravenous lactic acid after 14 minutes of CPR. Results At 10 minutes of CPR, cerebral ATP (99 plus minus 1.5%, control), blood flow (35 plus minus 3 mL/min per 100 g), O2 consumption (4.0 plus minus 0.2 mL/min per 100 g), and cerebral pH (7.05 plus minus.03) were unchanged from prearrest values (mean plus minus SEM). After 10 minutes of CPR in the control group, cerebral pH progressively fell (6.43 plus minus 0.10 at 90 minutes) in parallel with cerebral venous pH. In the bicarbonate group cerebral pH was maintained higher (6.91 plus minus 0.08). Cerebral blood flow, O2 consumption, and ATP were sustained near prearrest values in both groups. In the lactate group, however, the rate of decrease of cerebral pH was augmented (6.47 plus minus 0.06 by 30 minutes), and cerebral blood flow and metabolism were significantly reduced. Conclusions Cerebral pH decreased in parallel with blood pH when resuscitation was started immediately upon arrest even when cerebral O2 consumption and blood flow were near normal. Although cerebral metabolism was near normal during the first hour of CPR, systemic bicarbonate administration ameliorated the cerebral acidosis. This finding indicates that the blood-brain pH gradient is important at the subnormal cerebral perfusion pressures seen in CPR.

Original languageEnglish (US)
Pages (from-to)1028-1034
Number of pages7
JournalStroke
Volume26
Issue number6
DOIs
StatePublished - Jun 1995

ASJC Scopus subject areas

  • Clinical Neurology
  • Cardiology and Cardiovascular Medicine
  • Advanced and Specialized Nursing

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