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Difference in Acid-Base State between Venous and Arterial Blood during Cardiopulmonary Resuscitation

  • F. John Gennari
  • , Roger Barton
  • , Ernest Benjamin
  • , Thomas A. Paluch
  • , David R. Gentili
  • , Thomas J. Iberti
  • , Douglas C. Johnson
  • , David M. Systrom
  • , Joseph A. Chazan
  • , Max Harry Weil
  • , Eric C. Rackow
  • , Jay L. Falk
  • , Martin I. Griffel
  • , Arnold S. Relman
  • University of Vermont
  • University of Edinburgh
  • Icahn School of Medicine at Mount Sinai
  • Massachusetts General Hospital
  • Rhode Island Hospital
  • University of Health Sciences, The Chicago Medical School

Research output: Contribution to journalLetterpeer-review

10 Scopus citations

Abstract

To the Editor: The marked elevation in mixed venous partial pressure of carbon dioxide (PCO2) found during cardiopulmonary resuscitation by Weil and coworkers (July 17 issue)1 is an intriguing new observation, and clearly requires further studies to delineate its clinical importance. The authors and your accompanying editorial2 both offer explanations for the high PCO2. I am perplexed, however, because no one even raised for consideration what seems to be the most likely cause — abrupt restoration of oxidative metabolism and a resultant surge of carbon dioxide production as tissue oxygen delivery returns. More than 90 percent.

Original languageEnglish
Pages (from-to)1616-1618
Number of pages3
JournalNew England Journal of Medicine
Volume315
Issue number25
DOIs
StatePublished - Dec 18 1986

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