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  Vol. 117 No. 2, FEBRUARY 1966 TABLE OF CONTENTS
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Lactic Acidosis

ROBERT E. TRANQUADA, MD; WILLIAM J. GRANT, MD; CHARLES R. PETERSON, AB

Arch Intern Med. 1966;117(2):192-202.

Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

ALTHOUGH endogenous lactic acid has been recognized as a source of metabolic acidosis for many years in a variety of situations,1-5 it was not until the publication by Huckabee of his clinical observations of the significance of lactic acid acidosis 6,7 that great interest was stimulated in this condition. The demonstration that severe metabolic acidosis, frequently of fatal outcome, was a significant clinical problem has led to the increasing recognition of this situation in clinical practice.5,8-17

The definition of lactic acidosis remains arbitrary. Since the production of lactate is always accompanied by an equivalent appearance of hydrogen ion, significant elevation in blood lactate must be interpreted as lactic acidosis regardless of resultant arterial pH or bicarbonate levels. Qualifying factors include the degree of compensation for the metabolic acidosis, represented by arterial pH, eventual outcome (survival or fatality), the presence or absence of clinical symptoms of metabolic acidosis, . . . [Full Text PDF of this Article]


Author Affiliations

LOS ANGELES

From the departments of medicine, Los Angeles County Hospital and University of Southern California School of Medicine.


Footnotes

Received for publication June 28, 1965; accepted Sept 15.

Reprint requests to 2025 Zonal Ave, Los Angeles, Calif 90033 (Dr. Tranquada).



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