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Fetal acid-base physiology

Fetal acid-base physiology


Authors
Edward R Yeomans, MD
Susan M Ramin, MD
Section Editor
Charles J Lockwood, MD
Deputy Editor
Vanessa A Barss, MD
Disclosures
All topics are updated as new evidence becomes available and our peer review process is
complete.
Literature review current through: Oct 2012. | This topic last updated: Jul 20, 2012.
INTRODUCTION Normal fetal metabolism results in the production of acids which are
buffered to maintain extracellular pH within a critical range. Very small changes in pH may
significantly affect function of various fetal organ systems, such as the central nervous system
and the cardiovascular system [1]. The major buffers utilized by the fetus for neutralizing
hydrogen ion production are plasma bicarbonate and hemoglobin [2]. Inorganic phosphates and
erythrocyte bicarbonate are also potential buffers, although they play a lesser role in fetal acidbase homeostasis [2].
Fetal hypoxia can occur when maternal oxygenation is compromised, maternal perfusion of the
placenta is reduced, or delivery of oxygenated blood from the placenta to the fetus is impeded.
When adequate fetal oxygenation does not occur, complete oxidative metabolism of
carbohydrates to carbon dioxide (CO2) and water is impaired and metabolism proceeds along an
anaerobic pathway with production of organic acids, such as lactic acid, which are not readily
excreted or metabolized. Accumulation of lactic acid can deplete the buffer system and result in
metabolic acidosis.
Fetal acid-base physiology will be reviewed here. Interpretation of umbilical cord pH and blood
gas values assessed immediately after delivery is discussed elsewhere. (See "Umbilical cord
blood acid-base analysis".)
FETAL ACID-BASE PHYSIOLOGY The fetus produces both volatile (carbonic acid) and
nonvolatile acids (noncarbonic or organic acids).
Carbonic acid The fetus produces carbonic acid (H2CO3) during oxidative metabolism
(aerobic glycolysis). Since H2CO3 is formed primarily from CO2 via hydration in the presence
of erythrocyte carbonic anhydrase, the formation of carbonic acid is equivalent to CO2
generation [1]. The rate of CO2 production, in turn, is equivalent to fetal oxygen consumption
[3].

For the most part, the fetus can handle the amount of carbonic acid produced daily from aerobic
metabolism since carbonic acid dissociates to water and CO2, which readily diffuses across the
placenta. Diffusion of CO2 across the placenta is facilitated by a lower PCO2 in the mother
during pregnancy, secondary to hyperventilation [1].
Organic acids Noncarbonic or organic acids result from fetal anaerobic metabolism, which
occurs when placental transfer of oxygen is restricted. Unlike carbonic acid, the organic acids are
cleared very slowly across the placenta and therefore accumulate in the fetus. Metabolic
acidemia develops when the primary buffer, bicarbonate (HCO3), as well as other buffers
decrease to a critical level. The most important organic acids are lactic acid and ketoacids.
Buffers The fetus utilizes many different buffers to maintain pH in a very narrow range. The
two major buffers are bicarbonate and hemoglobin. Other buffers that play a lesser role include
inorganic phosphates, erythrocyte bicarbonate, and albumin [2].