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The fetus depends on the mother for placental exchange of oxygen and carbon dioxide.This in turn relies on adequate maternal blood gas concentrations, uterine blood supply, placental transfer and fetal gas transport.Disruption of any of these can cause fetal hypoxia, which, despite compensatory mechanisms, may lead to acidosis.When severe and acute (lasting hours), but especially if prolonged (days or weeks), hypoxia and therefore acidosis, are associated with significant morbidity and mortality with potential long term sequelae.Whether this damage is primarily due to reduced cell energy availability, as a result of hypoxia, or secondary to cell poisoning, as a result of acidosis, is unclear and indeed acidosis could simply be a marker of the cause and severity of the hypoxia.The very diVerent aetiologies of acute vs chronic acidosis and the possible consequences will be reviewed, whether directly caused by the acidosis or indirectly by the hypoxia What is acidosis?Acidosis means a high hydrogen ion concentration in the tissues.Acidaemia refers to a high hydrogen ion concentration in the blood and is the most easily measured indication of tissue acidosis.The unit most commonly used is pH, which is log to base 10 of the reciprocal of the hydrogen ion concentration.Whereas blood pH can change quickly, tissue pH is more stable.The cut oV taken to define acidaemia in adults is a pH of less than 7.36, but after labour and normal delivery much lower values commonly occur in the fetus (pH 7.00), often with no subsequent ill eVects.Studies looking at the pH of fetuses from cord blood samples taken antenatally and at delivery have established reference ranges.Other indices sometimes used to assess acidosis are the base excess or bicarbonate.Neither of these is measured by conventional blood gas machines but is calculated from the measured pH and pCO 2 .The major sources of hydrogen ions in the fetus are carbonic and lactic acids from aerobic and anaerobic metabolism, respectively.The removal of CO 2 (and so carbonic acid) from the fetus depends almost entirely on the placenta.Unlike in sheep, lactate does not normally seem to be an important substrate for the human fetus and lactic acid is usually either further metabolised or excreted transplacentally.The latter has been shown by analyses of
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Bobrow et al. (1999) studied this question.
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