Fetal acidosis can be acute or chronic and is caused by disruptions to placental exchange of oxygen and carbon dioxide between the fetus and mother. This exchange relies on adequate maternal blood gas concentrations, uterine blood supply, placental transfer, and fetal gas transport. Disruptions in any of these processes can lead to fetal hypoxia and acidosis, which is associated with significant morbidity, mortality, and potential long-term effects, especially if prolonged. Acidosis refers to a high concentration of hydrogen ions in the tissues or blood (acidaemia) and is commonly measured by pH levels, with levels below 7.36 in adults and 7.00 in fetuses after delivery indicating acidaemia.
Fetal acidosis can be acute or chronic and is caused by disruptions to placental exchange of oxygen and carbon dioxide between the fetus and mother. This exchange relies on adequate maternal blood gas concentrations, uterine blood supply, placental transfer, and fetal gas transport. Disruptions in any of these processes can lead to fetal hypoxia and acidosis, which is associated with significant morbidity, mortality, and potential long-term effects, especially if prolonged. Acidosis refers to a high concentration of hydrogen ions in the tissues or blood (acidaemia) and is commonly measured by pH levels, with levels below 7.36 in adults and 7.00 in fetuses after delivery indicating acidaemia.
Fetal acidosis can be acute or chronic and is caused by disruptions to placental exchange of oxygen and carbon dioxide between the fetus and mother. This exchange relies on adequate maternal blood gas concentrations, uterine blood supply, placental transfer, and fetal gas transport. Disruptions in any of these processes can lead to fetal hypoxia and acidosis, which is associated with significant morbidity, mortality, and potential long-term effects, especially if prolonged. Acidosis refers to a high concentration of hydrogen ions in the tissues or blood (acidaemia) and is commonly measured by pH levels, with levels below 7.36 in adults and 7.00 in fetuses after delivery indicating acidaemia.
Fetal acidosis can be acute or chronic and is caused by disruptions to placental exchange of oxygen and carbon dioxide between the fetus and mother. This exchange relies on adequate maternal blood gas concentrations, uterine blood supply, placental transfer, and fetal gas transport. Disruptions in any of these processes can lead to fetal hypoxia and acidosis, which is associated with significant morbidity, mortality, and potential long-term effects, especially if prolonged. Acidosis refers to a high concentration of hydrogen ions in the tissues or blood (acidaemia) and is commonly measured by pH levels, with levels below 7.36 in adults and 7.00 in fetuses after delivery indicating acidaemia.
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Fetal acidosis
• 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. • 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 • Whereas blood pH can change quickly, tissue pH is more stable • The cut off 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 effects etiologi ACUTE • Maternal : hypotension or hypovolaemia, such as haemorrhage, a vasovagal attack, or epidural anaesthesia will reduce the maternal blood supply and so oxygen delivery to the uterus, Uterine contractions can also interrupt the uterine blood flow by a pressure rise and if prolonged, as in hypertonus, may cause hypoxia and so acidosis • Placental : Abruption can disrupt the utero-placental circulation by separating and so tearing the uterine spiral arteries from the placenta • Fetal : Blood flow from the placenta to the fetus is often affected during labour and delivery by umbilical cord compression and this can sometimes happen before labour if there is reduced liquor or a true knot in the cord CHRONIC • Maternal : reduced oxygenation of maternal blood, such as in severe respiratory or cardiac disease, or reduced blood flow to the placenta as in connective tissue diseases—for example, systemic lupus erythematosus—and preeclampsia • Placental : Antenatal fetal blood sampling by ultrasound guided needle aspiration from the umbilical cord (cordocentesis) in pregnancies with fetal growth restriction (FGR) has shown hypoxia as a result of impaired placental transfer of oxygen. This is thought to result from inadequate trophoblast invasion of the myometrium in early pregnancy, leading to reduced perfusion of the intervillous spaces • Fetal : Anaemia from rhesus disease, parvovirus infection, thalassaemia or feto-maternal haemorrhage, when severe enough to reduce fetal haemoglobin concentrations below 40 g/l (equivalent to an oxygen content below 2 mmol/l), can lead to a fall in pH.8 9 Arterio- venous shunting in fetal tumours, serious cardiac structural abnormalities, or arrhythmias are other conditions which can lead to chronic acidosis by decreased oxygenation as a result of reduced fetoplacental blood flow.