Hyperventilation
- Probably due in part to progesterone stimulating the respiratory center
- Lung volume changes and altered compliance may also contribute
Thus,
- Chronic respiratory alkalosis which is compensated by renal excretion of bicarbonate
Typical blood gases results in the third trimester are:
- pH 7.43
- pCO2 33mmHg
- [HCO3] 21mmHg
- pO2 104 mmHg
Reduction in bicarbonate
--> Slightly reduced ability to buffer a metabolic acid load
Changes in ODC
Lower pCO2 would shift the oxygen dissociation curve to the left
But minimal change in pH
Increased 2,3 DPG levels during pregnancy
Overall,
- ODC is little altered in position
Hyperemesis
- Nausea and vomiting occur commonly in the first trimester
- May be severe (hyperemesis gravidarum) and intractable vomiting
--> Fluid loss and electrolyte disturbances
Typically causing metabolic alkalosis
NB:
- The actual acid-base effect of vomiting depends on the actual mix of acidic gastric fluid and alkaline intestinal secretions in the vomitus.
- Alkalosis does not always occur with prolonged vomiting.
Maternal Ketosis
The pregnant woman is prone to develop elevated ketone levels because:
- Fasting during pregnancy more rapidly results in hypoglycaemia and low insulin levels
- Insulin resistance develops as pregnancy progresses (probably due to placental hormones)
- Fasting ketosis develops in less than 16 hours in late pregnancy
* Compared to usually > 24 hours in the non-pregnant female
Ketones
- Ketones can cross the placenta and the foetus can adapt to use them as an energy source
- Ketones may be important in myelination in the developing central nervous system
- This mild ketosis that occurs with fasting does not seem to have any adverse effect on the mother
- Effect of ketosis on foetus is uncertain
However,
- Ketoacidosis due to maternal DM is more serious and has very serious adverse effect on the foetus
Others
Diuretic use may cause a metabolic alkalosis
--> a mixed alkalosis because the hyperventilation has already reduced the pCO2