Mechanism of Mild Respiratory Alkalosis in Pregnancy
Mild respiratory alkalosis in pregnancy is caused by progesterone-driven hyperventilation that increases minute ventilation by 20-40% above baseline, exceeding the elevated metabolic demands and resulting in enhanced CO₂ elimination with compensatory renal bicarbonate excretion. 1
Primary Hormonal Driver
Progesterone is the key mediator, directly increasing the sensitivity of central respiratory centers independent of chemoreceptor stimulation. 1 This hormonal effect begins early in pregnancy and progressively increases minute ventilation throughout gestation. 2
- The respiratory center stimulation by progesterone is the primary mechanism, not simply a response to increased metabolic needs. 2
- This represents a resetting of respiratory drive rather than a pathological process. 1
Metabolic-Ventilatory Mismatch
The progesterone-induced increase in ventilation exceeds the metabolic requirements of pregnancy, creating the alkalotic state:
- Maternal oxygen consumption rises by 20-33% in the third trimester to meet fetal, placental, and maternal organ demands. 1, 3
- However, minute ventilation increases by 20-40%, which is disproportionately higher than the metabolic increase. 1, 4
- This mismatch results in net carbon dioxide elimination beyond what would be needed for metabolic homeostasis alone. 1
Renal Compensation Mechanism
The kidneys respond to the respiratory alkalosis by excreting bicarbonate, producing a fully compensated state that is physiologically normal:
- Bicarbonate excretion reduces serum levels to approximately 18-21 mEq/L (compared to 22-26 mEq/L in non-pregnant adults). 1
- This compensation maintains pH in the near-normal range of 7.40-7.45. 1, 2
- The result is a chronic compensated respiratory alkalosis that persists throughout pregnancy. 5, 2
Expected Arterial Blood Gas Profile
The characteristic ABG findings in pregnancy reflect this compensated state 6, 1:
- PaCO₂: 28-32 mm Hg (versus 35-45 mm Hg in non-pregnant adults)
- Bicarbonate: 18-21 mEq/L (versus 22-26 mEq/L)
- pH: 7.40-7.45 (near-normal despite the alkalosis)
Important Clinical Caveats
Respiratory rate itself remains essentially unchanged during normal pregnancy; a rate >20 breaths per minute should prompt investigation for pathology rather than being attributed to normal physiological changes. 1 The increased minute ventilation is achieved primarily through increased tidal volume, not respiratory rate. 7
While this mild respiratory alkalosis is physiological and expected, severe maternal alkalosis can potentially harm a fetus with borderline reserve by decreasing uteroplacental blood circulation. 8, 7 However, the mild compensated alkalosis of normal pregnancy is not harmful and represents appropriate maternal adaptation. 2