ABG: Pregnancy

Obstetric Anesthesia, Physiology - Renal/Urine/Electrolytes

During the first trimester of pregnancy the arterial oxygenation increases from nonpregnant levels to 107 mmHg due to greater alveolar ventilation, the decline in PaCO2, and a lower AV oxygen difference (reducing the reduction in PaO2 due to venous admixture). Throughout pregnancy oxygen consumption increases and cardiac output increases to a lesser extent, lowering mixed venous oxygen content. Oxygenation further decreases in the supine position at midgestation because the FRC becomes less than the closing capacity leading to atelectasis.

Minute ventilation rises during pregnancy due to progesterone acting as a respiratory stimulant and as a result of increased carbon dioxide production (increased by 30%). pCO2 declines to approximately 30 mmHg by 12 weeks and stays constant through the remainder of pregnancy. This results in a respiratory alkalosis. Metabolic compensation for this reduces serum bicarbonate to approximately 20 mEq/L with a base excess of 2-3 mEq/L.

  • Arterial PaO2 is increased about 10 torr during pregnancy (increased minute ventilation)
  • PaCO2 is decreased about 10 torr during pregnancy.
  • PaCO2 is about 32 mmHg but pH is normalized secondary to a compensatory metabolic acidosis, with HCO3 decreasing from 25 meq/l to 21 meq/l


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