Estrogen is probably responsible for producing tissue edema, capillary congestion, and hyperplasia of mucous glands. The enlarging uterus and the hormonal effects produce anatomical changes to the thoracic cage. Diaphragm function remains normal and diaphragmatic excursion is not reduced. The increased circumference of the thoracic cage allows the vital capacity to remain unchanged, and the total lung capacity decreases only minimally by term. The increase in ventilation occurs because of increased metabolic CO 2 production as well as increased respiratory drive due to excessive serum progesterone level.
Respiratory rate remains relatively constant or increases slightly.
Arterial blood gases Physiological hyperventilation results in respiratory alkalosis with compensatory renal excretion of bicarbonate. Mild hypoxemia might occur in supine position. In active labor, hyperventilation increases, and tachypnea caused by pain and anxiety might result in marked hypocapnia and respiratory alkalosis, adversely affecting fetal oxygenation by reducing uterine blood flow. In some patients, severe pain and anxiety can lead to rapid, shallow breathing with alveolar hypoventilation, atelectasis, and mild hypoxemia. Thus a decreased PaO2 can be offset somewhat by increased blood hemoglobin concentration or by increased cardiac output.