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Pulmonary Disease and Pregnancy

Alterations in Pulmonary Physiology During Pregnancy

Pregnancy induces profound changes in the mother, resulting in significant alterations in normal physiology. The anatomical and functional changes affect the respiratory and cardiovascular systems. Management of respiratory diseases in pregnancy requires an understanding of these changes for interpretation of clinical and laboratory manifestations of disease states.

An image depicting asthma consensus guidelines to manage chronic asthma can be seen below.

Pulmonary disease and pregnancy. The graph depicts

Pulmonary disease and pregnancy. The graph depicts asthma consensus guidelines to manage chronic asthma. These guidelines are also generally used to treat pregnant patients with asthma.

Respiratory physiology

Anatomical changes

Hormonal changes in pregnancy affect the upper respiratory tract and airway mucosa, producing hyperemia, mucosal edema, hypersecretion, and increased mucosal friability. 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. As the uterus expands, the diaphragm is displaced cephalad by as much as 4 cm; the anteroposterior and transverse diameter of the thorax increases, which enlarges chest wall circumference. Diaphragm function remains normal, and diaphragmatic excursion is not reduced.

Pulmonary function

Anatomical changes to the thorax produce a progressive decrease in functional residual capacity, which is reduced 10-20% by term. The residual volume can decrease slightly during pregnancy, but this finding is not consistent; decreased expiratory reserve volume definitely changes. The increased circumference of the thoracic cage allows the vital capacity to remain unchanged, and the total lung capacity decreases only minimally by term. Hormonal changes do not significantly affect airway function. Pregnancy does not appear to change lung compliance, but chest wall and total respiratory compliance are reduced at term.


The minute ventilation increases significantly, beginning in the first trimester and reaching 20-40% above baseline at term. Alveolar ventilation increases by 50-70%. The increase in ventilation occurs because of increased metabolic carbon dioxide production and because of increased respiratory drive due to the high serum progesterone level. The tidal volume increases by 30-35%. The respiratory rate remains relatively constant or increases slightly.

Arterial blood gases

Physiological hyperventilation results in respiratory alkalosis with compensatory renal excretion of bicarbonate. The arterial carbon dioxide pressure reaches a plasma level of 28-32 mm Hg, and bicarbonate is decreased to 18-21 mmol/L, maintaining an arterial pH in the range of 7.40-7.47. Mild hypoxemia might occur when the patient is in the supine position. Oxygen consumption increases at the beginning of the first trimester and increases by 20-33% by term because of fetal demands and increased maternal metabolic processes.

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.

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