A lung which is partially destroyed or thrown out of function may suffice for the respiration of a normal individual, but be unable to respond to the added demands of pregnancy, particularly in the latter months, when the enlarged uterus restricts the mobility of the diaphragm.
—J. Whitridge Williams (1903)
As indicated by the above, it has long been appreciated that women in advanced pregnancy tolerate lung disease poorly. Nevertheless, pulmonary disorders are frequently encountered during pregnancy. Chronic asthma or an acute exacerbation is the most common and affects up to 8 percent of pregnant women. Moreover, asthma along with community-acquired pneumonia accounted for almost 10 percent of nonobstetrical antepartum hospitalizations in one managed care plan (Gazmararian, 2002). Pneumonia is also a frequent postpartum complication requiring readmission (Belfort, 2010). These and other pulmonary disorders are superimposed on several important pregnancy-induced changes of ventilatory physiology. For example, pregnant women, especially those in the last trimester, are susceptible to complications of severe acute pneumonitis as evidenced by the disparate number of maternal deaths during influenza pandemics.
The important and sometimes marked changes in the respiratory system induced by pregnancy are reviewed in Chapter 4 (Respiratory Tract), and values for associated tests can be found in the Appendix (Serum and Blood Constituents). Lung volumes and capacities that are measured directly to assess pulmonary pathophysiology may be significantly altered. In turn, these change gas concentrations and acid-base values in blood. Some of the physiological alterations induced by pregnancy were summarized by Wise and associates (2006):
Vital capacity and inspiratory capacity increase by approximately 20 percent by late pregnancy.
Expiratory reserve volume decreases from 1300 mL to approximately 1100 mL.
Tidal volume increases approximately 40 percent as a result of respiratory stimulation by progesterone.
Minute ventilation increases 30 to 40 percent due to increased tidal volume. As a result, arterial Po2 increases from 100 to 105 mm Hg.
Increasing metabolic demands cause a 30-percent rise in carbon dioxide (CO2) production. But, because of its concomitantly increased diffusion capacity and hyperventilation, the arterial Pco2 decreases from 40 to 32 mm Hg.
Residual volume decreases approximately 20 percent from 1500 mL to approximately 1200 mL.
Chest wall compliance is reduced by a third by the expanding uterus and increased intraabdominal pressure. This causes a 10- to 25-percent decrease in functional residual capacity—the sum of expiratory reserve and residual volumes.
In a longitudinal cohort study, Grindheim and colleagues (2012) also showed that forced vital capacity and peak expiratory flow rose progressively across pregnancy after 14 to 16 weeks’ gestation. The end result of these pregnancy-induced changes is substantively increased ventilation due to deeper but not more frequent breathing. These are thought to be stimulated by basal oxygen consumption as it rises incrementally from 20 to 40 mL/min in the second half of pregnancy.