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During pregnancy, pulmonary disorders are frequently encountered. In one study, asthma and community-acquired pneumonia accounted for almost 10 percent of nonobstetrical antepartum hospitalizations (Gazmararian, 2002). Pregnant women, especially those in the last trimester, tolerate lung disease poorly because of important pregnancy-induced changes in ventilatory physiology (Han, 2018). Lung volumes and capacities are significantly altered. In turn, these shift gas concentrations and acid-base values in blood. These important and sometimes marked changes are reviewed in Chapter 4 (p. 66), and normal values for blood gas can be found in the Appendix (p. 1232). Some of these can be summarized as follows:
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Vital capacity and inspiratory capacity increase by approximately 20 percent by late pregnancy.
Expiratory reserve volume declines from 1300 mL to approximately 1100 mL.
Progesterone-driven respiratory stimulation raises tidal volume approximately 40 percent.
Minute ventilation increases 30 to 40 percent due to higher tidal volume. As a result, arterial partial pressure of oxygen (Pao2) rises from 100 to 105 mm Hg.
Expanded metabolic demands cause a 30-percent increase in carbon dioxide (CO2) production. But, because of its concomitantly greater diffusion capacity and hyperventilation, the Paco2 is reduced from 40 to 32 mm Hg.
Residual volume diminishes approximately 20 percent from 1500 mL to 1200 mL.
An expanding uterus and higher intraabdominal pressure lower chest wall compliance by one third. This causes a 10- to 25-percent reduction in functional residual capacity—the sum of expiratory reserve and residual volumes.
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Beginning at 14 to 16 weeks’ gestation forced vital capacity and peak expiratory flow progressively increase (Grindheim, 2012). The result of these pregnancy-induced changes is substantively greater ventilation due to deeper but not more frequent breathing. This is thought to be stimulated by basal oxygen consumption, which incrementally rises from 20 to 40 mL/min in the second half of pregnancy.
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Asthma is a chronic inflammatory airway syndrome with a major hereditary component. Polymorphism genes on chromosome 5q that include cytokine gene clusters, β-adrenergic and glucocorticoid receptor genes, and the T-cell antigen receptor gene are associated with greater airway responsiveness and persistent subacute inflammation (Barnes, 2018). Racial differences are seen, and morbidity rates are disproportionately higher in black compared with white women (Kodadhala, 2018). Asthma is etiologically and clinically heterogeneous, and an environmental allergic stimulant such as influenza or cigarette smoke serves as a promoter for susceptible individuals.
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The hallmarks of asthma are reversible airway obstruction from bronchial smooth muscle contraction, vascular congestion, tenacious mucus, and mucosal edema. Stimuli cause acute infiltration of eosinophils, mast cells, and T lymphocytes. Inflammatory mediators produced by these and other cells include histamine, leukotrienes, prostaglandins, cytokines, immunoglobulin E (IgE), and many others. F-series prostaglandins and ergonovine exacerbate asthma, and these commonly used uterotonics are avoided if possible.
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