A number of acute and chronic pulmonary disorders are encountered during pregnancy. The most common is asthma, which affects up to 4 percent of women. Together with community-acquired pneumonia, it accounted for almost 10 percent of nonobstetrical antepartum hospitalizations in one managed care plan (Gazmararian and colleagues, 2002). Acute and chronic lung disorders are superimposed upon several important adaptive changes of pulmonary physiology and function during pregnancy. And although there is no evidence that pulmonary function is impaired because of pregnancy, advanced pregnancy may intensify the pathophysiological effects of some lung diseases. One example is the disparate number of maternal deaths during the influenza pandemics of 1918 and 1957. Another is the poor tolerance for pregnancy of women with severe chronic lung disease.
The important and sometimes marked changes in the respiratory system induced by pregnancy are found in Chapter 5, Respiratory Tract and the Appendix. Lung volumes and capacities that are measured directly to describe pulmonary pathophysiology may be significantly altered. In turn, these change the results of gas concentrations and acid-base values in blood. Some of the physiological changes induced by pregnancy were recently 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 the respiratory stimulant properties of progesterone
Minute ventilation increases about 30 to 40 percent due to increased tidal volume. Arterial pO2 also increases from 100 to 105 mm Hg
Carbon dioxide production increases approximately 30 percent, but diffusion capacity also increases, and with alveolar hyperventilation, the pCO2 decreases from 40 to 32 mm Hg
Residual volume decreases approximately 20 percent from 1500 mL to approximately 1200 mL
The expanding uterus and increased abdominal pressure cause chest wall compliance to be reduced by a third. Thus, the functional residual capacity—the sum of expiratory reserve and residual volumes—decreases by 10 to 25 percent.
The sum of these changes is substantively increased ventilation due to deeper but not more frequent breathing. These changes presumably are induced by basal oxygen consumption, which increases incrementally by 20 to 40 mL/min in the second half of pregnancy. The kidney increases bicarbonate excretion and serum levels decrease to approximately 15 to 20 meq/L, while pH is slightly alkalotic at 7.45.
Asthma is common in young women and therefore is seen frequently during pregnancy. Asthma prevalence increased steadily in many countries beginning in the mid-1970s but may have plateaued in the United States during the past decade (Eder and colleagues, 2006). According to Fanta (2009) and the National Center for Health Statistics (2007), almost 8 percent of the general population has asthma. Kwon and associates (2006) estimated asthma prevalence during pregnancy to range between 4 and 8 percent. Moreover, Namazy and Schatz (2005) reported that the prevalence in pregnant women appears to be increasing.
Asthma is a chronic inflammatory airway disorder with a major hereditary component. Increased airway responsiveness and persistent subacute inflammation have been associated with genes on chromosomes 5, 11, and 12 that include cytokine gene clusters, β-adrenergic and glucocorticoid receptor genes, and the T-cell antigen receptor gene (McFadden, 2005). There inevitably is an environmental allergic stimulant such as influenza or cigarette smoke in susceptible individuals (Hartert and colleagues, 2003).
The hallmarks of asthma are reversible airway obstruction from bronchial smooth muscle contraction, vascular congestion, tenacious mucus, and mucosal edema. There is airway inflammation and increased responsiveness to a number of stimuli including irritants, viral infections, aspirin, cold air, and exercise. Inflammation is caused by response of mast cells, eosinophils, lymphocytes, and bronchial epithelium. A number of inflammatory mediators by these and other cells include histamine, leukotrienes, prostaglandins, cytokines, and many others. IgE also plays a central role in pathophysiology (Strunk and Bloomberg, 2006). Because F-series prostaglandins and ergonovine exacerbate asthma, these commonly used obstetrical drugs should be avoided if possible.
Asthma represents a broad spectrum of clinical illness ranging from mild wheezing to severe bronchoconstriction. The functional result of acute bronchospasm is airway obstruction and decreased airflow. The work of breathing progressively increases, and patients present with chest tightness, wheezing, or breathlessness. Subsequent alterations in oxygenation primarily reflect ventilation–perfusion mismatching, because the distribution of airway narrowing is uneven.
The variations of asthma manifestations have led to a simple classification that considers severity as well as onset and duration of symptoms (Table 46-1). With persistent or worsening bronchial obstruction, stages progress as shown in Figure 46-1. Hypoxia initially is well compensated by hyperventilation, normal arterial pO2, decreased pCO2, and resultant respiratory alkalosis. As airway narrowing worsens, ventilation–perfusion defects increase, and arterial hypoxemia ensues. With severe obstruction, ventilation becomes impaired because fatigue causes early CO2 retention. Because of hyperventilation, this may only be seen initially as an arterial pCO2 returning to the normal range. With continuing obstruction, respiratory failure follows from fatigue.
Table 46-1. Classification of Asthma Severity
| Save Table
Table 46-1. Classification of Asthma Severity
>2 day/wk, not daily
>1/wk, not nightly
Short-acting β-agonist for symptoms
≥2 day/wk, but not >1×/day
Several times daily
Interference with normal activity
Normal between exacerbations
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