Minute ventilation increases 30 to 40 percent due to increased tidal volume. As a result, arterial P02 increases from 100 to 105 mm Hg.
5.
Increasing metabolic demands cause a 30-percent rise in carbon dioxide (C02) production. But, because of its concomitantly increased difusion capacity and hyperventilation, the arterial Peo2 decreases from 40 to 32 mm Hg.
6.
Residual volume decreases approximately 20 percent from 1500 mL to approximately 1200 mL.
7.
Chest wal 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 capacithe 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. hese are thought to be stimulated by basal oxygen consumption as it rises incrementally from 20 to 40 mLimin in the second half of pregnancy.
Reactive airway disease is seen frequently in young women and therefore oten complicates pregnancy. Asthma prevalence grew steadily in many countries beginning in the mid-1970s but may have plateaued in the United States with a prevalence in adults of approximately 10 percent (Barnes, 2015; Centers for Disease Control and Prevention, 201Oc, 2013). The estimated asthma prevalence during pregnancy ranges between 4 and 8 percent, and this appears to be rising (Kelly, 2015; Racusin, 2013). Finally, evidence is accruing that fetal and neonatal environmental exposures may contribute to the origins or mitigation of asthma (Grant, 2016; Litonjua, 2016; Spiegel, 2016).
Asthma is a chronic inlammatory airway syndrome with a major hereditary component. Increased airway responsiveness and persistent subacute inflammation are associated with polymorphism genes on chromosomes 5q that include cytokine gene clusters, 3-adrenergic and glucocorticoid receptor genes, and the T-cell antigen receptor gene (Barnes, 2015). Asthma is etiologically and clinically heterogeneous, and an environmental allergic stimulant such as influenza or cigarette smoke serves as a promoter for susceptible individuals (Bel, 2013).
he hallmarks of asthma are reversible airway obstruction from bronchial smooth muscle contraction, vascular congestion, tenacious mucus, and mucosal edema. Mucosal inlammation is characterized by infiltration with eosinophils, mast cells, and T lymphocytes. hese causes airway inflammation and increased responsiveness to numerous stimuli that include irritants, viral infections, aspirin, cold air, and exercise. Several inflammatory mediators produced by these and other cells include histamine, leukotrienes, prostaglandins, cytokines, IgE, and many others. Importantly, because F-series prostaglandins and ergonovine exacerbate asthma, these commonly used obstetrical drugs should be avoided if possible.