Asthma is a common chronic disorder of the airways characterized by variable and recurring symptoms and involving a complex interaction of airflow obstruction, bronchial hyperresponsiveness, and an underlying inflammation.¹

Asthma is reported to be one of the most common serious medical conditions to complicate pregnancy, and the prevalence of self-reported asthma in the United States is between 8.4% and 8.8%.² In a prospective study of 366 pregnancies in 330 women with asthma, asthma worsened in 35% of the women, improved in 28%, and remained unchanged in 33%. Asthma was significantly less frequent and severe during the last 4 weeks of pregnancy than during any other gestational interval.

In women whose asthma improved during pregnancy, the improvement was gradual with progressive pregnancy, whereas in women whose asthma worsened during pregnancy, there was an increase in asthma symptoms at between 29 and 36 weeks gestation. Asthma symptoms were uncommon during labor and delivery (L&D), occurring in only 10% of women, with approximately equal proportions of these women receiving either no treatment or inhaled bronchodilators. Asthma reverted to its prepregnancy course at 3 months postpartum in 73% of women. In 34 subjects prospectively studied for two successive pregnancies, significant concordance between the asthma course during the first and second pregnancies was observed.³

The dominant physiological event leading to clinical symptoms in asthma is airway narrowing, which subsequently interferes with airflow. Bronchial smooth muscle contraction (bronchoconstriction) occurs quickly during acute exacerbations of asthma, narrowing the airways, in response to exposure to a variety of stimuli, including allergens or irritants. Allergen-induced acute bronchoconstriction results from immunoglobulin E (IgE)–dependent release of mediators, which include histamine, tryptase, leukotrienes, and prostaglandins that directly contract airway smooth muscle, from mast cells.⁴ As the disease becomes more persistent and inflammation more progressive, further airflow limitation occurs due to factors such as edema, inflammation, mucus hypersecretion, and the formation of inspissated mucus plugs as well as structural changes, including hypertrophy and hyperplasia of the airway smooth muscle.⁵

During pregnancy, the upper airway undergoes mucosal changes secondary to elevated levels of estrogen and blood volume that may result in edema, hyperemia, hypersecretion, and a decrease in the pharyngeal diameter. Consequently, the patient may suffer from rhinitis of pregnancy, snoring, and/or sleep-disordered breathing. The upper airway changes may result in a higher Mallampati score, and thus a difficult airway.⁶

The functional residual capacity (FRC) decreases by approximately 20% to 30% (400–700 mL) as a result of a 4-cm upward displacement of the diaphragm, decreased downward excursion, and decreased outward chest recoil. This reduction in FRC is most notable around 24 weeks gestation and continues to decline thereafter, most notably in the supine position. There is also a 5% to 10% (200–350 mL) increase in the inspiratory capacity (IC). The overall total lung capacity (TLC) is relatively unchanged during pregnancy.^6,7

Due to the increase in progesterone-mediated minute ventilation during pregnancy, it is normal for a pregnant patient to have an arterial blood gas consistent with respiratory alkalosis. The pH can range from 7.42 to 7.46, the pCO₂ from 27 to 34 mmHg, and the PaO₂ from 100 to 106 mmHg.^6–8 These changes are evident as early as the first trimester and typically hit their bottom during the third trimester. The normal bicarbonate during pregnancy can plummet between 18 and 22 mEq/L during the third trimester. Any associated changes in blood gases during an acute asthma exacerbation are superimposed on the normal respiratory alkalosis of pregnancy. Therefore a PaCO₂ > 35 mmHg, a PaO₂ < 70 mmHg, or a pH < 7.35 associated with acute asthma exacerbation represent more severe compromise during pregnancy than in the nongravid state.

At term, the minute ventilation can rise by 20% to 50% from baseline. The increase in minute ventilation in pregnancy is attributed to a higher tidal volume of 450 to 650 mL per breath, with a relatively stable respiratory rate. The hyperventilation of pregnancy is further augmented during L&D, when pain and anxiety also increase minute ventilation. Up to 60 to 70% of normal pregnant women may complain of dyspnea in the absence of respiratory pathology, thought to be secondary to a heightened awareness to the augmented drive to breathe.^6,7

Routine measurements in spirometry, including the forced expiratory volume in 1 second (FEV1), forced vital capacity (FVC), and the peak expiratory flow (PEF), are unchanged when compared to nonpregnant patients. There is no significant expiratory airflow limitation as a result of pregnancy, despite changes in chest wall mechanics, upper-airway mucosa, and bronchoconstriction associated with a reduced PCO₂. During pregnancy, progesterone may have a bronchodilatory effect in these airways to balance the bronchoconstrictive changes described here, resulting in no overall change in expiratory airflow.^6,7

In patients presenting with new respiratory symptoms during pregnancy, the most common alternative diagnosis is dyspnea of pregnancy, which can be differentiated from asthma by its lack of cough, wheezing, chest tightness, or airway obstruction. Other differential diagnoses include cough due to gastroesophageal reflux or postnasal drip, bronchitis, laryngeal dysfunction, hyperventilation, pulmonary edema, and pulmonary embolism.^9,10

Symptoms and clinical signs of asthma should be assessed at each healthcare visit through physical examination and appropriate questions. A detailed symptom history should be taken, based on a short recall period (2–4 weeks). Assessment of the patient’s symptom history should include at least four key symptom expressions, including daytime asthma symptoms (wheezing, cough, chest tightness, or shortness of breath); nocturnal awakening as a result of asthma symptoms; frequency of use of short-acting beta agonists (SABAs) for relief of symptoms; and inability or difficulty performing normal activities (including exercise) due to asthma. Pulmonary function should be assessed periodically with spirometry or peak flow monitoring.

Spirometry should be measured at the time of initial assessment, after treatment is initiated and symptoms have stabilized, during a period of progressive or prolonged loss of asthma control, and at least every 1 to 2 years to assess the maintenance of airway function.^1,11 Peak flow monitoring during exacerbations will help determine their severity and guide therapeutic decisions in the home, clinician’s office, or Emergency Department.¹

The diagnosis of asthma in pregnancy is confirmed by the demonstration of a reduced FEV1 or ratio of FEV1 to FVC, with a 12% or greater improvement in FEV1 after the administration of inhaled albuterol.^1,10 In patients with a clinical picture that is consistent with new-onset asthma, in whom reversible airway obstruction cannot be demonstrated, a trial of asthma therapy is reasonable, and a positive response to asthma therapy can be used to diagnose asthma during pregnancy.¹⁰

A large study of 281,019 pregnancies reported that the pregnancies of women with asthma were more likely to be associated with miscarriage, antepartum hemorrhage, postpartum hemorrhage, anemia, depression, or cesarean delivery.¹² A retrospective cohort study revealed that women with asthma had higher odds of a number of complications of pregnancy, including preeclampsia, preterm birth, and pulmonary embolism.¹³ Most studies of asthma in pregnancy are retrospective and do not classify asthma severity. Prospective studies have demonstrated fewer significant adverse reactions, and that the gravid patient with mild or moderate asthma can have excellent maternal and infant outcomes.^14,15

Suboptimal control of asthma during pregnancy may be associated with increased maternal or fetal risk.¹⁵ A significant relationship has been reported between decreased FEV1 during pregnancy and increased risk of low birth weight and prematurity.¹⁶ The classification of asthma severity and administration of appropriate therapy tailored according to asthma severity can yield excellent infant and maternal outcomes.^14,15

All patients should receive education regarding the relationship between asthma and pregnancy. They should be taught about proper techniques for specific inhalers, adherence to medication, and control of potential environmental triggers. Patients should be provided with a self-treatment action plan that provides a schedule for maintenance medication and doses of rescue therapy for increased symptoms and explains how to recognize severe asthma exacerbation and when to seek urgent or emergency care. Asthma control can be improved with appropriate management of common coexisting conditions such as rhinitis, sinusitis, and gastroesophageal reflux that can aggravate asthma. Pregnant asthmatics that smoke should be informed of the potential adverse effects of smoking on their asthma control as well as the potential adverse effects of smoking on the fetus, thus smoking cessation should be recommended. Patients should receive advice on controlling potential environmental triggers and measures for reducing exposure to allergens based on the results of allergy testing, particularly perennial indoor inhalant allergens.^1,17

The medical management of asthma in pregnant asthma patients is similar to that of nonpregnant ones. The therapy consists of long-term-control medications and rescue therapy. Long-term-control medications are used for maintenance therapy to prevent manifestations of asthma and include inhaled corticosteroids, long-acting beta-agonists (LABAs), leukotriene receptor antagonists, and theophylline. The appropriate therapy for patients who are not already on controller medications is determined by classifying the severity of the patient’s asthma (Table 20-1).