Maternal adaptations to pregnancy: Dyspnea and other physiologic respiratory changes

INTRODUCTION — Dyspnea, or breathing discomfort, is common during pregnancy. It is usually a physiologic result of pregnancy itself but can be caused by new or underlying cardiac or pulmonary disease.

This topic will discuss the normal changes in the respiratory system in pregnant people and physiologic dyspnea of pregnancy, as well as initial considerations for the differential diagnosis of nonphysiologic dyspnea during pregnancy and immediately postpartum. The definition, pathophysiology, and general approach to evaluation of acute and chronic nonphysiologic dyspnea in adults are reviewed in detail separately:

●(See "Physiology of dyspnea".)

●(See "Approach to the adult with dyspnea in the emergency department".)

●(See "Approach to the patient with dyspnea".)

PHYSIOLOGIC PULMONARY CHANGES IN PREGNANCY — Distinguishing physiologic dyspnea of pregnancy from other causes requires an understanding of the normal cardiovascular and pulmonary changes that occur during pregnancy [1-4]. The most striking normal cardiovascular changes in pregnancy are increased blood volume (figure 1)and increased cardiac output (figure 2). (See "Maternal adaptations to pregnancy: Hematologic changes" and "Maternal adaptations to pregnancy: Cardiovascular and hemodynamic changes".):

The normal pulmonary changes (described in the following sections) result in compensated respiratory alkalosis, with a lower partial pressure of carbon dioxide (PCO₂) and a higher partial pressure of oxygen (PO₂) compared with the nonpregnant state. The lower PCO₂ supplies a diffusion gradient, which may help the fetus eliminate waste from aerobic metabolism.

Interestingly, healthy patients carrying twins appear to have similar respiratory function as those with a singleton pregnancy [5].

Chest — Outward flaring of the ribs begins early in pregnancy. The subcostal angle changes from 68 to as much as 103 degrees [6,7], and the chest diameter can increase ≥2 cm [8]. The change in chest wall configuration may be partly related to hormone-induced relaxation of ligamentous attachments to the lower ribs [9,10].

Diaphragm — The progressively enlarging uterus raises the diaphragm 4 cm above its usual resting position [11]. Diaphragmatic excursion during respiration is not impaired, and increases by up to 2 cm.

Lung volumes and flow rates — Functional residual capacity (FRC) decreases by approximately 20 percent during the latter half of pregnancy, due to a decrease in both expiratory reserve volume (ERV) and residual volume (figure 3) [12,13].

Variable changes in vital capacity (VC) and total lung capacity (TLC) occur, but they are generally small and probably not clinically significant.

Airway function and flow rates are preserved during pregnancy, as reflected by an unchanged forced expiratory volume in one second (FEV1) and an unchanged FEV1/FVC ratio.

Diffusing capacity — Minor changes of little clinical importance have been described in diffusing capacity for carbon monoxide: an increase during the first trimester followed by a decrease until 24 to 27 weeks of gestation [14].

Ventilation — Resting minute ventilation rises by nearly 50 percent at term. This is primarily due to a larger tidal volume (increased up to 40 percent), whereas the respiratory rate remains essentially unchanged [15]. The increase in ventilation is greater than the corresponding increase in oxygen consumption (approximately 20 percent) (figure 4) [13].

Higher progesterone levels during pregnancy are probably responsible for the rise in ventilation above that explained by the enhanced metabolic requirements. Progesterone is a stimulant of respiration and respiratory drive, and its concentration gradually rises from approximately 25 ng/mL at 6 weeks to 150 ng/mL at term [16].

Gas exchange and arterial blood gases — As a result of the progesterone-induced increase in alveolar ventilation, arterial PCO₂ (PaCO₂) falls to a plateau of 27 to 32 mmHg during pregnancy. This respiratory alkalosis is followed by compensatory renal excretion of bicarbonate so that the resultant arterial pH is normal to slightly alkalotic (usually between 7.40 and 7.45) [17]. (See "Simple and mixed acid-base disorders", section on 'Compensatory respiratory and renal responses'.)

Maternal oxygenation is preserved during pregnancy. In fact, maternal PaO₂ is generally increased because of hyperventilation, ranging from 106 to 108 mmHg in the first trimester to 101 to 104 mmHg in the third trimester [18,19]. Interpretation of the PaO₂ is accomplished most easily by looking at the alveolar-arterial (A-a) oxygen difference, which takes the PaCO₂ into account when calculating the alveolar PO₂ (calculator 1) [20]. The normal A-a gradient varies with age and can be estimated from the following equation [20,21]:

Oxygen consumption — Among healthy pregnant people, maximal O₂ consumption (VO₂max) is preserved throughout pregnancy and may increase during the second trimester with values 20 percent above baseline at term, secondary to an increase in maternal myocardial O₂ demand and renal O₂ consumption, increased work to ventilate the lung in pregnancy, and fetal metabolic demands [22-24].

Upper respiratory tract mucosa — The upper respiratory mucosa during pregnancy shows hyperemia, glandular hyperactivity, increased phagocytic activity, and increased mucopolysaccharide content on pathologic examination [25]. Pregnant people often experience nasal stuffiness and epistaxis, possibly as a result of these changes. (See "Recognition and management of allergic disease during pregnancy", section on 'Pregnancy rhinitis'.)

PHYSIOLOGIC DYSPNEA OF PREGNANCY — Sixty to 75 percent of pregnant people experience episodic dyspnea (often described as "air hunger") during the course of normal pregnancy [13,26,27] (see "Approach to the patient with dyspnea", section on 'Descriptors of breathing discomfort'). It commonly starts during the first or second trimester, becomes more frequent during the second trimester, and then generally stabilizes during the third trimester (figure 5). The severity, which can be quantified with various scales (table 1A-B), tends to increase along with the frequency [27].

The mechanism is not entirely clear. Because it initially occurs while the uterus is still relatively small, it cannot be attributed solely to upward pressure on the diaphragm. Progesterone-induced hyperventilation is likely to be at least partially responsible, perhaps due to the increase in ventilation above the level needed to meet the rise in metabolic demand. Clinical observations are consistent with this hypothesis. In one observational study, dyspnea during pregnancy correlated with a low partial pressure of carbon dioxide in arterial blood (PaCO₂), and the individuals most likely to experience dyspnea were those who had relatively high baseline (ie, nonpregnant) PaCO₂ values [28]. Two small studies of males reported increased ventilation during treatment with medroxyprogesterone acetate [29,30]. (See "Physiology of dyspnea".)

An echocardiographic study investigating possible cardiac factors contributing to dyspnea of pregnancy compared 30 pregnant patients who had significant dyspnea requiring an emergency department visit with 30 pregnant patients without dyspnea [31]. Studies at 38 weeks of gestation showed a slight but statistically significant increase in septal and posterior wall thickness and pulmonary artery pressure in those with dyspnea. There were also echocardiographic changes suggesting subtle diastolic dysfunction. However, the values for pregnant patients with dyspnea were not outside of the normal range, and whether these patients with significant dyspnea were representative of those with less severe dyspnea of pregnancy is not known.

APPROACH TO DIFFERENTIAL DIAGNOSIS — When a pregnant or recently pregnant patient reports dyspnea, distinguishing between underlying disease (eg, asthma) (table 2), a new problem (eg, pulmonary embolism, peripartum cardiomyopathy, infection), and progesterone-induced hyperventilation (dyspnea of pregnancy) can be a difficult diagnostic problem [1-4,32].

A key principle is that dyspnea of pregnancy is an isolated finding; it is not accompanied by other signs and symptoms such as cough, wheezing, fever, tachypnea, pleuritic or other chest pain, hemoptysis, sputum production, hypoxemia, tachycardia, irregular heart rhythm, or immunoglobulin E (IgE)-mediated reactions (eg, urticaria). It typically begins in the first or second trimester and gradually progresses. Imaging, pulse oximetry, and laboratory test results are normal for pregnancy.

The differential diagnosis is also influenced by the stage of pregnancy. In the first half of pregnancy, the differential diagnosis, other than dyspnea of pregnancy, is similar to that in nonpregnant patients. Later in pregnancy (especially the third trimester) or postpartum, pregnancy-related etiologies, such as preeclampsia with severe features, peripartum cardiomyopathy, pulmonary or amniotic fluid embolism, and sepsis, should also be considered.

Indications for urgent evaluation — We advise urgent evaluation of patients presenting with moderate or severe acute dyspnea in whom there is concern for pulmonary embolism, pulmonary edema, pneumothorax, upper airway obstruction, significant asthma exacerbation, heart failure, cardiac tamponade, myocardial ischemia, angioedema, or anaphylaxis. These patients may have heart rate >120 beats/minute, respiratory rate >24 breaths/minute, oxygen saturation (SpO₂) <95 percent on pulse oximetry [33], use of accessory respiratory muscles, difficulty speaking full sentences, stridor, asymmetric breath sounds or percussion, diffuse crackles (also known as rales), diaphoresis, neck or substernal chest pain, cyanosis, hemoptysis, depressed or agitated mental status, or oropharyngeal swelling.

If the clinician does not have the training and experience to diagnose and treat these disorders, then consultation should be obtained from a maternal-fetal medicine or pulmonary specialist who can see the patient immediately, or the patient can be referred to an emergency department. (See "Approach to the adult with dyspnea in the emergency department".)

Initial history and physical examination — The source of dyspnea in most patients is either the respiratory or cardiovascular system, but more than one process may be occurring in a given patient. Other factors unrelated to the lungs or heart should also be considered as etiologic or contributing factors, including severe anemia [34] (see "Anemia in pregnancy"). The general approach to the evaluation of patients with acute and chronic dyspnea is discussed in detail separately (see "Approach to the adult with dyspnea in the emergency department" and "Approach to the patient with dyspnea"). The following discussion focuses on the evaluation of patients who develop dyspnea during pregnancy or within six weeks postpartum.

●Is the patient known to have underlying asthma or other pulmonary disease? – The most common underlying disorder potentially causing dyspnea in females of child-bearing age is asthma. There is no predictable effect of pregnancy on preexisting asthma, as approximately equal percentages of patients experience worsening, improvement, or no change in the course of their asthma during pregnancy. Pregnant patients with mild asthma can often be managed by their primary care clinician. Those with moderate to severe asthma, or a less common underlying pulmonary disease, ideally should be managed by a pulmonary specialist and/or a maternal-fetal medicine specialist. (See "Asthma in pregnancy: Clinical course and physiologic changes".)

●Is the patient known to have underlying heart disease? – The most common underlying heart diseases with the potential to cause dyspnea during pregnancy are congenital heart disease and valvular heart disease. Dyspnea may be worse at night or when lying down. Pregnant patients with underlying heart disease should be managed by a cardiologist and often by a maternal-fetal medicine specialist as well. (See "Pregnancy in women with congenital heart disease: General principles" and "Pregnancy and valve disease".)

●Did dyspnea develop acutely? – Physiologic dyspnea during pregnancy has a gradual onset. Causes of acute-onset dyspnea in pregnancy include:

•Pulmonary embolism – In addition to the sudden onset of dyspnea, other common findings suggesting pulmonary embolism are tachypnea and pleuritic chest pain, which do not occur with normal dyspnea of pregnancy. Heart rate may increase above the elevated baseline rate of normal pregnancy. Oxygen saturation by pulse oximetry is often low with acute pulmonary embolism, but normal oxygen saturation does not exclude this diagnosis. (See "Pulmonary embolism in pregnancy: Clinical presentation and diagnosis".)

•Acute upper airway obstruction – Acute dyspnea from upper airway obstruction is a symptom of anaphylaxis and is often accompanied by other symptoms of an acute IgE-mediated hypersensitivity reaction (eg, flushing, pruritus, urticaria, angioedema, tachycardia, hypotension). A history of exposure to a causative agent (table 3) and simultaneous hypersensitivity symptoms suggest anaphylaxis. (See "Anaphylaxis during pregnancy and delivery".)

Additional causes of acute upper airway obstruction include central airway obstruction (typically intraluminal compromise from intrinsic or extrinsic compression from a benign or malignant tumor), foreign body, food obstruction, and infection. Again, the history typically helps distinguish among these entities. (See "Clinical presentation, diagnostic evaluation, and management of malignant central airway obstruction in adults".)

•Spontaneous pneumothorax – Spontaneous pneumothorax is characterized by the sudden onset of dyspnea and pleuritic chest pain. The peak age of occurrence is the early 20s; risk factors include smoking, thoracic endometriosis, and previous personal or family history of spontaneous pneumothorax. However, the disorder is much more common in males. (See "Pneumothorax in adults: Epidemiology and etiology".)

•Arrhythmia or coronary artery ischemia or dissection – A rapid or irregular heartbeat accompanying the onset of dyspnea can suggest a supraventricular or ventricular tachyarrhythmia, whereas cardiac ischemia from either atherosclerotic coronary artery disease or coronary artery dissection is often associated with chest pain or pressure. (See "Clinical features and diagnosis of coronary heart disease in women" and "Coronary artery disease and myocardial infarction in young people" and "Spontaneous coronary artery dissection".)

●Is a new cough present? – Physiologic dyspnea of pregnancy is not associated with cough. Patients with a new cough are further evaluated for the following disorders based on their symptoms.

•Respiratory infection – Acute cough is most commonly due to an acute respiratory infection (eg, rhinovirus, coronavirus, influenza or parainfluenza); acute bronchitis is a possibility when cough is accompanied by wheezing. Active pulmonary tuberculosis is less common and can present with the additional symptoms of fever, weight loss, night sweats, and malaise. (See "Asthma in pregnancy: Clinical course and physiologic changes" and "Clinical evaluation and diagnostic testing for community-acquired pneumonia in adults" and "Tuberculosis disease (active tuberculosis) in pregnancy".)

•Asthma – An asthma exacerbation may present with new or worsening dyspnea, cough, and/or wheezing. A history of asthma or asthma symptoms antedating pregnancy may suggest asthma as the cause of dyspnea during pregnancy, although occasional patients present with new-onset asthma while pregnant. Evidence of reversible airflow obstruction on pulmonary function testing supports the diagnosis of asthma. (See "Asthma in pregnancy: Clinical course and physiologic changes".)

•Cardiac disorders with pulmonary venous hypertension – Cardiac disorders with pulmonary venous hypertension can present with acute cough and wheezing. Pulmonary venous hypertension should be suspected in patients with underlying cardiac disease (including preeclampsia) that is potentially associated with elevated left atrial pressure, or if crackles are present on chest auscultation in the absence of known parenchymal lung disease. The diagnosis of myocardial or valvular heart disease can be confirmed by echocardiography.

•Other causes of acute cough – These include an acute exacerbation of underlying chronic pulmonary disease, acute respiratory distress syndrome, and, rarely, pulmonary embolism.

●Is a subacute/chronic cough present? – Cough that has been present for longer than three weeks can be considered subacute or chronic. Common causes include upper airway cough syndrome, asthma, and chronic gastroesophageal reflux.

Upper airway cough syndrome typically responds to empiric treatment for postnasal drip; asthma can often be suspected based on previous history and physical examination and can be diagnosed with pulmonary function testing; and gastroesophageal reflux can be suspected based on history, diagnosed based on barium swallow, or empirically treated. (See "Causes and epidemiology of subacute and chronic cough in adults".)

●Is chest auscultation abnormal? – The lungs should be clear in patients with physiologic dyspnea. Wheezing, rales (crackles), and focal findings are not normal.

•Wheezing – Wheezing indicates airflow obstruction and, in the reproductive age group, is most suggestive of underlying asthma or acute bronchitis. Wheezing typically results from airway obstruction caused by bronchoconstriction, airway inflammation, or excessive mucus production and/or poor clearance [35-38]. Asthma is typically diagnosed by a combination of history, physical examination, and demonstration of reversible airflow obstruction on pulmonary function testing. Other less common causes of wheezing include chronic obstructive pulmonary disease, extrathoracic disease (eg, anaphylaxis or vocal cord edema or paralysis), or other intrathoracic disorders affecting airway patency. These discussions are presented in detail elsewhere.

-(See "Asthma in adolescents and adults: Evaluation and diagnosis".)

-(See "Chronic obstructive pulmonary disease: Diagnosis and staging".)

-(See "Evaluation of wheezing illnesses other than asthma in adults".)

•Rales (crackles) – Rales are indicative of abnormalities affecting the distal lung parenchyma, such as interstitial pulmonary edema from left ventricular failure or mitral stenosis, or a variety of forms of interstitial lung disease. Pulmonary edema represents a final common pathway of several complications of pregnancy and the peripartum period, including:

-Preeclampsia with severe features – Pulmonary edema can occur due to a combination of factors, including capillary leak, left heart failure, acute severe hypertension, iatrogenic volume overload, and hypoalbuminemia, and is a common cause of dyspnea in the third trimester. (See "Preeclampsia: Clinical features and diagnosis", section on 'Pulmonary edema' and "Eclampsia".)

-Iatrogenic fluid overload – Patients receiving magnesium sulfate for preeclampsia or fetal neuroprotection, oxytocin for induction of labor, or glucocorticoids for fetal maturation are prone to iatrogenic fluid overload. The risk of pulmonary edema increases with the number of concomitant processes (eg, a patient with a twin gestation induced for preterm preeclampsia with severe features may be receiving magnesium sulfate, oxytocin, and glucocorticoids). (See "Preeclampsia: Intrapartum and postpartum management and long-term prognosis", section on 'Fluids'.)

-Heart failure – Pulmonary edema may be secondary to acquired or congenital heart disease. Acquired heart disease may be preexisting or related to pregnancy. (See "Management of heart failure during pregnancy" and "Acquired heart disease and pregnancy" and "Pregnancy in women with congenital heart disease: General principles".)

-Acute respiratory distress syndrome (ARDS) – ARDS may be the result of amniotic fluid embolism, sepsis, or severe acute respiratory syndrome coronavirus 2 [SARS-CoV-2]). (See "Amniotic fluid embolism" and "Acute respiratory failure during pregnancy and the peripartum period" and "COVID-19: Clinical features".)

-Tocolytic-induced pulmonary edema – Beta-agonists (eg, terbutaline) are commonly used for tocolysis. Fluid overload is probably the major pathogenic factor in tocolytic-related pulmonary edema, although cardiac dysfunction and increased capillary permeability may also contribute. (See "Acute respiratory failure during pregnancy and the peripartum period", section on 'Tocolytics'.)

•Focal rales with or without consolidation – Focal rales, either with or without consolidation, suggest pneumonia. Associated common signs and symptoms include cough, fever, pleuritic chest pain, dyspnea, and sputum production. (See "Clinical evaluation and diagnostic testing for community-acquired pneumonia in adults".)

●Are pain and/or other symptoms present? – Physiologic dyspnea is not accompanied by pain or other symptoms.

Thoracic tumors and pulmonary emboli may present with dyspnea and chest pain, hemoptysis, cough, or wheezing [39]. Dyspnea accompanied by fever and cough suggests an infectious process (eg, bronchitis, pneumonia). Heart failure affecting right ventricular filling pressures is associated with peripheral edema and prominent neck veins. (See "Clinical manifestations of lung cancer" and "Clinical evaluation and diagnostic testing for community-acquired pneumonia in adults" and "Rheumatic mitral stenosis: Clinical manifestations and diagnosis" and "Right ventricular myocardial infarction".)

●Did dyspnea present or worsen near term? – Physiologic dyspnea typically begins in the first or second trimester. Patients with peripartum cardiomyopathy commonly complain of dyspnea, but onset is typically gradual and after 36 weeks of gestation; affected patients usually present during the first four to five months postpartum [32,40]. Other frequent symptoms include cough, orthopnea, paroxysmal nocturnal dyspnea, pedal edema, dizziness, and hemoptysis. Nonspecific fatigue, chest discomfort, or abdominal pain may confuse the initial evaluation due to the occurrence of similar symptoms during normal pregnancy. Common examination findings include edema, tachycardia or arrhythmias, tachypnea, jugular venous distension, and rales [40]. (See "Peripartum cardiomyopathy: Etiology, clinical manifestations, and diagnosis".)

Severe anemia can impair oxygen delivery, leading to dyspnea from a variety of mechanisms. Severe anemia before delivery is most common during the late second and the third trimester as a result of obstetric hemorrhage or iron deficiency. (See "Anemia in pregnancy".)

Dyspnea related to obesity is commonly associated with a sense of increased effort to breathe or work of breathing. It may worsen near term due to the enlarging uterus and deconditioning during pregnancy.

●What medications is the patient taking? – A variety of medications have pulmonary toxicity. Patients should be queried about their medication history in case they are taking one of the many medications that can lead to respiratory complications. (See "Pulmonary disease induced by cardiovascular drugs" and "Overview of pleuropulmonary diseases associated with rheumatoid arthritis", section on 'Drug-induced lung toxicity'.)

●What is the patient's family, social, and occupational history? – Some pulmonary disorders in females of childbearing age have a well-defined phenotype and genetic component (eg, alpha-1 antitrypsin deficiency, cystic fibrosis). Some disorders, such as sarcoidosis, have a less well-defined phenotype but the family history is sometimes positive, even though the specific genetic components have not been well defined.

Social history may provide clues for an occupation-related lung disease or exposure to cigarette smoke, dusts, or fumes. The most common acquired occupational lung diseases include occupational asthma, bronchitis, bronchiolitis, hypersensitivity pneumonitis, acute toxic inhalant syndromes, pneumoconioses, and tumors.

Initial laboratory and imaging tests — The history and physical examination described above lead to accurate diagnoses in most patients with dyspnea. Ancillary studies are briefly mentioned below and discussed in detail separately. (See "Approach to the adult with dyspnea in the emergency department", section on 'History'.)

●All pregnant patients are evaluated for anemia at the first prenatal visit, at the beginning of the third trimester, and during/after episodes of significant bleeding.

●When the initial evaluation is suggestive of pulmonary embolism, clinicians should have a low threshold for objective testing; one approach is shown in the algorithm (algorithm 1) and discussed in detail separately. (See "Pulmonary embolism in pregnancy: Clinical presentation and diagnosis", section on 'Diagnostic imaging'.)

Because D-dimer levels normally increase during pregnancy, measurement of D-dimer has limited utility for diagnosis of pulmonary embolism during pregnancy and is not routinely measured. (See "Pulmonary embolism in pregnancy: Clinical presentation and diagnosis", section on 'D-dimer'.)

●When the initial evaluation is not suggestive of pulmonary embolism, the choice of tests is determined by symptoms and examination findings. As an example, a patient with wheezing and no other symptoms may only require spirometry for the diagnosis of asthma (demonstration of airflow obstruction that improves following an inhaled bronchodilator), but a patient with wheezing and cough may require both spirometry and a chest radiograph to evaluate for infection. (See "Asthma in adolescents and adults: Evaluation and diagnosis".)

A chest radiograph should be obtained in patients with suspected pneumonia or other parenchymal lung disease. The amount of fetal radiation exposure from a chest radiograph is not known to have adverse fetal consequences [41]. Nevertheless, chest radiography during pregnancy should be performed only when clearly medically indicated, and the mother's abdomen should be appropriately shielded. (See "Clinical evaluation and diagnostic testing for community-acquired pneumonia in adults" and "Diagnostic imaging in pregnant and lactating patients".)

●Echocardiography is generally performed when heart failure or pulmonary hypertension is suspected based on clinical findings, brain natriuretic peptide (BNP) or N-terminal proBNP levels, cardiomegaly on chest radiograph, or when the cause of dyspnea remains unclear after initial evaluation. BNP levels are not affected by pregnancy, with typical values of <50 pg/mL and median levels of approximately 20 pg/mL throughout pregnancy [42]. (See "Approach to the patient with dyspnea", section on 'Pulmonary hypertension suggested by echocardiography'.)

●Arterial blood gas analysis is typically not necessary except in selected individuals (eg, suspicion of hypercapnia).

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Respiratory disease in pregnancy".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5^th to 6^th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10^th to 12^th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

●Basics topics (see "Patient education: Shortness of breath (The Basics)" and "Patient education: Pregnancy symptoms (The Basics)")

●Beyond the Basics topics (see "Patient education: Shortness of breath (dyspnea) (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

●Clinical presentation – Approximately two-thirds of pregnant people experience a sensation of dyspnea (often described as "air hunger"). This symptom commonly starts during the first or second trimester; the frequency rises during the second trimester and then generally stabilizes during the third trimester. (See 'Physiologic dyspnea of pregnancy' above.)

●Physiologic versus nonphysiologic dyspnea – Physiologic dyspnea of pregnancy is an isolated finding related, in part, to progesterone-induced hyperventilation; it is not accompanied by other signs and symptoms of cardiopulmonary disease, such as cough, wheezing, fever, tachypnea, pleuritic or other chest pain, hemoptysis, hypoxemia, tachycardia, an irregular heart rhythm, or immunoglobulin E (IgE)-mediated reactions. It typically begins with gradual onset in the first or second trimester. Imaging, pulse oximetry, and laboratory test results are normal for pregnancy. (See 'Approach to differential diagnosis' above.)

●Diagnostic evaluation – When a pregnant patient reports dyspnea, the clinician should consider the entire clinical picture to distinguish whether the symptoms are due to a new acute disorder (eg, pulmonary embolism), exacerbation of an underlying disease (eg, asthma), or physiologic progesterone-induced hyperventilation. (See 'Approach to differential diagnosis' above.)

•Alarm signs and symptoms – Clues to the need for an urgent evaluation include heart rate >120 beats/minute, respiratory rate >24 breaths/minute, pulse oxygen saturation (SpO₂) <95 percent, use of accessory respiratory muscles, difficulty speaking in full sentences, stridor, asymmetric breath sounds or percussion, diffuse rales, diaphoresis, neck or substernal chest pain, cyanosis, hemoptysis, depressed or agitated mental status, and oropharyngeal swelling. (See 'Indications for urgent evaluation' above.)

•Initial approach – The history and physical examination lead to accurate diagnoses in most patients with dyspnea. For patients in whom additional information is needed to make a diagnosis, but are not thought to have a pulmonary embolus, chest radiography and/or pulmonary function testing are typically the first tests obtained (table 4). Hematocrit or hemoglobin should also be checked to assess whether moderate or severe anemia may be causing or contributing to dyspnea. (See 'Initial laboratory and imaging tests' above.)

•Additional testing – Additional testing can include imaging for patients with suspected pulmonary embolus (algorithm 1), or brain natriuretic peptide levels or echocardiography for patients with a suspected cardiac cause of dyspnea. (See 'Approach to differential diagnosis' above.)