Dyspnea during pregnancy

May 11, 1998

The development of dyspnea in the pregnant woman raises the question of whether the patient has some form of underlying cardiac or pulmonary disease, or whether the dyspnea is due to the pregnancy itself. Making this assessment requires an understanding of the cardiopulmonary changes that occur during normal pregnancy as well as a recognition of the syndrome of dyspnea during normal pregnancy.

CARDIAC CHANGES DURING PREGNANCY — The most striking cardiovascular changes during pregnancy include increases in circulating blood volume and cardiac output [1,2,3]. (See "Systemic hemodynamics and renal function in pregnancy"). Blood volume starts to rise during the first trimester and eventually reaches a maximum that is 40 to 50 percent above the baseline, nonpregnant blood volume. Because plasma volume increases more than red cell mass, the hematocrit generally falls, resulting in the physiologic "anemia of pregnancy" (show figure 1).

Cardiac output also starts to rise in the first trimester, reaching a peak at 20 to 32 weeks gestation that is 30 to 50 percent above baseline (show figure 2) [3,4]. Although the increase in cardiac output is initially due to a rise in stroke volume, the increase is maintained later in pregnancy by an increase in heart rate, as stroke volume falls during the third trimester. A decrease in systemic vascular resistance accompanies the increase in cardiac output. Blood pressure during pregnancy is often notable for a rise in pulse pressure due to an unchanged systolic pressure accompanied by a decrease in diastolic pressure.

RESPIRATORY SYSTEM FUNCTION DURING PREGNANCY — Although the progressively enlarging uterus causes diaphragm position to rise up to 4 cm above its usual resting position, diaphragmatic excursion during respiration is not impaired [5]. Functional residual capacity (FRC) decreases approximately 20 percent during the latter half of pregnancy, due to a decrease in both expiratory reserve volume (ERV) and residual volume (RV) (show figure 3) [6,7]. Variable and generally minor changes in vital capacity (VC) and total lung capacity (TLC) have also been observed, but the magnitude of these changes suggests they are not likely to be clinically significant.

Airway function is preserved during pregnancy, as reflected by an unchanged forced expiratory volume in one second (FEV1) and an unchanged FEV1/FVC ratio. Minor changes, which are of little clinical importance, have been described in diffusing capacity for carbon monoxide (DLCO): an increase during the first trimester followed by a decrease until weeks 24 to 27 [8].

Ventilation and respiratory drive — Perhaps the most striking change in respiratory physiology during pregnancy is an increase in resting minute ventilation, which rises by nearly 50 percent at term. This is primarily due to a larger tidal volume, whereas the respiratory rate remains essentially unchanged [9]. The increase in ventilation is greater than the corresponding elevation in oxygen consumption (approximately 20 percent) (show figure 4) [7].

Increased levels of progesterone during pregnancy are thought to be responsible for the rise in ventilation above that explained by the enhanced metabolic requirements. Progesterone is a known stimulant of respiration and respiratory drive, and its levels rise gradually rise from approximately 25 ng/mL at six weeks to 150 ng/mL at term [10].

Arterial blood gases and acid-base status — As a result of the progesterone-induced increase in alveolar ventilation, arterial PCO2 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 to 7.45 [11]. (See "Simple and mixed acid-base disorders", section on Compensatory responses).

Maternal oxygenation is preserved during pregnancy. In fact, the maternal arterial PO2 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 [12,13]. Interpretation of the arterial PO2 must take into account the corresponding level of PCO2, which is generally accomplished most easily by calculation of the alveolar-arterial oxygen difference.

DYSPNEA OF PREGNANCY — During the course of a normal and uncomplicated pregnancy, as many as 60 to 70 percent of women experience a sensation of dyspnea, which is commonly described as a feeling of air hunger [7,14]. This symptom commonly starts during the first or second trimester, before it can be explained by an increase in abdominal girth. The frequency of dyspnea rises during the second trimester and is reasonably stable during the third trimester (show figure 5).

The mechanism of dyspnea during normal pregnancy is not entirely clear. It is likely that progesterone-induced hyperventilation is at least partially responsible, perhaps due to the increase in ventilation above the level needed to meet the rise in metabolic demand. The following observations from one report are consistent with this hypothesis: the presence of dyspnea during pregnancy correlated with a low PCO2; and the women most likely to experience dyspnea were those who had relatively high baseline (ie, nonpregnant) values for PCO2 [15]. (See "Physiology of dyspnea").

EVALUATION OF DYSPNEA DURING PREGNANCY — When a pregnant woman complains of dyspnea, distinguishing between underlying disease and progesterone-induced hyperventilation can be a difficult diagnostic problem. Although almost any cardiac or pulmonary disorder or severe anemia can cause dyspnea, the pulmonary diseases most likely to cause dyspnea during pregnancy are asthma and pulmonary embolism. (See "Approach to the patient with dyspnea" and see "ATS guidelines: Dyspnea: Mechanisms; assessment; and management-I").

  •  A previous history of asthma is a helpful clue when considering asthma as the cause of dyspnea during pregnancy; however, occasional patients present with new onset asthma while pregnant. (See "Pregnancy in patients with asthma"). Useful objective findings include the presence of wheezing on chest examination and airflow obstruction on pulmonary function testing.

  •  Pulmonary embolism is typically characterized by the sudden onset of dyspnea as opposed to the gradual onset of dyspnea due to hyperventilation. Other common findings suggesting pulmonary embolism are pleuritic chest pain and hemoptysis, neither of which is part of the  syndrome of dyspnea during pregnancy. (See "Venous thromboembolism in pregnancy").

  •  An additional historical feature that is helpful, if present, is cough. Cough is common with primary pulmonary disorders and with cardiac diseases causing pulmonary venous hypertension, but is not expected with the syndrome of dyspnea during pregnancy.

  •  Acute respiratory distress syndrome (ARDS) is an uncommon cause of dyspnea during pregnancy, occurring with approximately 0.3 percent of deliveries [16]. ARDS is generally associated with complications of pregnancy such as toxemia, leukoagglutinin reactions, amniotic fluid embolism, or premature labor treated with tocolytic agents. (See "Transfusion-related acute lung injury (pulmonary leukoagglutinin reactions)" and see "Amniotic fluid embolism").

Besides spirometry and arterial blood gases, neither of which is contraindicated during pregnancy, the other major diagnostic tests often considered are chest radiography and radionuclide lung scanning. The amount of radiation exposure to the fetus from a chest radiograph is extremely small and thought to be unlikely to have adverse fetal consequences [17].

Nevertheless, chest radiography during pregnancy should be done only when there is a good medical reason, and appropriate shielding of the mother's abdomen should be used. Similarly, radionuclide lung scanning, which requires use of technetium-labeled macroaggregates of albumin (for the perfusion scan) and inhaled xenon (for the ventilation scan), is also thought to pose little risk to the fetus, but again should only be used when there is a serious consideration of pulmonary embolic disease [18,19]. The radiation dosage can be limited by performing the perfusion scan without the ventilation scan whenever possible, and/or by reducing the perfusion agent dose [20]. (See "Diagnostic imaging procedures during pregnancy").