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1/18/2018 Dyspnea during pregnancy

Dyspnea during pregnancy

Dyspnea during pregnancy

Author Section Editors Deputy Editor

Steven E Weinberger, Charles J Lockwood, Vanessa A Barss, MD
Peter J Barnes, DM,


Last literature review version 19.3: Fri Sep 30 00:00:00 GMT

2011 | This topic last updated: Fri Dec 10 00:00:00 GMT
2010 (More)
INTRODUCTION — Dyspnea is common during pregnancy. The
development of dyspnea in the pregnant woman raises the
question as to whether she has some form of underlying cardiac
or pulmonary disease or whether her 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 recognition of the syndrome of
dyspnea during normal pregnancy [1-4].



Cardiovascular changes — The most striking cardiovascular

changes during pregnancy are increases in blood volume and
cardiac output [5-7].

Blood volume — 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" (figure 1). (See
"Hematologic changes in pregnancy".)

Cardiac output — Cardiac output also starts to rise in the

first trimester, reaching a peak at 20 to 32 weeks of
gestation that is 30 to 50 percent above baseline (figure 2)
[7,8]. 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.

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(See "Maternal cardiovascular and hemodynamic

adaptations to pregnancy".)

Respiratory changes — The normal respiratory tract changes

during pregnancy result in a compensated respiratory alkalosis,
with a higher PO2 and a lower PCO2 than in the nonpregnant
state. The lower PCO2 is thought to provide a diffusion gradient
that may facilitate the fetus' ability to eliminate waste from
aerobic metabolism. (See "Respiratory tract changes during

Elevation of the diaphragm — 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 since chest wall
mobility increases and there is flaring of the ribs [9].

Decreased FRC and stable FEV1 — Functional residual

capacity (FRC) decreases approximately 20 percent during
the latter half of pregnancy, due to a decrease in both
19.3 expiratory reserve volume (ERV) and residual volume (RV)
(figure 3) [10,11]. 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.
Laboratory and imaging tests
INFORMATION FOR PATIENTS Airway function is preserved during pregnancy, as reflected
SUMMARY AND by an unchanged forced expiratory volume in one second
RECOMMENDATIONS (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
GRAPHICSView All increase during the first trimester followed by a decrease
until 24 to 27 weeks of gestation [12].
Physiologic anemia of
pregnancy Increased ventilation and respiratory drive — Perhaps
Hemodynamics in pregnancy the most striking change in respiratory physiology during
Pulmonary function in pregnancy is an increase in resting minute ventilation,
pregnancy which rises by nearly 50 percent at term. This is primarily
Ventilation in pregnancy due to a larger tidal volume, whereas the respiratory rate
remains essentially unchanged [13]. The increase in
Dyspnea during pregnancy
ventilation is greater than the corresponding elevation in
oxygen consumption (approximately 20 percent) (figure 4)
Dyspnea differential [11].
Increased levels of progesterone during pregnancy are
Acquired heart disease and
thought to be responsible for the rise in ventilation above
that explained by the enhanced metabolic requirements.
Amniotic fluid embolism Progesterone is a known stimulant of respiration and
respiratory drive, and its levels gradually rise from
Anaphylaxis in pregnant and approximately 25 ng/mL at six weeks to 150 ng/mL at term
breastfeeding women [14].
Approach to the patient with
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Respiratory acidosis and increased arterial O2 tension

— 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
TOPIC OUTLINE (usually between 7.40 to 7.45) [15]. (See "Simple and
INTRODUCTION mixed acid-base disorders", section on 'Compensatory
respiratory and renal responses'.)
Maternal oxygenation is preserved during pregnancy. In
fact, the maternal arterial oxygen tension (PaO2) is
Cardiovascular changes
generally increased because of hyperventilation, ranging
Respiratory changes
from 106 to 108 mmHg in the first trimester to 101 to 104
DYSPNEA OF PREGNANCY mmHg in the third trimester [16,17]. Interpretation of the
EVALUATION OF PREGNANT arterial PO2 must take into account the corresponding level
WOMEN WITH DYSPNEA of PCO2, which is generally accomplished most easily by
History and physical calculation of the alveolar-arterial oxygen difference.
- Is dyspnea of acute or gradual DYSPNEA OF PREGNANCY — Sixty to 70 percent of women
onset? experience a sensation of dyspnea (often described as "air
hunger") during the course of normal pregnancy [11,18]. This
symptom commonly starts during the first or second trimester,
the frequency rises during the second trimester, and then is
reasonably stable during the third trimester (figure 5). Dyspnea
of pregnancy is usually worse when the pregnant woman is in the
sitting position, and is not associated with exercise.

The mechanism of dyspnea during normal pregnancy is not

entirely clear. It occurs while the uterus is still relatively small,
thus it cannot be attributed solely to an increase in abdominal
girth. 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, 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 [19]. (See
"Physiology of dyspnea".)


DYSPNEA — When a pregnant woman complains of dyspnea,
distinguishing between underlying disease (table 1) and
progesterone-induced hyperventilation can be a difficult
diagnostic problem [1-4]. These issues are reviewed briefly
below. The general approach to evaluation of dyspneic patients is
discussed in detail separately. (See "Approach to the patient with

History and physical examination

Is dyspnea of acute or gradual onset? — Physiologic

dyspnea during pregnancy has a gradual onset. In contrast,
pulmonary embolism is characterized by the sudden onset of

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dyspnea. Other common findings suggesting pulmonary embolism

are tachypnea, pleuritic chest pain, and hemoptysis, which do not
occur with normal dyspnea of pregnancy. Heart rate may increase
above the elevated baseline rate of normal pregnancy.

Spontaneous pneumothorax is also characterized by the sudden

onset of dyspnea and pleuritic chest pain. The peak age of
occurrence is in the early 20s; risk factors include smoking,
thoracic endometriosis, and previous or family history of
spontaneous pneumothorax. The disorder is much more common
in men. (See "Primary spontaneous pneumothorax in adults".)

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,
itching, urticaria, angioedema, tachycardia, hypotension). (See
"Anaphylaxis in pregnant and breastfeeding women".)

Acute cardiac tamponade is sudden in onset, may be associated

with chest pain, tachypnea, and dyspnea, and is life-threatening
if not promptly treated. The jugular venous pressure is markedly
elevated, and may be associated with venous distension in the
forehead and scalp. The heart sounds are often muted.
Hypotension is common due to the decline in cardiac output. (See
"Cardiac tamponade".)

Acute dyspnea can also be a sign of coronary artery ischemia or

dissection or an arrhythmia (see "Clinical features and diagnosis
of coronary heart disease in women").

Is cough or wheezing present? — Physiological dyspnea of

pregnancy is not associated with cough or wheezing.

Acute cough is most commonly due to an acute respiratory tract

infection. Other considerations include an acute exacerbation of
underlying chronic pulmonary disease, pneumonia, and
pulmonary embolism. Cough that has been present longer than
three weeks is either subacute or chronic. (See "Evaluation of
subacute and chronic cough in adults".)

Cough and wheezing are also common symptoms of asthma and

cardiac diseases with pulmonary venous hypertension. A history
of asthma symptoms, especially antedating pregnancy, suggests
asthma as the cause of dyspnea during pregnancy; although
occasional patients present with new onset asthma while
pregnant. Evidence of airflow obstruction on pulmonary function
testing supports the diagnosis of asthma. (See "Physiology and
clinical course of asthma in pregnancy".)

Is the chest clear on auscultation? — The lungs should be

clear in women with physiological dyspnea. Crackles (rales) are
indicative of abnormalities affecting the distal lung parenchyma,
such as interstitial pulmonary edema from left ventricular failure.
Heart failure affecting right ventricular filling pressures is
associated with peripheral edema and prominent neck veins.
Pulmonary edema represents a final common pathway of several
complications of pregnancy and the peripartum period:

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Severe preeclampsia/eclampsia (see "Clinical features,

diagnosis, and long-term prognosis of preeclampsia" and

Tocolytic-induced pulmonary edema (see "Pulmonary

pearls: A 24 year-old woman with pulmonary edema after
labor and delivery")

Cardiac disease (which may be acquired or congenital,

preexisting, or related to pregnancy) (See "Management of
heart failure in pregnancy" and "Acquired heart disease and
pregnancy" and "Pregnancy in women with congenital heart
disease: General principles".)

Amniotic fluid embolism (see "Amniotic fluid embolism


Focal rales with or without consolidation may also be

suggestive of pneumonia. Associated common signs and
symptoms include cough, fever, pleuritic chest pain,
dyspnea, and sputum production. (See "Diagnostic
approach to community-acquired pneumonia in adults".)

Are 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 [20]. Dyspnea accompanied by
fever and cough suggests an infectious process (eg, bronchitis,
pneumonia). (See "Overview of the risk factors, pathology, and
clinical manifestations of lung cancer" and "Diagnostic approach
to community-acquired pneumonia in adults".)

Is onset early in gestation or near term? — Physiologic

dyspnea typically begins in the first or second trimester. Women
with peripartum cardiomyopathy commonly complain of dyspnea,
but onset is rarely before 36 weeks of gestation, and affected
patients usually present during the first four to five months
postpartum. Other frequent symptoms include cough, orthopnea,
paroxysmal nocturnal dyspnea, and hemoptysis. Nonspecific
fatigue, chest discomfort, or abdominal pain may confuse the
initial evaluation due to the occurrence of similar symptoms
during normal pregnancy. (See "Peripartum cardiomyopathy".)

Laboratory and imaging tests — The history and physical

examination lead to accurate diagnoses in most patients with
dyspnea; chest radiography and pulmonary function testing
should be the first tests obtained in the majority of cases in which
additional information is required. Brain natriuretic peptide (BNP)
levels may be useful in pregnant women with a suspected cardiac
cause of dyspnea.

Spirometry is useful for diagnosis of asthma and can be

performed safely during pregnancy. The diagnosis of
asthma is based upon the presence or history of respiratory
symptoms consistent with asthma (most commonly episodic
cough, wheezing, or dyspnea provoked by typical triggers),
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combined with the demonstration of variable expiratory

airflow obstruction. (See "Diagnosis of asthma in
adolescents and adults".)

The amount of radiation exposure to the fetus from a chest

radiograph is extremely small and not known to have
adverse fetal consequences [21]. 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. A chest radiograph
should be obtained in patients with suspected pneumonia or
lung lesions. (See "Diagnostic imaging procedures during
pregnancy", section on 'Procedures using ionizing
radiation' and "Diagnostic approach to community-acquired
pneumonia in adults".)

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. (See
"Diagnostic imaging procedures during pregnancy", section
on 'Ventilation-perfusion and helical CT'.)

BNP levels are not affected by pregnancy, with typical

values of <50 pg/mL and median levels of approximately 20
pg/mL throughout pregnancy [22]. Thus, BNP levels may be
useful in the patient with suspected ventricular dysfunction
as the cause of dyspnea.

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 5th to 6th 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
10th to 12th grade reading level and are best for patients who
want in-depth information and are comfortable with some medical

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 information: Shortness of breath

(dyspnea) (The Basics)")

Beyond the Basics topics (see "Patient information:

Shortness of breath (dyspnea)")

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Two-thirds of pregnant women experience a sensation of

dyspnea (often described as "air hunger"), which starts
gradually during the first or second trimester. (See
'Dyspnea of pregnancy' above.)

When a pregnant woman complains of dyspnea, the

clinician should determine whether her symptoms are due
to an underlying disease (table 1) or physiologic
progesterone-induced hyperventilation. (See 'Evaluation of
pregnant women with dyspnea' above.)

Physiologic dyspnea of pregnancy is of gradual onset;

sudden onset or presence of cough, wheezing, rales, chest
pain, fever, or hemoptysis suggests a pathologic process
that requires further evaluation. (See 'Evaluation of
pregnant women with dyspnea' above.)

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