Review Article

Obstetric Medicine
2015, Vol. 8(3) 126–132
! The Author(s) 2015
Acute respiratory failure in pregnancy Reprints and permissions:
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DOI: 10.1177/1753495X15589223
Stephen E Lapinsky obm.sagepub.com

Abstract
Respiratory failure affects up to 0.2% of pregnancies, more commonly in the postpartum period. Altered maternal respiratory physiology affects the
assessment and management of these patients. Respiratory failure may result from pregnancy-specific conditions such as preeclampsia, amniotic fluid
embolism or peripartum cardiomyopathy. Pregnancy may increase the risk or severity of other conditions, including thromboembolism, asthma, viral
pneumonitis, and gastric acid aspiration. Management during pregnancy is similar to the nonpregnant patient. Endotracheal intubation in pregnancy carries
an increased risk, due to airway edema and rapid oxygen desaturation following apnea. Few data are available to direct prolonged mechanical ventilation in
pregnancy. Chest wall compliance is reduced, perhaps permitting slightly higher airway pressures. Optimizing oxygenation is important, but data on the use
of permissive hypercapnia are limited. Delivery of the fetus does not always improve maternal respiratory function, but should be considered if benefit to
the fetus is anticipated.

Keywords
Pregnancy, obstetric, respiratory failure, mechanical ventilation

Inadequate gas exchange due to pulmonary or extra-pulmonary con- Causes of respiratory failure in pregnancy
ditions may produce hypoxemic (type 1) or hypercapnic (type 2)
respiratory failure. Respiratory failure may complicate about 0.1% Respiratory failure may be caused by several pregnancy-specific com-
to 0.2% of pregnancies. The pregnant patient is at risk of various plications, as well as by other conditions, some of which may be exa-
pregnancy-specific conditions as well as other diseases, which may pre- cerbated by pregnancy (Table 1). The more common conditions are
cipitate respiratory failure (Table 1). Maternal hypoxemia and hyper- reviewed, with a brief outline of specific management in pregnancy.
capnia carry potential risks for the fetus. This review discusses the
causes, risks, and management of respiratory failure in pregnancy.
Asthma
Respiratory physiologic changes in Asthma affects 4% to 8% of the general population and is a common
pregnancy pulmonary disorder in pregnancy. Approximately a third of asthmatics
remain unchanged during pregnancy, while a similar proportion deteri-
Hormonal changes in pregnancy affect the upper respiratory tract and orate or improve.8 Asthma during pregnancy is associated with adverse
cause airway hyperemia and edema.1 The diaphragm is displaced effects, including an increased incidence of preterm labor, low neonatal
upwards by up to 4 cm, but the potential loss of lung volume is birth weight, increased perinatal mortality, and an association with
offset by widening of the anteroposterior and transverse thoracic diam- preeclampsia, chronic hypertension, and complicated labor.9,10
eters. Functional residual capacity (FRC) decreases by 10% to 25% by Management of the acute asthmatic attack during pregnancy is not
term.2 The vital capacity remains unchanged, and total lung capacity different to management in the non-pregnant patient. A large body of
decreases only minimally. Measurements of airflow (FEV1) and lung literature exists demonstrating the lack of teratogenicity of drugs used
compliance are not altered during pregnancy, but chest wall and total in the pharmacotherapy of asthma in pregnancy. In general, the risks
respiratory compliance are reduced in the third trimester.3 of poorly controlled asthma far outweigh the possible adverse effects of
Minute ventilation increases progressively during pregnancy, begin- drug therapy.11,12 Selective short-acting beta2-agonists have demon-
ning in the first trimester and reaching 20% to 40% above baseline by strated an acceptable safety profile for the fetus,13 although nonselec-
term. An increase in respiratory drive is caused by elevated serum tive beta-agonists such as epinephrine carry a risk of uterine
progesterone levels, producing an increase in tidal volume with very vasoconstriction and are probably best avoided for treatment of
little change in respiratory rate.4 A respiratory alkalosis develops asthma. Systemic corticosteroids are indicated in similar circumstances
with compensatory renal excretion of bicarbonate, with PaCO2 falling to the nonpregnant patient; however, intrauterine growth restriction
to 28 to 32 mmHg (3.8–4.3 kPa) and plasma bicarbonate falling to has been documented, associated with either the use of corticosteroids
18 to 21 mEq/L.5 Alveolar-to-arterial oxygen tension differences or with asthma severity.14 Halogenated corticosteroids (such as pred-
(PAO2-PaO2) are usually unchanged by pregnancy, although mild nisolone, prednisone) do not cross the placenta to a significant degree,
hypoxemia may develop in the supine position as FRC diminishes so fetal and neonatal adrenal suppression is not a major concern with
near term. Oxygen consumption is increased, beginning in the first these drugs.
trimester and reaching 20% to 33% above baseline by the third
trimester. The combination of a reduced FRC and increased oxygen
consumption cause the pregnant patient to the rapidly develop hypoxia Mount Sinai Hospital and the Interdepartmental Division of Critical Care,
in response to hypoventilation or apnea.6 University of Toronto, Toronto, Canada
Alkalosis may worsen fetal oxygenation by reducing uterine blood
flow.7 This can occur during hyperventilation related to labor as well Corresponding author:
as due to a metabolic alkalosis that can be produced by volume deple- Stephen Lapinsky, Mount Sinai Hospital and the Interdepartmental Division
tion and vomiting. Adequate pain relief blunts this ventilatory of Critical Care, University of Toronto, 600 University Ave #18-214,
response, and can correct the hyperventilation associated with active Toronto M5G 1X5, Canada.
labor. Email: [email protected]
Lapinsky 127

Labor and delivery carry some risks for asthmatic patients, partly by physicians or the patient to obtain a chest radiograph, due to
due to the drugs commonly administered. Narcotics other than fen- inappropriate concern of radiation exposure (Table 2). Antibacterial
tanyl may release histamine, which can worsen bronchospasm. therapy is similar to treatment in the nonpregnant patient, although
Oxytocin is the optimal agent for labor induction and for postpartum drugs such as tetracyclines and quinolones should be avoided if
hemorrhage, but 15-methyl prostaglandin F2-alpha, methylergonovine, possible.19
and ergonovine may cause bronchospasm and should be avoided in Viral pneumonia carries a risk of significant morbidity in preg-
asthmatics if possible. nancy, with increased mortality rates compared with the general popu-
lation. In influenza pandemics, the maternal mortality rate has
consistently been higher than the general population. Vaccination of
Pulmonary infections pregnant women is strongly recommended.20 The 2009 influenza A
(H1N1) pandemic was associated with a high incidence of severe dis-
The pregnant woman is at risk of increased susceptibility or increased ease in pregnant women, with significant mortality.21 Amantadine has
severity of some infections. Changes occur in a pregnant woman’s been used in pregnancy as treatment and as prophylaxis, and oselta-
immune system to allow tolerance to paternally derived fetal antigens. mivir was used quite extensively in pregnancy in the 2009 epidemic.22
Down regulation of cell-mediated immunity occurs, balanced by an Varicella pneumonia is also associated with significant morbidity and
intact or upregulated humoral immune response.15,16 mortality during pregnancy. In one review, a 35% mortality rate was
Pneumonia is a significant cause of maternal and fetal morbidity reported in pregnancy, compared with 10% in other adults23 although
and mortality.17,18 The incidence does not appear to be higher than not all prospective studies have confirmed this increased risk in preg-
that in the general population. Pregnancy is associated with an nancy. Treatment with acyclovir is necessary and reduces mortality in
increased risk of complications of pneumonia, including respiratory gravid patients.24
failure. Pneumonia may produce pregnancy complications, including Although fungal pneumonias are uncommon in pregnancy,
preterm labor, small-for-gestational-age, and intrauterine and neonatal coccidioidomycosis is more likely to disseminate in pregnancy.25
death.17–19 Bacterial pneumonia has a similar microbiologic spectrum This occurs particularly in the third trimester and has been
to the usual community-acquired pneumonia in nonpregnant patients. attributed to subtle impairment of cell-mediated immunity and to a
The diagnosis of pneumonia can often be delayed because of reluctance stimulatory effect of progesterone and 17-beta-estradiols on fungal
proliferation.26 Amphotericin is the accepted therapy for disseminated
coccidioidomycosis.

Table 1. Causes of acute respiratory failure in the obstetric

patient. Pulmonary edema
Specific to pregnancy Pulmonary edema due to preeclampsia Due to the cardiac physiological changes of pregnancy, women with
ARDS due to chorioamnionitis pre-existing heart disease are at risk of cardiac decompensation. Those
ARDS related to placental abruption with cyanotic disease, left heart valvular stenotic lesions, or systolic
Peripartum cardiomyopathy dysfunction are at most risk27 with pulmonary edema occurring during
Amniotic fluid embolism pregnancy or postpartum, related to large shifts in intravascular
Tocolytic-associated pulmonary edema volume associated with delivery. The rise in cardiac output and heart
Trophoblastic embolism rate that occur during gestation increase the gradient across a stenotic
Risk increased by Venous thromboembolism mitral valve.28 In contrast, the reduced systemic vascular resistance
pregnancy Gastric acid aspiration (SVR) of pregnancy mitigates the effects of mitral and aortic regurgi-
Transfusion related acute lung injury tation and of the left-to-right intracardiac shunts, but worsens the
Asthma effects of Eisenmenger’s syndrome and uncorrected tetralogy of
ARDS due to sepsis, often pyelonephritis Fallot. Changes in SVR and cardiac output induced by pregnancy
Pneumonia (e.g. varicella, fungal) can alter fractional shunts producing hypoxemia, and precipitating
Stenotic valvular heart disease, pulmonary pulmonary edema. Specific to pregnancy is the condition of peripartum
hypertension cardiomyopathy, a disorder that occurs in 1 of 1300 to 15,000 deliv-
eries. This condition may present with congestive heart failure, and is
Nonspecific conditions Trauma
associated with a risk of pulmonary and systemic embolization.29
Drugs/toxins
Preeclampsia can result in pulmonary edema, which occurs in
Pancreatitis
about 2.9% of patients with this condition.30 The hemodynamic

Table 2. Risk of radiation exposure from common chest radiographic investigations.38,42,43,82

Maternal breast Fetal radiation exposure
exposure
mGy mGy rad Comments

Investigation
Chest radiograph 0.2 0.010 0.001 Minimal risk to fetus
Ventilation-perfusion scan 51.5 0.20–1.0 0.02–0.10 If perfusion normal, avoid ventilation scan
CT chest /angiogram 10–18 0.1–0.8 0.01–0.10 The larger the fetus, the greater the exposure
Adverse effect
Increase risk of childhood leukemia 420–50 42–5 May be reached with abdominal-pelvic CT scan
Teratogenicity 4100–200 410–20 Levels reached with radiation therapy
Neurological developmental abnormalities 4100 410 Most vulnerable period 8–15 weeks gestation
128 Obstetric Medicine 8(3)

findings in preeclampsia include normal or low left ventricular preload, Amniotic fluid embolism
increased afterload, with a normal or low cardiac output. Systolic and
diastolic function may be impaired.31 When pulmonary edema occurs, The syndrome of amniotic fluid embolism occurs in about 7.7 per
it usually presents in the postpartum period, related to fluid adminis- 100,000 pregnancies.47 This most often occurs related to labor and
tration at delivery and return of blood from the contracting uterus to delivery or after uterine manipulation, and is characterized by devel-
the central circulation. Other contributing effects include the low col- opment of severe dyspnea and hypoxemia, followed by seizures and
loid oncotic pressure and abnormal vascular permeability. cardiovascular collapse or arrest. Those who survive the initial event
Pulmonary edema may sometimes occur during the systemic may develop disseminated intravascular coagulation and ARDS.48
administration of beta2-sympathomimetic agents used to inhibit pre- Risk factors for amniotic fluid embolism include older maternal age,
mature labor.32 It usually presents at least 24 h after initiation of beta- high parity, cesarean section, low uterine segment laceration, and
adrenergic therapy, and treatment often only requires discontinuation meconium staining of amniotic fluid. The mechanism of amniotic
of beta-adrenergic therapy but furosemide is usually administered. fluid embolism involves traumatic opening of uterine vessels, as sug-
Pulmonary edema may also complicate tocolysis with calcium channel gested by data from a U.S. registry of cases, where 78% of the patients
blockers.33 had ruptured membranes and several had just undergone intrauterine
procedures.49 Fetal squamous cells are found in the maternal pulmon-
ary circulation at autopsy, but this finding is not specific for the syn-
Pulmonary thromboembolic disease drome as fetal cells may be recovered from pulmonary artery catheters
in symptom-free patients with other diagnoses.50 Hemodynamically,
Although venous thromboembolism is not common in pregnancy, the mechanism involves the acute development of pulmonary hyper-
occurring with an incidence of about 0.6–2 per 1000 deliveries,34 this tension followed by left ventricular dysfunction.51 These effects may be
incidence is about five times as great as in matched nongravid controls. caused by constituents of amniotic fluid, including leukotrienes and
Pulmonary thromboembolism is a leading cause of maternal mortal- arachidonic acid metabolites. In view of some similarities to anaphyl-
ity,34,35 accounting for about 10% of pregnancy-related deaths in the axis it has been suggested that the disorder be renamed anaphylactoid
United States.36 The risk for thrombosis is increased in pregnancy, syndrome of pregnancy.49 Recent evidence suggests a possible patho-
because of the increase in coagulation factors (V, VIII, X, and von genic and prognostic role for low C1 esterase inhibitor levels.52
Willebrand factor), a fall in protein S levels,37 uterine compression of Radiographically, the patients usually develop bilateral pulmonary
the inferior vena cava and the left iliac vein, and local trauma to pelvic infiltrates.
veins during delivery. The peak incidence of thromboembolism is in the There is no treatment specific for amniotic fluid embolism, and
postpartum period, especially after cesarean section. management consists of supportive care for the associated dissemi-
The initial diagnostic test for venous thrombosis should be duplex nated intravascular coagulation and left ventricular and respiratory
ultrasonography if symptoms or signs of DVT are present.38 failure. If the fetus survives the initial event, it should be promptly
Radiological investigations can be performed safely in pregnancy delivered. In cases of imminent maternal demise, emergency postmor-
(Table 2). The diagnosis of pulmonary embolism in pregnant women tem or periresuscitative cesarean section should be performed, as in
can utilize ventilation-perfusion (V/Q) scanning or CT pulmonary other instances of cardiopulmonary resuscitation in pregnancy.53 The
angiography. Radiation exposure for a standard technetium- maternal mortality rate has been reported as high as 86% but in more
labeled macroaggregated albumin perfusion scan is about 0.18 mGy recent reports, as low as 22%.47 Amniotic fluid embolism may account
(18 mrad),39 which can be reduced by halving the dose without signifi- for 14% of all maternal deaths.49
cantly impairing resolution. The ventilation portion of the study can be
avoided if perfusion is normal. Computed tomographic (CT) angiog-
raphy is associated with similarly low radiation doses to the fetus.40,41 Acute respiratory distress syndrome
In addition to the potential fetal risks of radiation exposure, significant
maternal breast radiation exposure may occur particularly with CT The pregnant patient is at risk of developing acute lung injury from
scans (Table 2). Breast tissue of women under 40 years has relatively pregnancy-associated complications as well as other conditions.54
high radiosensitivity and the proliferative pregnant breast tissue Acute respiratory distress syndrome (ARDS) in not uncommon in
may be more susceptible to radiation exposure, although limited evi- pregnancy and is a leading cause of maternal death (Table 1).55 The
dence exists to support this concern.42,43 V/Q scanning in pregnancy pregnant state may predispose to the development ARDS by a number
is usually associated with high-quality scans, due to the patients’ of mechanisms, including the increased circulating blood volume, the
younger age and lack of co-morbidity, while CT-angiography may reduced serum albumin level,54 a possible upregulation of components
be technically suboptimal, due to the increased cardiac output in of the acute inflammatory response56 and increased capillary leak.
pregnancy. Noncontrast magnetic resonance imaging can image There are few differences in the management of the pregnant
pelvic and lower extremity veins, gadolinium being preferably avoided patient who has ARDS compared with one who is not pregnant.
in pregnancy.38 Survival from ARDS appears to be as good as or better than that in
Low molecular weight heparin (LMWH) is safe in pregnancy and the general population, likely because of these patients’ young age, lack
is associated with fewer adverse effects than unfractionated heparin.44 of comorbidity, and the reversibility of many of the predisposing con-
A weight-adjusted dosing regimen should be used,45 and some ditions, with an anticipated 40% to 75% survival rate.57
authors suggest titrating the dose to achieve anti-factor Xa levels Gastric acid aspiration is an important cause of maternal acute
of 0.5 to 1.2 U/mL 3 to 6 h after injection.34 Treatment is usually lung injury. The increased risk in pregnancy is related to the increased
given for at least 6 weeks postpartum (a minimum duration of intra-abdominal pressure caused by the enlarged uterus, the effect of
3 months). LMWH should be held 24 h prior to delivery or neuraxial progesterone lowering the tone of the esophageal sphincter, as well as
anesthesia (for twice daily dosing). Warfarin is usually avoided in use of the supine position for delivery. About two thirds of cases of
pregnancy for this indication as it crosses the placenta and causes aspiration occur in the delivery suite. All pregnant patients should be
nasal, ophthalmologic, and central nervous system abnormalities. considered to have a full stomach. Aspiration of gastric contents with
Temporary, retrievable IVC filters may be placed during pregnancy pH 2.5 or lower causes chemical pneumonitis with permeability edema.
with limited fetal radiation exposure, the major concern being extrin- Transfusion related acute lung injury (TRALI) is a complication of
sic compression of the IVC by the uterus. Thrombolytic therapy has blood component therapy, which may occur in pregnancy.58 The clin-
been used successfully in life-threatening thromboembolism during ical presentation is of sudden onset of dyspnea during, or within 6 h, of
pregnancy, with a complication rate similar to that in nonpregnant transfusion of plasma-containing blood products. The clinical picture
women.46 is indistinguishable from ARDS from other causes, and the differential
Lapinsky 129

diagnosis includes circulatory fluid overload. Management is support- edema and friability can adversely affect visualisation and increase
ive and most patients improve within a few days, although fatal out- the risk of bleeding. Nasal intubation should be avoided and a smaller
comes may occur. size endotracheal tube may be required. Preoxygenation is important,
but overventilation and respiratory alkalosis must be avoided. The risk
of aspiration should always be considered.
Restrictive lung disease
Interstitial lung diseases (ILD) are not very common in woman in their Noninvasive ventilation
childbearing years, as most diseases affect an older demographic. There
are conditions which may occur in this age-group and some, including Noninvasive ventilation is well suited to short-term ventilatory sup-
lymphangioleiomyomatosis and systemic lupus erythematosus, may port, and avoids the potential complications of endotracheal intub-
worsen as a result of pregnancy. Physiologically, a concern in the ation and the associated sedation. This modality has a role in
woman with ILD in pregnancy is hypoxemia and difficulty in meeting obstetric respiratory complications which reverse rapidly.66 The
the increased oxygen requirements of pregnancy. The increased cardiac major concern with this form of ventilator support is the risk of aspir-
output of pregnancy (and therefore shortened alveolar capillary transit ation. Noninvasive ventilation should therefore only be used in the
time) in the face of a diffusion defect, predisposes to hypoxemia. pregnant patient who is alert, protecting her airway and where there
Women with chest wall restrictive disease (e.g. kyphoscoliosis) or is an expectation of a relatively brief need for mechanical ventilation.
neuromuscular weakness may not be able to meet the increased venti-
lation requirements of pregnancy, putting them at risk of respiratory
failure. Due to the lack of pulmonary parenchymal disease, oxygen- Invasive mechanical ventilation
ation problems are less of a concern.
Marked obesity may also reduce lung volumes, potentially impact- Prolonged mechanical ventilation of pregnant patients in the ICU is
ing on pregnancy. Some physiological effects of pregnancy (e.g. upper relatively uncommon, and few data are available to guide manage-
airway edema) may predispose to the development of obstructive sleep ment. Hyperventilation and alkalosis should be avoided to prevent
apnea (OSA), while other physiological effects (e.g. respiratory stimu- uterine vasoconstriction.67 Lung protective ventilation, sometimes pro-
lation by progesterone) may be protective.59 Obstructive sleep apnea ducing permissive hypercapnia, has not been assessed in pregnancy.
during pregnancy may be associated with gestational hypertensive dis- Chest wall compliance is reduced by the enlarging uterus, and the
orders, gestational diabetes, and fetal growth restriction.59 usual pressure limits (e.g. plateau pressure of 35 cmH2O) may not be
Few data exist on the management and outcome in patients with appropriate. Slightly higher airway pressures (without increased trans-
restrictive lung disease, but it appears reasonably well tolerated in pulmonary pressure) may be needed to achieve appropriate tidal vol-
pregnancy.60,51 Small case series have described successful pregnancy umes in pregnant women near term.
outcome in women with vital capacities less than 40% predicted.60–62 Blood gas abnormalities may adversely affect the fetus.68
Successful pregnancy in such patients requires an experienced, multi- Oxygenation should be optimized to ensure adequate fetal oxygen-
disciplinary team approach. Assessment may require pulmonary func- ation. A maternal oxygenation goal of pO2 greater than 70 mmHg
tion testing, arterial blood gases and echocardiography. Nocturnal has been suggested.69,70 However, a short-term study of controlled
hypercapnia may precede daytime ventilatory failure in patients with maternal hypoxemia (585%) using inhalation of 10% oxygen demon-
neuromuscular disease, and a sleep study with CO2 monitoring may be strated no adverse effects on fetal monitoring.71 Maternal oxygen sat-
of value to identify patients at risk.61 If associated pulmonary hyper- uration is only one factor contributing to fetal oxygenation, placental
tension exists in these patients, this increases maternal risk signifi- perfusion usually playing a more significant role.
cantly. Noninvasive ventilation has been used to support respiratory While excessive hypocapnia may cause fetal harm by reducing pla-
function through the latter part of pregnancy and during labour.62 In cental perfusion,72 the effects of hypercapnia on the fetus are less clear.
all these patient groups, additional intercurrent illness such as pneu- Maternal CO2 levels are normally reduced to about 27 to 34 mmHg,
monia or influenza could result in significant respiratory compromise. producing a gradient to facilitate placental excretion of fetal CO2.
Permissive hypercapnia has not been evaluated in pregnancy, and
maternal hypercapnia could produce fetal respiratory acidosis. This
Cystic fibrosis acidosis likely does not have the same ominous implications for the
fetus as the lactic acidosis produced by hypoxemia, which implies sig-
With improved treatment of cystic fibrosis (CF), median survival has nificant tissue hypoxemia.73 Small clinical studies have evaluated the
increased and pregnancy is not uncommon, despite the frequent infer- short-term effect of mild hypercapnia in pregnancy. Women undergo-
tility of women with this condition. Pregnancy in CF patients has been ing cesarean delivery were subjected to mild hypocapnia (mean
associated with adverse fetal and maternal outcomes.63 From a fetal 23 mmHg) or mild hypercapnia (39.3 mmHg).74 Hypocapnia produced
perspective, preterm labor and perinatal death rate are increased. a lower Apgar score and delayed neonatal breathing. Another small
Pregnancy has little effect on patients with stable CF, although poor study compared ventilated women delivered with mild hypercapnia
outcomes have been seen in those with severe disease.64 An FEV1 (mean CO2 57.6 mmHg) with ventilated women with mild hypocapnia
below 60% of predicted and the presence of pulmonary hypertension (mean CO2 26.4 mmHg) and women managed with a local anesthesia
are poor prognostic factors for both mother and infant. block (mean CO2 30.1 mmHg).75 The hypercapnic group had a statis-
tically significantly higher Apgar score at delivery. If necessary, mild
hypercapnia with PaCO2 maintained less than 60 mmHg, has been
Ventilatory management in the pregnant recommended for pregnancy.76 It should be noted that the right shift
of the haemoglobin oxygen dissociation curve caused by acidosis may
patient negate the beneficial oxygen-carrying characteristics of fetal
Intubation haemoglobin.

Endotracheal intubation in the pregnant patient carries considerable

risk. Failed intubation is 8 times more common in the obstetric popu- Nonconventional support
lation than in other anesthetic intubations.65 The reduced FRC and
increased oxygen consumption in pregnancy cause rapid oxygen desat- Few data are available to support the use of interventions such as
uration during apnea or hypoventilation.6 Upper airway mucosal inhaled nitric oxide, prone positioning and high-frequency oscillation
130 Obstetric Medicine 8(3)

in pregnancy, although these modalities have been used successfully 5. Lucius H, Gahlenbeck HO, Kleine O, et al. Respiratory functions,
and described in case reports and small series. The 2009 H1N1 influ- buffer system, and electrolyte concentrations of blood during
enza epidemic resulted in a marked increased utilization of extracor- human pregnancy. Respir Physiol 1970; 9: 311–317.
poreal life-support for ARDS, including pregnant patients with 6. Archer GW and Marx GF. Arterial oxygen tension during apnoea
reasonably good outcome.77 in parturient women. Br J Anaesth 1974; 46: 358–360.
7. Buss DD, Bisgard GE, Rawlings CA, et al. Uteroplacental blood
flow during alkalosis in the sheep. Am J Physiol 1975; 228:
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8. Stenius-Aarniala B, Piirilä P and Teramo K. Asthma and preg-
It has been suggested that delivery of the pregnant patient with respira- nancy: a prospective study of 198 pregnancies. Thorax 1988; 43:
tory failure will result in improvement in the mother’s condition.78 12–18.
However, a significant benefit to the mother has not been consistently 9. National Asthma Education Program, National Institutes of
demonstrated.79,80 If the fetus is at a viable gestation and is at risk due Health. Working Group report on: Managing of asthma during
to intractable maternal hypoxia, there may well be a benefit to the fetus pregnancy: Recommendations for pharmacological treatment.
in delivery. The mode of delivery should be determined by standard http://www.nhlbi.nih.gov/files/docs/resources/lung/astpreg_
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higher mortality in these patients.81 Delivery should not be performed (ACOG) and The American College of Allergy, Asthma and
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The author(s) declared no potential conflicts of interest with respect to nancy. Thorax 2001; 56: 398–405.
the research, authorship, and/or publication of this article. 20. Skowronski DM and De Serres G. Is routine influenza immuniza-
tion warranted in early pregnancy? Vaccine 2009; 27: 4754–4770.
21. Jamieson DJ, Honein MA, Rasmussen SA, et al. H1N1 2009 influ-
Funding enza virus infection during pregnancy in the USA. Lancet 2009;
This research received no specific grant from any funding agency in the 374: 429–430.
public, commercial, or not-for-profit sectors. 22. Tanaka T, Nakajima K, Murashima A, et al. Safety of neuramin-
idase inhibitors against novel influenza A (H1N1) in pregnant and
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Stephen Lapinsky acyclovir for varicella pneumonia in otherwise healthy adults:
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Contributorship 24. Broussard RC, Payne DK and George RB. Treatment with acyclo-
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25. Stevens DA. Coccidioidomycosis. N Engl J Med 1995; 332:
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