PREGNANCY AND LUNG
Cardiopulmonary Physiology in Pregnancy
- Profound changes occur in
the cardiovascular system early in pregnancy. By the early second
trimester, circulating blood volume increases 40-50%. This is due to an
increase in both the circulation red cell mass and an even larger increase
in the plasma volume.
- The larger increase in
plasma volume leads to a dilutional anemia and a decrease in the serum
colloid oncotic pressure.
- These changes increase the
susceptibility of pregnant patients to the development of pulmonary edema.
- The cardiac output also
increases by about 30-45% by the early second trimester. In patients with
underlying cardiac disease this further worsens the tendency toward
pulmonary edema.
- Gas exchange is also
affected by pregnancy. Minute ventilation is increased during pregnancy
(primarily an increase in tidal volume with a normal respiratory rate) for
2 reasons. First, oxygen consumption and carbon dioxide production
increase 20-30% by the third trimester and up to 100% during labor,
necessitating increased minute ventilation to maintain normal acid base
status. In addition, progesterone directly stimulates the central
respiratory center causing a further increase in minute ventilation. The
net effect is a mild chronic respiratory alkalosis with a decrease in the
arterial PaCO2, a slight increase in the PaO2 (alveolar gas equation), a
slightly elevated pH and a slightly decreased HCO3 (renal compensation).
- FRC decreases substantially
during pregnancy due to increased pressure from the gravid abdomen. This
results in an increased susceptibility to atelectasis especially in the
supine position. This may lead to mild arterial hypoxemia if blood gases
are measured supine.
Pulmonary Problems During Pregnancy
Asthma
While there is no
evidence that the inflammation underlying asthma is worse during pregnancy, the
increased minute ventilatory requirements often worsen the symptoms of asthma.
The fetus is especially susceptible to maternal hypoxemia so exacerbations of
asthma must be treated early and aggressively. Therapy is no different than in
the non-pregnant patient. Close follow up is essential.
Pulmonary Embolism
The risk of pulmonary
embolism is substantially increased during the peripartum period. A high
clinical suspicion must be maintained and heparin prophylaxis should be
considered in patients with additional risk factors.
ARDS
Perhaps, because of
the higher hydrostatic and lower oncotic pressures associated with pregnancy,
pregnant patients are at increased risk of developing hypoxemia and even ARDS
with systemic infections. Again concern for maternal and fetal oxygenation in
the face of an already increased maternal cardiac output and oxygen consumption
necessitates early aggressive supportive care.
Aspiration
Mechanical factors
associated with the gravid uterus as well as hormonal effects which tend to
lower esophageal sphincter tone increase the risk of aspiration of gastric
contents late in pregnancy.
Tocolytic Induced Pulmonary Edema
The systemic use of
(2 agonists (terbutaline, salbutamol) to interrupt preterm labor is associated
with a substantial risk of pulmonary edema. The pathogenesis is unknown.
Pulmonary edema generally develops within 72 hours of the initiation of
therapy. It resolves within 24 hours of discontinuation of the drug. The pulmonary
edema may be sever leading to respiratory failure. Given their disputed
efficacy, some authors have recommended against the use of these agents.
Amniotic Fluid Embolism
This is a rare but
catastrophic complication of pregnancy which presents as the acute onset of
dyspnea, cyanosis and tachypnea during or immediately after labor. Mechanical
obstruction or cytokine mediated constriction of the pulmonary vasculature
leads to acute cardiorespiratory collapse which is often fatal. Risk factors
include advanced maternal age, multiparity, amniotomy, c-section, and IUDs.
Airway Management
Endotracheal
intubation is more difficult in the pregnant patients for multiple reasons.
First, mild upper airway edema which narrows the caliber of the airway. Second,
the risk of aspiration during endotracheal intubation is increased. Finally the
rate of oxygen consumption is increased, limiting the efficacy of
preoxygenation.
Cardiac Disease
The cardiopulmonary
changes of pregnancy increase the susceptibility of patients with cardiac
disease to pulmonary edema as outlined above. In addition, peripartum
cardiomyopathy, an idiopathic diffuse cardiomyopathy may occur in the third
trimester or in the 3-6 months post partum. It is therefore important to
exclude pre-existing or new cardiac disease as a cause of dyspnea in the
peripartum period.
Acute Respiratory Failure in the Peripartum Period
Often clinicians are faced with a patient in the peripartum period with
acute hypoxemic respiratory failure and a diffuse infiltrate on chest x-ray. As
in other patient populations, the approach to these patients includes
supportive care, often with intubation and mechanical ventilation, followed by
pulmonary artery catheterization to distinguish high versus low pressure
pulmonary edema. However, the differential diagnosis in this scenario is
slightly different. A specific history of tocolytic use should be sought.
Respiratory failure during or immediately after labor should raise the suspicion
of amniotic fluid embolism. Echocardiography should be done early to exclude a
peripartum cardiomyopathy. A careful search for infection should be performed
given the increased propensity to ARDS in response to sepsis. Finally, a
history of witnessed aspiration events should be sought.
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