PREGNANCY AND LUNG

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.