This entry focuses on lung disease during pregnancy.
Hyperventilation is a characteristic feature of pregnancy. During pregnancy, the enlarging uterus causes a progressive upward displacement of the diaphragm, to a maximum of 4 cm. This displacement, however, does not impair diaphragmatic function. The diameter of the chest increases by approximately 2 cm; flaring of the ribs and widening of the rib cage with a subsequent increased angle below the ribs—subcostal angle (up to 50%). Despite these changes, respiratory muscle
function appears unchanged. The pregnant woman’s ability to move air in and out of the lung remains unrestrained.
The levels of the hormone progesterone increase throughout pregnancy. Placental progesterone stimulates the brain’s respiratory centers to increase minute ventilation. The increase in minute ventilation increases the amount of oxygen available to the fetus. Minute ventilation increases by 20-50% before the end of the first trimester and remains the same throughout the duration of the pregnancy. This increased minute ventilation is the result of a marked increase in tidal volume; the respiratory rate remains unchanged throughout pregnancy. Thus, hyperventilation is due to deeper, not more frequent breathing.
Anxiety and uterine contractions associated with labor and delivery further increase the physiologic hyperventilation of pregnancy. Oxygen consumption can double during pregnancy and triples during uterine contractions. Pain relief via intravenous sedation and epidural analgesia can minimize this laborand deliveryinduced hyperventilation.
Shortness of breath or dyspnea is a common feature among 60-70% of normal, healthy pregnant women and is a normal physiologic response in gravid (women in their first pregnancy) patients. The exact cause of dyspnea is not well understood. It occurs in the 1st and 2nd trimesters and plateaus or improves as term approaches. Dyspnea occurs before the upward displacement of the diaphragm. Thus, it is unlikely that the growing uterus plays a significant role in the development of dyspnea. Physiologic dyspnea has been attributed to progesterone’s stimulatory effects on the inspiratory neural drive. Others suggest it is due to an increased awareness of the physiologic hyperventilation. Furthermore, increase chemosensitivity may also contribute to dyspnea of pregnancy. Regardless of the exact cause, it remains unlikely that dyspnea of pregnancy is caused by the mechanical burden of the enlarging fetus.
Pneumonia is the most common nonobstetric infectious cause of death during pregnancy and the puerperium. The pathogens involved in pneumonias of pregnant women are similar to those identified in nonpregnant women. Most cases of pneumonia during pregnancy are due to bacteria. The most common bacterial pathogen in community acquired pneumonia in pregnant women is the gram-positive diplococcus, Streptococcus pneumoniae. Onset is abrupt and dramatic. Symptoms include fever, chills, pleuritic chest pain, and productive cough with purulent sputum.
Viral pneumonias are also common in pregnant women. Influenza is the most common viral pathogen of pneumonia in pregnancy. Of the three major antigenic types, Type A is most often associated with human illness and epidemics. After a short incubation period, symptoms develop and include general malaise, headache, fever, chills, and upper respiratory symptoms. While initially the respiratory examination may not be remarkable, pregnant women can rapidly develop respiratory failure.
During the course of pneumonia, adverse maternal and fetal effects can occur. Maternal complications can be severe. The most serious complications include bacterial superinfection, respiratory failure, and adult respiratory distress syndrome. Premature labor and delivery is another obstetric problem that can occur including the possible transmission of viral agents to the fetus and newborn. Premature labor may develop during pneumonia as a result of prostaglandin production or from the woman’s inflammatory response to the underlying infection. While the transplacental passage of the influenza virus has been documented, it has not been identified as a teratogen (cause of birth defects).
Asthma occurs in 4% of gravid women, and complicates up to 1.5% of pregnancies, representing the most common obstructive pulmonary disease seen in pregnancy. Asthma is a chronic disease with acute exacerbations; it is characterized by reversible airway obstruction, airway inflammation, and airway hyperresponsiveness to stimuli such as allergens, viruses, exercise, and cold air. Hyperreactive airways result in bronchospasm, mucosal edema, and mucus plugging, producing symptoms of cough, wheezing, dyspnea, and chest tightness.
Poorly controlled asthma is associated with maternal and fetal complications, while well-controlled asthma poses little threat. Maternal decrease in blood oxygen (hypoxemia) is associated with increased incidence of intrauterine growth retardation, prematurity, low birthweight, perinatal mortality, and maternal hypertension. The primary goal in managing the pregnant patient with asthma is to prevent hypoxemia while minimizing the risk to the mother and fetus of adverse effects from medications. Controlling asthma in a pregnant patient should be addressed as in a nonpregnant individual. One of the first steps is to identify triggers that initiate or worsen asthma for a particular person. Triggers may include allergens, exercise, cold air, infections, emotional stress, irritants, gastroesophageal reflux, and drugs such as aspirin.
AMNIOTIC FLUID EMBOLISMS IN PREGNANCY
Amniotic fluid obstruction by clot or debris (embolism) is an uncommon obstetric complication, present in 1/8,000 to 1/80,000 pregnancies. However, it is frequently a fatal event, with a mortality rate in mothers of 50-60% within 1 hour after the onset of symptoms. Permanent neurological damage is suffered by 70% of survivors. This process is triggered by the sudden obstruction (embolization) of amniotic fluid or fetal debris into the maternal blood flow system (venous circulation). Initial alterations in blood flow and pressure (hemodynamics) and oxygenation can be seen and are then followed by abnormalities in blood clotting (coagulopathy). The most common presentation is sudden breathlessness (dyspnea) and hypotension (low blood pressure) followed by cardiorespiratory arrest. The diagnosis does not depend on the detection of fetal debris in the blood vessels (vasculature), but rather on the basis of clinical presentation, since not all patients will have these objective findings.
The neonatal outcome is usually greater than maternal outcome, with 80% of neonates surviving delivery if they are alive at the onset of the event. However, 50% of these neonates suffer permanent neurological damage. In patients who survive amniotic fluid embolism, no recurrence in subsequent deliveries has been reported.
For a pregnant woman with any breathing (pulmonary) complication, the primary goal is to prevent reduced blood oxygen (hypoxemia) and maintain adequate oxygenation for both mother and fetus. Pregnancy may exacerbate or ameliorate other pulmonary diseases. For care providers, it is important to be familiar with the various respiratory infections that may be found among this population. Is it essential to know which antibiotics are contraindicated (not recommended) during pregnancy and to monitor patients on medications to minimize adverse effects. This information is critical in order to provide accurate counseling and education to patients. Finally, it is important to understand that any dyspnea the woman is experiencing will resolve postpartum. As the level of progesterone returns to normal, the increased minute ventilation will also return to baseline.
SEE ALSO: Asthma, Pregnancy
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- Oberstein, E. M., Marder, A., Pitts, S., & Glassberg, M. K. (2002). Pulmonary complications in pregnancy, part 1: Infections and asthma. Journal of Respiratory Diseases, 23, 41-53.
- Oberstein, E. M., Marder, A., Pitts, S., & Glassberg, M. K. (2002). Pulmonary complications in pregnancy, part 2: Emboli and other diseases. Journal of Respiratory Diseases, 23, 175-181.
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- Venkataraman, M. T., & Shanies, H. M. (1997). Pregnancy and asthma. Journal of Asthma, 34, 265-271.
- excessive progesterone and respiratory distress
- mucosal edema pneumonia
- progressive worsening asthma and the incidence of respiratory infections
- puerperial infection