Physiologic Changes in Pregnancy

Hormonal changes in pregnancy affect the upper respiratory tract and cause airway hyperemia and edema resulting in symptoms of rhinitis. Estrogens are likely responsible for many of these effects because they produce capillary congestion and mucous gland hyperplasia. Changes to the thoracic cage result from both the enlarging uterus and the hormonal effects producing ligamentous laxity. The diaphragm is displaced cephalad by up to 4 cm, but the potential loss of lung capacity is partially offset by an increase in the anteroposterior and transverse diameters and by widening of the subcostal angle (Figure 76-1). Despite these anatomic changes, diaphragmatic function remains normal, diaphragmatic excursion is not reduced, and the maximum transdiaphragmatic inspiratory pressures that can be generated near term are similar to values generated by patients who are not pregnant. The changes in the chest wall return to normal within 6 months of delivery, although the costal angle may remain widened.

Figure 76-1 Pulmonary physiology in pregnancy: anatomic and functional effects of pregnancy that influence pulmonary physiology.

These changes in the thorax produce a progressive decrease in functional residual capacity (FRC) by 10% to 25% by term (Figure 76-2). Residual volume decreases slightly, but the major change is in expiratory reserve volume. These alterations are measurable as early as 16 to 24 weeks of gestation and progress to term. The increased diameter of the thoracic cage and the preserved respiratory muscle function allow the vital capacity to remain unchanged, and total lung capacity decreases only minimally. Measurements of airflow and lung compliance are not affected, but chest wall and total respiratory compliance are reduced in the third trimester because of the chest wall changes and increased abdominal pressure. Inconsistencies in results reported for diffusing capacity during pregnancy likely arise from the effects of anemia, variable changes in intravascular volume, and the increase in cardiac output. A small increase may be noted in early pregnancy with a subsequent decrease to normal values by term.

Figure 76-2 Physiologic changes in pregnancy. Shown are some of the physiologic changes that occur during pregnancy and the postpartum period.

(From Lapinsky SE, Kruczynski K, Slutsky AS: Critical care in the pregnant patient, Am J Respir Crit Care Med 152:427–490, 1995.)

Minute ventilation increases greatly in pregnancy, beginning in the first trimester and reaching 20% to 40% above baseline at term (Figure 76-2), produced mainly by an increase in tidal volume of approximately 30% to 35%. These changes are mediated by the increase in respiratory drive that results from elevated serum progesterone levels. A respiratory alkalosis with compensatory renal excretion of bicarbonate results, with arterial carbon dioxide tension (PaCO₂) falling to 28 to 32 mm Hg and plasma bicarbonate falling to 18 to 21 mEq/L. Alveolar-arterial oxygen tension difference (PO₂[A−a]) is similar to nonpregnant values, and mean PaO₂ usually exceeds 100 mm Hg at sea level throughout pregnancy. Mild hypoxemia and an increased PO₂(A−a) may develop in the supine position because of airway closure, because FRC diminishes near term. One study suggests that shunt is normally increased in the third trimester to approximately 15% and is not changed significantly by posture. Oxygen consumption increases, beginning in the first trimester, and reaches 20% to 33% above baseline by the third trimester because of fetal demands and maternal metabolic processes. The combination of a reduced FRC and increased oxygen consumption lowers oxygen reserve, which renders the pregnant patient susceptible to the rapid development of hypoxia in response to hypoventilation or apnea.

During labor, hyperventilation increases, and tachypnea (caused by pain or anxiety) may result in marked respiratory alkalosis, augmented in some patients by volume depletion or vomiting. Alkalosis adversely affects fetal oxygenation by reducing uterine blood flow. In some patients, severe pain and anxiety may lead to rapid, shallow breathing with alveolar hypoventilation, atelectasis, and mild hypoxemia. Achieving adequate pain relief with narcotics or epidural analgesia blunts the ventilatory response and can correct the gas exchange abnormalities associated with active labor. The pregnancy-associated changes in lung function reverse significantly in the first 72 hours postpartum and return to baseline within a few weeks.

Changes occur to the pregnant woman’s immune system, to facilitate tolerance to paternally derived fetal antigens. Some suppression of cell-mediated immunity occurs; maternal lymphocytes demonstrate a diminished proliferative response to soluble antigens and to allogeneic lymphocytes, and decreased numbers of T-helper cells have been documented. These effects are balanced by an intact or slightly enhanced humoral immune response. These alterations to maternal immunity result in a predisposition to more severe manifestations of some viral and fungal infections.

Dyspnea in Pregnancy

Dyspnea is a common complaint in women who have otherwise normal pregnancies. It may develop in the first or second trimester, and 70% of women complain of dyspnea by the third trimester. The mechanism is not clear but likely represents a normal awareness of increased ventilation; the physiologic increase in minute ventilation results in increased motor cortical stimulation of the respiratory center. The diagnosis of this benign condition is based on the presence of isolated dyspnea not usually affecting daily activities, the absence of associated symptoms, and the exclusion of other, pathologic conditions. Pregnancy also can be associated with increased exercise-induced dyspnea.

Pregnancy-Specific Disorders

Amniotic Fluid Embolism

Amniotic fluid embolism is a rare obstetric complication (between 1 in 8000 and 1 in 80,000 live births) that carries a mortality rate of 10% to 86% and may account for 10% of maternal deaths. Amniotic fluid embolism is usually associated with labor and delivery, but it may also occur with uterine manipulations or uterine trauma or in the early postpartum period. The mechanism seems to involve amniotic fluid that enters the vascular circulation through endocervical veins or uterine tears. Particulate cellular contents and humoral factors in the amniotic fluid produce acute pulmonary hypertension, predominantly by causing vascular spasm (Figure 76-3). Acute right ventricular dysfunction results from the increased afterload and myocardial dysfunction mediated by humoral factors, associated with secondary left ventricular (LV) failure. The cardiovascular changes of amniotic fluid embolism may resemble those of anaphylaxis, and sensitivity to amniotic fluid contents may be responsible.

Figure 76-3 Pathophysiology of amniotic fluid embolism: proposed pathophysiologic mechanisms for the development of circulatory shock caused by amniotic fluid embolism. RV, right ventricular.

The clinical presentation usually involves the sudden onset of severe dyspnea, hypoxemia, and cardiovascular collapse, often accompanied by seizures. Less common presentations include hemorrhage caused by disseminated intravascular coagulation (DIC) and fetal distress. Up to one half of patients may die within the first hour, and cardiac arrest during this period is common.

The diagnosis of amniotic fluid embolism is usually made on the basis of observing the typical clinical picture. Fetal squames in a wedged pulmonary capillary aspirate have been used to confirm the diagnosis, but this is not a specific finding. Less invasive diagnostic tests, such as maternal serum zinc coproporphyrin or sialyl-Tn levels, have been investigated but are not currently in use. The differential diagnosis includes septic shock, pulmonary thromboembolism, abruptio placentae (placental abruption), tension pneumothorax, and myocardial ischemia.

Treatment and Prognosis

Treatment of the pregnant patient with amniotic fluid embolism involves routine resuscitative and supportive measures, with prompt attention to adequate oxygenation, mechanical ventilation, and inotropic support. No specific therapy has been shown to be effective, but some suggest a role for corticosteroids. In view of the inconsistent hemodynamic findings, invasive monitoring may be of value. Survivors of the initial resuscitation are likely to experience the complications of DIC or acute respiratory distress syndrome (ARDS). Neurologic damage caused by hypotension and hypoxemia is common.

Preeclampsia and Pulmonary Edema

Pulmonary edema may rarely occur in association with preeclampsia (i.e., perhaps 3% of preeclamptic patients). The preeclamptic patient is usually volume-depleted, and pulmonary edema usually occurs in the early postpartum period, often associated with aggressive, intrapartum fluid replacement. Other factors that may contribute to the pathogenesis include reduced serum albumin, elevated LV afterload, and systolic and diastolic myocardial dysfunction (Figure 76-4). Increased capillary permeability may also occur, aggravated by concomitant conditions such as sepsis, placental abruption, or massive hemorrhage.

Figure 76-4 Pathophysiologic mechanisms responsible for the development of pulmonary edema in preeclampsia.

Pulmonary edema has been described in chronically hypertensive, obese, pregnant patients in whom preeclampsia develops. Diastolic LV dysfunction results from both the hypertension and the obesity, and pulmonary edema is precipitated by volume overload of pregnancy and hemodynamic stresses of preeclampsia.

Preeclampsia is characterized by hypertension, proteinuria, and peripheral edema, usually in the third trimester. The presentation of pulmonary edema is with acute respiratory distress in the preeclamptic patient, often in the early postpartum period.

Treatment and Prognosis

The standard approach is to restrict fluid, administer diuretics cautiously, and provide ventilatory support if necessary. Invasive monitoring may be useful if inotropic or vasodilator therapy becomes necessary, particularly in the patient with renal dysfunction. Aggressive diuresis must be avoided because filling pressures should not be reduced to the point of compromising cardiac output and reducing placental perfusion. Volume replacement may be necessary in preeclampsia, particularly if vasodilators are used, because these patients may be extremely volume-depleted. Excessive fluid replacement, however, may precipitate pulmonary or cerebral edema. The ultimate treatment of preeclampsia is delivery of the fetus.