Critical Care Medicine in Pregnancy

Management of the critically ill pregnant patient is a situation with which few intensive care physicians gain significant expertise. The usual clinical approach may be altered by the physiologic changes induced by pregnancy, by the relatively uncommon pregnancy-specific conditions, and by perceived limitations on therapy produced by the presence of a fetus (Fig. 81.1).

Figure 81.1 Approach to the assessment and management of the critically ill obstetric patient.

Physiologic Changes in Pregnancy

The pregnant woman undergoes a number of physiologic changes affecting various systems relevant to critical care management. From a respiratory perspective, the upper airways develop edema and hyperemia, which may be relevant during endotracheal intubation. Changes in lung volumes occur, with a 10% to 25% decrease in functional residual capacity (FRC), whereas total lung capacity decreases only minimally as the thoracic cage widens to compensate.¹ Forced expiratory volume in 1 second (FEV₁) is not altered by the pregnant state. Lung compliance remains unchanged, but chest wall and total respiratory compliance are reduced.²

The rising progesterone level stimulates an increase in ventilation. Tidal volume and minute ventilation increase from the first trimester, reaching 20% to 40% above baseline by term (Table 81.1).³ A mild respiratory alkalosis is produced with compensatory renal excretion of bicarbonate (PaCO₂ 28 to 32 mm Hg; HCO₃⁻ 18 to 21 mEq/L). Oxygen consumption increases because of the demands of the fetus and maternal metabolic processes, reaching levels up to 33% above baseline by term. Arterial PO₂ remains normal throughout pregnancy, but mild hypoxemia caused by an increased alveolar-arterial oxygen tension difference may develop in the supine position, as FRC diminishes near term.

Table 81.1

Physiologic Changes in Late Pregnancy

Parameter	Change
Respiratory
Functional residual capacity	Decreased 10-25%
Minute ventilation	Increased 20-40%
Arterial partial pressure of oxygen	No change
Arterial partial pressure of carbon dioxide	Reduced to 28-32 mm Hg
Serum bicarbonate	Reduced to 18-21 mEq/L
Cardiac
Heart rate	Increased 10-30%
Pulmonary capillary wedge pressure	No change
Cardiac output	Increased 30-50%
Systemic vascular resistance	Decreased 20-30%
Pulmonary vascular resistance	Decreased 20-30%
Renal
Glomerular filtration rate	Increased 50%
Creatinine	Decreased (24-68 µmol/L; 0.29-0.77 mg/dL)

Maternal blood volume and cardiac output increase through pregnancy, reaching a peak at 30% to 50% above baseline levels by about 28 weeks (Fig. 81.2).⁴ Hemodynamic measurements by pulmonary artery catheter in the near-term patient demonstrate the increased cardiac output, with a reduced systemic vascular resistance and pulmonary vascular resistance (see Table 81.1).⁵ During labor and continuing into the immediate postpartum period, cardiac output is further augmented by the return of 300 to 500 mL of blood to the central circulation.⁶

Figure 81.2 Graphic representation of some of the physiologic changes that occur in pregnancy. CO, cardiac output; FRC, functional residual capacity; GFR, glomerular filtration rate; , minute ventilation. (From Lapinsky SE, Kruczynski K, Slutsky AS: Critical care in the pregnant patient. Am J Respir Crit Care Med 1995;152:427-455.)

Oxygen delivery to the fetus is dependent on the maternal arterial oxygen content and the uterine blood flow. Maternal hypotension, alkalosis (e.g., hyperventilation), and endogenous or exogenous catecholamines can vasoconstrict the uterine artery and adversely affect fetal oxygenation.⁷ Uterine blood flow is also reduced transiently by uterine contractions. Although umbilical venous blood returning to the fetus has a relatively low oxygen tension, a high oxygen content is maintained by the left shift of the oxygen dissociation curve of fetal hemoglobin.

Glomerular filtration rate increases early in pregnancy, reaching a value 50% above prepregnancy levels in the second trimester, and remains elevated throughout pregnancy (see Fig. 81.2).⁸ The normal serum creatinine level is therefore in the range of 0.5 to 0.7 mg/dL (45 to 60 µmol/L). As pregnancy progresses, mild ureteric dilation and mild hydronephrosis may occur as a result of uterine compression and smooth muscle relaxation.

Pregnancy is associated with a reduced lower esophageal sphincter pressure, reaching a nadir at 36 weeks. The position of the stomach is displaced, further decreasing the effectiveness of the gastroesophageal sphincter and reducing gastric emptying. The pregnant woman should therefore always be considered at risk for aspiration of stomach contents, regardless of the time elapsed since her last meal.

The increase in plasma volume is associated with a lesser increase in red blood cell mass causing a physiologic anemia, with a hematocrit of 32% to 34% by the third trimester. A mild leukocytosis occurs with white blood cell count rising further during labor. Platelet counts are usually unchanged, although a condition of benign mild thrombocytopenia may occur.⁹ Procoagulant factors rise, contributing to the hypercoagulable state of pregnancy. The erythrocyte sedimentation rate (ESR) rises related to increased levels of plasma globulins.

Critical Care Management

General Care

Table 81.2

Risk of Fetal Radiation Exposure Resulting from Radiologic Studies in the Critically Ill Pregnant Patient

Investigation	Fetal Radiation Exposure (mGy)
Chest radiograph (with abdomen shielded)	0.01
Ventilation-perfusion scan
Perfusion	0.1-1
Ventilation	0.1-0.4
CT pulmonary angiogram	0.1-4
CT scan of pelvis and abdomen	30-50
Radiation effect on fetus
Teratogenicity	50-100
Oncogenicity	20-50

CT, computed tomography.

The adverse effects of fetal exposure to radiation include oncogenicity and teratogenicity. A twofold increased risk of childhood leukemia may result from fetal exposure in the range of 20 to 50 mGy (2 to 5 rads). Most intensive care unit (ICU) procedures can be carried out well below these levels of exposure to the fetus (see Table 81.2). Teratogenicity does not appear to occur at these radiation doses, requiring radiation exposure greater than 50 to 100 mGy (5 to 10 rads). Nonetheless, every effort should be made to minimize uterine exposure, particularly in the first trimester.

Drug Therapy in Pregnancy

Pharmacotherapy during pregnancy requires consideration of the altered drug clearance, metabolism, and volume of distribution of drugs in pregnancy, and the potential pharmacologic and teratogenic effects on the embryo. A detailed description of drug therapy in pregnancy is beyond the scope of this chapter. Consultation with an obstetrician and pharmacist is essential, and several excellent resources are available.12,13 Some common ICU drugs are discussed briefly as follows.

Catecholamines

Catecholamines commonly used in the ICU such as dobutamine, dopamine, norepinephrine, and epinephrine all have the potential to reduce uterine blood flow. Both ephedrine and phenylephrine boluses are used for transient hypotension induced by neuraxial anesthesia. Nonpharmacologic maneuvers such as volume replacement and left lateral positioning are essential to the management of hypotension, and the rapidity of correction of blood pressure may be more important than the specific inotropic agent used. If vasopressor infusion therapy is required to support maternal hemodynamics, this therapy should not be withheld because of concerns for potential adverse effects on the fetus.

Sedation, Analgesia, and Neuromuscular Blockade

Little data exist on the preferred drugs for prolonged sedation, analgesia, or neuromuscular blockade in pregnancy. Benzodiazepine use in early pregnancy has been associated with a small risk of congenital malformations, mainly cleft lip and palate. Midazolam crosses the placenta to a lesser degree than diazepam, which can accumulate in the fetus at levels greater than in the mother. Propofol has been used as an induction agent for cesarean section, but a single case report describes the development of non–anion gap acidosis in two pregnant women receiving propofol infusion for neurosurgical procedures.¹⁴ Congenital malformations have not been demonstrated with use of narcotic analgesics such as morphine, meperidine, and fentanyl. The majority of nondepolarizing neuromuscular blocking agents have been shown to cross the placenta including pancuronium, vecuronium, and atracurium, but transfer is unlikely to have clinical effects on the fetus in the short term. Nevertheless, if sedative or paralyzing agents are used in the pregnant woman, this information must be communicated to the neonatologist, who should anticipate the need for ventilatory support for the fetus.

Antibiotics

Antibiotic regimens similar to those used in the nonpregnant patient are appropriate, with some precautions. Quinolones should probably be avoided because of the potential risk of arthropathy. Tetracyclines produce adverse effects on fetal teeth and bone, and aminoglycosides and sulfonamides should be used with caution.

Fetal Oxygenation and Monitoring

Attention to interventions aimed at optimizing fetal oxygenation is important in the management of any critically ill pregnant patient. Depending on gestational age, delivery of the fetus may be the most appropriate intervention. Uteroplacental oxygen delivery can be optimized by increasing oxygen carrying capacity—by blood transfusion, improving maternal cardiac output, and optimizing maternal oxygenation. The simple maneuver of tilting the patient to the left lateral position to increase cardiac output should always be considered.¹⁰

Continuous electronic monitoring of fetal heart rate (FHR) can be used to identify changes in fetal physiology. Abnormal patterns of FHR have been described with good sensitivity but varying specificity for fetal distress. Fetal tachycardia may occur in the presence of maternal infection or chorioamnionitis, but fetal bradycardia or sinusoidal variation in FHR are more ominous, suggesting fetal hypoxia. Changes in FHR occur in response to uterine activity. Early decelerations coinciding with contractions are benign, but late decelerations beginning beyond the peak in contraction and persisting after the contraction may indicate fetal compromise, particularly if associated with a reduced beat-to-beat variation. Fetal compromise may occur as a result of uteroplacental or fetal pathology but may also indicate maternal illness with reduced uterine oxygen delivery. The fetus may be further assessed by an ultrasound biophysical profile that evaluates factors such as spontaneous movement, breathing action, and amniotic fluid volume. A normal biophysical profile carries a good prognosis.

Hemodynamic Monitoring

In general the indications for use of the pulmonary artery catheter are similar to those in nonobstetric patients, and pregnancy is not a contraindication to invasive hemodynamic monitoring. An awareness of the normal cardiovascular physiologic changes in pregnancy (discussed earlier) is necessary in order to correctly interpret the hemodynamic data obtained.

Ventilatory Support

Noninvasive Ventilation

Noninvasive ventilation avoids the adverse effects of endotracheal intubation, such as airway trauma, the increased risk of nosocomial pneumonia, and the complications associated with sedation. This modality is ideally suited to short-term ventilatory support, which is the case in many obstetric complications that reverse rapidly. The major concern with mask ventilation in pregnancy is the risk of aspiration because of the increased intra-abdominal pressure, delayed gastric emptying, and reduced lower esophageal sphincter tone accompanying pregnancy. Noninvasive ventilation should therefore be reserved for the patient who is alert, protecting her airway, and has an expectation of a relatively brief requirement for mechanical ventilatory support.

Airway Management

Failed intubation is more common in the obstetric population than in other anesthetic intubations.¹⁵ The reduced oxygen reserve caused by diminished FRC and increased oxygen consumption produces rapid desaturation in response to apnea or hypoventilation.¹⁶ Preoxygenation with 100% oxygen is beneficial, but respiratory alkalosis must be avoided. In view of the delayed gastric emptying and elevated intra-abdominal pressure, the pregnant patient should always be considered to have a full stomach and appropriate precautions should be taken. Upper airway hyperemia and edema may reduce visualization and necessitate use of a smaller endotracheal tube. The risk of bleeding is increased and nasal intubation should be avoided.

Mechanical Ventilation

The normal PaCO₂ of about 30 mm Hg in late pregnancy should be considered in the interpretation of arterial blood gases when decisions are made to institute ventilatory support. Data on the prolonged mechanical ventilation of pregnant patients are limited. Hyperventilation should be avoided because this adversely affects uterine blood flow ¹⁷ because of the resulting alkalemia as well as the effect of positive-pressure ventilation in reducing cardiac output. The current ventilatory approach of avoiding excessive lung stretch by pressure limitation and permissive hypercapnia has not been assessed in pregnancy. The usual pressure limits (e.g., plateau pressure of 35 cm H₂O) may not be applicable in the near-term patient, in whom chest wall compliance is reduced. Transpulmonary pressures may not be elevated at a plateau pressure of 35 cm H₂O, and higher ventilatory pressures may be acceptable in pregnant patients near term. Although late pregnancy is associated with a mild respiratory alkalosis, maternal hypercapnia up to 60 mm Hg in the presence of adequate oxygenation does not appear to be detrimental to the fetus.¹⁸ Maternal hypercapnia and respiratory acidosis may produce fetal acidosis, but this does not have the same ominous implications as fetal acidosis due to lactic acidosis resulting from fetal hypoxia.¹⁹ However, acidosis produces a right shift of the hemoglobin oxygen dissociation curve, which may negate the beneficial oxygen-carrying characteristics of fetal hemoglobin. If marked respiratory acidosis results from permissive hypercapnia, treatment with bicarbonate may improve maternal and fetal acidemia.