Key Clinical Questions
What are physiologic changes of pregnancy pertinent to critical care?
What are common reasons for pregnant women to require critical care?
What factors impact airway intubation during pregnancy?
What issues arise in hemodynamic monitoring during pregnancy?
What vasopressors can and should be used during pregnancy?
Are there special considerations for resuscitation during pregnancy?
Introduction
The majority of critical care admissions for pregnant and peripartum women are for obstetric disorders, primarily hypertensive complications (particularly hemorrhagic stroke) or intrapartum hemorrhage. Medical indications, such as sepsis, respiratory failure, cardiomyopathy, or ischemic stroke are less common. Maternal mortality in developed nations remains rare (10 to 16 per 10,000 births); however the proportion attributable to medical disorders has been increasing as women with underlying medical conditions and older women conceive, perhaps with assisted reproductive technology. Standard scoring systems, such as APACHE scores, overestimate mortality in pregnant and peripartum women, particularly if they have an obstetric indication for critical care. Delivery or surgery may contribute to rapid improvement. A small proportion of obstetric patients require critical care. Hospitalists and intensivists may have limited experience managing these patients.
Virtually every organ system adapts to accommodate pregnancy and delivery. Hemodynamic alterations prepare for blood loss of one-half to one liter at delivery. Blood volume increases by 50% (Table 222-1).
Direction of Change | Percentage of Change or Normal Range in Pregnancy | |
---|---|---|
Blood volume | ↑ | 30–40% increase |
Heart rate | ↑ | Increases by 10–20 bpm |
Cardiac output | ↑ | 30–60% increase |
Systemic vascular resistance | ↓ | 25–30% decrease |
Blood pressure | ↓ | 10–15 mm Hg decrease in first two trimesters |
Colloid oncotic pressure | ↓ | 10–15% decrease |
Total lung capacity | ↓ | 4–5% decrease |
Functional residual capacity | ↓ | 20% decrease |
Diffusion capacity | ↔ | No change |
Tidal volume | ↑ | Increased |
Respiratory rate | ↔ | No change |
Minute ventilation | ↑ | 50% increase |
PaO2 | ↑ | Average 100–105 |
PcaCo2 | ↓ | Average 28–32 |
pH | ↑ | Mild respiratory alkalosis |
A-a gradient | ↑ | Increase in late gestation to approximately 20 |
Protein S | ↓ | |
Activated Protein C resistance, fibrinogen, factor V, VIII, IX, X, | ↑ | |
Plasminogen activator inhibitor type 1 and 2 | ↑ | |
Activity of tissue plasminogen | ↓ |
Cardiac output increases by 30% to 50% and total peripheral resistance decreases by 20%, leading to blood pressure declining by 10 to 15 mm Hg in the first half of pregnancy, then returning to baseline in the second half. Diastolic blood pressure decreases more than systolic; pulse pressure is widened. Central venous pressure (CVP) and pulmonary capillary wedge pressure (PCWP) remain unchanged. Blood flow distribution is altered such that up to 25% of maternal cardiac output is directed to the uterus, 20% to kidneys, with an increase in breast flow. When supine, women in the second half of pregnancy experience aortocaval compression (termed supine hypotensive syndrome), in which cardiac output may drop by 30%. Left lateral decubitus positioning relieves aortocaval compression and improves venous return and cardiac output.
Maternal respiratory adaptations help optimize fetal oxygenation. Initial changes are progesterone mediated with diaphragmatic elevation contributing to changes later in pregnancy. Minute ventilation increases 30% to 60% by increased tidal volume; respiratory rate remains unchanged. Tachypnea is abnormal and warrants investigation! Diaphragmatic elevation leads to a 20% reduction in functional residual capacity by late pregnancy. Given that diaphragmatic excursion is usually unchanged in pregnancy, this drop in functional residual capacity is counterbalanced by an increase in inspiratory capacity and the resultant effect is no significant change in total lung capacity. On the other hand, oxygen consumption is significantly increased during pregnancy and rises further during labor and delivery. For those reasons, oxygen reserve is reduced in pregnancy. Arterial blood gas testing reveals a compensated respiratory alkalosis due to the above described changes and enhanced renal bicarbonate excretion. PaO2 is typically 100 to 105 mm Hg during pregnancy and PaCO2 decreases to 28 to 32 mm Hg. Maternal pulse oximetry greater than 95% is desirable in order to maintain a PaO2 greater than 70 mm Hg and optimize placental oxygen diffusion.
Hematologic changes also occur in pregnancy with a progressive activation of the hemostatic system to prepare the parturient for the hemostatic challenge of delivery. The anticoagulant activity of protein S is reduced and activated protein C resistance rises. Procoagulant activity is increased, with higher concentrations of fibrinogen and factors V, VIII, IX, and X, leading to enhanced thrombin production. On the other hand, fibrinolysis is decreased as a result of increased activity of plasminogen activator inhibitor type 1 and type 2 and decreased activity of tissue plasminogen. Shortcomings of these changes are an increase in the risk of venous thromboembolism (VTE) antepartum until six weeks postpartum.
Obstetric indications include preeclampsia and related complications: eclampsia, HELLP (hemolysis, elevated liver enzymes, low platelets), hypertensive crisis, pulmonary edema, oliguric renal failure, and cerebral hemorrhage. All of these complications would meet criteria for severe preeclampsia and would warrant urgent delivery. Close collaboration with obstetrics is essential for optimal maternal (and fetal/neonatal) outcome. Although often maternal manifestations of preeclampsia are quickly reversible with delivery and judicious fluid and blood pressure management, they may persist or even worsen in the postpartum period, requiring ongoing vigilance. While still pregnant, blood pressure goals must minimize maternal hypertensive complications, which are more likely above 160 mm Hg systolic and 110 mm Hg diastolic, while maintaining sufficient uteroplacental flow. Blood pressure reduction should be attempted promptly with caution in pregnant women given the potential for impaired uteroplacental flow and fetal compromise. Options include intravenous labetalol or hydralazine, noting that hydralazine has been associated with greater hypotension in this setting. Short-acting oral nifedipine may be useful if intravenous access is delayed but may also precipitously lower the blood pressure. Magnesium sulfate infusion is superior to phenytoin and benzodiazepines for preventing seizures in preeclampsia and reducing recurrence of eclamptic seizures. Given that most seizures are self-limited, there are limited studies comparing different drugs; however, benzodiazepines may be helpful for acute seizure treatment, noting risk of neonatal respiratory depression.
Additional obstetric conditions warranting critical care include acute fatty liver of pregnancy, peripartum cardiomyopathy, amniotic fluid embolism, and placental abruption and hemorrhage. Acute fatty liver of pregnancy (AFLP) is rare, estimated to occur in 1 in 13,000 deliveries, but carries a high mortality. Manifestations may include fulminant hepatic failure with hypoglycemia, coagulopathy, and renal failure; about half of cases are associated with preeclampsia. It may initially be difficult to differentiate AFLP from HELLP syndrome (defined as transaminases greater than twice the upper limit of normal and platelet count less than 100,000 per mm3), but AFLP should be suspected in patients with otherwise unexplained hypoglycemia and severe hepatic dysfunction. Liver transplantation may be necessary. Recurrence rates are significant in subsequent pregnancies.
Peripartum cardiomyopathy is defined as dilated cardiomyopathy with no other known cause, with onset in the last month of pregnancy or within five months postpartum. Rates vary markedly across the world, with highest rates reported in Africa. The etiology has not fully been defined. Risk factors include advanced maternal age, multiple gestations, preeclampsia, and African descent. Treatment includes standard congestive heart failure management, including vasodilators, diuretics, and sodium restriction. Prior to delivery, hydralazine and nitrates should be used rather than angiotensin converting enzyme inhibitors, which have adverse fetal renal effects at all stages of gestation. After delivery, enalapril and captopril are considered compatible with breastfeeding. Anticoagulation should be initiated if ejection fraction is less than 35%, mural thrombus is present on imaging, or atrial fibrillation is observed, as thrombosis is a major cause of mortality in these patients. Up to half of women recover ventricular function to baseline levels within six months, with variable persistent dysfunction ranging from mild to fatal in the other half. Recurrence rates are high, and women warrant careful counseling and surveillance regarding future pregnancies.