Hematologic Changes

Maternal plasma volume increases ~50% above baseline by 30 to 34 weeks of pregnancy. Red blood cell mass also increases throughout gestation, but to only 18% to 30% more than nonpregnancy levels. These two phenomena result in a physiologic anemia, with the nadir of hemoglobin concentration (usually between 11 and 12 g/dL) at approximately 30 weeks of gestation. White blood cell counts during pregnancy also may increase (secondary to increased numbers of circulating granulocytes), with the upper limits of a pregnant woman’s normal white blood cell count being in the 15,000 to 16,000/μL range. Platelet counts remain greater than 150,000/μL during gestation, despite increased platelet turnover and a slightly shortened platelet life span.

Pregnancy has been described as a hypercoagulable state for the most part because of estrogen-induced increases in hepatic production of clotting factors I (fibrinogen), VII, IX, and X. Although pregnant patients have normal bleeding and clotting times, they are at increased risk for venous thromboembolism. This is particularly true in the puerperium (i.e., childbirth to 3 to 6 weeks postpartum) when injury to large pelvic veins or venous stasis in lower extremity veins is likely to occur. Any pregnant patient in whom there is prolonged restriction to activity should be considered a candidate for prophylaxis of deep venous thrombosis and should be fitted with pneumatic compression stockings or receive prophylactic anticoagulation (enoxaparin 40 mg subcutaneous daily, dalteparin 5000 IU mg subcutaneous daily, or heparin 5000 to 10,000 units subcutaneous twice per day).

Hemodynamic Changes

Blood pressure normally decreases during pregnancy secondary to decreased peripheral vascular resistance, an effect of circulating progesterone. The lowest values are seen at 24 to 28 weeks of gestation. Mean systolic blood pressure measures 5 to 10 mm Hg below baseline, whereas diastolic blood pressure falls slightly more, 10 to 15 mm Hg. Mean maternal heart rate increases at the beginning of the third trimester. Cardiac output is increased by 10 weeks of gestation secondary to increased stroke volume and later, in the third trimester, because of an increased heart rate (+15%). In large part, other changes in hemodynamic parameters result from the increased plasma volume associated with pregnancy (Table 28.1).

When a pregnant patient lies supine, the gravid uterus compresses the inferior vena cava leading to decreased venous return and cardiac output. Normally, peripheral vascular resistance increases to compensate for the decreased venous return. However, in up to 10% of pregnant patients, this protective mechanism fails. These patients have supine hypotension of pregnancy and become lightheaded or syncopal when supine. Maternal hemodynamics are optimized when the patient is placed in a left lateral recumbent position. Because blood pressure during pregnancy can vary with postural changes, serial blood pressure measurements should be obtained consistently with the pregnant patient in one position, with the cuff and heart at the same height from the floor.

Physical Findings Attributable to Pregnancy

Pregnant patients often have dependent edema secondary to decreased colloid oncotic pressure, increased lower extremity venous pressure, and obstruction of lymphatic flow by the gravid uterus. The first heart sound is often split, and a third heart sound can be auscultated in most pregnant patients secondary to increased plasma volume. Although almost all pregnant patients have a systolic ejection murmur secondary to increased flow across the aortic and pulmonic valves, diastolic murmurs are not considered physiologic during pregnancy. Electrocardiography often demonstrates a 15-degree left axis deviation because of elevation of the heart by the gravid uterus. Echocardiography may demonstrate functional tricuspid regurgitation secondary to a dilated tricuspid valve annulus. Chest radiographs will typically reveal an enlarged cardiac silhouette secondary to hypervolemia.

Postpartum Hemodynamic Fluctuations

Maternal blood loss from vaginal delivery of a singleton gestation averages ~500 mL. It can be two times that for a cesarean delivery. In the postpartum period, the mother mobilizes extracellular fluid, resulting in a postpartum diuresis equivalent to approximately 3 kg of weight loss. Despite the blood loss and diuresis, stroke volume and cardiac output remain elevated because of increased venous return. The clinical significance of these changes is manifested in a subclass of preeclamptic patients (see Chapter 72) as follows: (1) before delivery they have generalized vasospasm and intravascular volume depletion, (2) postpartum they mobilize their extracellular fluid as expected, (3) they often fail to diurese secondary to restricted renal blood flow, and (4) this places them at high risk for pulmonary or cerebral edema.

Respiratory Changes

Alterations in maternal lung volumes, respiratory mechanics, and arterial blood gas values precede elevation of the diaphragm because of the gravid uterus. Respiratory rate does not change during pregnancy, but tidal volume expands by 30% to 40%. This results in an increased minute ventilation beginning in the first trimester. Progesterone acting on the central respiratory center modulates these changes. Although gravid women frequently report a mild pregnancy-associated dyspnea, their forced expiratory volume in 1 second (FEV₁) is not decreased. Arterial pH remains at 7.40 during pregnancy, whereas Pao₂ is normally elevated at 104 to 108 mm Hg (as a result of chronic hypocapnia via the alveolar gas equation [Equation 12 in Box 1.1 in Chapter 1]), and Paco₂ is normally decreased at 27 to 32 mm Hg (secondary to the increased minute ventilation and increased alveolar ventilation [Box 1.1 in Chapter 1]). Increased renal excretion of bicarbonate (normal serum levels in pregnancy are 18 to 21 mEq/L) compensates for decreased Paco₂ and maintains the neutral pH. The lower maternal Paco₂ facilitates fetal-maternal CO₂ diffusion.

Renal Changes

Expanded plasma volume and decreased systemic vascular resistance result in increased renal plasma flow (+75%) and glomerular filtration rate (+30% to 50%) during pregnancy. A normal creatinine clearance during pregnancy is 150 to 200 mL/minute, and serum creatinine values decrease to 0.5 to 0.6 mg/dL. Glycosuria is not abnormal during pregnancy secondary to increased filtration of glucose. It is important to consider the increased renal clearance of drugs when dosing patients during pregnancy. Although strict guidelines cannot be provided, obtaining drug levels when applicable is recommended.

Gastrointestinal Changes

The smooth muscle relaxing effects of progesterone result in delayed gastric emptying, gastroesophageal sphincter relaxation, and esophageal reflux. These predispose pregnant patients to aspiration during emergency endotracheal intubation. Portal venous compression during pregnancy increases the likelihood of portal hypertension in patients with underlying chronic liver disease. Clinical presentations of this condition range from hemorrhoids to esophageal varices.

Drug Therapy

Most drugs used in critical care have not been studied extensively in the pregnant population so that little is known regarding their adverse effects on the human fetus. Although the potential risks on the fetus must be considered, as a general rule, the need to treat critical illness to restore maternal well-being should far outweigh these considerations. All drugs are assigned to categories representing degrees of fetal risk (Table 28.2). These categories are indicated in parentheses for the drugs discussed in the following sections.