Section 4: Subspecialty Management
Chapter 57: Anesthesia for Obstetrics

Cardiovascular Changes

The cardiovascular system is progressively stressed during pregnancy and parturition (Table 57–3, Figs. 57–3 and 57–4). Many of the changes appear during the first trimester of pregnancy (increase in cardiac output of 22% and decrease in systemic vascular resistance [SVR] by 30% at 8 weeks‘ gestation). 13  The changes continue into the second and early third trimester of pregnancy, when cardiac output increases to approximately 30 to 40 percent above nonpregnant values. 14, 15  The increase in cardiac output during pregnancy is primarily a result of an increase in stroke volume (by about 30%), with a more modest increase in heart rate (10–15 beats per minute [bpm]) 13  noted. Arterial blood pressure does not change during normal pregnancy because of a decrease in peripheral vascular resistance. Early reports suggested that cardiac output decreased markedly during the third trimester. These reports, however, studied gravid patients in the supine position. Lees and associates 14, 16  and Ueland et al 17  showed that this marked decrease in cardiac output occurring after 28 weeks of pregnancy in subjects in the supine position was caused by obstruction of the inferior vena cava by the gravid uterus. Decreased venous return and reduced cardiac output were not seen in subjects in the lateral position, which eliminates this obstruction.

TABLE 57–3. Hemodynamic Changes in Pregnancy

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FIGURE 57–3 Maternal cardiovascular changes during pregnancy and labor from studies on patients in the lateral and supine positions. (From Mangano426 )

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FIGURE 57–4 Effects of uterine contractions on cardiac output, stroke volume, and heart rate during labor. Values represent percent increases from control measurements in late pregnancy. (From Mangano426 )

Maternal blood volume increases markedly during pregnancy (Fig. 57–5). 18, 19  Near term, blood volume has increased approximately 35 to 40 percent, (i.e., by more than 1,000 mL). Plasma volume increases from 40 mL/kg before pregnancy to 70 mL/kg during late pregnancy, and red blood cell volume increases from 25 to 30 mL/kg. The latter increases at a slower rate than the former, accounting for the relative anemia of pregnancy. Although the dilutional anemia of pregnancy decreases the oxygen-carrying capacity of the blood, several factors compensate for this, including an increase in maternal partial pressure of arterial oxygen (see Table 57–1), a decrease in blood viscosity, an increase in cardiac output, and a rightward shift in the maternal oxyhemoglobin dissociation curve (see Table 57–2). 10  As a result, transport of oxygen to important organs increases during pregnancy.

TABLE 57–1. Maternal Respiratory Changes at Term

TABLE 57–2. P50 Values of Nonpregnant, Pregnant, and Preeclamptic Subjects

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FIGURE 57–5 Percent of increase in the volume of plasma, red blood cells (RBC), and total blood during pregnancy, labor, and the puerperium. (From Bonica424 )

The increased blood volume and cardiac output may produce changes in the cardiac examination of the pregnant patient. Auscultation may reveal a wide, loud split first sound and a soft systolic ejection murmur caused by increased blood flow and vasodilation. 20  The position of the heart is usually altered by the elevated diaphragm at term gestation. This displaces the point of maximum impulse to the left and changes the axis of the heart on the electrocardiogram to the left. 20  The electrocardiogram may show minor, nonspecific ST-, T-, and Q-wave changes and benign arrythmias. 20  These normal findings should be differentiated from those indicating heart disease. Signs of significant heart disease in the pregnant woman include true cardiac enlargement, severe arrhythmias, systolic murmur greater than grade 3, or significant diastolic murmur.

The pain and apprehension of labor adds to cardiac work during pregnancy and increases stroke volume and cardiac output by 45 percent over prelabor values. 21, 22  Blood pressure increases during painful labor. Additional stresses are imposed by uterine contractions, which cause, in effect, an autotransfusion. With each uterine contraction, blood from the body of the uterus is pushed into the central circulation, and blood volume and cardiac output increase by 10 to 25 percent. 22, 23  After delivery, the same autotransfusion occurs. In addition to an increase in central blood volume, obstruction of the vena cava is relieved. As a result, there is a marked increase (up to 80% of prelabor values) in stroke volume and cardiac output immediately postpartum. Patients with limited cardiac reserve may experience cardiac failure at this time.

Despite the increase in blood volume and cardiac output, the parturient at term is susceptible to hypotension when supine. When the patient is supine, the gravid uterus partially or completely compresses the aorta and inferior vena cava, leading to decreased venous return, decreased cardiac output, hypotension, and reduced uterine blood flow (Figs. 57–6, 57–7, and 57–8). 24, 25, 26, 27, 28  Up to 10 percent of pregnant patients near term develop signs of shock (hypotension, pallor, sweating, nausea, vomiting, changes in cerebration) when they assume this position. Compensatory mechanisms include increased sympathetic tone and collateral routes (paravertebral veins to azygos vein) to improve venous return during obstruction of the vena cava. Caval compression also increases uterine venous back pressure, which further decreases uterine blood flow. Compression of the aorta is not associated with maternal symptoms but does cause arterial hypotension in the lower extremities and uterine arteries, which can further decrease uterine blood flow and impair uteroplacental perfusion. 29 

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FIGURE 57–6 Venogram in the supine position just before cesarean section. (A) Dye has been injected into both femoral veins but does not reach the inferior vena cava, traversing instead the paravertebral veins. (B) Same patient just after cesarean section. The dye now easily reaches the inferior vena cava. (From Kerr et al27 )

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FIGURE 57–7 Schematic of lateral angiograms obtained from two women lying in the supine position. In the nonpregnant woman (left), there is a clear gap between the vertebral column and the aorta. Note the uniform width of the aorta. In the pregnant patient near term (right) the aorta is clearly displaced in the dorsal direction, encroaching on the shadow of the spine. The aorta is narrowed at the level of the lumbar lordosis. (From Bieniarz et al427 )

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FIGURE 57–8 Serial hemodynamic studies in a patient who exhibited supine hypotension. After the patient had lain supine for 6 minutes, a profound fall in arterial pressure and heart rate was seen. (From Kerr26 )

The anesthesiologist must recognize the importance of the aortocaval compression syndrome and the potential for its adverse effects to be exaggerated by anesthesia. Drugs causing vasodilation, such as potent inhaled agents, and particularly anesthetic techniques causing sympathetic blockade (subarachnoid or epidural anesthesia) exacerbate decreased venous return to the heart when the vena cava is obstructed. Aortocaval compression must be prevented. Displacement of the uterus off the great vessels can be accomplished by manually displacing the uterus to the left. During labor, the patient should be positioned either on her side or with a left tilt. During delivery, the operating or delivery table can be tilted laterally to the left, or a small pillow or foam rubber wedge can be used to elevate the patient‘s right buttock and back about 10 to 15 cm.

The pregnant woman at term is in a hypercoagulable state owing to increases in factors VII, VIII, X, and plasma fibrinogen. 30  Estimates of blood loss at delivery vary but may be around 500 mL for an uncomplicated vaginal delivery. Blood loss during cesarean delivery varies widely, with 500 to 1400 mL being reported. 31, 32