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PHYSIOLOGIC CHANGES OF PREGNANCY

Maternal changes in pregnancy occur as a result of hormonal alterations, mechanical effects of the gravid uterus, increased metabolic and oxygen requirements, metabolic demands of the fetoplacental unit, and hemodynamic alterations associated with the placental circulation. Such changes become more significant as pregnancy progresses, and they have major implications for anesthetic management, especially in high-risk parturients.

Cardiovascular System

The cardiovascular system adjusts throughout pregnancy to meet the changes that occur. Hemodynamic and maternal cardiovascular changes in pregnancy are outlined in Table 58-1 . Although the physiologic changes in the cardiovascular system appear to begin in the first trimester, these changes continue into the second and third trimesters, when cardiac output increases by approximately 40% of nonpregnant values. Cardiac output increases from the fifth week of pregnancy and reaches its maximum levels at approximately 32 weeks,
TABLE 58-1 -- Cardiovascular changes in pregnancy
Parameter Change Amount (%)
Heart rate Increased 20–30
Stroke volume Increased 20–50
Cardiac output Increased 30–50
Contractility Variable ±10
Central venous pressure Unchanged
Pulmonary capillary wedge pressure Unchanged
Systemic vascular resistance Decreased 20
Systemic blood pressure Slight decrease Midtrimester 10–15 mm Hg, then rises
Pulmonary vascular resistance Decreased 30
Pulmonary artery pressure Slight decrease
From Birnbach DJ, Gatt SP, Datta S (eds): Textbook of Obstetric Anesthesia. New York, Churchill Livingstone, 2000, p 34.

after which there is only a slight increase until labor, delivery, and the postpartum period.[5] Approximately 50% of the increase in cardiac output has occurred by the eighth week of pregnancy.[6] Although this increase in cardiac output is due to an increase in both stroke volume and heart rate, the more important factor is stroke volume, which increases by 20% to 50% at term from nonpregnant values. Changes in heart rate are extremely difficult to reliably quantify, but it is thought that the approximately 20% increase in heart rate is present by the fourth week of pregnancy. Although the normal variability in heart rate does not change in pregnancy, there does appear to be a reduction in the sympathetic component.[7] Tachyarrhythmias are more common, especially later in pregnancy as a result of both hormonal and autonomic factors.[8]

Because of the decrease in peripheral vascular resistance, arterial blood pressure does not change in a normal pregnant patient. Although it was originally thought that cardiac output decreases during the third trimester, we now know that this decrease is due to effects of the supine position in the patient at term.[9] Ueland and colleagues demonstrated that the fall in cardiac output was due to obstruction of the inferior vena cava by the gravid uterus and did not occur when women were placed in the lateral position.[10] A venogram performed before and after cesarean delivery ( Fig. 58-1 ) demonstrates this phenomenon. Despite the increase in blood volume and cardiac output, parturients at term are susceptible to hypotension, especially when in the supine position. Up to 10% of pregnant patients at term show signs of shock when assuming the supine position. This phenomenon has been termed the supine hypotension syndrome. To compensate, collateral routes of venous return develop, including the paravertebral veins to the azygos vein. Unlike compression of the vena cava, compression of the aorta is not associated with maternal symptoms in a healthy


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Figure 58-1 A, Venogram in a term patient in the supine position before cesarean section. Radiopaque dye injected into the femoral veins fails to reach the inferior vena cava (IVC) but reaches the paravertebral veins. B, After cesarean section, blood is seen in the IVC. (From Kerr MG, Scott DB, Samuel E: Studies of the inferior vena cava in late pregnancy. BMJ 1:532, 1964.)

parturient, but it may be associated with decreased utero-placental perfusion.[11] Anesthetics and drugs that cause vasodilation or anesthetic techniques that cause sympathectomy (neuraxial techniques) may exacerbate aortocaval compression. In the operating room, a small pillow or "wedge" should be used to provide left uterine displacement of approximately 15 to 20 degrees. This angle can be increased as necessary by increasing the wedge or tilting the table.

The changes in blood volume and cardiac output usually have clinical implications for parturients who have concomitant cardiac disease, but they may also have an impact on healthy parturients. Many pregnant patients will complain of symptoms suggestive of cardiovascular disease at term, including shortness of breath, palpitations, dizziness, edema, and poor exercise tolerance.[12] Physical examination of the patient may also be abnormal when compared with the prepregnant state, with auscultation commonly revealing a wide loud split first heart sound, an S3 sound, and a soft systolic ejection murmur. As illustrated in Table 58-2 , pregnancy has numerous effects on cardiac evaluation, including changes in the electrocardiogram, chest radiograph, and echocardiogram. Although these minor changes occur in healthy pregnant women at term, symptoms and signs such as chest pain, syncope, severe arrhythmias, systolic murmur more than grade 3, or diastolic murmur suggest severe disease and warrant further investigation.[13] A gradual return to the prepregnancy blood volume occurs at 6 to 9 weeks postpartum.

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