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UTEROPLACENTAL ANATOMY
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The uterine blood supply is derived from the uterine arteries with a minor contribution from the ovarian arteries. Maternal blood destined for the placenta travels through the spiral branches of the uterine arteries before reaching the intervillous space, the outermost limit of the maternal portion of the placenta. Maternal blood pools in the intervillous space, surrounding projections of fetal tissue, known as villi, which contain fetal capillaries (Figure 152-1). These capillaries receive deoxygenated blood from the fetus via two umbilical arteries. It is here, in the terminal villi, that the maternal–fetal exchange of nutrients, respiratory gases, fetal waste, and other substances occurs. Maternal blood returns to maternal circulation via the uterine veins, and oxygenated fetal blood travels back to the fetus via the umbilical vein.
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UTEROPLACENTAL BLOOD FLOW
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In the nonpregnant female, the uterus receives blood at about 50–100 mL/min; compare this to a term pregnancy, wherein uterine blood flow is 500–900 mL/min, or about 10% of maternal cardiac output. Of this 10%, the majority (80%–90%) supplies the placenta with the remainder going to the myometrium and nonplacental endometrium. In order to accommodate this large increase in blood flow, the spiral arteries of the uterus undergo extensive growth and remodeling. The elastic and muscular portions of the arteries are replaced, first by cytotrophoblasts and then by fibroid cells. This replacement of the tunica media results in maximal vasodilation, such that uterine arterial pressure is dependent on maternal blood pressure and cardiac output. The vasculature does maintain intrinsic responsiveness to α-adrenergic agents and, possibly, β-adrenergic agents, affecting uterine vascular resistance. In sum, uterine blood flow is determined as follows:
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Note that uterine perfusion pressure = uterine arterial pressure – uterine venous pressure.
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In examining this equation, three relationships are evident. First, any factor that causes maternal hypotension will decrease uterine arterial pressure and thereby decrease uterine blood flow. Aortocaval compression, hypovolemia and the sympathetic blockade caused by neuraxial anesthesia are possible causes of maternal hypotension. Second, an increase in uterine venous pressure will decrease uterine blood flow. Vena cava compression, certain drugs (e.g., cocaine, oxytocin), uterine contractions or hypertonus, and skeletal muscle hypertonus (e.g., seizure, Valsalva) are all possible causes of increased uterine venous pressure. Finally, an increase in uterine vascular resistance will decrease uterine blood flow. Endogenous catecholamine release, vasopressin release (e.g., secondary to hypovolemia), exogenous vasopressors (e.g., phenylephrine, ephedrine, high concentrations of local anesthetics), and compression of endometrial spiral arterioles during uterine contractions all increase uterine vascular resistance.
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EFFECTS OF ANESTHETIC AGENTS ON UTEROPLACENTAL BLOOD FLOW