UTERINE BLOOD FLOW

Uterine blood flow increases progressively during pregnancy and reaches a mean value of 500 to 700 mL by term. Blood flow through the uterine vessels is high and has low resistance; this change in resistance occurs most dramatically after 20 weeks of gestation.^[33] Uterine blood flow lacks autoregulation (vessels are maximally dilated during pregnancy), and uterine artery flow is therefore dependent on maternal blood pressure and cardiac output. Any factors that alter blood flow through the uterus will adversely affect the fetal blood supply. Uterine blood flow is determined by the following relationship:





Uterine blood flow decreases during periods of maternal hypotension, which can occur as a result of hypovolemia, hemorrhage, aortocaval compression, and sympathetic blockade. Similarly, uterine hypercontractility (or conditions that increase the frequency or duration of uterine contractions) and changes in uterine vascular tone, as seen in hypertensive states, may also adversely affect blood flow.

Anesthetics may dramatically influence uterine blood flow either by alterations in perfusion pressure or by changes in uterine vascular resistance. Sympathetic blockade after neuraxial techniques may reduce maternal blood pressure, and the decrease in pressure will affect uterine blood flow. This response may be exaggerated in patients who are not adequately prehydrated. Fluid preloading before neuraxial anesthesia does not completely avoid maternal hypotension, but it does increase maternal cardiac output; thus, it may preserve uteroplacental blood flow. ^[34] Studies have demonstrated that maternal cardiac output correlates with the uterine artery pulsatility index and umbilical artery pH.^{[35] [36]} High concentrations of volatile anesthetics during general anesthesia may cause systemic vasodilatation and produce depressant effects on the myocardium. Aortocaval compression may further compound these effects.

Vasopressors with direct α-adrenergic receptor activity (such as phenylephrine) have been associated in animal studies with increased intrinsic vascular resistance and, as a consequence, a reduction in uterine blood flow.^[37] There has been renewed interest in phenylephrine as a vasopressor for use in routine clinical practice; studies have demonstrated that this drug can be used safely in healthy parturients and is as efficacious as ephedrine in maintaining maternal blood pressure and umbilical artery pH values.^{[38] [39] [40]} Although a recent study has suggested that combination therapy with ephedrine and phenylephrine is optimal,^[41] ephedrine is still probably the vasopressor of choice.^[42] Its mixed α- and β-adrenergic effects cause an increase in arterial blood pressure that is secondary to increased cardiac output and increased peripheral vascular resistance. Studies in pregnant ewes have demonstrated that ephedrine is superior to metaraminol and methoxamine in maintaining uteroplacental blood flow.^[43]