The uterine arteries provide the uterus with ~ 700 cc/min of maternal blood. The fetus receives blood through two uterine arteries, and returns it via a single uterine vein. Placental vasculature normally exists in a vasodilated state (although not maximally so, as is classically taught), probably secondary to nitric oxide release. Note that many studies of uterine blood flow rely on the S/D ratio, which is the ratio of maximal velocity during systole divided by the minimal velocity during diastole – an elevated S/D ratio is associated with poor placental perfusion.
By far the most important determinant of UBF. Affected by positioning (ex. aortocaval compression), sympathectomy, hypovolemia.
In animal models (pregnant ewe), pain impacts uterine blood flow via two mechanisms – an increase in circulating catecholamines (which reduce blood flow [Shnider SM et al. Anesthesiology 50: 524, 1979]), and via hyperventilation. [Levinson G et al. Anesthesiology 40: 340, 1974]
Temporarily reduces uterine blood flow, and can cause total cessation when pressures exceed 35 mm Hg.
The impact of regional anesthesia on uterine blood flow is controversial. Decreases in catecholamines have the potential to increase uterine blood flow, however hypotension, when present, may counteract these effects.
Effect of Pharmacologic Agents
No change in uterine blood flow (sheep studies [Alon E et al. Anesthesiology 78: 562, 1993])
Minimal change in uterine blood flow (sheep studies [Fresno L et al. Vet J 177: 94, 2008])
No change in uterine blood flow using 0.5-0.7 mg/kg (sheep studies [Craft JB Jr. et al. Am J Obs Gyn 146: 429, 1993])
Isoflurane preserves uterine blood flow despite the decrease in MAP, most likely due to uterine vasodilation. [Palahniuk RJ and Shnider SM. Anesthesiology 41: 462, 1974]
Even low doses of epinephrine (15 ucg bolus) have been shown to decrease uterine blood flow in sheep. [Hood DD et al. Anesthesiology 64: 610, 1986]
Placental Gas Exchange
The oxygen dissociation curve is left-shifted in the fetus (which encourages uptake of oxygen from maternal supplies), and the average [Hgb] in the fetus is 17 g/dL, thus while fetal pO2 is only ~ 30 mm Hg, oxygen content is almost identical to that of its mother. A healthy fetus can safely tolerate a 50% reduction in oxygen delivery. [Wilkening RB and Meschia G. Am J Physiol 244: H749, 1983]
CO2 exchange depends on concentration gradients and uterine blood flow. Note that maternal hypocapnea can cause fetal hypoxia and acidosis secondary to vasoconstriction, decreased venous return (hypocapnea is usually the result of hyperventilation and increased thoracic pressure), and left shift of the maternal oxygen dissociation curve (CO2 leads to unloading of O2, hypocapnea leads to retention of O2).