[Maternal-fetal cardiovascular effect of spinal anesthesia]

Despite of a chronic volume overload the left ventricle function of pregnant women is preserved by both afterload reduction (arterial vasodilatation) and a facilitation of heart filling through an increase in peripheral venous tone. Fetal oxygenation results from an equilibrium between placental and umbilical blood flows. During regional anaesthesia the sympathetic blockade leads to a peripheral vasodilatation (mainly in the capacitive territories) which is the cause of arterial hypotension through a decrease in cardiac output. Placental flow may therefore be altered by the reduced perfusion pressure and/or a reflex or pharmacological vasoconstriction. Hypotension is an infrequent event during labor epidural analgesia. However the incidence of hypotension is higher during regional anaesthesia for cesarean section, up to 35% following intrathecal injection of local anaesthetic. Prevention of hypotension requires (i) release of aortocaval compression by gravid uterus (ii) volume preloading (15 min i.v. infusion of crystalloid, 20 ml.kg-1 with ephedrine, 15 mg if spinal anaesthesia is chosen), and (iii) limitation of plain local anaesthetic dosage (epinephrine, 1:200,000 with fentanyl, sufentanil or clonidine). Hypotension must be promptly reversed to avoid placental and umbilical flow alteration. Titrated doses of vasopressors are useful, either ephedrine or phenylephrine. Finally regional anaesthesia is beneficial for the mother and the fetus through a reduction in plasma catecholamines, provided that arterial pressure remains unchanged. Thus during pregnancy-induced hypertension (PIH) epidural analgesia leads to an improvement of the reduced placental blood flow. However PIH renders the women susceptible to sympathetic blockade and the fetus easily vulnerable to an additional stress factor like acute decrease in placental flow due to hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)