Spinal anesthesia-induced hypotension (SAIH) occurs frequently, particularly in the elderly and in patients undergoing caesarean section. SAIH is caused by arterial and venous vasodilatation resulting from the sympathetic block along with a paradoxical activation of cardioinhibitory receptors. Bradycardia after spinal anesthesia (SA) must always be treated as a warning sign of an important hemodynamic compromise. Fluid preloading (before initiation of the SA) with colloids such as hydroxyethyl starch (HES) effectively reduces the incidence and severity of arterial hypotension, whereas crystalloid preloading is not indicated. Co-loading with crystalloid or colloid is as equally effective to HES preloading, provided that the speed of administration is adequate (ie, bolus over 5 to 10 minutes). Ephedrine has traditionally been considered the vasoconstrictor of choice, especially for use during SAIH associated with bradycardia. Phenylephrine, a α1 adrenergic receptor agonist, is increasingly used to treat SAIH and its prophylactic administration (ie, immediately after intrathecal injection of local anesthetics) has been shown to decrease the incidence of arterial hypotension. The role of norepinephrine as a possible alternative to phenylephrine seems promising. Other drugs, such as serotonin receptor antagonists (ondansetron), have been shown to limit the blood pressure drop after SA by inhibiting the Bezold-Jarisch reflex (BJR), but further studies are needed before their widespread use can be recommended.
Keywords: arterial hypotension; ondansetron; phenylephrine; spinal anesthesia; vasopressor.
© 2020 Ferré et al.