In North America, norepinephrine, ephedrine, and epinephrine have been recommended as first-choice vasopressors for the treatment of spinal hypotension during cesarean delivery. However, in international consensus guidelines, epinephrine was recommended for circulatory collapse only. Phenylephrine infusion is an important therapeutic strategy for preventing spinal-induced hypotension (SIH) in cesarean delivery, as it decreases the incidence of hypotension, nausea, and vomiting. However, high doses may reduce maternal heart rate and cardiac output in a dose-dependent manner. Ephedrine, previously considered the first-choice drug, has both α and β receptor agonistic activity and causes norepinephrine release from sympathetic neurons. Its β1 effect increases heart rate and contractility, but may cause undesirable tachycardia. Tachyphylaxis can develop with repeated doses. Norepinephrine, the biosynthetic precursor of epinephrine, has both potent α and weak β agonist effects, tending to cause bradycardia. Despite a lower incidence of hypotension with prophylactic norepinephrine, PSH still occurs in up to 30% of parturients undergoing cesarean section. The administration of a bolus dose of epinephrine prior to continuous infusion is an unusual practice in obstetric anesthesia, but has been reported to be safe in other contexts and in pregnant women when used for hemodynamic support. Epinephrine has both potent α- and β-adrenoceptor agonist activity. Its β effects could offset reflex decreases in maternal HR and CO during spinal anesthesia for cesarean delivery. Although some studies compared epinephrine infusion with phenylephrine, it remains unclear whether adding an initial bolus of epinephrine before infusion offers superior maternal hemodynamic stability compared to infusion alone.
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Incidence of post-spinal hypotension
Timeframe: up to 2 hours after spinal anesthesia