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An alternative explanation for the inferior neonatal outcome with noradrenaline?

In a recent issue of Anaesthesia, Mohta et al. compared noradrenaline and phenylephrine to treat postspinal hypotension during caesarean section in 90 women [1]. Bolus noradrenaline 5 lg or phenylephrine 100 lg was used to maintain maternal blood pressure higher than 80% of baseline. They reported statistically fewer requirements to maintain maternal blood pressure, as well as a lower umbilical artery pH, for noradrenaline. The authors attributed such inferior neonatal outcome to, presumably, placental transfer and the fetal metabolic effects of noradrenaline. At first glance, this study warns us of the potential neonatal risk when administering noradrenaline, however, somedetails of the study attracted our attention. Firstly, in any discussion comparing noradrenaline with phenylephrine, it is important to consider the doses used of both vasopressors. In a previous dose–response study by Ngan Kee, the potency ratio of noradrenaline vs. phenylephrine, when used as a bolus to treat a first episode of hypotension, was approximately 13:1 [2]. Alternatively, as calculated by Mohta et al. themselves in another study it was 11.3:1 [3]. Therefore, noradrenaline 5 lg is almost certainly less potent than phenylephrine 100 lg. Theoretically, more boluses of noradrenaline should be required in this study; however, somewhat unexpectedly, a contrary result was reported, with a median [range] of 1 [1– 5] boluses for noradrenaline and 2 [1–9] boluses for phenylephrine, respectively; p = 0.01. As all the recruited women were healthy, uncomplicated, parturients, who received a consistent haemodynamic management regimen and blood pressure goal, we are confused by such seemingly paradoxical results. Secondly, if fewer noradrenaline boluses were administered, as reported in the study, in combination with the lower potency of noradrenaline 5 lg compared with phenylephrine 100 lg, the overall blood pressure might be maintained at a lower level in the noradrenaline group, albeit higher than 80% of baseline. Despite this, the blood pressure was found to be no different between the groups at each time-point, although the statistical analysis for overall blood pressure throughout the observational period, from intrathecal injection to delivery, was not available for both drugs in Mohta et al.’s study. As uteroplacental perfusion is highly dependent on maternal blood pressure, is it possible that, the lower umbilical artery and umbilical vein pH values might reflect the overall lower maternal blood pressure and reduced uteroplacental perfusion? Finally, a possibly minor issue. If the time-point zero in figures 2 and 3 indicate baseline systolic arterial pressure and heart rate values immediately before spinal anaesthesia, then such values are not consistent with those shown in Table 2. We are unclear as to the underlying reasons for this, and wondered whether the authors could explain?