Hypotension during spinal anaesthesia for caesarean section.

Abstract

I read Yokose et al.'s observational study about the predictive ability of non-invasive haemodynamic parameters for hypotension during Caesarean section with interest 1. In contrast to our study of pulse oximetry perfusion index to predict spinal hypotension 2, the authors found that pre-anaesthetic heart rate, but not perfusion index (PI) derived from pulse oximetry, was a predictor of spinal-induced hypotension during caesarean section. Since psychological stress and anxiety can induce sympathetic activation, which generates peripheral vasoconstriction and decreases PI, the authors were unsure whether PI was predictive for hypotension. Similarly, heart rate variability (HRV) was not found to be a predictor of hypotension, which the authors attribute to HRV's being affected by psychological stress. I am uncertain, then, why heart rate – itself subject to alteration by sympathetic activity – should be predictive when PI and HRV were not found to be. Perfusion index can be used to assess peripheral perfusion dynamics caused by changes in peripheral vascular tone. In our study 2, baseline haemodynamic variables and PI were simultaneously recorded with the subjects lying down on the operating table and before the preload of colloid, the mean (SD) baseline PI being 4.0 (2.3), smaller than that reported by Yokose et al. Since vascular tone is regulated by sympathetic and endothelial pathways, PI in our study could have been affected by these. However, normal pregnancy is characterised by a decrease in systemic vascular resistance (SVR) due to reduction in endothelial vascular tone 3, and so peripheral vascular tone decreases, even though there is compensatory dependence on sympathetic vasoconstriction for the control of vascular tone. Compared with parturients with low baseline PI, patients with high baseline PI in our study were more multiparous. Since the magnitude of the decrease in SVR is greater in multiparous women than nulliparous 4, we considered that higher baseline PI reflected lower peripheral vascular tone, and so greater dependence on sympathetic activity to maintain blood pressure. We found that parturients with high baseline PI showed a marked decrease in PI after spinal anaesthesia, compared with those with low baseline PI in whom changes were not significant. Sumikura et al. reported a decrease in PI of the finger and an increase in PI of the toe after spinal anaesthesia, indicating a reduction in peripheral perfusion in the upper part of the body because of a blood shift to the lower part of the body 5. Since endothelial regulation is not altered by spinal anaesthesia, we considered that parturients with high baseline PI were likely to develop hypotension because pooling of more blood in the lower part of the body due to low vascular tone. A variety of factors are considered to be associated with spinal-induced hypotension during caesarean section. Our results suggest that haemodynamic changes after spinal anaesthesia for caesarean section are influenced by not only volume status and sympathetic activity, but also endothelial-dependent vascular tone, and we invite Yokose et al. to comment on this.