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      Effect of prophylactic ondansetron and/or continuous infusion of phenylephrine on spinal anesthesia-induced hypotension

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          Abstract

          Sir, We read with interest the article by Ortiz-Gómez et al. reporting the effect of prophylactic ondansetron and/or continuous infusion of phenylephrine on spinal anesthesia-induced hypotension; we acknowledge their work.[1] The investigators reported, in a double-blind, randomized, placebo-controlled trial, a reduction of 50% in the incidence of maternal hypotension during elective caesarean delivery. We appreciate that the authors mentioned the usually forgotten reverse Bainbridge reflex with the well cited one study by Bezold-Jarisch in an attempt to probably explain the prophylactic effect of ondansetron on the hypotension associated with spinal anesthesia.[2] At the same time we must mention that ondansetron, expected to inhibit hypotension and bradycardia via inhibiting the Bezold-Jarisch reflex, triggered many cases of severe bradycardia and even cardiac arrest.[3] We do not fully share with the authors the opinion when they stated that the main contributors to hypotension with sympathetic nerve blockade are the decreases in cardiac output and systemic vascular resistance. Studies have proven many years before the publication of the article in question that the typical hemodynamic effects of spinal anesthesia in healthy pregnant women are a decrease in the systemic vascular resistance and a compensatory increase in cardiac output, which might increase again after fetal extraction by cancellation of uterine aortocaval compression syndrome.[4] These scientific facts are made possible by the utilization of minimally or noninvasive monitoring of cardiac output whose increase is the result of a partial rise in stroke volume and tachycardia.[4 5] Thus, phenylephrine is the first-line vasopressor from physiological point of view, regardless of the effect of both phenylephrine and ephedrine on the fetal acid-base status.[4 5] However, when hypotension is associated with bradycardia, ephedrine becomes the recommended option.[5] We do have also a great concern about the results reporting significant differences between the groups in heart rate. After a thorough glance to these findings, we noticed that atropine was not administered at all in the control and ondansetron groups but was given in 25.4% and 19.1% in phenylephrine and ondansetron plus phenylephrine groups, respectively. For us this is a proof that bradycardia seen in the latter two groups was a reactional response to blood hypertension caused by continuous phenylephrine infusion and mediated by arterial baroreceptors.[2] Another direct implication is that the phenylephrine dosage used in the present trial was causing hypertension rather than preventing hypotension as was the aim of the investigators. Last but not least, pregnant women are now classified ASA 2 instead of ASA 1 according to the recent ASA classification update.[6] In fact, physiological changes related to pregnancy influence perioperative management and outcome. We wonder how the trial was carried out to give solutions for spinal anesthesia-induced hypotension, and at the same time, we remark in the demographic and anesthetic data that dural puncture to skin incision and skin incision to fetal extraction are both lasting for 10 min in average. This means that delivery took in the study several minutes which is known to have possible negative impacts on maternal and fetal prognosis even under spinal anesthesia. Finally, we really appreciate the authors’ initiative to accomplish this work which will certainly help to clarify and animate the debate about spinal anesthesia-induced hypotension as was suggested by meta-analyses.[7] Financial support and sponsorship None. Conflicts of interest There are no conflicts of interest.

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          Most cited references 6

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          International consensus statement on the management of hypotension with vasopressors during caesarean section under spinal anaesthesia

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            Maternal haemodynamic changes during spinal anaesthesia for caesarean section.

            Maternal haemodynamic changes during spinal anaesthesia for caesarean section have traditionally been evaluated by noninvasive blood pressure and heart rate. Recent publications have addressed the importance of cardiac output measurement in the assessment of the maternal circulation. In this review, a physiological approach is suggested for the prevention and treatment of haemodynamic instability during caesarean section in healthy women and in those with preeclampsia or cardiac disease. A better understanding of the maternal haemodynamic effects of spinal anaesthesia and the effects of vasopressors has emerged from the monitoring of cardiac output during caesarean section in healthy women and in those with severe preeclampsia or cardiac disease. Based on maternal physiological arguments, phenylephrine is the vasopressor of choice in healthy pregnant women. New work demonstrating cardiac dysfunction in some women with severe preeclampsia has implications for risk assessment and anaesthesia. Recent publications suggest that combined spinal-epidural and continuous spinal anaesthesia is well tolerated in pregnant women with cardiac disease. The most frequent response to spinal anaesthesia for elective caesarean section is a marked decrease in systemic vascular resistance and partial compensation from increased stroke volume and heart rate. Early administration of phenylephrine by bolus or continuous infusion is indicated in most cases. Recent work has expanded our knowledge of the therapeutic range of phenylephrine and indicates that the heart rate response to vasopressors is a good surrogate marker for cardiac output. Further research should examine haemodynamic changes during spinal anaesthesia in high-risk pregnant women with early onset preeclampsia or cardiac disease.
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              Effects of prophylactic ondansetron on spinal anesthesia-induced hypotension: a meta-analysis

               Y. WANG,  J Zheng,  L Gao (2015)
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                Author and article information

                Affiliations
                Department of Anesthesia and Intensive Care, Teaching Hospital of Sahloul, University of Medicine, Sousse, Tunisia
                [1 ]Department of Anesthesia and Intensive Care, Teaching Hospital of Farhat Hached, University of Medicine Ibn Al Jazzar, Sousse, Tunisia
                [2 ]Department of Anesthesia and Intensive Care, Teaching Hospital of Taher Sfar Mahdia, University of Medicine Fattouma Bourguiba, Monastir, Tunisia
                Author notes
                Address for correspondence: Dr. Salah Mhamdi, Department of Anesthesia and Intensive Care, Teaching Hospital of Sahloul, Sousse, Tunisia. E-mail: dr_mhamdi@ 123456yahoo.fr
                Journal
                Saudi J Anaesth
                Saudi J Anaesth
                SJA
                Saudi Journal of Anaesthesia
                Medknow Publications & Media Pvt Ltd (India )
                1658-354X
                0975-3125
                Oct-Dec 2018
                : 12
                : 4
                : 656-657
                SJA-12-656
                10.4103/sja.SJA_371_18
                6180680
                30429759
                Copyright: © 2018 Saudi Journal of Anesthesia

                This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms.

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                Anesthesiology & Pain management

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