Journal: Anesthesiology 108(5):802-811, 2008
Reprint: D23 Department of Anesthesia, University of Cape Town and New Groote Schuur Hospital, Anzio Road, Observatory, Cape Town 7925, South Africa (RA Dywe, FCA(SA))
Faculty Disclosure: Abstracted by J. Joyce, who has nothing to disclose.
Only since 1995, when the first randomized trial on the use of regional versus general anesthesia for cesarean delivery in severe preeclampsia was published, has spinal anesthesia (SA) been con¬sidered an option in this high-risk group of patients. As recently as 1998, an editorial recommended that epidural anesthesia is preferable to SA for cesarean delivery, even if the patient has not received epidural anesthesia in labor. It was therefore decided to investigate cardiac output (CO) changes during SA for cesarean delivery in severe pre-eclampsia. The hypothesis was that SA would result in clinically insignificant change in CO in these patients, other than at the time of oxytocin administration. Also studied were the hemodynamic responses to vasopressors and to delivery and oxytocin. In addi¬tion, an assessment was made of the hemodynamics of recovery from SA.
This observational study describes the maternal hemodynamic response to SA for cesarean delivery in 15 patients with severe preeclampsia, using phenylephrine as the first choice vasopressor, as is the current practice in healthy patients during SA for cesarean delivery. This study confirms the hypothesis that CO decreases were clinically insignificant during the procedure. The requirement for vasopressors was low, in keeping with the existing literature, which suggests a lower requirement than in normal parturients.
In the current study, when target values of mean arterial pressure (MAP) for vasopressor administra¬tion (a 20% decrease in blood pressure) were reached, CO had not decreased significantly, and in many cases had increased. This suggests that main¬taining blood pressure at the baseline level in this patient population during SA may not be optimal practice, especially considering the risk of worsening hypertension in patients with severe preeclampsia. Furthermore, phenylephrine, administered in re¬sponse to a 20% decrease in baseline MAP, did not increase CO. In several cases, CO decreased.
Fluid preloading increased CO in the preeclamptic group in a recent study, but not in healthy patients. The use of ephedrine increased both MAP and systemic vascular resistance. At delivery, increases in the CO of preeclamptic patients were due only to increases in HR; stroke volume did not increase, in contrast with the healthy patients. Of particular clinical relevance was the finding that in the healthy patients, hemodynamic values returned to baseline after recovery from SA, whereas the stroke index and cardiac index in the preeclamptic group were significantly lower than presurgery levels.
This observational study showed that SA was associated with modest afterload reduction and minimal CO changes. Phenylephrine did not improve CO, and further work is required to establish whether a mixed α, β agonist is the preferred vasopressor, from both the maternal and the fetal point of view. |
