We are gratified, but not surprised, by the interest in our recent article,1 given that we examined one of the oldest recommendations regarding maternal position for cesarean delivery. In their letters, Riley et al.2 and Shayegan et al.3 correctly note that cardiac output was slightly lower among women kept supine, and that more phenylephrine was required (probably related). The goal of anesthetic management, however, is not to maintain specific hemodynamic parameters, but rather to maintain adequate or optimal conditions for mother and fetus. There is no evidence that the lower cardiac output or increased phenylephrine requirements caused any injury, nor any plausible mechanism by which these levels of cardiac output should be harmful. It is probable, as suggested by Dyer et al.4 in their work on the effects of phenylephrine as the vasopressor for management of spinal hypotension, that the maternal cardiac output may be significantly higher than it needs to be, especially once spinal anesthesia is established. In fact, Dyer et al. proposed that phenylephrine is the optimal vasopressor to use during spinal anesthesia because it decreases cardiac output, offsetting the increase in cardiac output that results from the decreased systemic vascular resistance.4 Because the purpose of maternal cardiac output is to maintain maternal and fetal homeostasis, any increase above this level may be “unnecessary.” Looking at specific numbers, in our study, using the NICOM cardiac output monitor (Cheetah Medical Inc., USA), maternal cardiac output before spinal anesthesia was 8.1 l/min in the supine position and 8.4 l/min in the tilted position; this increased to over 9 l/min in both groups after spinal anesthesia.1 Therefore, the measured “decrease” in cardiac output with higher phenylephrine dosing, both in our study1 and in Dyer et al.’s4 (where boluses were given) may be mostly a return to prespinal baseline due to restoration of systemic vascular resistance.
Riley et al.2 are correct that some women may benefit from tilting or other forms of uterine displacement. Indeed, uterine displacement can and should be used in women who develop severe or unresponsive hypotension after spinal anesthesia, and perhaps in women with a history of supine hypotension during the pregnancy. Despite decades of practice and tradition, however, the evidence that the tilt maneuver, regardless of the degree at which it was provided, actually improves maternal or fetal conditions with contemporary neuraxial anesthesia practice is almost nonexistent. It may not be appropriate to subject all women to a maneuver that they do not feel comfortable with, and most surgeons dislike, when very few of them benefit. Clinicians also should acknowledge that 15° of left tilt is not achieved reliably in practice, and therefore, most cesarean deliveries around the world are performed under conditions very similar to those evaluated in our supine study group.
Regarding the accuracy of using base excess as our primary outcome, we agree with Shayegan et al.3 that using the calculated value of base excess derived from the measured values for both carbon dioxide pressure and pH is valid. Our goal was to acknowledge the difference between the “calculated” nature of base excess from the “measured” nature of pH, and emphasize our belief that base excess results in a better assessment of fetal acid-base status than pH, given that the latter is affected by acute changes in partial pressure of carbon dioxide.
Shayegan et al.3 also questioned our decision to exclude from our study women with a greater than 10-yr history of diabetes due to concerns about autonomic neuropathy; we acknowledge that the onset of diabetic autonomic neuropathy is highly variable, and that subclinical signs may be detected relatively early in the course of the disease. This approach was essentially an empirical decision to ensure that patients who were likely to have significant clinical symptoms not be included. In reality, because the study was conducted at NewYork Presbyterian/the Allen Hospital, a community hospital serving a healthy, low-risk obstetric population, very few diabetic patients were enrolled, and these few women had gestational diabetes only. We agree that the physiologic mechanisms underlying supine hypotensive syndrome are obviously distinct from the mechanisms underlying hypotension due to neuraxial anesthesia, although the former may be additive with the latter.
In the third letter addressed here, Dr. Daoud5 asked if the umbilical cord was double-clamped prior to sampling, to prevent equilibration with ongoing placental metabolism. Because it is standard practice for obtaining umbilical cord blood samples to perform double clamping, this was not specified, but indeed this was the case. In addition, although we acknowledge that the protocol as described on www.clinicaltrials.gov states that the time frame for sampling was within 2 h of birth, sampling of the umbilical cord blood occurred within minutes of birth. As is the clinical practice in our institution, a second circulating nurse is assigned to collect these samples and assist the pediatrician.
To answer Dr. Daoud’s questions about cardiac output measurements and data analysis, baseline cardiac output (before spinal anesthesia was induced) was determined in all women, in both the tilted and supine positions. The mean values were 8.1 l/min in the supine position and 8.4 l/min in the tilted position. These values, determined in both positions for each subject, were the values compared (appropriately) by paired t test. Subsequently, cardiac output and other hemodynamic value comparisons after spinal anesthesia were not paired, given that each subject only received one intervention (i.e., tilt or supine position).
Of note, time intervals between induction to delivery and uterine incision to delivery were recorded for each subject, and as expected there were no differences between groups (data not reported). Similarly, there was no difference between groups with respect to maternal sensory block levels (data not reported). We agree with Dr. Daoud that the rebound hypertension after a single dose of ephedrine 10 mg intravenously in the woman with a blood pressure of 44/22 mmHg occurring 6 min after spinal anesthesia initiation was unexpected; however, this was unlikely to have been due to a drug error. Last, with regards to the 2014 American Society of Anesthesiologists House of Delegates classification considering all pregnant women to be American Society of Anesthesiologists physical status II, our study was designed before this opinion was published.
Finally, if not for the long history and tradition of the tilt maneuver, based on limited and poor evidence, as detailed in a recent review by two of us,6 the results of our study would certainly be interpreted quite differently. Indeed, if tilt/displacement were not the traditional practice, and a clinical study was conducted demonstrating a moderate increase in cardiac output, and/or a moderate decrease in phenylephrine requirements by tilting all women 15o, with no effect on outcome, we doubt clinicians would adopt such a maneuver.
We are not suggesting that a single study is sufficient to support a widespread change in obstetric anesthesia practice. We would like to see our results confirmed in further studies on healthy parturients and extended to higher-risk patients (obesity, preeclampsia, etc.) by ourselves and others. It is certainly desirable to induce uterine displacement via tilt or otherwise in symptomatic women. In our own practice, we have almost completely abandoned the tilt maneuver in healthy women, with no obvious deleterious effect. We hope to present our experience and data on maternal and neonatal outcomes in the absence of tilt in the future.
The authors wish to acknowledge NICOM, Cheetah Medical Inc., Vancouver, Washington, for providing NICOM monitors and disposable sensors for the conduct of the investigation.
The authors declare no competing interests.