We agree that the reference mean arterial pressure (MAP) measured during the preoperative consultation might have overestimated their “normal” daytime MAP due to a potential “white coat” effect, and that this overestimation may have affected our conclusions. Although it would have been appealing to obtain an automated ambulatory MAP measurement during sleep the day before surgery using noninvasive finger cuff technology as recently proposed,3 we unfortunately don’t have access to this device at our hospital (yet). It is also important to note that at least 40% of our studied population had chronic hypertension, and in a large randomized controlled trial conducted in chronic hypertensive patients, Wu et al.4 demonstrated that maintaining a MAP between 80 and 95 mmHg decreased the incidence of acute kidney injury (AKI). Additionally, a separate guideline recommendation article also suggests that maintaining a MAP higher than the general threshold of 65 mmHg seems appropriate for preventing AKI in hypertensive patients.5 As a result, we felt that maintaining a MAP at a minimum of 80 mmHg in our study can be justified, although future research always has the potential to adjust our current perioperative goals.
The discrepancy between the estimated and the observed total duration of intraoperative case time with hypotension in the control group can likely be explained by a lack of compliance on the part of clinicians in that group. Although the anesthesiologists intended to maintain a median MAP value of 80 mmHg, it is easy to understand that MAP values between 75 to 79 mmHg may not have necessarily elicited an immediate response. This phenomenon has already been well described by Sessler et al.6 in their triple-low alerts study and recently by Maheshwari et al.7 in the hypotension prediction index study. Both studies reported that most of the system alerts were not subsequently followed by an appropriate response in accordance with the predefined algorithm. It was also possible that sometimes clinicians may have simply ignored the alert. Therefore, we feel that despite an individualized hemodynamic management protocol designed to maintain MAP within 90% of baseline MAP, clinicians may have intermittently not reacted to MAP values just below that target levels.
Last, we agree with Soussi et al. that brief repetitive episodes of less than 1 to 2 min of hypotension versus prolonged episodes could differ in risk of end-organ damage, despite a similar cumulative duration of hypotension. However, our small study was not designed to answer this important question, and it should be investigated in the future with an appropriately powered and designed protocol.
Drs. Joosten and Rinehart are consultants for Edwards Lifesciences (Irvine, California) and have ownership interest in Perceptive Medical, Inc. (Newport Beach, California), which is developing closed-loop physiologic management systems. In addition, Dr. Rinehart has ownership interest in Sironis (Newport Beach, California), and Sironis has developed a fluid closed-loop system that has been licensed to Edwards Lifesciences and was used in this study as a decision support system (assisted fluid management). The closed-loop system for vasopressor administration used in this study is new and is the sole creation of two of the authors (Drs. Joosten and Rinehart). Dr. Van der Linden has received, within the past 5 yr, fees for lectures and consultancies from Fresenius Kabi GmbH (Bad Homburg, Germany), Aguettant Medical SA (Lyon, France), Nordic Pharma (Antwerpen, Belgium), and Vifor Pharma (Antwerpen, Belgium). The other authors declare no competing interests.