To the Editor:
We read with great interest the randomized controlled trial published recently by Joosten et al. in Anesthesiology.1 This study assessed the ability of a closed-loop system for the titration of a norepinephrine infusion combined with a fluid-management decision support system to decrease the percentage of intraoperative time at risk for tissue hypoperfusion when compared with a “traditional” manually controlled goal-directed hemodynamic optimization. The authors reported that patients in the computer-assisted group had significantly less total intraoperative time with hypotension (primary outcome), less oscillation in mean arterial pressure (MAP) during surgery, and a higher mean cardiac index at the end of the procedure—while also receiving less total norepinephrine by infusion and having a lower fluid balance.1
We congratulate the authors for having performed such innovative research on perioperative hemodynamic optimization to improve patient’s postoperative outcome. Nonetheless, we have a few comments and questions.
In this study, the median [interquartile range] minimum “individualized” MAP target (within 10% of baseline) was significantly higher (81 [76 to 81] mmHg) than expected based on recommendations by the Perioperative Quality Initiative consensus on intraoperative blood pressure, risk, and outcomes for elective surgery (i.e., MAP greater than 60 to 70 mmHg).2 We suspect that the MAP measured during the preoperative screening, defined as “baseline” (90 [85 to 90] mmHg), might be an overestimate of the individual normal daytime MAP due to the “white coat” effect, known to affect up to 30% of subjects.3 This point is even more important because general anesthesia represents a state of reduced sympathetic nervous system and metabolic activities during which the MAP threshold for adequate organ perfusion is likely reduced in comparison with daytime. A potential more physiologic approach was reported by Saugel et al.,4 who suggest that automated ambulatory measurement of MAP during physiologic sleep is a more relevant target during general anesthesia. As a consequence of the high level of MAP triggering intervention in the current study, the reported reduction in the duration of intraoperative hypotension in the computer-assisted group (−21.1% [95% CI, −15.9 to −27.6%]) was potentially overestimated.
In their sample calculation, the authors estimated the control group to have a total duration of 12 ± 8% of intraoperative case time with hypotension based on their previous data. However, the control group experienced hypotension at nearly twice the anticipated rate (21.5% [14.5 to 31.8]). If this is indeed well-established standard of care, it would be helpful to understand the authors’ insight into potential causes of this significant discrepancy with their initial estimate.
Last and not least, in their rationale, the authors mentioned the finding by Walsh et al.5 regarding the increase in risk associated with every 5 min spent under the MAP threshold of 55 mmHg. The current presentation of the results (cumulative duration of hypotension) does not distinguish between repetitive brief (e.g., less than 1 to 2 min) episodes of hypotension versus prolonged episodes, which probably differ in risk for end organ damage and therefore clinical relevance. Would such an analysis (i.e., filtering out very short durations of hypotension) modify the conclusions of the authors?
Dr. Cholley has received honoraria for participation on advisory boards and lecturing fees from Edwards Lifesciences (Irvine, California), Orion Pharma (Espoo, Finland), Amomed (Wien, Austria), and Nordic Pharma (Paris, France). Dr. McCluskey has received honoraria from Edwards Lifesciences for advisory work and speaker’s support. The other authors declare no competing interests.