Nothing in our article1 suggests that some patients cannot safely be maintained at intraoperative mean arterial pressures less than 65 mmHg. For example, some patients come to surgery with pressures at about that level and will presumably tolerate at least somewhat lower ones. Similarly, some patients may require higher pressures—presumably those with conditions that restrict organ perfusion. Importantly, the article to which Saugel and colleagues refer evaluated myocardial injury and acute kidney injury; we have previously reported associations between mean arterial pressure and 30-day all-cause mortality, and the thresholds are somewhat higher.2 Harm thresholds for other organs might differ.
As Saugel and colleagues note, a strength of our analysis was inclusion of a large and diverse patient population. Furthermore, the acuity of Cleveland Clinic patients is high. The 57,300 patients we studied thus presumably included a fair number of patients who might be especially sensitive to hypotension. To the extent that some special-risk patients require higher blood pressures to perfuse key organs, we would expect that the curves relating mean arterial pressure and injury would gradually increase starting at relatively high pressures. In fact, they do not: the remarkable feature of figure 1 is that the risk of myocardial injury is essentially constant until mean arterial pressure reaches about 65 mmHg, and then increases steeply—on a logit scale no less. The curves for percentage change from baseline have a similar pattern. The relationship between mean arterial pressure and acute kidney injury looks almost the same, with risk being relatively constant until mean arterial pressure reaches 65 mmHg and then shooting up (fig. 2). Overall mortality decreases to a mean arterial pressure of 80 mmHg, and then increases sharply (fig. 3).2 The threshold pressures triggering injury are thus far more notable for sharp corners than gradual increases.
Saugel and colleagues note that organ perfusion rather than blood pressure is the variable of interest, and suggest that “pressure targets can only be set individually considering outflow pressure of different organ systems, cardiac output, vascular resistance, and blood flow autoregulation in the context of chronic hypertension and other comorbidities.” The trouble, of course, is that perfusion of sensitive organs including the gut, kidneys, and heart cannot be evaluated clinically. In real life, clinicians thus titrate hemodynamic management to blood pressure—which is exactly why evidence-based population thresholds are valuable.
Our point is not that any particular intraoperative mean arterial pressure is safe for everyone. Clinical care should be evidence based and include reasonable extrapolations from population-based studies that are appropriate for individual patients. In some cases, optimal care will target mean arterial pressures well above 65 mmHg; occasionally it might be lower. But absent information specific to individual patients, our results suggest that mean arterial pressure should rarely be allowed to decrease below 65 mmHg. This threshold is a population-based lower limit. Optimal pressure may well be greater.
Dr. Sessler is a consultant for Edwards Lifesciences, Irvine, California. The Department of Outcomes Research (Anesthesio logy Institute, Cleveland Clinic, Cleveland, Ohio) is funded by Edwards and Sotera, San Diego, California. Dr. Salmasi declares no competing interests.