Is a Mean Arterial Pressure Less Than 65 mm Hg an Appropriate Indicator of the Quality of Anesthesia Care?

Abstract

See Article, p 946 Physician anesthesiologists have understood for more than a century the importance of blood pressure management during anesthesia.1 There has been divergent opinion during the ensuing decades, however, on what blood pressure constitutes “hypotension” with no clear consensus.2 Implementation of electronic health records has allowed for analysis of large hemodynamic data sets linked to patient outcomes. Multiple investigators have hence evaluated various blood pressure cut-offs in relationship to organ injury finding an association between a mean arterial pressure (MAP) <65 mm Hg and acute kidney injury, myocardial infarction, and mortality in selected populations of adults undergoing noncardiac surgery.3–5 The results of these retrospective analysis supports the hypothesis that hypotension might represent a potentially modifiable risk factor for poor patient outcome after noncardiac surgery and thus an indicator of clinician skill. These findings have fostered consideration of a MAP <65 mm Hg for ≥15 minutes as an internal quality improvement measure by the Anesthesia Quality Institute (measure ID IIM025) and as a future qualified clinical data registry (QCDR) measure for the Center for Medicare & Medicaid Services Merit-Based Incentive Payment System (MIPS) program (measure ID EPREOP31). The study by Sessler et al6 in this issue of Anesthesia & Analgesia has important implications on interpreting whether a MAP <65 mm Hg is indeed a suitable measure of intraoperative quality of care. Their study involved analysis of electronic anesthesia records collected during a 10-year period at a single institution from 25,702 adult patients undergoing general anesthesia for noncardiac surgery lasting at least 1 hour. Blood pressure was monitored either directly with an arterial catheter (35% of cases) or with oscillometry. Whether less frequent measurement of blood pressure with the latter method rather than continuous monitoring confounds the relationship between MAP <65 mm Hg and adverse outcomes is not clear. Certainly, the different frequency of recording blood pressure could influence the promptness of intervention, as well as the potential for unrecognized hypotension when measurements occur at 5 or more-minute intervals. Regardless, in their investigation Sessler et al6 limited the analysis to anesthetics administered by a certified registered nurse anesthetist (CRNA) medically directed by an anesthesiologist. Since medical direction by an anesthesiologist is a prevalent model of anesthetic care in the United States, it is a reasonable approach to focus on the provider most likely to immediately intervene for hypotension. Analysis was restricted to cases where a single CRNA was present for 80% of the case and it only considered CRNAs who logged >200 cases during the study period. The study’s analysis was based on 110,391 hours of anesthesia and 99 CRNAs whom provided on average (mean ± standard deviation [SD]) 260 ± 124 cases lasting 4.3 ± 1.8 hours. Using various statistical approaches the authors had 4 basic aims. First, they attempted to develop a multivariate model to predict hypotension based on preoperative patient characteristics and medical history but excluded the provider as a variable. Second, they calculated the observed versus predicted amount of MAP <65 mm Hg for each case and then summarize excess hypotension as the difference between these 2 variables. Third, they determined the amount of MAP <65 mm Hg on a case basis associated with complications. For this, they used a composite complication end-point consisting of myocardial injury (troponin ≥0.03 ng/mL), stroke, acute kidney injury, infections, readmission to their facilities, or death. Their final goal was to assess the range of minutes and excess MAP <65 mm Hg for each CRNA and whether this was associated with the composite complication end-point. The authors found that MAP <65 mm Hg was common with nearly 70% of cases having at least 1 minute of MAP <65 mm Hg. The average minutes of MAP <65 mm Hg was (mean ± SD) 13 ± 23 minutes with a median (interquartile range) of 4 (0, 15) minutes. Regarding their first aim, they were unable to accurately predict hypotension based on preoperative data. Introducing CRNA into the modeling as a random effect suggested that inter-CRNA minutes of MAP <65 mm Hg represented a small portion of the variance in predicting this end-point. In other words, minutes of MAP <65 mm Hg is not a strong performance indicator between CRNAs medically directed by an anesthesiologist. Both actual and excess minutes of MAP <65 mm Hg were associated with the adjusted risk of the composite complication outcome confirming the findings of other studies.3–5 Each 10 minutes of MAP <65 mm Hg was associated with a 3.8% higher odds of a major complication (95% confidence interval [CI], 2.1-5.6; P < .0001). Cases in the highest quartile of excess minutes of MAP <65 mm Hg (>24 minutes above predicted) had approximately a 31% higher odds for complications compared to patients without hypotension (odds ratio, 1.31, 95% CI, 1.16-1.47; P < .0001). Patients in the third quartile (10–24 minutes) of excess hypotension had an odds ratio of 1.27 (95% CI, 1.12-1.44; P = .0002) for a complication compared with no hypotension. Nonetheless, there was no association in confounder-adjusted models for an individual CRNA’s average amount of excess MAP <65 mm Hg and complications as a continuous exposure (P = .09) or as quintiles (P = .30). These results were confirmed in sensitivity analysis. They conclude that while MAP <65 mm Hg is associated with complications, the average amount of blood pressure below this cutoff varied only slightly between CRNAs and it was insufficient to account for differences in complications. The authors appropriately temper their conclusions as representing analysis from a single, tertiary medical center making generalizability of the results untested. The results, though, raise questions about whether a MAP <65 mm Hg during anesthesia for noncardiac surgery is an appropriate quality indicator. The support for this measure is derived from retrospective data analysis and represents an association but not a causal relationship with acute kidney injury, myocardial infarction, or mortality.3–5 Notably, a recent investigation that included intra- and postoperative hemodynamic data suggests that hypotension after, rather than during surgery is a stronger predictor of myocardial injury.7 Support for avoiding hypotension during noncardiac surgery as a strategy for improving outcomes comes from the 9-center Intraoperative Norepinephrine to Control Arterial Pressure (INPRESS) study.8 In that study, high-risk patients (n = 298) undergoing noncardiac surgery under general anesthesia were randomized to maintain systolic blood pressure within 10% of a reference values versus standard practice of maintaining >80 mm Hg or 40% of a reference value. Patients in the intervention arm had a lower frequency of the composite outcome of systemic inflammatory response syndrome and dysfunction of at least 1 organ system by day 7 after surgery compared with the standard care arm (38.1% vs 51.7%; P = .02). That study did not specifically address the risks and benefits of maintaining MAP >65 mm Hg. Blood pressure data reported every 30 minutes as supplemental data from that study suggests that the median MAP, even in the standard care group, may have been >65 mm Hg. Rather than an empiric MAP cutoff derived from population-based data, our group has advocated for an individualized approach for defining hypotension based on bed-side monitoring of cerebral blood flow autoregulation.9 Interestingly, we have found is that the median MAP at the lower limit of cerebral blood flow autoregulation during cardiopulmonary bypass is 66 mm Hg and during shoulder surgery in the lateral decubitus position 65 mm Hg. What is striking, though, is the breadth of the CIs at this cutoff: 43–90 mm Hg during cardiac surgery and 55–75 mm Hg during noncardiac surgery. Thus, a MAP <65 mm Hg for defining hypotension may be sufficient for ensuring cerebral autoregulation for the “average patient” but it may be too high or too low for others. Moreover, experimentally, kidneys have a higher blood pressure cutoff for autoregulation than the brain, and perfusion is also dependent on cardiac output.10 In that laboratory investigation, when MAP was at the lower limit of cerebral blood flow autoregulation, renal blood flow was 75% of baseline. One could argue in favor of the quality measure of MAP <65 mm Hg if there is no harm with the treatment needed to meet this goal. Data from the INPRESS study and our own experience suggests that a higher dose of vasoconstrictive drugs do not lead to a higher frequency of complications.8,11 The potential harms of an empiric MAP target of 65 mm Hg is that it may represent hypotension in individuals whose lower limit of cerebral autoregulation is higher. Further, we have found that the cumulative magnitude and duration that MAP is above the upper limit of cerebral autoregulation is associated with delirium.12 Thus, simply keeping every patient’s MAP “high” could potentially have unintended consequences. The study by Sessler et al6 should prompt debate on the appropriateness of a MAP <65 mm Hg for >15 minutes as an indicator of the quality of anesthesia care during noncardiac surgery (Table). A MAP <65 mm Hg may or may not be a modifiable risk factor for adverse events. Conversely, it may simply be an epiphenomenon identifying patients at high risk for complications regardless of blood pressure management during the anesthetic. If true, a MAP <65 mm Hg for ≥15 minutes may simply identify an anesthesiologist caring for more complex and “sicker” patients. The inclusion of a quality measure based on evidence obtained only from retrospective database analysis is reminiscent of our specialty’s travails with a strategy of administration of β-adrenergic receptor blocking drugs to reduce perioperative myocardial infarction after noncardiac surgery. This practice was subsequently refuted as causing more deaths and strokes in an adequately powered prospective randomized, placebo controlled study.13 In the absence of evidence from such appropriately designed studies, judging anesthesia provider clinical performance based on associations derived from retrospective data base analysis will likely remain imprecise. Further, with a care team model of anesthesiologist medical direction of CRNAs, this measure will more likely reflect performance of the team and not necessarily an individual physician. The challenges of developing anesthesiologist-specific quality dashboards is underscored by investigations of large databases of patients undergoing cardiac surgery. Those investigations have emphasized that major postoperative complications and mortality are more dependent on patient, surgeon, and institutional characteristics than individual anesthesiologist.14,15 Those observations further confound using such outcomes for judging anesthesiologist quality of perioperative care. Table. - Arguments For and Against a MAP <65 mm Hg for ≥15 min as Quality Indicator for Individual Anesthesiologist Pro • Retrospective database analysis from a limited number of tertiary care centers have linked this MAP cutoff with organ injury and mortality. • Objective data are easily collected from electronic anesthesia records. • Data linked to individual provider easily transferred to quality reporting platforms. Con • Validation using data from a wide variety of medical practices representing academic and private groups of varying sizes from across the United States and containing adequate numbers of women and underrepresented minorities is lacking. • Insufficient evidence that prospectively maintaining MAP above this threshold reduces complications and mortality. • When applied to care provided by anesthesiologist medical direction of CRNAs, the metric reflects results of the anesthesia team model more than individual anesthesiologist. • Metric may identify anesthesiologist caring for higher risk and “sicker” patients, thus potentially discouraging care of such patients to improve externally monitored quality of care. • Fails to consider the impact of postoperative hemodynamic events or other complications on the risk for acute kidney injury, myocardial infarction, and mortality. • Single threshold for defining hypotension based on population averages fails to precisely identify what MAP for an individual patient compromises organ perfusion. Abbreviations: CRNA, certified registered nurse anesthetist; MAP, mean arterial pressure. DISCLOSURES Name: Eric Kamenetsky, MD. Contribution: This author helped with the concepts, literature review, and writing of this article. Conflicts of Interest: None. Name: Charles W. Hogue, MD, FAHA. Contribution: This author helped with the concepts of this study and writing of the article. Conflicts of Interest: C. W. Hogue has served as a consultant and provided lectures for Medtronic, Inc (Boulder, CO) and Edwards Lifescience (Irvine, CA). He serves on a data safety and monitoring committee for Merck, Inc (Kenilworth, NJ). This manuscript was handled by: Richard C. Prielipp, MD.