Blood Pressure During Cardiopulmonary Bypass: HowLow Is Too Low?Hilary P. Grocott, MD, FRCPC, FASE

Unquestionably, major advancements in the care ofcardiac surgical patients have been made in thepast half century since cardiopulmonary bypass

(CPB) brought about the advent of modern-day cardiacsurgery. However, despite improvements in surgical tech-nique, mechanical advances in the conduct of CPB, and anever-evolving understanding of cardiovascular physiologyand pharmacology, several fundamental questions in car-diac anesthesia persist. The target arterial blood pressureduring CPB to maintain homeostasis during surgery is oneof these questions. There have been several well-intentionedattempts to address this issue, but most studies have beenlimited by significant patient heterogeneity or other deficien-cies in study design and statistical power.1 So, despite decadesdebating about what is the optimal blood pressure duringCPB, the answer remains elusive.

In this issue of Anesthesia & Analgesia, Joshi et al.2 havereported a major advancement in our understanding ofblood pressure management during CPB, thereby offeringsome hope that we could soon have a more definitiveapproach to defining this important physiologic parameter.In this sophisticated study, they utilized near-infraredspectroscopy (NIRS) measurements of regional cerebraloxygen saturation (Scto2) to determine cerebral autoregu-latory thresholds. By using cerebral oximetry to examine anindividual’s Scto2 responses to various changes in bloodpressure, they were able to define, in real-time, the specificcerebral lower limit of autoregulation (LLA). By definition,a patient’s cerebral autoregulation is intact when there is apoor correlation between perfusion pressure and cerebralblood flow (CBF), and is lost when CBF becomes pressurepassive. The LLA is a threshold when the mathematicalcorrelation between CBF and blood pressure transitionsfrom near zero to that approaching one. In their study, thetransition was defined when the correlation was �0.4,which is a generally well-accepted threshold.3 Although

their ability to define the LLA was not perfect, it doesprovide a major step in moving this field forward.

In the absence of any specific monitoring, the usual,albeit arbitrary, LLA has typically been depicted to beapproximately 50 mm Hg. This popular concept, however,has previously been argued to be in error.4 Accordingly, ithas been contested that this 50 mm Hg LLA should not beused. But, however elegant these arguments may be, withoutmore objective confirmation, we have largely procrastinatedin making any meaningful change in our consideration of it.As such, it remains a repeatedly described threshold despitethe tenuous data on which it was originally based.5,6 Theuncertainty of any specific blood pressure target based on thistraditional LLA approach is further accentuated in the cardiacsurgery population where hypertension is highly prevalent.In the absence of real-time data on CBF responses to bloodpressure, the conventional approach has been to use a higherLLA target in patients with chronic hypertension, predicatedby the assumption that these patients have a rightward shift intheir autoregulatory curve.7 However, the degree to which theLLA is shifted, if at all, has always been uncertain. As a result,anesthesiologists have been unable to reliably determinewhen an individual’s blood pressure may be too low.

The implication of what Joshi et al. describe is that wehave largely been inaccurate in our estimation of where theLLA is, with there being a wide range to this threshold inmost of our patients, regardless of their baseline bloodpressure condition. Even in the absence of significantpreexisting hypertension, interpatient heterogeneity aloneappears to question the validity of any arbitrary bloodpressure above which patients should be maintained. Fur-thermore, when superimposed on variable degrees of cere-brovascular disease, it is likely even more difficult to definehypotension with any unifying number.8

The question we are then faced with is, Where do we gofrom here? For example, will actually knowing, and inter-vening based on, the LLA make any difference to patientoutcome? This will require considerable study to determinewhat outcomes could be expected to be improved. Becausethis finding intuitively has direct relevance to the brain, alogical principle effect of utilizing the LLA to target hemo-dynamic management would be to reduce neurologic dys-function. An example of how this may have an impact haspreviously been described by these same investigators in anobservational study that identified impaired autoregula-tion during rewarming from hypothermic bypass.9 Theyhighlighted that those with impaired autoregulation may

From the Departments of Anesthesia & Perioperative Medicine and Surgery,University of Manitoba, Winnipeg, Manitoba, Canada.

Accepted for publication December 2, 2011.

The author declares no conflicts of interest.

Reprints will not be available from the author.

Address correspondence to Hilary P. Grocott, MD, FRCPC, FASE, Depart-ment of Anesthesia & Perioperative Medicine, University of Manitoba, St.Boniface Hospital, CR3008-369 Tache Ave., Winnipeg, MB, Canada R2H2A6. Address e-mail to hgrocott@sbgh.mb.ca.

Copyright © 2012 International Anesthesia Research SocietyDOI: 10.1213/ANE.0b013e3182456fbb

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be at risk for other cerebral complications, such as strokeand/or transient ischemic attacks. Thus, using LLA deter-minations could identify high-risk patients and also openup the possibility of intervening to optimize CBF to attenu-ate these adverse outcomes.

It is not clear, however, as to the scope of what neurologicoutcomes (i.e., stroke, encephalopathy, delirium, cognitivedysfunction) might be influenced by using a real-time LLA-guided assessment and intervention. A relationship betweenlower CPB pressure and increased stroke risk in cardiacsurgical patients with severe aortic atherosclerosis has previ-ously been reported.10,11 It was postulated that the lowerpressure in those patients exposed to excess atheromatousemboli increased the risk of cerebral ischemia secondary to areduction in blood flow in the pressure-dependent cerebralcollateral vessels.12 However, it is unlikely that using aglobal cerebral LLA target would be expected to influenceregional thromboembolic events per se or that NIRS wouldbe able to identify these relatively small at-risk regionswithin the brain. However, if aortic atherosclerosis isindicative of severe diffuse cerebrovascular disease, then itcould have an impact on overall stroke risk. That is, itwould be far more likely to have an impact on the generalsequelae of impaired CBF. For example, watershed strokes(secondary to global cerebral hypoperfusion) have previ-ously been shown to occur more frequently in patientsmanaged during CPB with a lower (than their prebypassbaseline) blood pressure.13 Maintaining a blood pressurewell above the LLA might reduce these types of watershed(hypoperfusion) stroke events. As for more subtle neuro-logic deficits, there is also evidence that prolonged hypo-tension could also have an impact on delirium.14 Findingthe optimal pressure for patients has the theoretical poten-tial to mitigate all of these subtypes of neurologic compli-cations, but the evidence thus far, is weak.

Other non-neurologic outcomes could also be influencedwith this information. Murkin et al.,15 in an interventionaltrial using NIRS to optimize Scto2 (with one interventionbeing blood pressure manipulation), described an improve-ment in their major morbidity composite outcome. Thatstudy essentially described the brain as a potential sentinelor index organ serving to identify “at-risk” situations whenScto2 was low.16,17 However, it is well known that there isa hierarchy of organ blood flow, and what is an optimalblood pressure (and flow) for the brain may not be the samefor other major organs (such as the kidney or other splanch-nic organs).18 Because of its inherent autoregulation, as wellas the body’s preferential perfusion of the brain at theexpense of other organs, it may be that despite having anormal brain oxygen saturation, the other organs havesignificant impairment in their own blood flow and tissueoxygen delivery.19

It is important to understand the context, and limita-tions, in which the brain can be considered an index organ.First, it is the only organ that is readily accessible to thepenetration and reflection of light wavelengths used inNIRS cerebral oximetry technology.20 It is easy to postulatethat a more favorable non-neurologic outcome effect mightbe expected if tissue oximetry signals were used to targetinterventions by a monitor focused on the kidney or gut, forexample. In effect, rather than the brain being an early

warning system, it should more appropriately be consid-ered the opposite of a “canary in a coal mine” (in effect,being the last to go) because it is highly likely that once thebrain desaturates, the other organs have long since beenexposed to compromised blood flow and oxygenation.Thus, using the cerebral LLA as a target that might influ-ence other outcomes is a potential limitation to the datapresented by Joshi et al. However, it is not so much alimitation in their study design per se, but in the potentialclinical utilization of this information.

One further caveat to this study relates to the limitationthat the technology and the software that they used tocollect and analyze the LAA data are not commerciallyavailable. Although commercialization in some relatedform is likely to occur, it will not be known how this mightimpact patient care until it is more widely available in amore user-friendly mode. Importantly, however, cerebraloximetry, irrespective of whether specific NIRS-guideddetermination of autoregulation becomes available, is in-creasingly being used in the day-to-day management ofcardiac and other surgical patients and has shown greatpromise.19,21 Its ease of application and the intuitive informa-tion it provides in reflecting both cerebral oxygen supply anddemand issues can be applied to multiple physiologic param-eters other than just blood pressure. However, the ultimateimpact of this technology will need to be determined inlarger-scale prospective controlled trials.

The information presented by Joshi et al. shows greatpromise, but until we have more data related to its impacton patient outcomes, the question of “how low is too low”a blood pressure remains incompletely answered.

DISCLOSURESName: Hilary P. Grocott, MD, FRCPC, FASE.Contribution: Hilary P. Grocott, MD, FRCPC, FASE, wroteand approved this manuscript.

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