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Ann Thorac Surg 1995;60:1156-1157
© 1995 The Society of Thoracic Surgeons
Department of Anesthesiology and Section of Cardiothoracic Surgery, Department of Surgery, Department of Neurosurgical Research, Mayo Clinic 200 First St SW, Rochester, MN 55905
To the Editor:
Our recent article, ``Cerebral Blood Flow During Cardiac Operations: Comparison of Kety-Schmidt and Xenon-133 Clearance Methods'' [1] was accompanied by an editorial [2] whose authors are intimately familiar with 133Xe methodology through their own research efforts.
Their comments were not unexpected, but warrant a response in the hopes of providing some degree of balance in the apparent controversy highlighted by their comments. We certainly agree with Young and associates that all indirect measurements of cerebral blood flow (CBF) in humans relying on the Fick principle must be viewed as an index of the truth; the controversy, if there is one, is simply which index most closely mirrors the quantitative (not qualitative) truth.
We do not intend to address each of the detailed criticisms in the editorial, because the careful reader will find that nearly all of these were adequately addressed in our article. There are two exceptions: First, Young and colleagues' scrutiny of our data identified an error we failed to recognize. Under hypothermic cardiopulmonary bypass (CPB) conditions, they calculated an inappropriate discrepancy in the arteriovenous oxygen content difference (AVDO2) from the CBF and cerebral metabolic rate for oxygen (CMRO2) values reported for the Kety-Schmidt and 133Xe washout methods. A single AVDO2 was determined during the middle of each measurement period and that value was used to calculate CMRO2 by both techniques; we incorrectly reported the value of CMRO2 at 27°C using 133Xe as 0.47 +/- 0.24 mL • 100 g-1 • min-1. If AVDO2 is calculated from the incorrect value, it is different from the AVDO2 calculated from the Kety-Schmidt measurements under the same conditions. The value for CMRO2 obtained with 133Xe at 27°C should have been reported as 0.33 +/- 0.13 mL • 100 g-1 • min-1, as identical AVDO2 values were used to calculate CMRO2 by both techniques. The measurement of CBF by 133Xe at 27°C and all other reported measurements of CBF and CMRO2 are correct. We apologize for this mathematical error and appreciate Young and colleagues' identification of it but note that it does not change the statistical significance of our values at hypothermia or the interpretation of our data.
Second, our ``remarkable failure to cite. . . an especially important validation study'' (conducted in the laboratory of one of the editorial's authors) [3] was, if a failure, deliberate. That study was in canines; our report was in humans. In their investigation, they eliminated almost all possibility of extracranial contamination by surgical removal of the soft tissues interposed between the gamma detector and the brain and used shielding to minimize radiation contamination from noncerebral sites. These methods do not reflect the use of 133Xe in clinical investigation. Additionally, their study also relied on sequential rather than simultaneous comparative measurements, and finally, the saturation period (9.5 minutes) for the Kety-Schmidt measurements was inadequate to allow equilibration to occur. Therefore, although that investigation was interesting and valid, it is not appropriate for comparison with our findings; hence our ``remarkable failure.''
In addition to responding to those specific points, we wish to offer a more generic response to the criticisms either implied or stated in the editorial. First, in the absence of CPB, the Kety-Schmidt method for measuring CBF is universally accepted as the ``gold standard'' for the indirect measurement of CBF in humans and for evaluating the validity of any other indirect CBF measurement technique. Young and colleagues seem to suggest that the use of CPB may invalidate the Kety-Schmidt method, but offer no data (or references) to support such a proposal. Certainly, if that is their contention, it is their obligation, not ours, to justify such an unexpected and unexplained variance from the norm introduced by the use of CPB.
Second, although brain blood flow is subject to a variety of variables that might be influenced by CPB, brain metabolic rate is remarkably stable under a wide variety of such influences (eg, arterial carbon dioxide tension, hematocrit, perfusion pressure, arterial oxygen tension). There is absolutely no reason to expect that brain metabolic rate is altered by CPB per se-such a concept defies common sense. Accordingly, one should examine and compare the values for brain metabolic rate calculated from CBF measurements using the two methods in question. With the Kety-Schmidt method, measurements are consistent at equivalent temperatures under bypass and nonbypass conditions. Our reported values are precisely what one would predict based on non-CPB studies in humans and multiple studies (with and without CPB) in laboratory animals [4–7]. By contrast, using the modified 133Xe washout measurements, all calculated metabolic rates are approximately 50% of expected (consistent with the CBF measurements) and, once again, defy common sense-both physiologically and pharmacologically.
Finally, we agree that the Kety-Schmidt method is a cumbersome, time-consuming, invasive, and difficult measurement technique relative to the ease of the modified 133Xe washout technique. We agree further that if one is interested only in direction or relative changes in CBF (and metabolic rate), both techniques are equally valid. But if quantitative information is the goal of one's efforts, then the Kety-Schmidt technique must still be considered the ``gold standard''-including during CPB-until proven otherwise.
References
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