Affiliations: Clinic of Anesthesiology, Ludwig Maximilians University, Munich, Germany,
University of Pittsburgh, Pittsburgh, PA,
Yale University, New Haven, CT
Correspondence to: Markus Rehm, MD, Ludwig-Maximilians University, Clinic of Anesthesiology, Nussbaumstr 20, 80336 Munich, Germany; e-mail: Markus.Rehm@med.uni-muenchen.de
The article presented by Gómez and colleagues1 is very interesting and well documented, stating that analbuminemic rats are not more susceptible to hypercapnia-induced hemodynamic instability or changes of pH. This can be interpreted as a clear contradiction to the classical acid-base analysis in which albumin constitutes a buffer. One would have expected the albumin group to produce lower carbon dioxide-caused changes of pH due to the higher buffer capacity, but that obviously did not occur. However, the identical changes of pH are understandable using the modern concept of Stewart because only the Pco2 is changed equally in both groups. The total amount of weak acids and the strong ion difference remain, at different levels, constant. Therefore, a quantitative change of solely one independent variable can only induce equal quantitative changes of the pH. This is a very interesting and important finding of this study, unfortunately only scarcely discussed by the authors.
However, the conclusions drawn in the editorial to this article with the striking title “Another nail in albumin’s coffin” by Lewis Kaplan2are at least confusing. It is not possible to deduce that administration of albumin in the critically ill, especially with lung injury or ARDS, can no longer be supported from this study. It is a well-known fact that genetical analbuminemia requires a tremendous adaptation in order to survive this defect.3Analbuminemia in the fetus is associated with an increased prevalence of miscarriage and neonatal death.4
Until today, only 39 cases of analbuminemia have been reported.3 The main compensatory mechanism of this defect is an increase in the synthesis of nonalbumin proteins (such as α-1, α-2 or β-globulins), to the effect that the total serum protein level is usually only marginally lower than in healthy patients. These other proteins are also thought to take over many of the functions of albumin.5–6 In genetical analbuminemia, these compensation mechanisms have time to develop intrauterinely, in contrast to the acutely occurring hypoalbuminemia in critical ill patients.
Hence, in the study of Gómez and colleagues,1 it would have been interesting to “analbuminate” healthy rats. These animals should cope much worse with hypercapnia or hypocapnia than the genetical (compensated) analbuminemic rats. However, this shortcoming disallows a transfer to critical ill patients, who have not compensated their acute loss of albumin, nor does their condition favor a rapid compensation. Therefore, by missing the point by so much, instead of hitting the proverbial nail on the head (and into the coffin), the editorial has in fact hit his own thumb!
A study by Dr. Jacob and Dr. Rehm (Anesthesiology 2006; 104:1223–1231) was performed using a grant provided by ZLB Behring, Marburg, Germany. Otherwise, the authors have no conflicts of interest to disclose.
The authors have no conflicts of interest to disclose.
We are rather puzzled by the letter from Dr. Rehm and colleagues concerning our recent article in CHEST (May 2007)1 on the effects of hypercapnea on BP in hypoalbuminemic and Nagase analbuminemic rats. The authors’ contention that “a quantitative change of solely one independent variable can only induce equal quantitative changes of the pH” is entirely unsupported by our data. In fact, as stated in the “Materials and Methods” section of our article, we calculated buffer capacity as the reciprocal of the slope of Pco2/pH. Thus, our results showing differences in buffer capacity across different groups is prima facie evidence that the authors’ assertion is false. As to the suggestion that we include a group of animals with acquired hypoalbuminemia rather than genetic hypoalbuminemia, Dr. Rehm and colleagues appear to have missed the fact that we did just that. While our “elderly” hypoalbuminemic rats were not critically ill, they do represent a model of hypoalbuminemia that is much closer to the clinical state. The limitations of our model were discussed in our article.
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