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New Haven, CT
Correspondence to: Lewis J. Kaplan, MD, FCCP, Associate Professor of Surgery and Director, Surgical ICU and Surgical Critical Care Fellowship, Yale University School of Medicine, 330 Cedar St, BB-310, New Haven, CT 06520; e-mail: Lewis.Kaplan{at}yale.edu
In this issue of CHEST (see page 1295),1 one finds another important investigation that addresses one of the fundamental tenets of acid-base physiology: the role of albumin as a buffer base. Few therapies have entrenched themselves in medicine with the same tenacity as albumin administration. According to conventional wisdom, albumin functions as a buffer base and should, therefore, blunt the acidosis generated by increases in PCO2. In an elegantly designed investigation, Gomez and colleagues1 varied PCO2 in rodents with either normal albumin, hypoalbuminemia, or analbuminemia. If albumin serves this central buffer base role, then for a given increase in PCO2, the effects of acidosis (principally hypotension) should be proportional to the decrement in albumin from normal. Despite identifying a decreased buffer capacity in the hypoalbuminemic and analbuminemic rats, no such BP effect was observed. This observation casts further doubts onto the time-honored practice of albumin administration in the critically ill, as one can no longer support such a practice on the basis of acidosis buffering in the setting of permissive hypercapnia for lung injury or ARDS.2
The authors1 explored nitric oxide (NO) production as a potential explanation for the lack of BP effect in groups with different albumin concentrations. No differences in NO production were identified, with all groups increasing NO production with hypercapnia. While baseline nitrite levels were diminished in rats with decreased albumin, NO production in response to hypercapnia and acidosis increased in these groups to a greater extent than in their normoalbuminemic counterparts. Thus, the data suggest an increased endothelial sensitivity to NO in the presence of decreased buffer capacity and acidosis. Such a mechanism would support mean arterial pressure and organ-based perfusion pressure. This group has a long-standing interest in acid-base physiology based on physicochemical principles3 and utilized this model to ascertain additional data underlying the mechanism of acid-base homeostasis with abnormal albumin concentrations, modeling the clinical circumstance.
Utilizing the principles of charge balance determining acid-base balance espoused by Peter Stewart in 1983,4 Gomez et al1 identified that the normal acid-base balance manifested in each of the groups relied on different arrangements of plasma charge. In particular, the analbuminemic rats balanced their reduced albumin charge with a reduced plasma strong ion difference (SID). This seemingly simple observation carries important implications. Perhaps most important is that the reduced SID represents a homeostatic adaptation to reduced plasma weak acid change (principally albumin), instead of a mixed acid-base disorder. Recognizing this adaptive mechanism allows the clinician to refrain from attempting to "repair" an unrecognized balanced acid-base state, reducing iatrogenically induced deranged physiology.
An important accompaniment to the reduced SID is an increase in unmeasured anions identified as the strong ion gap (SIG). While the origin of the unmeasured anions remains opaque, their presence is undeniable. An increased SIG correlates with early mortality after injury,5 but its significance in the baseline steady-state of the analbuminemic rats is less morbid, and likely represents an appropriate baseline for reduced plasma weak acids in the absence of pathology. It is a straightforward extension to apply the Stewart approach to interrogate hypoalbuminemic patients in the ICU prior to therapeutic decision making with regard to acid-base balance, and a calculator is available on the Internet.6 The authors are to be congratulated on further defining the mechanisms underpinning acid-base balance and guiding future clinical study. Accordingly, translating their data into clinical practice is straightforward with regard to understanding the components of normal and deranged pH. The extension to abandoning albumin supplementation to buttress buffer base is strongly supported by their data, but will likely require human data to convince current users prior to putting the final nail in the coffin.
Footnotes
Dr. Kaplan is Associate Professor of Surgery and Director, Surgical ICU and Surgical Critical Care Fellowship, Yale University School of Medicine.
The author has no conflict of interest to disclose.
References
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  G. S. Martin and L. J. Kaplan "Nailing" the Evidence Chest, December 1, 2007; 132(6): 2055 - 2056. [Full Text] [PDF]
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D. Chappell, M. Jacob, M. Rehm, J. A. Kellum, and J. L. Gomez Genetical Analbuminemia Is Not an Appropriate Model for Hypoalbuminemia in Critically Ill Patients Chest, November 1, 2007; 132(5): 1717 - 1718. [Full Text] [PDF]
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