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Effects of Hypercapnea on BP in RatsResponse FREE TO VIEW

Edward M. Omron, MD, MPH, FCCP
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Affiliations: Novi, MI,  University of Pittsburgh, Pittsburgh, PA,  Yale University, New Haven, CT

Correspondence to: Edward M. Omron, MD, MPH, FCCP, Pulmonary and Critical Care Specialists, 39650 Orchard Hill Place, Suite 100, 48375-5331; e-mail: edofiron@gmail.com



Chest. 2007;132(5):1717. doi:10.1378/chest.07-1247
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I read with great interest the recent article in CHEST (May 2007) by Gómez et al,1who investigated the effects of hypercapnea on BP in hypoalbuminemic and analbuminemic rats. I congratulate the authors on an intriguing exploration of physicochemical principles, but I disagree with one of their main conclusions that “the presence of a lower SIDa [apparent strong ion difference] in the NAR [Nagase analbuminemic mutant Sprague-Dawley] rats… is consistent with a reduction in the ‘set point’ for SIDa to maintain acid-base equilibrium in the face of a reduced weak acid content.” This simple statement has immense practical implications for intensivists who apply physicochemical analysis at the bedside. Hypoalbuminemia per se does indeed change the buffering capacity2 but cannot significantly reduce or change the plasma buffer base or effective strong ion difference (the more relevant physicochemical parameters), contrary to the authors’ suggestion. A primary change of one independent variable (albumin) will not affect the other independent variables (plasma buffer base or Pco2) in a physicochemical system.3 To change any of the independent variables, an intervention must be introduced from outside the system (ie, altering the minute ventilation, renal intervention, or the accumulation of unmeasured acids). These are secondary physiologic adaptations and not consequences of the “laws of chemistry.” Each of these possibilities may explain the lower baseline SIDa and effective strong ion difference in NAR rats. In the special case of analbuminemic rats, at baseline conditions the reduction in SIDa represents a compensated but markedly deranged metabolic acid-base status. The question is not whether the clinician calls this state a mixed acid-base disorder or normal compensation, but whether an intervention is necessary to restore standard-state conditions. In the NAR rats, the answer is obviously no, but in a critically ill patient with lactic acidosis, hypoalbuminemia, hyperchloremia, and hyponatremia the answer is yes.

The author has no conflict of interest to disclose.

The authors have reported to the ACCP that no significant conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Gómez, JL, Gunnerson, KJ, Song, M, et al (2007) Effects of hypercapnea on BP in hypoalbuminemic and Nagase analbuminemic rats.Chest131,1295-1300. [PubMed] [CrossRef]
 
Fencl, V, Jabor, A, Kazda, A, et al Diagnosis of metabolic acid-base disturbances in critically ill patients.Am J Respir Crit Care Med2000;162,2246-2251. [PubMed]
 
Fencl, V, Leith, DE Stewart’s quantitative acid-base chemistry: applications in biology and medicine.Respir Physiol1993;91,1-16. [PubMed]
 
To the Editor:

We thank Dr. Omron for his letter regarding our recent article in CHEST (May 2007),1and we certainly agree that our observations regarding changes in baseline strong ion difference (SID) in analbuminemic rats have “practical implications for intensivists who apply physicochemical analysis at the bedside.” However, we are surprised that Dr. Omron has interpreted our comments to suggest that hypoalbuminemia can directly alter SID. Instead, we stated that “we speculate that the normal physiologic response to hypoalbuminemia is to lower the SIDa [apparent SID] ….” Indeed, these physiologic responses, or “secondary physiologic adaptations” as Dr. Omron refers to them, would necessarily involve changes in strong ions most likely via the action of the kidney. Changes in SID are well known to occur as a result of long-term changes in Pco2 but have not been described as a consequence of changes in weak acids such as albumin. Importantly, the metabolic component of acid-base balance, quantified by base excess, comprises both SID and total weak acids2; thus, as opposed to Dr. Omron’s assertion, hypoalbuminemia per se does significantly change the base excess (for every gram-per-deciliter change in albumin level, base excess changes by approximately 3 mEq).,23 This has important “practical implications” because if one considers these changes in SID to be “pathologic” instead of “physiologic,” one will be tempted to treat them. Our study did not and could not address therapy but we cannot share Dr. Omron’s certainty that changes in SID in the critically ill should always be treated. Instead, we would only offer the time-honored clinical advice that we should treat patients, their diseases, and symptoms, and not merely numbers.

References
Gómez, JL, Gunnerson, KJ, Song, M, et al Effects of hypercapnea on BP in hypoalbuminemic and Nagase analbuminemic rats.Chest2007;131,1295-1300. [PubMed] [CrossRef]
 
Kellum, JA Clinical review: reunification of acid-base physiology.Crit Care2005;9,500-507. [PubMed]
 
Wooten, EW Calculation of physiological acid-base parameters in multicompartment systems with application to human blood.J Appl Physiol2003;95,2333-2344. [PubMed]
 

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References

Gómez, JL, Gunnerson, KJ, Song, M, et al (2007) Effects of hypercapnea on BP in hypoalbuminemic and Nagase analbuminemic rats.Chest131,1295-1300. [PubMed] [CrossRef]
 
Fencl, V, Jabor, A, Kazda, A, et al Diagnosis of metabolic acid-base disturbances in critically ill patients.Am J Respir Crit Care Med2000;162,2246-2251. [PubMed]
 
Fencl, V, Leith, DE Stewart’s quantitative acid-base chemistry: applications in biology and medicine.Respir Physiol1993;91,1-16. [PubMed]
 
Gómez, JL, Gunnerson, KJ, Song, M, et al Effects of hypercapnea on BP in hypoalbuminemic and Nagase analbuminemic rats.Chest2007;131,1295-1300. [PubMed] [CrossRef]
 
Kellum, JA Clinical review: reunification of acid-base physiology.Crit Care2005;9,500-507. [PubMed]
 
Wooten, EW Calculation of physiological acid-base parameters in multicompartment systems with application to human blood.J Appl Physiol2003;95,2333-2344. [PubMed]
 
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