Affiliations: National Naval Medical Center Bethesda, MD,
The Alfred Hospital Victoria, Australia
Correspondence to: LCDR Edward M. Omron, MC, USNR, FCCP, Pulmonary Medicine Department, National Naval Medical Center, 8901 Wisconsin Ave, Bethesda, MD 20889; email: enomron@Bethesda.med.navy.mil
I read with interest the study by Holland et al (August 2003)1–
describing the metabolic acid-base status in patients with acute exacerbations of adult cystic fibrosis (CF) and COPD. I congratulate them on an interesting descriptive study of acid-base status and electrolytes in COPD and CF. However, I disagree with their conclusion that “metabolic alkalosis contributes to hypercapnic respiratory failure with acute exacerbations of CF.” No arterial blood gas or electrolyte data are provided to establish a premorbid baseline in either the COPD or CF groups to support the inference that one or both groups are indeed in acute hypercapnic respiratory failure. The arterial blood gas and electrolyte data on presentation in both groups could be interpreted as chronic hypercapnic respiratory failure with appropriate compensatory metabolic alkalosis. In fact, the mean inorganic strong ion difference (Na++K+−Cl−) in both the CF and COPD groups is approximately equal (45.7 mmol/L and 45.1 mmol/L or milliequivalents per liter, respectively) and consistent with appropriate renal compensation for chronic hypercapnea.2
An equal mean inorganic strong ion difference between the CF and COPD groups reveals that the magnitude of the metabolic alkalosis attributed to electrolyte differences is equal in both groups and does not account for the minor difference in mean pH. The CF group manifested a more severe hypoalbuminemia (less plasma weak-acid content) relative to the COPD group, and fully accounts for the alkaline difference in mean pH between the groups when assessed by physicochemical analysis.3
The inference of the author is of clinical concern since overzealous correction of a compensatory metabolic alkalosis may unmask a severe respiratory acidosis. As well, aggressive ventilation for chronic hypercapnic respiratory failure may unmask a severe metabolic alkalosis. Insufficient data are present to support the conclusion that a metabolic alkalosis in adult CF in this setting contributes to hypercapnic respiratory failure.
We thank Dr. Omron for his interest in our article examining acid-base status in patients with cystic fibrosis (CF) and COPD.1
His comments focus on two main points: whether the differences in acid-base balance do in fact represent a primary metabolic alkalosis in addition to respiratory acidosis in the CF group, and what the mechanism of the observed changes may be.
In the setting of an acute exacerbation of lung disease accompanied by hypercapnia, we observed a significantly more alkaline pH in the CF group than in the group of patients with COPD. Although the mean difference in pH between the groups was modest in absolute terms, we noted that 13 of 14 patients with CF (93%) had a pH > 7.4, which would be an unusual feature of a partially compensated respiratory acidosis. In addition, in 13 of 14 of the patients with CF (93%), the observed renal response to elevated Paco2 was greater than would be expected to compensate for a chronic respiratory acidosis.2
We therefore feel confident that the observed differences indicate both primary metabolic alkalosis and primary respiratory acidosis in the patients with CF.
This was a cross-sectional study in which we described acid-base status in hypercapnic patients with CF and COPD presenting with an acute exacerbation of lung disease. As such, our article did not aim to determine the cause of the observed metabolic alkalosis in CF. We concur with Dr. Omron that hypoalbuminemia may play an important role in acid-base disturbance, and the data we presented support this hypothesis. However, in the light of previous work showing an association between chloride depletion and metabolic alkalosis in children with CF,3–
along with observed changes in cerebrospinal fluid chloride levels with changes in plasma chloride,4
the contribution of electrolyte status requires evaluation. We are currently conducting further work in this area.
We agree with Dr. Omron that the clinical implications of this study are as yet unclear. It is possible that correction of metabolic alkalosis in this patient group may not be advantageous; however, this has not been examined. In addition, the effects of noninvasive ventilation on respiratory drive in patients with metabolic alkalosis are unknown. These issues are yet to be examined in clinical trials. It is clear, however, that acid-base analysis in patients with multisystem diseases such as CF needs to encompass more than a cursory glance at Paco2.
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