Article Text

Download PDFPDF

Salt depletion and hypoalbuminaemia in cystic fibrosis may add to hypercapnia in acute respiratory failure
  1. S J Kelly
  1. Specialist Registrar, Adult Cystic Fibrosis Unit, Northern General Hospital, Sheffield, UK,

Statistics from

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

Patients admitted over a 1 year period with acute exacerbations of cystic fibrosis (CF) and hypercapnia (Paco2 ⩾45 mm Hg, n=14) were compared with a control group with hypercapnic exacerbations of COPD (n=49). The CF group were significantly younger (23 v 69 years) with a lower body mass index (18.3 kg/m2v 25.0 kg/m2) but no significant difference in FEV1 (% predicted 27 v 34).

Using the Stinebaugh and Austin reference diagram for acid-base classification, a mixed respiratory acidosis and metabolic alkalosis was present in 71% of patients with CF and in only 22% of those with COPD (p<0.01). Both the plasma chloride and sodium levels were significantly lower in the CF group, together with a greater degree of hypoalbuminaemia.

Metabolic alkalosis is associated with sodium and chloride depletion and is likely to relate to the basic chloride channel defect in CF. A low albumin level may also contribute to a metabolic alkalosis due to its role as a weak non-volatile acid. Resulting respiratory compensation for this metabolic alkalosis results in hypoventilation and increased hypercapnia. This study is the first to show a significant role for a metabolic alkalosis in contributing to hypercapnic respiratory failure in patients with CF. Attention to fluid and electrolyte replacement in this group may aid treatment.

View Abstract