Acid–base patterns in acute severe asthma

Abstract

Background and objectives: Acid–base status in acute severe asthma (ASA) remains undefined; some studies report complete absence of metabolic acidosis, whereas others describe it as present in one fourth of patients or more. Conclusion discrepancies would therefore appear to derive from differences in assessment methodology. Only a systematic approach centering on patient clinical findings can correctly establish true acid–base disorder prevalence levels. Methods: This study examines acid–base patterns in ASA (314 patients), taking into account both natural history of disease and treatment, in patients free of other diseases altering acid–base status. Data were collected from patients admitted for ASA without prior history of chronic bronchitis, emphysema, kidney or liver disease, heart failure, uncontrolled diabetes mellitus or gastrointestinal illness. Informed consent was obtained for all patients, after study protocol approval by the Institutional Review Board. Results: Arterial blood gases, plasma electrolytes, lactate levels, and FEV1 were measured on arrival. Severe airway obstruction was found with FEV1 values of 25.6 ± 10.0%, substantial hypoxemia (PaO2 66.1 ± 11.9 mmHg) and increased A-a O2 gradient (39.3 ± 12.3 mmHg) breathing room air. While respiratory alkalosis occurred in patients with better preservation of FEV1, respiratory acidosis was observed with more severe airway obstruction, as was increased lactate in the majority of patients, independent of PaO2 and PaCO2 levels. Conclusions: Predominant acid–base patterns observed in ASA in this patient population included primary hypocapnia, or less frequently, primary hypercapnia. Lactic acidosis occurred in 11% of patients and presented consistently as a mixed acid–base disorder. These findings suggest lactic acidosis results from the combined effects of both ASA and medication-related sympathetic effects.