부산대학교 도서관

Background and Objective: Raised blood lactate secondary to high dose β2‐agonist treatment has been reported in asthma exacerbations but has not been investigated during acute exacerbations of COPD (AECOPD). We explored associations of blood lactate measurements with disease outcomes and β2‐agonist treatments during AECOPD. Methods: Retrospective (n = 199) and prospective studies (n = 142) of patients hospitalized with AECOPD were conducted. The retrospective cohort was identified via medical records and the prospective cohort was recruited during hospitalization for AECOPD. Baseline demographics, comorbidities, β2‐agonist treatment, biochemical measurements and clinical outcomes were compared between patients with normal (≤2.0 mmol/L) versus elevated lactate (>2.0 mmol/L). Regression analyses examined associations of lactate measurements with β2‐agonist dosages. Results: Demographic data and comorbidities were similar between high versus normal lactate groups in both cohorts. The populations were elderly (mean >70 years), predominantly male (>60%) with reduced FEV1 (%) 48.2 ± 19 (prospective cohort). Lactate was elevated in approximately 50% of patients during AECOPD and not related to evidence of sepsis. In the prospective cohort, patients with high lactate had more tachypnoea, tachycardia, acidosis and hyperglycaemia (p < 0.05) and received more non‐invasive ventilation (37% vs. 9.7%, p < 0.001, prospective cohort). There was a trend to longer hospitalization (6 vs. 5 days, p = 0.06, prospective cohort). Higher cumulative β2‐agonist dosages were linked to elevated lactate levels (OR 1.04, p = 0.01). Conclusion: Elevated lactate during AECOPD was common, unrelated to sepsis and correlated with high cumulative doses of β2‐agonists. Raised lactate may indicate excessive β2‐agonist treatment and should now be investigated as a possible biomarker. β2‐Agonists can cause lactic acidosis but this has not been studied in AECOPD. Lactate was elevated in ~50% of people hospitalized with AECOPD and associated with metabolic abnormalities, higher rates of NIV and cumulative β2‐agonist dosages. Injudicious salbutamol may be driving apparent clinical deterioration via lactic acidosis. [ABSTRACT FROM AUTHOR]