OBJECTIVE: To evaluate arterial lactate levels during treatment of acute severe asthma (ASA) and the prognostic value of arterial hyperlactatemia in ASA. DESIGN: Prospective study. SETTING: A respiratory intensive care unit (ICU) of a university hospital. PATIENTS: 29 consecutive patients admitted to the ICU for ASA not intubated on admission and with a peak expiratory flow (PEF) < 150 l/min or an arterial carbondioxide tension (PaCO2) > 40 mm Hg. All patients received standardized treatment during the first 24 h including i.v. and nebulized salbutamol, i.v. theophylline, and dexamethasone. MEASUREMENTS AND RESULTS: Arterial lactate levels were serially measured by an enzymatic method during the first 24 h following admission. On admission, the mean arterial lactate level was 3.1 +/- 0.38 mmol/l (range 1.1-10.4); 17 patients (59%) had arterial hyperlactatemia with a lactate level > 2 mmol/l. No difference was found in lactate levels between patients with progressively worsening asthma and those with an acute onset of severe asthma. No correlation was found between arterial lactate levels on admission, on the one hand, and respiratory rate (RR), heart rate, PEF, pH, PaCO2, arterial oxygen tension, potassium, phosphorus, creatine kinase, or transaminase values on admission, on the other hand. All patients developed an important but transient increase in arterial lactate levels during treatment, with a peak at 7.72 +/- 0.46 mmol/l and a mean elevation of 4.62 +/- 0.45 mmol/l (range 0.4-12.1), from the initial admission value contrasting with a significant clinical improvement assessed by RR, PEF, and arterial blood gas parameters. CONCLUSION: This study suggests that, in ASA, arterial hyperlactatemia is frequently present on admission to the ICU. Delayed hyperlactatemia is a constant finding during treatment of ASA. Initial or delayed hyperlactatemia seems of no prognostic value because none of the patients required mechanical ventilation. The effects of therapy for acute asthma on lactate metabolism still need to be studied.
OBJECTIVE: To evaluate arterial lactate levels during treatment of acute severe asthma (ASA) and the prognostic value of arterial hyperlactatemia in ASA. DESIGN: Prospective study. SETTING: A respiratory intensive care unit (ICU) of a university hospital. PATIENTS: 29 consecutive patients admitted to the ICU for ASA not intubated on admission and with a peak expiratory flow (PEF) < 150 l/min or an arterial carbondioxide tension (PaCO2) > 40 mm Hg. All patients received standardized treatment during the first 24 h including i.v. and nebulized salbutamol, i.v. theophylline, and dexamethasone. MEASUREMENTS AND RESULTS: Arterial lactate levels were serially measured by an enzymatic method during the first 24 h following admission. On admission, the mean arterial lactate level was 3.1 +/- 0.38 mmol/l (range 1.1-10.4); 17 patients (59%) had arterial hyperlactatemia with a lactate level > 2 mmol/l. No difference was found in lactate levels between patients with progressively worsening asthma and those with an acute onset of severe asthma. No correlation was found between arterial lactate levels on admission, on the one hand, and respiratory rate (RR), heart rate, PEF, pH, PaCO2, arterial oxygen tension, potassium, phosphorus, creatine kinase, or transaminase values on admission, on the other hand. All patients developed an important but transient increase in arterial lactate levels during treatment, with a peak at 7.72 +/- 0.46 mmol/l and a mean elevation of 4.62 +/- 0.45 mmol/l (range 0.4-12.1), from the initial admission value contrasting with a significant clinical improvement assessed by RR, PEF, and arterial blood gas parameters. CONCLUSION: This study suggests that, in ASA, arterial hyperlactatemia is frequently present on admission to the ICU. Delayed hyperlactatemia is a constant finding during treatment of ASA. Initial or delayed hyperlactatemia seems of no prognostic value because none of the patients required mechanical ventilation. The effects of therapy for acute asthma on lactate metabolism still need to be studied.
Authors: Lars W Andersen; Julie Mackenhauer; Jonathan C Roberts; Katherine M Berg; Michael N Cocchi; Michael W Donnino Journal: Mayo Clin Proc Date: 2013-10 Impact factor: 7.616
Authors: Alina G Liedtke; Sebastiano A G Lava; Gregorio P Milani; Carlo Agostoni; Viola Gilardi; Mario G Bianchetti; Giorgio Treglia; Pietro B Faré Journal: J Clin Med Date: 2019-12-27 Impact factor: 4.241