Thursday, March 17, 2011
TOPIC DISCUSSION: Lactate levels and B2 agonists? any connection
Lactic acidosis has been reported in many cases in severe asthma due to production by over worked respiratory muscles. However, there is some thought that the b2 agonist agents might induce lactic acidosis or just elevated lactate levels. Even patients who are not asthmatics who get these agents have had similar reports. So far, lactic acidosis occurring in association with β-2 agonist treatments such as salbutamol, ritodrine, meta-proterenol, and albuterol have been reported, and its mechanism remains poorly understood. In one study, healthy volunteers without respiratory distress who were given intravenous infusions of either salbutamol or rimiterol had dose-related increases in lactic acid levels. In the absence of any clinical signs of circulatory shock or severe hypoxia , this would be considered a type B acidosis. β-2 Receptor activation produces excess glycogenolysis and lipolysis. Increased glycogenolysis eventually leads to increased concentrations of pyruvate. Pyruvate is converted to acetyl CoA, which enters the citric acid cycle. If pyruvate does not enter this aerobic pathway, it is converted to lactate instead, thereby potentially causing lactic acidosis.
An emergency medicine evaluation of this event was done prospectively. In total, 18 subjects who presented to an emergency department were enrolled in the study. All patients were treated with albuterol; four puffs (100 microg/puff) at 10 minute intervals, delivered by a pressurised metered dose inhaler into a spacer device over a 2 hour period. At the end of treatment, mean plasma lactate level 2.94 mmol/l was significantly higher (p = 0.001) than baseline. Of the 18 patients, nine (50%) showed lactate levels > or = 2.5 mmol/l (four patients presented values > 4 mmol/l); however, there were no significant differences in the airway response between groups. Their conclusions: "This study confirmed previous observations that high lactate concentrations can develop during the first hours of inhaled beta agonist treatment. The presence of a previous hyperadrenergic state may predispose to the development of this condition. A significant improvement in lung function was associated with elevated lactate levels."
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