Aerosolized β2-adrenergic agonists achieve therapeutic levels in the pulmonary edema fluid of ventilated patients with acute respiratory failure

K Atabai, LB Ware, ME Snider, P Koch, B Daniel… - Intensive care …, 2002 - Springer
K Atabai, LB Ware, ME Snider, P Koch, B Daniel, TJ Nuckton, MA Matthay
Intensive care medicine, 2002Springer
Objective. Experimental studies demonstrate that β-adrenergic agonists markedly stimulate
alveolar fluid clearance if concentrations of 10–6 M are achieved in alveolar fluid. However,
no studies have determined whether aerosolized β-adrenergic agonists are delivered to the
distal air spaces of the lung in therapeutic concentrations in patients with pulmonary edema.
Design and setting. This retrospective study measured albuterol levels in the pulmonary
edema fluid and plasma from mechanically ventilated patients with pulmonary edema from a …
Abstract
Objective. Experimental studies demonstrate that β-adrenergic agonists markedly stimulate alveolar fluid clearance if concentrations of 10–6 M are achieved in alveolar fluid. However, no studies have determined whether aerosolized β-adrenergic agonists are delivered to the distal air spaces of the lung in therapeutic concentrations in patients with pulmonary edema.
Design and setting. This retrospective study measured albuterol levels in the pulmonary edema fluid and plasma from mechanically ventilated patients with pulmonary edema from a hydrostatic mechanism (n=10) or from acute lung injury (n=12).
Measurements and results. After a total aerosolized albuterol dose of 4.2±3.2 mg in the prior 6 h the median pulmonary edema fluid albuterol level was 1,250 ng/ml (10–6 M) in patients with hydrostatic pulmonary edema; after 3.5±2.6 mg the figure was 1,240 ng/ml (10–6 M) in patients with pulmonary edema from acute lung injury. Plasma albuterol levels were much lower, with a median of 5.2 ng/ml (0.01×10–6 M) in patients with hydrostatic pulmonary edema and 3.1 ng/ml (0.01×10–6 M) in patients with pulmonary edema from acute lung injury.
Conclusions. These results provide the first evidence that levels of β-adrenergic agonists that are physiologically efficacious in experimental models can be achieved with conventional delivery systems in ventilated, critically ill patients with acute respiratory failure from pulmonary edema.
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