Abstract

In this issue of Anesthesia & Analgesia, Naganobu et al. (1) report that, in dogs, 20 mg/kg epinephrine given endobronchially in combination with 2 mL distilled water increased both epinephrine plasma levels and arterial blood pressure significantly more than did 2 mL normal saline as diluent of 20 mg/kg endobronchial epinephrine, indicating that distilled water provided a “solvent drag” for endobronchial epinephrine. Although distilled water administered into the endobronchial tree transiently decreased partial-pressure oxygen more than did normal saline, these changes are acceptable because of the profound benefit of the more rapid and extensive epinephrine effects. Endobronchial drug administration may be a simple and rapid alternative during cardiopulmonary resuscitation (CPR), when endotracheal intubation is performed before IV cannulation (2), when the time interval to IV access is prolonged, or when attempts to establish IV access are unsuccessful (3). Thus, endobronchial drug delivery may be of advantage whenever intubation is performed before IV access has been obtained. Endobronchial drug administration strategy during CPR is not as simple as during stable cardiocirculatory conditions because of dependence on many factors, including drug conversion or degradation by lung tissue, drug structure and lung permeability, ventilation/perfusion ratio of the lung, drug dilution with saline or water, volume of dilution carrier, and depth of drug administration into the bronchial tree (4 ‐9). The European Resuscitation Council therefore recommends the administration of drugs via an endotracheal tube (with normal saline as diluent) during CPR only as a second-line approach because of impaired absorption and unpredictable pharmacodynamics (10), whereas the American Heart Association CPR guidelines take a more liberal approach and state that endobronchial drugs (with normal saline or distilled water as diluent) should be administered if venous access is delayed (11).

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