Paret and colleagues speculate that the effects of endotracheal adrenaline may cause ß₂-mediated hypotension that could be deleterious during cardiac arrest. In our study, the frequency of initial decrease in blood pressure did not differ after airway administration of adrenaline compared with intravenous administration. Blood pressure decreased by 10% in 4 of 34 patients 30 seconds after airway-administered adrenaline but also decreased by 10% in 6 of 34 patients after intravenously administered adrenaline (P > 0.2). This indicates that the blood pressure decrease is not related to the route of adrenaline administration but may be associated with the plasma adrenaline levels achieved. In fact, initial plasma adrenaline levels were not different 30 seconds after airway adrenaline or 30 seconds after intravenous adrenaline (P = 0.1; Figure).

View larger version (18K): [in this window] [in a new window]   Figure. Time course of plasma adrenaline levels. Levels were measured in six patients (top) after central intravenous adrenaline administration (CV) and application directly into the endotracheal tube (ET) and in seven patients (bottom) after central intravenous and peripheral bronchial (PB) administration by way of a wedged catheter. The bold line represents the median.

The blood pressure decrease at low plasma levels was immediately opposed by -receptor–mediated vasoconstriction at rapidly increasing plasma adrenaline levels (Figure). The blood pressure decreases observed by McCrirrick and Kestin were probably caused by the anesthesia technique because the endotracheal adrenaline dose of 30 µg was too low to produce any effects (1). In dogs, blood pressure decreases persisted for 30 minutes after endotracheal administration of adrenaline (2). We speculate that this effect was associated with low plasma adrenaline levels because of poor effectiveness of the adrenaline administration technique. In our study, plasma adrenaline levels also remained low after airway administration of adrenaline in 4 of 13 patients (Figure). However, as stated in our report, spontaneous plasma adrenaline levels in cardiac arrest are even higher than the maximum plasma levels achieved in our study (Figure). It is extremely unlikely that adrenaline administration during cardiac arrest could cause the ß₂-mediated vasodilatatory effects that might occur in patients with spontaneous circulation at low plasma adrenaline levels. Therefore, vasodilatatory effects after airway adrenaline do not appear to be clinically relevant.

In contrast, the unreliable adrenaline absorption from the lungs does represent a relevant clinical problem. The course of plasma adrenaline levels varied considerably after airway administration of adrenaline (Figure), and a greater variation could be expected during cardiac arrest. We doubt that higher endotracheal adrenaline doses would result in more reliable adrenaline absorption from the lungs. Therefore, our data may encourage researchers to consider more reliable routes for adrenaline administration in adults (for example, the intraosseous route) and to investigate alternative vasopressors that are absorbed more reliably.