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Medical School, Hannover, Germany
To the Editor:
Vaknin et al. (1) observed vasodilatory effects of endotracheal adrenaline in hypertensive dogs. As recently stated in a response to a letter from this group, we are convinced that these effects are not clinically relevant (2). Undoubtedly, ß-mediated effects depend on adrenaline plasma levels and not on the route adrenaline is administered. Patients with cardiac arrest have very high spontaneous adrenaline plasma levels (3). Therefore, it is extremely unlikely that adrenaline administration during cardiac arrest causes any vasodilatory effects that could occur at low adrenaline plasma levels under spontaneous circulation.
Vaknin et al. (1) speculated that ß-blockers abolished vasodilatory effects in the patients of our study (1,4). Twenty of 34 patients were not on ß-blockers. Why did all dogs have blood pressure decreases for at least 10 min (1) compared with a few seconds in only 4 of 34 patients (4) when more than twice the airway adrenaline dose was given to the animals?
Unlike ß-adrenergic effects, the variable effectiveness of airway adrenaline (4) could indeed be deleterious during cardiac arrest. This encourages us to also consider the more reliable intraosseous route in adults and vasopressors that are absorbed more reliably from the lungs (5).
References
The Chaim Sheba Medical Center, Ramat-Gan, Israel
In Response:
We thank Drs. Raymondos and Panning for their interest in our study. The observations they made in their letter, however, indicate that they misunderstood the intent and direction of our investigation. The study protocol made no pretensions of being valid during cardiac arrest. Rather, our aim was to clarify the well-documented deleterious side effect of a significant decrease in blood pressure immediately after endotracheal adrenaline administration that had been shown by their group (1), as well as by other clinical and laboratory studies (2,3). Furthermore, a recent editorial by Tang (4) has pointed out the detrimental effects of adrenaline and expressed the hope of finding a more specific short-acting 
-adrenergic agonist as an alternative drug during resuscitation.
Drs. Raymondos and Panning note that 20 of 34 patients in their study were not on ß-blockers. It was precisely this limitation of their study that we pointed out in our letter (5): no correlation had been made between the hemodynamic response of patients who were treated with ß-blockers versus those who were not.
As to the difference in hemodynamic responses between dogs and humans, it is well established that the response to catecholamines has an extremely large individual variation, even among humans (6). This is why we propound a need for the further study of pharmacokinetic and pharmacodynamic effects of endotracheal adrenaline in humans in search for a safer and more predictable alternative.
Whatever the mechanism of the decrease of blood pressure that is associated with endotracheal adrenaline, the clinical implications still prevail. Thus, we are gratified that Drs. Raymondos and Panning have written that they are encouraged to reconsider their recommendation of supporting the airways as an alternative route for adrenaline during resuscitation in adults in their original paper (1) in favor of the intraosseous route and the use of vasopressors that are absorbed more reliably from the lungs.
References
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