Bradycardia during hypoxaemic airway crises. Does atropine treat the patient or the anaesthetist?

Abstract

Bradycardia is commonly seen in the late stages of failing airway management when it is a response to worsening hypoxaemia. The aetiology of hypoxaemic bradycardia is either a vagally-mediated reflex resulting from hypoxia [1] or a direct consequence of myocardial hypoxia [2]. Recent discussion between the authors, regarding the management of this haemodynamic complication in the context of an obstructed airway in adults, highlighted differences between what we believe to be the most appropriate approach and the interventions commonly instituted in simulated airway emergencies, reported in clinical cases and recommended in standard advanced life support protocols. Given that in a patient with an obstructed upper airway, it is profound oxygen desaturation that leads to bradycardia, the most appropriate response is to relieve the hypoxaemia. Our collective experience suggested that many clinicians would also concurrently administer intravenous atropine as a positive chronotrope, as occurred, for example, in the case of Elaine Bromiley [3]. The rationale for atropine administration in this situation is to maintain cardiac output and prevent bradycardia progressing to asystole. One might also speculate, however, that confronted with the prospect of failing to restore airway patency, administering atropine for bradycardia could also be motivated by the alleviation of stress that is derived from identifying an immediately remediable problem requiring a familiar intervention and the intuitive appeal of restoring normal physiological values. However, we do not believe atropine administration in this situation is actually beneficial to the patient. We contend that, in addition to not addressing the cause of the bradycardia, administration of atropine might be a potentially harmful intervention in this context for the following reasons. Firstly, it is a potential distraction that might divert attention from, and delay restoration of, adequate alveolar oxygen delivery, particularly when the number of available staff is limited. This is especially relevant given that delays in performing emergency front-of-neck airway are recognised to contribute to patient morbidity and mortality in cases of upper airway obstruction [4]. Secondly, when bradycardia is due to direct cardiac cellular hypoxia, rather than a vagal response, antimuscarinics would not be expected to increase heart rate anyway. Finally, in a situation where the patient’s oxygen reserves are being consumed rapidly without adequate (or perhaps any) replenishment, the increased heart rate will increase oxygen consumption and accelerate depletion of the limited remaining oxygen reserves. This will potentially worsen myocardial ischaemia and cardiac output, decreasemixed venous oxygen content (further compromising the oxygen content of blood delivered to other organs, including the brain) and thereby worsen hypoxic brain injury and hasten progression to cardiac arrest. For example, there may be enough reserve oxygen to maintain cardiac contractility for 1 min when the heart rate is 60 bpm or, alternatively, up to double this period when the heart rate is 30 bpm. Clinical trials supporting this concept are lacking, but animal studies show that onset of hypoxic cardiac arrest ismore rapid when atropine is used to increase the heart rate [5]. Hypoxic bradycardia may, therefore, represent a protective reflex and, like many other areas of acute medicine, slavish adherence to normal physiology by artificial means could be counter-productive. In cases of hypoxic bradycardia, standard textbooks of anaesthesia, critical care and emergency medicine rightly advocate relieving the cause of the problem by restoring oxygenation, but leave open the question as to whether bradycardia should be concurrently managed using chronotropes. In our opinion, the administration of atropine at this point is a medical displacement activity which is at best