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Bradycardia during critical care intubation: mechanisms, significance and atropine
  1. Peter Jones1,
  2. Stéphane Dauger2,
  3. Mark J Peters1
  1. 1Critical Care Group – Portex Unit, Institute of Child Health, University College London, London, UK
  2. 2APHP, Service de Réanimation et Surveillance Continue Pédiatriques, Hôpital Robert Debré et Université Paris-Diderot Paris VII, Paris, France
  1. Correspondence to Dr Peter Jones, Critical Care Group – Portex Unit, Institute of Child Health, University College London, 30 Guilford Street, London WC1N 1EH, UK peter.jones{at}rdb.aphp.fr

Abstract

Bradycardia occurs during the intubation of some critically ill children as a result of vagal stimulation due to hypoxia and/or laryngeal stimulation; such ‘stable’ bradycardia is accompanied by selective vasoconstriction. Some induction drugs also induce bradycardia which may be accompanied by vasodilatation which is also a feature of certain pathologies, which influence the progression to ‘unstable’ bradycardia, which does not respond to re-oxygenation and a pause in laryngoscopy. Preintubation atropine diminishes the overall incidence of stable bradycardia during routine anaesthesia. However, clinical studies of critical care intubation show that atropine does not prevent all episodes of bradycardia and specifically cannot affect vasodilatation. As such, there is insufficient evidence to support a recommendation for the indiscriminate use of atropine for intubation during critical care illness, including simple neonatal respiratory distress. Atropine is appropriate during septic or late stage hypovolaemic shock where abnormal vasomotor tone and bradycardia may potentially set up a negative feedback loop of cardiac hypo-oxygenation and hypoperfusion and during premedication when using suxamethonium.

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Footnotes

  • Competing interests None.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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