Role of carotid-body chemoreceptors and their reflex interactions in bradycardia and cardiac arrest

Lancet. 1979 Apr 7;1(8119):764-7. doi: 10.1016/s0140-6736(79)91218-2.


Stimulation of the carotid-body chemo-receptors by asphyxia during an apnoeic episode may contribute to the vagally mediated cardiac arrest and sudden death that sometimes occurs in man. Apnoeic asphyxia may be induced centrally or reflexly by stimulation of upper airways receptors. Conditions associated with apnoeic asphyxia and in which the risk is likely to be greatest include intubation, laryngoscopy and bronchoscopy; accidents involving underwater swimming; inhalation of sympathomimetic amines in aerosols by asthmatic patients; and chronic hypoventilation syndromes. These reflexes may be responsible for some victims of sudden infant death syndrome. Stimulation of the carotid bodies normally produces hyperventilation and bradycardia. When apnoea occurs centrally or reflexly, carotid chemoreceptor excitation resulting from asphyxia now causes a much enhanced bradycardia and even cardiac arrest, but paradoxically does not usually affect respiration. These reflexes and their interactions normally serve protective and purposeful functions, but may under certain circumstances become exaggerated and put the patient's life at risk.

MeSH terms

  • Animals
  • Apnea / physiopathology
  • Arteries / innervation
  • Asphyxia / physiopathology
  • Bradycardia / etiology*
  • Bradycardia / prevention & control
  • Carotid Body / physiopathology*
  • Chemoreceptor Cells / physiopathology*
  • Death, Sudden / etiology*
  • Face / innervation
  • Heart / innervation
  • Heart Arrest / etiology*
  • Heart Arrest / prevention & control
  • Humans
  • Reflex / physiology*
  • Respiration
  • Respiratory System / innervation
  • Trigeminal Nerve / physiopathology
  • Vagus Nerve / physiopathology