Hyperventilation, cerebral perfusion, and syncope

J Appl Physiol (1985). 2014 Apr 1;116(7):844-51. doi: 10.1152/japplphysiol.00637.2013. Epub 2013 Nov 21.


This review summarizes evidence in humans for an association between hyperventilation (HV)-induced hypocapnia and a reduction in cerebral perfusion leading to syncope defined as transient loss of consciousness (TLOC). The cerebral vasculature is sensitive to changes in both the arterial carbon dioxide (PaCO2) and oxygen (PaO2) partial pressures so that hypercapnia/hypoxia increases and hypocapnia/hyperoxia reduces global cerebral blood flow. Cerebral hypoperfusion and TLOC have been associated with hypocapnia related to HV. Notwithstanding pronounced cerebrovascular effects of PaCO2 the contribution of a low PaCO2 to the early postural reduction in middle cerebral artery blood velocity is transient. HV together with postural stress does not reduce cerebral perfusion to such an extent that TLOC develops. However when HV is combined with cardiovascular stressors like cold immersion or reduced cardiac output brain perfusion becomes jeopardized. Whether, in patients with cardiovascular disease and/or defect, cerebral blood flow cerebral control HV-induced hypocapnia elicits cerebral hypoperfusion, leading to TLOC, remains to be established.

Keywords: cardiac output; cerebral blood flow; cerebral metabolism; cerebral oxygenation; diabetes; vascular conductance.

Publication types

  • Review

MeSH terms

  • Age Factors
  • Blood Flow Velocity
  • Carbon Dioxide / blood
  • Cerebrovascular Circulation*
  • Chemoreceptor Cells / metabolism
  • Humans
  • Hyperventilation / blood
  • Hyperventilation / complications*
  • Hyperventilation / physiopathology
  • Hypocapnia / blood
  • Hypocapnia / etiology*
  • Hypocapnia / physiopathology
  • Middle Cerebral Artery / physiopathology*
  • Oxygen / blood
  • Syncope / blood
  • Syncope / etiology*
  • Syncope / physiopathology


  • Carbon Dioxide
  • Oxygen