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Hyperventilation, cerebral perfusion, and syncope.

R V Immink1, F C Pott, N H Secher

  • 1Laboratory for Clinical Cardiovascular Physiology, Department of Anatomy, Embryology, and Physiology, AMC Center for Heart Failure Research, Academic Medical Centre, University of Amsterdam, Amsterdam, the Netherlands;

Journal of Applied Physiology (Bethesda, Md. : 1985)
|November 23, 2013
PubMed
Summary
This summary is machine-generated.

Hyperventilation (HV) can cause hypocapnia, reducing brain blood flow and potentially leading to syncope (transient loss of consciousness). However, HV alone or with postural stress is unlikely to cause TLOC.

Keywords:
cardiac outputcerebral blood flowcerebral metabolismcerebral oxygenationdiabetesvascular conductance

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Area of Science:

  • Neuroscience
  • Cardiovascular Physiology

Background:

  • Cerebral blood flow is sensitive to arterial blood gases, specifically PaCO2 and PaO2.
  • Hyperventilation (HV) induces hypocapnia, which can decrease cerebral perfusion.

Purpose of the Study:

  • To review human evidence linking hypocapnia from HV to reduced cerebral perfusion and syncope (transient loss of consciousness - TLOC).

Main Methods:

  • Review of existing human studies examining the relationship between hyperventilation, hypocapnia, cerebral blood flow, and TLOC.

Main Results:

  • Hypocapnia from HV is associated with reduced cerebral perfusion and TLOC.
  • The effect of low PaCO2 on cerebral blood flow reduction during postural changes is transient.
  • HV combined with cardiovascular stressors (e.g., cold immersion, reduced cardiac output) can compromise brain perfusion.

Conclusions:

  • While HV-induced hypocapnia can reduce cerebral perfusion, its role in TLOC, especially in individuals with cardiovascular conditions, requires further investigation.