Hyperventilation, cerebral perfusion, and syncope

TY - JOUR

T1 - Hyperventilation, cerebral perfusion, and syncope

AU - Immink, R V

AU - Pott, F C

AU - Secher, N H

AU - van Lieshout, J J

PY - 2014/4/1

Y1 - 2014/4/1

N2 - 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.

AB - 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.

KW - Age Factors

KW - Blood Flow Velocity

KW - Carbon Dioxide

KW - Cerebrovascular Circulation

KW - Chemoreceptor Cells

KW - Humans

KW - Hyperventilation

KW - Hypocapnia

KW - Middle Cerebral Artery

KW - Oxygen

KW - Syncope

U2 - 10.1152/japplphysiol.00637.2013

DO - 10.1152/japplphysiol.00637.2013

M3 - Journal article

C2 - 24265279

SN - 8750-7587

VL - 116

SP - 844

EP - 851

JO - Journal of Applied Physiology

JF - Journal of Applied Physiology

IS - 7

ER -