Journal of Applied Physiology
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J Appl Physiol 94: 833-848, 2003; doi:10.1152/japplphysiol.00260.2002
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Vol. 94, Issue 3, 833-848, March 2003

INVITED REVIEW
Syncope, cerebral perfusion, and oxygenation

Johannes J. Van Lieshout1,2, Wouter Wieling1,2, John M. Karemaker1,3, and Niels H. Secher4,5

1 Cardiovascular Research Institute Amsterdam and Departments of 2 Medicine and 3 Physiology, Academic Medical Center, University of Amsterdam, 1105 AZ Amsterdam, The Netherlands; and 4 The Copenhagen Muscle Research Center and 5 Department of Anesthesia, Rigshospitalet, University of Copenhagen, DK-2100 Copenhagen, Denmark

During standing, both the position of the cerebral circulation and the reductions in mean arterial pressure (MAP) and cardiac output challenge cerebral autoregulatory (CA) mechanisms. Syncope is most often associated with the upright position and can be provoked by any condition that jeopardizes cerebral blood flow (CBF) and regional cerebral tissue oxygenation (cO2Hb). Reflex (vasovagal) responses, cardiac arrhythmias, and autonomic failure are common causes. An important defense against a critical reduction in the central blood volume is that of muscle activity ("the muscle pump"), and if it is not applied even normal humans faint. Continuous tracking of CBF by transcranial Doppler-determined cerebral blood velocity (Vmean) and near-infrared spectroscopy-determined cO2Hb contribute to understanding the cerebrovascular adjustments to postural stress; e.g., MAP does not necessarily reflect the cerebrovascular phenomena associated with (pre)syncope. CA may be interpreted as a frequency-dependent phenomenon with attenuated transfer of oscillations in MAP to Vmean at low frequencies. The clinical implication is that CA does not respond to rapid changes in MAP; e.g., there is a transient fall in Vmean on standing up and therefore a feeling of lightheadedness that even healthy humans sometimes experience. In subjects with recurrent vasovagal syncope, dynamic CA seems not different from that of healthy controls even during the last minutes before the syncope. Redistribution of cardiac output may affect cerebral perfusion by increased cerebral vascular resistance, supporting the view that cerebral perfusion depends on arterial inflow pressure provided that there is a sufficient cardiac output.

arrhythmia; blood pressure; cerebral blood flow; vasovagal; cardiac output


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