Effects of orthostasis on cerebral blood flow and oxygenation - Prof. Lieshout скачать в хорошем качестве

Effects of orthostasis on cerebral blood flow and oxygenation - Prof. Lieshout

Invited Session "The Brain at Work" at ECSS Barcelona 2013 Effect of orthostasis on cerebral blood flow and oxygenation Van Lieshout, J. Dpt Internal Medicine & Laboratory for Clinical Cardiovascular Physiology Upon either passive or active assumption of the upright body position, the first circulatory event is a gravitational displacement of blood away from the thorax to dependent regions of the body with a fall in venous return. Depending on the type of orthostatic stress (i.e. active standing vs. passive head-up tilt or simulated orthostatic stress by lower body negative pressure) approximately one half to one litre of blood is transferred to the regions below the diaphragm. Orthostatic pooling of venous blood begins immediately and the total transfer is almost complete within 3-5 min depending on the investigated body region. In addition to this transfer of thoracic blood, the central blood volume is affected by transcapillary filtration of fluid into the interstitial spaces in the dependent parts of the body. The circulatory adjustment to active standing up includes an initial ~30 s lasting fluctuation in mean arterial pressure (MAP) followed in 1-2 min by a phase of relative stability. Initially, MAP drops some 25 mmHg as total peripheral resistance falls ~40% for 6 to 8 s unrelated to orthostasis or straining and attributed to the instantaneous increase in vascular conductance of the active leg muscles. This transient and rapid fall in MAP is likely to explain the feelings of light-headedness that even healthy humans sometimes experience shortly after standing up, and may even cause recurrent transient loss of consciousness (TLOC). When standing, both the position of the cerebral circulation and the reductions in MAP and cardiac output challenge cerebrovascular autoregulatory mechanisms and cerebral perfusion and oxygenation decrease. The mechanisms underlying the postural reduction in cerebral perfusion are as yet incompletely understood. The role of systemic pressure/flow control, static and dynamic cerebrovascular autoregulation and the carbon dioxide (CO2) responsiveness of the brain vasculature will be discussed. With exercise the initial increase in cerebral blood flow is blunted at higher exercise intensities by a hyperventilation-induced lowering of the arterial CO2 partial pressure and subsequent cerebral vasoconstriction. For exercise-related fainting the key question is whether TLOC developed during or after stopping exercise.