http://circ.ahajournals.org/content/111/22/2997

To survive in the world, humans must possess the ability to make moment by moment alterations that permit their internal environment to remain stable despite dramatic changes in their external environment. This includes not only changes in ambient temperature, humidity, and barometric pressure but also the ability to react quickly to the presence of perceived danger. The principal neural mechanisms by which this “homeostasis” is maintained and regulated are governed by the hypothalamus via its 2 effector systems, which include the Autonomic Nervous System (ANS) and the endocrine system.

The ANS provides the principal means for both the short- and long-term responses to changes in position (the renin-angiotensin-aldosterone system also plays a role but over a longer time frame). In the normal person, approximately 25% to 30% of blood volume is located in the thorax when they are supine (lying on back, face upward). On standing, there is a gravity-mediated downward displacement of roughly 300 to 800 mL of blood to the vasculature of the abdomen and lower extremities.This represents a volume drop of between 25% and 30%, half of which occurs within the first few minutes of standing. This sudden redistribution of blood results in a fall in venous return to the heart. Because the heart can only pump the blood that it receives, this causes a fall in stroke volume of ≈40% and a decline in arterial pressure. 

While standing, contractions of the leg muscles (in conjunction with the venous valve system) actively pump blood back to the heart and move the venous HIP closer to the level of the right atrium. In addition, standing produces a substantial increase in the transmural capillary pressure present in the dependent areas of the body, which causes a rise in fluid filtration into tissue spaces. This process reaches a steady state after ≈30 minutes of upright posture and can produce a decline in plasma volume of up to 10%.Successful maintenance of upright posture (and cerebral perfusion) requires the interplay of several cardiovascular regulatory systems. Orthostatic stabilization occurs within 1 minute. The exact response to postural change differs with standing (an active process) compared with responses seen during head-up tilt (a more passive process).

Standing is a much more active process that is accompanied by contractions of muscles of both the leg and abdomen, which produces a compression of both capacitance and resistance vessels and results in an elevation in peripheral vascular resistance. This increase is sufficient to cause a transient increase in both right atrial pressure and cardiac output, which in turn causes an activation of the low-pressure receptors of the heart. Continued upright posture also activates a series of neurohormonal changes, the exact extent of which depend on the patient’s volume status. The greater the volume depletion, the greater the degree of activation of the renin-angiotensin-aldosterone system (and vasopressin). However, one of the most important aspects of the body’s ability to compensate for continued orthostatic stress is the influence of arterial baroreceptors (particularly the carotid sinus) on peripheral vascular resistance. At any given moment, ≈5% of the body’s blood is in the capillaries, 8% is in the heart, 12% is in the pulmonary vasculature, 15% is in the arterial system, and 60% is in the venous system. The inability of any one of these mechanisms to operate adequately (or in a coordinated manner) may result in a failure of the body to compensate to either an initial or prolonged orthostatic challenge. This, in turn, would result in systemic hypotension, which, if sufficiently profound, could lead to cerebral hypoperfusion and subsequent loss of consciousness.