question: why does restricting blood flow to an area make your veins pop out even more in that area?
comment: Pressure. Veins are "drain pipes" for the blood that has already been pumped through the body to get back to the heart. They are low pressure compared to the higher pressure in the arteries. By pinching them off and restricting this pressure, the veins dilate (expand and "pop out"). So you are not really restricting blood flow to the area unless you are putting pressure against an artery. You are actually restricting blood flow from moving away from the area below it.
passages: If the blood viscosity increases (gets thicker), the result is an increase in arterial pressure. Certain medical conditions can change the viscosity of the blood. For instance, anemia (low red blood cell concentration), reduces viscosity, whereas increased red blood cell concentration increases viscosity. It had been thought that aspirin and related "blood thinner" drugs decreased the viscosity of blood, but instead studies found that they act by reducing the tendency of the blood to clot.
  
  Section::::Blood vessels.:Wall tension.
   Veins are adapted to an environment of low pressure and low flow. In order to bypass the coronary obstruction and restore blood flow, veins are transferred and integrated into the arterial circulation, where they exposed to high pressure and flow. These new hemodynamic conditions cause intimal hyperplasia and atherosclerosis that cause intermediate and late vein graft failure. The idea of placing an external support on the vein graft was first suggested in 1963. The rational was that it will protect the vein from intimal damage and thrombosis by aiding with the adaptation of the vein toward the arterial environment.
  
  Section::::Method.
   The vascular wall consists of amongst others the vascular smooth muscle cells, endothelial cells that line the lumen, and elastic fibers and other extracellular matrix elements. Physical forces form an important part of the adaptation mechanisms of small arteries: Blood pressure causes distension of the matrix elements, but also induces contraction of the smooth muscle cells and production of more cells and more matrix. Blood flow is sensed by the endothelial cells, which release factors such as nitric oxide that cause relaxation and remodeling towards larger diameters. Forces, cells, and matrix, therefore, form a triangle of mutual effects that underlie vascular adaptation.
   Additional return flow may be generated by the movement of skeletal muscles, which can compress veins and push blood through the valves in veins toward the right atrium.
  
  The blood circulation was famously described by William Harvey in 1628.
  
  Section::::Physiology.:Production and degradation of blood cells.
   Section::::Vascular recruitment in the lung.
  
  Vascular recruitment in the lung (i.e., in the pulmonary microcirculation) may be noteworthy to healthcare professionals in emergency medicine, because it may increase evidence of lung injury, and increase pulmonary capillary protein leak.
  
  Section::::Vascular recruitment in the brain.
  
  Vascular recruitment in the brain is thought to lead to new capillaries and increase the cerebral blood flow.
  
  Section::::Controversy.
  
  The existence of vascular recruitment in response to a stimulus has been disputed by some researchers. However, most researchers accept that vascular recruitment exists.
   Vasodilation
  
  Vasodilation is the widening of blood vessels. It results from relaxation of smooth muscle cells within the vessel walls, in particular in the large veins, large arteries, and smaller arterioles. The process is the opposite of vasoconstriction, which is the narrowing of blood vessels.
   Under normal conditions, to avoid atherogenesis, thrombosis, smooth muscle proliferation and endothelial apoptosis, shear stress maintains its magnitude and direction within an acceptable range. In some cases occurring due to blood hammer, shear stress reaches larger values. While the direction of the stress may also change by the reverse flow, depending on the hemodynamic conditions. Therefore, this situation can lead to atherosclerosis disease.
  
  Section::::Blood vessels.:Capacitance.
  
  Veins are described as the "capacitance vessels" of the body because over 70% of the blood volume resides in the venous system. Veins are more compliant than arteries and expand to accommodate changing volume.
   Fåhræus effect
  
  The Fåhræus effect is the decrease in average concentration of red blood cells in human blood as the diameter of the glass tube in which it is flowing decreases. In other words, in blood vessels with diameters less than 500 micrometers, the hematocrit decreases with decreasing capillary diameter. The Fåhræus effect definitely influences the Fåhræus–Lindqvist effect, which describes the dependence of apparent viscosity of blood on the capillary size, but the former is not the only cause of the latter.
  
  Section::::History.
   The major regulator of vascular resistance in the body is regulation of vessel radius. In humans, there is very little pressure change as blood flows from the aorta to the large arteries, but the small arteries and arterioles are the site of about 70% of the pressure drop, and are the main regulators of SVR. When environmental changes occur (e.g. exercise, immersion in water), neuronal and hormonal signals, including binding of norepinephrine and epinephrine to the α1 receptor on vascular smooth muscles, cause either vasoconstriction or vasodilation. Because resistance is inversely proportional to the fourth power of vessel radius, changes to arteriole diameter can result in large increases or decreases in vascular resistance.
   Extravasation is the leakage of intravenously (IV) infused, and potentially damaging, medications into the extravascular tissue around the site of infusion. The leakage can occur through brittle veins in the elderly, through previous venipuncture access, or through direct leakage from wrongly positioned venous access devices. When the leakage is not of harmful consequence it is known as infiltration. Extravasation of medication during intravenous therapy is an adverse event related to therapy that, depending on the medication, amount of exposure, and location, can potentially cause serious injury and permanent harm, such as tissue necrosis. Milder consequences of extravasation include irritation, characterized by symptoms of pain and inflammation, with the clinical signs of warmth, erythema, or tenderness.
   When blood vessels dilate, the flow of blood is increased due to a decrease in vascular resistance and increase in cardiac output. Therefore, dilation of arterial blood vessels (mainly the arterioles) decreases blood pressure. The response may be intrinsic (due to local processes in the surrounding tissue) or extrinsic (due to hormones or the nervous system). In addition, the response may be localized to a specific organ (depending on the metabolic needs of a particular tissue, as during strenuous exercise), or it may be systemic (seen throughout the entire systemic circulation).
   The principal buffers for increased volumes include CSF and, to a lesser extent, blood volume. These buffers respond to increases in volume of the remaining intracranial constituents. For example, an increase in lesion volume (e.g., epidural hematoma) will be compensated by the downward displacement of CSF and venous blood.
  
  The Monro–Kellie hypothesis is named after Edinburgh doctors Alexander Monro and George Kellie.
  
  Section::::Diagnosis.
   There are three main theories as to the anatomical cause; the first has to do with the geometry of the veins, wherein the vein on the left side connects to the larger outflowing vein at a right angle, which tends to fail; the second is that valves that are supposed to prevent backflow fail (venous insufficiency); the third is that pressure in upstream arteries creates a “nutcracker” syndrome.
  
  Section::::Pathophysiology.
   Since 1873, when a hypertonic solution was injected into the large penile vein in an attempt to treat impotence and resulting in reduced venous drainage away from the corpora cavernosa, there has been much controversy concerning the most ideal milieu for applying Pascal’s law as it relates to this area of study.
   Blood viscosity increases as blood is more hemoconcentrated, and decreases as blood is more dilute. The greater the viscosity of blood, the larger the resistance will be. In the body, blood viscosity increases as red blood cell concentration increases, thus more hemodilute blood will flow more readily, while more hemoconcentrated blood will flow more slowly.
   BULLET::::- Baroreceptors in low pressure receptor zones (mainly in the venae cavae and the pulmonary veins, and in the atria) result in feedback by regulating the secretion of antidiuretic hormone (ADH/Vasopressin), renin and aldosterone. The resultant increase in blood volume results in an increased cardiac output by the Frank–Starling law of the heart, in turn increasing arterial blood pressure.
  
  These different mechanisms are not necessarily independent of each other, as indicated by the link between the RAS and aldosterone release. When blood pressure falls many physiological cascades commence in order to return the blood pressure to a more appropriate level.
   Blood plasma volume may be expanded by or drained to extravascular fluid when there are changes in Starling forces across capillary walls. For example, when blood pressure drops in circulatory shock, Starling forces drive fluid into the interstitium, causing third spacing.
  
  Standing still for a prolonged period will cause an increase in transcapillary hydrostatic pressure. As a result, approximately 12% of blood plasma volume will cross into the extravascular compartment. This causes an increase in hematocrit, serum total protein, blood viscosity and, as a result of increased concentration of coagulation factors, it causes orthostatic hypercoagulability.
  
  Section::::History.
   The capacitance, also known as compliance, of the arterio-vascular channels that carry the blood also controls cardiac output. As the body's blood vessels actively expand and contract, the resistance to blood flow increases and decreases respectively. Thin-walled veins have about eighteen times the capacitance of thick-walled arteries because they are able to carry more blood by virtue of being more distensible.
   Vasodilation is a similar process mediated by antagonistically acting mediators. The most prominent vasodilator is nitric oxide (termed endothelium-derived relaxing factor for this reason).
  
  Section::::Function.:Blood flow.
   BULLET::::5. Gravity: The effects of gravity on venous return seem paradoxical because when a person stands up, hydrostatic forces cause the right atrial pressure to decrease and the venous pressure in the dependent limbs to increase. This increases the pressure gradient for venous return from the dependent limbs to the right atrium; however, venous return actually decreases. The reason for this is when a person initially stands, cardiac output and arterial pressure decrease (because right atrial pressure falls). The flow through the entire systemic circulation falls because arterial pressure falls more than right atrial pressure; therefore the pressure gradient driving flow throughout the entire circulatory system is decreased.
   Vasoconstriction is the narrowing of the blood vessels resulting from contraction of the muscular wall of the vessels, in particular the large arteries and small arterioles. The process is the opposite of vasodilation, the widening of blood vessels. The process is particularly important in staunching hemorrhage and acute blood loss. When blood vessels constrict, the flow of blood is restricted or decreased, thus retaining body heat or increasing vascular resistance. This makes the skin turn paler because less blood reaches the surface, reducing the radiation of heat. On a larger level, vasoconstriction is one mechanism by which the body regulates and maintains mean arterial pressure.
   Venous collapse is important during exercise, when muscular compression of leg veins is used to pump blood against gravity up to the heart, and in therapeutic compression of leg veins for the treatment of deep-vein thrombosis 
  
  partial vessel collapse occurs in vessels which undergo conditions of higher external pressure relative to the fluid within and can be difficult to predict mathematically. As such, devices such as a Starling Resistor are often used to predict fluid flow under these conditions.
   Mean systemic pressure increases if there is an increase in blood volume or if there is a decrease in venous compliance (where blood is shifted from the veins to the arteries). An increase in mean systemic pressure is reflected in a shift of the vascular function curve to the right. Mean systemic pressure is decreased by a decrease in blood volume or by an increase in venous compliance (where blood is shifted from the arteries to the veins). A decrease in mean systemic pressure is reflected in a shift of the vascular function curve to the left.
  
  Section::::Calculations involving MSP.
   When demand for oxygen in the myocardium is increased, the vascular resistance of the coronary arteries has the ability to reduce, and this can increase the volume of blood passing through the blood vessels. This reduction occurs because the arteries dilate, which causes an increase in the diameter of the lumen. The greatest potential for this change is normally in the branches (arterioles) of the coronary artery that penetrate the myocardium, rather than those on the surface of the heart.
  
  Section::::Measurement.
   In addition to these blood vessels, the microcirculation also includes lymphatic capillaries and collecting ducts. The main functions of the microcirculation are the delivery of oxygen and nutrients and the removal of carbon dioxide (CO). It also serves to regulate blood flow and tissue perfusion thereby affecting blood pressure and responses to inflammation which can include edema (swelling).
  
  Section::::Function.:Regulation.
  
raw_presuppositions: Restricting blood flow to an area makes the veins pop out. Veins pop because you are restricting blood flow to the area.
raw_corrections: When the veins pop out, a person is most likely restricting blood flow from leaving rather than restricting it to reaching an area. Veins pop because you are restricting blood from moving away from the area.