The higher blood pressure is often indicative of a severe form of peripheral vascular disease, reduced Impedance, increased atherosclerosis and reduced lumen in extremities with large blood vessel.

Blood pressure measurement is normally higher in small distal arteries compared to large proximal arteries. Likewise, atherosclerosis normally begins in large proximal arteries, particularly along curvatures and bifurcations, but atherosclerosis is rare in small peripheral arteries and arterioles. This cannot be explained in terms of classical hemodynamic theory, which assumes that blood pressure is directly related to the contractile force exerted by cardiac contraction, so that the blood pressure reading should be identical throughout the arterial tree, as if hemodynamic physiology is analogous to the "static" hydraulic brake system of an automobile. However, hemodynamic blood flow is "dynamic" as opposed to "static." This is what causes the confusion.

The key to understanding hemodynamic physiology is the "non-Newtonian" nature of mammalian blood. The "non-Newtonian" blood flow in arteries is totally different from "Newtonian" water flow in pipes.

When water is accelerated in pipes, it causes turbulence that exaggerates flow resistance. Increases in the acceleration of water flow in pipes causes exponential increases in turbulent flow resistance. in other words, the harder water is forced forward in a pipe, the greater the flow resistance that opposes the forward flow of the water. This explains why water can only be delivered to homes at relatively low rates, so that bathtubs and swimming pools fill slowly.

Blood flow in arteries is totally different. When the heart contracts, it accelerates blood flow velocity from zero to 125 cm/sec within 0.1 second. There is negligible turbulent flow resistance in mammalian blood because mammalian blood cells spontaneously form "aggregate" patterns (stacks of red cells) that inhibit turbulences, and therefore eliminate turbulent flow resistance. Thus, blood flow is truly "laminar" and free from turbulent flow resistance. This explains the extreme efficiency of mammalian hemodynamic physiology, and why mammals enjoy superior exercise tolerance compared to reptiles.

When the mammalian heart contracts, it expels its contents in less than a tenth of a second, because there is no flow resistance. The muscular/elastic arterial tree expands its volume in order to accommodate the volume of blood ejected by the heart. The arterial tree then functions as a "secondary heart" that slowly contracts to restore its resting volume. In so doing it propels blood forward toward peripheral capillary beds. This blood flow is "non-Newtonian" so that it entails negligible flow resistance. It is extremely efficient.

However, in the immediate aftermath of cardiac contraction, as the heart muscle relaxes, the forward flow of blood momentarily reverses. This momentary "backward flow" of blood in the proximal aorta causes the aortic valve to snap shut, causing the second heart sound (the first heart sound is caused by mitral valve closure when the left ventricle begins to contract). The decreased diameter of the distal aorta exaggerates this brief reversal of blood flow, and initiates a wave of pulsatile turbulence that propagates throughout the arterial tree during diastole. This pulsatile turbulent waves generate lateral forces which press on the interior walls of arteries that are perceived as the "palpable pulse." These turbulent lateral forces are measured as "blood pressure" by conventional monitoring devices. This causes great confusion.

The decreasing diameter in distal arteries and arterioles exaggerates the turbulent lateral forces generated by the traveling waves of pulsatile turbulence. This explains why blood pressure readings are higher in large proximal arteries than small distal arteries.

Blood pressure reading are misleading because blood pressure is NOT the "driving force" that propels blood toward capillary beds. On the contrary, high blood pressure is typically caused by abnormal increases in capillary flow resistance that pathologically alters diastolic pulsatile turbulence and exaggerates blood pressure.

Trauma patients suffer pain and anxiety that increase sympathetic tone and activity, which "closes" the capillary gate and increases capillary flow resistance. This simultaneously elevates blood pressure and undermines tissue perfusion and tissue oxygenation. This explains why blood pressure measurement often seems re-assuringly "normal" in trauma patients, especially when it is measured in small distal arteries, even though their tissue perfusion and tissue oxygenation is decreased to critical levels, so that they are near death. Furtermore, the conventional "Riva-Rocci" technique cannot detect blood pressure below 40 torr. This explains why blood pressure "disappears" in large proximal arteries even though blood pressure remains detectable in small peripheral arteries.

I am presently toiling to complete and publish a pair of books that summarize recent advances in the stress theory of Hans Selye. The recent discovery and description of the "mammalian stress mechanism" enables Selye's "Unified Theory of Medicine" that explains the true nature of mammalian hemodynamic physiology and pathophysiology. www.stressmechanism.com

Detailed info seen above. I would add simply that peripheral vasoconstriction occurs during trauma when blood is shunted towards the key organs. Also of note when measuring blood pressure keep in mind that in order to externally compress an artery all the surrounding soft tissue needs to be compressed too and hence readings from the thigh can be difficult to interpret.