In the theory of arterial stiffness the aorta and its major branches are seen as a reservoir that can absorb the stroke volume pumped in by the heart to release it in a gradual way during systole. The German term is Windkessel effect. When we become older the elastance of this Windkessel decreases and the aorta becomes stiffer. The blood ejected by the heart can no longer be buffered in the aorta and will penetrate the branches of the arterial tree causing an increase in pulsatility. 

Where the aorta and its main branches have a high elasticity, this is assumed less in the distal arterial branches. Here the stiffness becomes larger and the elastance less. These differences, according to the theory of arterial stiffness, explains why pulsatility increases towards periphery. It assumes non-linearity: the vessels have less resistance to blood flow during systole as during diastole. In peripheral arteries this will cause an increase in pulse pressure (the difference between systolic and diastolic pressure). 

Because this arterial stifness in the periphery, pressure waves traveling from the heart to the periphery are reflected in opposite direction. This effect increases the pressure at a given location in the arterial tree in a rather complex way, depending on the timing of forward versus backward traveling waves. This explains why, after a first rapid increase, there is a dip in the systolic pressure during the second phase of systole.

Issues unexplained

There are issues with the theory of arterial stiffness. In the first place it does not take into account the branching of the arterial tree: although individual arteries become stiffer there number increase exponentially making the total cross-sectional area manifold larger than at the origin of the aorta. The arterial tree should be seen as a funnel, the blood being pumped in at the narrow end and being distributed along a multitude of small arteries and arterioles. 

Furthermore, the theory of arterial stiffness assumes energy loss during systole: the energy of heart contraction faces reflecting waves from a multitude of branching points: blood flow has to wait for diastole.

Finally, the theory of arterial stiffness does not explain how blood is distributed over the arterial tree. The general view is that arterioles open or close depending on local metabolic activity allowing blood to flow in at demand. Can blood reach remote capillary systems? Only when arterioles in proximal tissues are relatively closed. Can blood reach tissues under unfavorable conditions such as high tissue pressures? Only when tissues under more favorable conditions adopt a high arteriolar vascular tone.

Elaborate technical apparatus measure the forward and backward traveling waves and calculate a value for arterial stiffness (e.g. the augmentation index). Measurements of arterial stiffness have been shown to correlate with cardiovascular disease: the larger the arterial stiffness, the higher the risk for myocardial infarction and stroke. Is arterial stiffness indeed a passive process or may active contraction within the arteries' muscular layers be involved? This question leads us to the theory of arterial acceleration.

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