Harvey with a modern twist: How and why conducting arteries amplify the pressure wave originating from the heart

Current views on cardiovascular physiology differ little from that published by William Harvey in 1628: the heart delivers all energy for blood circulation, forcing its contents into the aorta, via arteries, arterioles and capillaries into the venous system that collects the blood and returns it to the right side of the heart. Similarly, blood from the right side passes through pulmonary arteries and arterioles to pulmonary veins before returning to the left side of the heart. However, from aorta to capillaries there is a great increase in overall cross-sectional area. The arterial system can be seen as a funnel, the heart pumping blood into its narrow end. Theoretically, this implies that pulsatile energy delivered by the heart dilutes significantly along its way through the arterial tree. Also, unfavorable tissue conditions, such as elevated pressure, impede proper perfusion when blood can pass just as easy through adjacent capillary systems. Finally, blood will experience more resistance to flow for capillary systems more distant to the heart due to its longer trajectory. This implies that capillary systems closer to the heart are more easily perfused than more distant ones. In reality, the pulse from the heart has been shown to increase and accelerate towards periphery. This, together with transcranial Doppler observations on the variation in wave morphology in intracranial arteries, for instance during CO2-reactivity testing and during cardiac arrhythmia, has led to the theory of arterial acceleration: at stroke onset, the arterial pressure wave resulting from myocardial contraction is enhanced by a short-lasting and well-synchronised contraction within the smooth muscle layers of conducting arteries. This results in a temporary 'stiffening' of the arterial tree by which cardiac pressure during early systole is amplified and distributed into all the body's capillary systems. This theory would overcome all theoretical and observational concerns sketched above. Such arterial acceleration limited to the first 100-150 ms of every heart beat would augment, accelerate and distribute the pulse generated by heart contraction over the full length and branching of the arterial tree, thereby enforcing a widespread tissue perfusion. It is obvious that the theory of arterial acceleration is a major shift of paradigm forcing us to reconsider many aspects of cardiovascular physiology. Moreover, it improves our understanding how blood expelled by the heart through the small lumen of the aortic notch has sufficient energy to reach every nook and cranny of our body. (C) 2014 Elsevier Ltd. All rights reserved.