Although the Windkessel model accurately captures much of arterial behavior, its main limitation is that it does not account for wave reflection within the arterial circulation.

With each ventricular ejection, a pulse wave propagates down the arterial system. At points where the vessel characteristics change (such as branch points or high-resistance arterioles) part of the energy from the wave is reflected back toward the heart.

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The reflected energy waves have a dual effect:

1. They augment arterial pressure (positive effect on pressure)

2. They impede forward flow (negative effect on ventricular ejection).

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The net effect on both pressure augmentation and the degree to which forward flow is impeded is governed by two factors. First, how fast the pressure wave travels through arteries (velocity), and second, the magnitude of the wave reflection.  

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The velocity of pressure waves travel through arteries is known as the pulse wave velocity (PWV).  PWV increases when arteries become stiffer and is determined by the elastic properties of the arterial wall, wall thickness, vessel diameter, and blood density (which remains relatively constant).  The relationship is described by the Moens-Korteweg equation: PWV = √(Eh/2ρR), where E is the elastic modulus (stiffness) of the arterial wall, h is wall thickness, R is arterial radius, and ρ is blood density.

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The magnitude of wave reflection depends on the degree of impedance mismatch at the reflection site.  Impedance can be thought of as the intrinsic opposition of the vessel to pulsatile flow.  Wave reflections occur at multiple sites of impedance mismatch throughout the arterial tree—including branch points, changes in vessel diameter, and transitions in arterial wall properties.  For example, when peripheral vasoconstriction occurs within arterioles, impedance mismatch increases at the arterioles, enhancing wave reflection. 

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The timing of reflected wave arrival determines its hemodynamic impact. In young, compliant arteries with low PWV, reflected waves return during diastole, augmenting diastolic pressure and coronary perfusion. With arterial stiffening and increased PWV, reflected waves arrive earlier—during mid-to-late systole—augmenting systolic pressure and increasing cardiac workload.

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In young, healthy individuals with compliant arteries, pulse wave velocity is slow (approximately 5 m/s), so reflected waves return to the aortic root during diastole, augmenting diastolic pressure and enhancing coronary perfusion.  This beneficial timing occurs because the reflected wave arrives after aortic valve closure, providing a "boosting" effect to coronary blood flow.  This is demonstrated in the figure below. 

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With aging or arterial stiffening, pulse wave velocity increases dramatically (up to 20 m/s), causing reflected waves to arrive earlier—during mid-to-late systole rather than diastole. This earlier arrival produces several adverse hemodynamic consequences: it increases systolic pressure and left ventricular afterload, reduces diastolic pressure augmentation (thereby decreasing coronary perfusion), and widens central pulse pressure.

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​Heart rate also modulates this effect: at lower heart rates, systole lasts longer, providing more time for reflected waves to arrive before aortic valve closure. This prolongs the period during which reflected waves can augment central systolic pressure. For any given pulse wave velocity, a slower heart rate therefore increases the magnitude of central systolic pressure augmentation.

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The clinical significance of these changes can be appreciated by comparing central aortic pressure and flow waveforms between individuals with normal versus reduced arterial compliance. In stiff arteries, the pressure waveform shows a pronounced mid-to-late systolic component, reflecting the earlier arrival of reflected waves, while flow patterns demonstrate reduced forward flow efficiency.

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​​​​​​​​​​​​​​The upper panel of the figure above shows pressure waveforms recorded at six sequential locations along the arterial tree. Note that the pressure waveform becomes progressively "peakier" and narrower as it travels distally.  At each location along the arterial tree, the forward (ejected) wave and backward (reflected) wave synchronize differently. At the ascending aorta, these waves synchronize late, producing a lower systolic peak. At peripheral sites, they synchronize earlier, producing higher systolic peaks—even though mean arterial pressure remains nearly constant throughout.

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The lower panel shows flow velocity: As waveforms reflect backwards faster and converge with forward moving waves, the flow is reduced, despite a higher pulse pressure.  In other words, early wave reflection increases afterload and reduces flow efficiency, despite an apparently higher systolic pressure.  

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What is the benefit of this phenomenon? 

Pulse pressure amplification keeps central (aortic) systolic pressure and pulse pressure low while allowing higher pressures in the periphery.  This is beneficial because:

• The heart "sees" the central aortic pressure, not peripheral pressure—so lower central pressure means reduced left ventricular afterload and myocardial oxygen demand.

• The normal amplification between the aortic root and brachial artery shields the heart from excessive pulsatile stress.
   

With aging, central aortic stiffness increases disproportionately compared to peripheral arteries, reducing the stiffness gradient and diminishing pulse pressure amplification. This results in higher central systolic pressure, increased left ventricular workload, and is a significant predictor of cardiovascular risk including cardiac hypertrophy and heart failure.

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