Response to “Central Blood Pressure Physiology” a (More) Critical Review (Schultz et al.)

To the Editor: The major theme of my review1 was to question whether newer indicators of pulse wave transmission add substantially to the information intrinsically included in traditional brachial systolic blood pressure (BP). This time-honored indicator contains information about arterial stiffness and impedance, propagation of pressure waves, and cardiac function. Appreciation of these important nuances is low and instead, attention has turned to devices that report data about pulse wave transmission and arterial structure-function relationships. These newer indicators are inexorably linked to brachial systolic BP for a variety of reason, not the least of which is that they are calibrated by brachial cuff systolic BP. The literature promoting the clinical promise of these new techniques requires a hard second look; my skepticism about the level of understanding and appropriate use of these newer indicators is not unique.2 I also expressed my concern about our use of outdated or poorly validated models with questionable assumptions, perhaps including standard wave reflection principles. A secondary aim of the review was to spark new discussion about alternative models for pulsatile flow and its variation within and between individuals. The important commentary provided by Schultz, Davies, and Sharman3 is modest evidence that I succeeded in achieving this aim. For clarity, I used standard wave reflection terminology and although I included data to indicate that there were problems with the standard model, I failed to articulate the alternative models, in part because of the scope and direction of the article. As my critics have so clearly elucidated, however, it is high time to reevaluate the concept of wave reflection. Subtle observations, including the relative invariability of timing landmarks in the arterial contour suggests that wave reflection models are problematic.4 We can corroborate and extend these observations. Schultz et al. proposes an alternate model that includes a pressure reservoir (Windkessel) and an “excess pressure” component related to transmission parameters.5 A few other points deserve commentary. First, is there wave summation? The simple answer is yes because any second systolic peak (P2) or backward pressure wave resulting from a downstream impedance or capacitance change is additive with the first systolic peak (P1). The timing of the second systolic peak is relatively fixed but a change as small as 20–30ms can have a small effect on the magnitude of P2 because it occurs during the period of rapid pressure descent that follows P1. What is very clear is that the old concept of a reflected wave returning to the aortic root in early diastole in younger people and late-systole in older people is simply not correct. Secondly, Schultz has refuted my comments that aortic valve closure and cerebral perfusion could be at least partially dependent on the height of the late-systolic pressure boost. They and others have focused more recently on the properties of forward-traveling negative-pressure (expansion or “suction”) waves determined by a complex system of wave intensity analysis.6 In my opinion, their findings do not fully exclude late-systolic pressure augmentation as a contributing factor in both valve closure and in support of forward blood flow to the brain. The author declared no conflict of interest.