Arterial pulse pressure (PP) is defined as the absolute difference between systolic and diastolic blood pressure. Its relationship to other cardiovascular variables and its strong predictive value for clinical vascular events has resulted in PP becoming the focus of much research into the mechanisms that underlie its generation, as it is an attractive target for both non-drug and pharmacological therapies. The clinical relevance of PP is reviewed here, as are its determinants. Particular reference is made to the relationship between central arterial PP and aortic dimensions.
Determinants of Pulse Pressure
Aortic, or central, PP is dependent predominantly on stroke volume (SV) and arterial compliance (AC) (of both the proximal large conduit vessels and the distal arterial tree). Compliance is defined as the capacity of a fluid-filled vessel to change volume relative to the accompanying change in internal pressure. Hence, it is the inverse of stiffness, and the relationship with PP can be simplified to compliance = stroke volume/pulse pressure or PP = SV/AC. Although the relationship is more complex than this, it aids in appreciating the age-related rise in PP due, in part, to the increased arterial stiffness seen in the elderly and accompanied by some decline in left ventricular SV. The proximal aorta, because of the relatively high content of elastin within its walls compared with the distal, more muscular, arteries, accounts for the majority of the systemic circulation’s compliance.
The distal circulation also plays a role in the generation of central PP, as it is the site of pulse wave reflections that is particularly prevalent at points of bifurcation or other branching. Pulse waves arising as a result of left ventricular contraction are propagated in an anterograde fashion and result in changes in arterial blood pressure and blood flow velocity. A fraction of each wave is reflected from the distal circulation and travels in a retrograde direction towards the proximal vasculature, where the summation of forward- and backward-travelling waves culminates in the final measured blood pressure or blood flow velocity. The timing of this augmentation of central pressure during the cardiac cycles is dependent on pulse wave velocity, which increases with increasing arterial stiffening. As such, the peak of the reflected wave influences the final composite PP at a relatively earlier point in the cardiac cycle when the peripheral circulation is stiffer because of an accelerated pulse wave velocity. Following on from this concept is the fact that heart rate will influence central PP by altering the duration of the cardiac cycle and subsequently the relative timing of the reflected wavefronts.1,2
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