michigan hypertension core curriculum - State of Michigan

side of the vascular tree. Arterial BV is determined by the difference in the BV ejected by the heart/unit
of time (cardiac output, C.O.) and the outflow through the arterial resistance vessels into the venous
capacitance vessels (peripheral runoff). When C.O. and peripheral runoff are balanced, arterial BV and
arterial pressure remain constant. If C.O. increases but peripheral runoff doesn’t rise commensurately,
then arterial BV rises and BP also increases.
Arterial elasticity is an important determinant of the rise in SBP that occurs for any given increase
in BV. Generally speaking, arterial elasticity is inversely related to age; that is, younger persons have
greater arterial elasticity and with advancing age arterial elasticity declines. Arterial compliance is
determined by elastic properties of the large conduit vessels. Arterial compliance is dV/dP - the change
in pressure that occurs with a given change in arterial volume. It should be clear that the greater the
arterial elasticity, the smaller the rise in systolic pressure during the systolic ejection phase of the cardiac
cycle. Conversely, lesser arterial elasticity causes a greater rise in systolic BP during the systolic ejection
phase. This also places an extra burden of work on the myocardium to maintain cardiac output, in part
because the systolic ejection phase is prolonged under these circumstances.
B. Physiological Factors: Cardiac output (stroke volume [SV] * heart rate [HR]) and peripheral
arterial resistance, largely determined at the level of the arterioles, are the major physiological factors
involved in the determination of arterial BP.
C. Age-Related Changes in the Aortic Conduit Vessel
There is an age-related reduction in arterial elasticity. This means that the rise in SBP is going
to be greater because, for a given stroke volume, less of the SV is “stored” in the stiffer aorta. Pressure
waves travel faster in stiff/less elastic arterial blood vessels leading to increased pressure wave reflection
from the peripheral arterial vasculature. Thus, SBP rises to a greater degree than would be seen in a
younger person with greater arterial elasticity for any given level of stroke volume. Also, because less of
the SV is “stored” in the aorta during the systolic ejection phase, there is a greater run-off of the stroke
volume to the periphery. Thus, BP falls to a lower level during diastole. These physiologic changes in
the vasculature underlie the higher levels of SBP, lower levels of DBP, and widening of the pulse pressure
that have been well documented with advancing age. Accordingly, the stiffening of the vasculature
places an increased work burden on the myocardium, in part attributable to lengthening of the systolic
ejection phase.
The normal aortic distension that occurs when blood is ejected from the heart is mediated by the
aortic elastin fibers located in the media of the vessel wall. However, with advancing age and elevated
blood pressure, aortic elastin fibers fragment thus transferring the pulsatile aortic stress to collagen fibers.
This leads to aortic stiffening, a process that is further accelerated by diabetes mellitus and arterial wall
calcification. Plausibly the fragmented elastin fibers with their plethora of calcium binding sites plausibly
contribute to arterial wall calcification. Chronic kidney disease, smoking, and diabetes mellitus also
contribute to calcium deposition in the media of the arterial wall. Figure 3 displays the hemodynamic
consequences of aortic stiffening
26 Hypertension Core Curriculum