In the aorta and arteries the pressure is pulsatile. The maximum pressure is the systolic arterial pressure (about 120 mmHg) and the minimum is the diastolic arterial pressure (about 70 mmHg). The difference between diastolic and systolic is the pulse pressure, normally about 50 mmHg.
The aortic pressure wave changes in magnitude and shape occur as it travels through the arterial system. The shape of the pressure wave narrows and high frequency features such as the incisura (end systolic notch) become dampened as it moves distally. Initially systolic pressures increase as the pressure waves travel from aorta distally through the large arteries. At the femoral arteries systolic pressures have risen by 20 mmHg, and by the time pressure waves have reached the foot systolic pressures are 40 mmHg higher than in the aorta. Pressure pulsations begin to become attenuated in the smaller arteries and are finally reduced to a steady pressure with a mean level of 30-35 mmHg by the arterioles, ready for the capillary beds (Figure CR.12). The changes in the shape of the pressure waves are mainly due to the visco-elastic properties of the arterial walls. While the increases in systolic pressure are thought to be due to factors affecting the propagation of the pressure waves through the vessels, such as reflection, resonance and changes in the velocity of propagation.
Figure CR.12 Pressure related to vessel size
Mean arterial pressure (MAP) is the value obtained when the pressure is averaged over time and can be obtained from the product of cardiac output and systemic vascular resistance. Since the pressure varies cyclically, MAP can be determined by integrating a pressure signal over the duration of one cycle (this gives the shaded area shown in Figure CR.13). The mean pressure is then given by the value of this integral divided by time. An estimate of mean arterial pressure may be made by taking the diastolic plus one-third of the pulse pressure. Thus, for a systolic pressure of 120 mmHg and a diastolic of 70 mmHg, the mean pressure (MAP) is given by:
The factors affecting MAP are summarized in Figure CR. 14.
The elasticity of the arterial walls provides an essential mechanism for maintaining forward blood flow during diastole. When the aorta and arteries are distended during systole the elasticity of the walls store kinetic energy from the ejected blood. This stored energy is then returned in diastole by the recoil of the vessel walls. A useful measure of arterial elasticity is the arterial compliance (Ca). Compliance (as in the respiratory system) is the change in arterial blood volume produced by a unit change in arterial blood pressure. Thus, easily distended arteries have a high compliance, and stiff arteries have a low compliance. The reciprocal relationship between Ca and arterial elastance (Ea) should be noted as Ea is used in describing left ventricular performance.
In vitro—the pressure-volume curves of post mortem aorta preparations have been plotted for different age groups. This is approximately linear in the young normal subject, the gradient of the curve being equal to Ca. With age the arterial walls increase in stiffness and the gradient decreases to a fraction of its value in young subjects. In addition, the compliance curve becomes curvilinear in the working arterial pressure range (Figure CR.15)
Pi = Systolic pressure PU = Dinslolic piSHUriff
In vivo—the end systolic points from different ventricular pressure-volume loops can be plotted for a given subject. This gives an arterial elastance curve in which the gradient is equal to Ea.
Determinants of Systolic and Diastolic Pressures
The factors determining systolic and diastolic pressures are summarized in Figure CR. 16:
• Arterial blood volume (ABV)
• Stroke volume
• Systemic vascular resistance
• Arterial compliance
The arterial system can be visualized as an elastic vessel containing a varying volume of blood. This volume (ABV) varies with the injection of each stroke volume and the 'run off of blood into the peripheral vessels. The arterial pressure at any instant, is then given by the relationship between the arterial compliance and ABV. This instantaneous value for arterial pressure should be differentiated from mean arterial pressure (MAP), which is averaged over time.
The determination of systolic and diastolic pressures can be examined by extending the electrical circuit analogy used previously to relate MAP to cardiac output and systemic vascular resistance (SVR). Arterial compliance (Ca) is added as a 'shunt' capacitance across
SVR to give a parallel resistance-capacitance (RC) circuit (Figure CR.17). This is fed by a continual series of current pulses (stroke volumes). Each pulse of current divides between the SVR and Ca. Ca charges to a maximum voltage (systolic pressure) during a current pulse and discharges to a minimum (diastolic pressure) in between pulses. For a given pulse amplitude these maximum and minimum values will be determined by the parallel RC time constant. The effects of SVR and Ca on systolic and diastolic arterial pressures are illustrated by the following notes:
• Ca reduces the peak current through SVR by 'shunting' current away from SVR. Thus, increasing Ca (compliant arteries) leads to reduced systolic pressures
• Increased Ca also increases the RC time constant, giving a more gradual fall of pressure during diastole and reduced pulse pressures
• Decreased Ca (stiff arteries) gives reduced shunted current, giving increased peak current through SVR and higher systolic pressures
• Decreasing Ca also decreases the RC time constant, allowing a more rapid fall in pressure during diastole and increased pulse pressures
• When arterial compliance is decreased as with age or disease, the arterial pressure-volume curve becomes non linear. The effect of this on systolic and diastolic pressures can be seen by comparing the arterial pressure waves produced (P0 and Pi) by the same stroke volume, using the normal and decreased arterial compliance curves shown in Figure CR.18. Projecting the stroke volume variation on the normal compliance curve produces the pressure signal, P0. Repeating this with the decreased compliance curve gives arterial pressure signal P1. It can be seen that systolic pressure is increased disproportionately compared with diastolic pressure
Age ai disease m
Figure CR.18 Effect of compliance on systolic and diastolic pressures
Figure CR.18 Effect of compliance on systolic and diastolic pressures
• Increased SVR as occurs in chronic hypertension, produces non linearity in the pressure-volume curve like the effects of age on the arterial compliance curve. This produces similar increases in systolic and pulse pressures. Increased SVR increases the time constant slowing the rate of diastolic pressure fall
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