C

Compliance; resistance Resistance exchange

Fig. 1. Oversimplified description of the macro- and microcirculation. A semiquantitative evaluation of the extent of endothelium and medial layer function is indicated from + to +++ [1-4].

as an elastic reservoir (Windkessel function), and (3), following the systolic ejection of blood on the aortic wall, a shock wave acutely develops, resulting in the rapid propagation of this wave along the arterial tree. Only points 2 and 3 of this description are detailed in this paragraph.

At the end of ventricular ejection, the pressure in the aorta falls much more slowly than in the left ventricle because the large central arteries, and particularly the aorta, are elastic, and thus act as a reservoir during systole, storing part of the ejected blood, which is then forced out into the peripheral vessels, during diastole. More specifically, the pulsatile load is borne primarily by elastic-containing central arteries, which fulfill the bulk of the cushioning function by expanding during systole to store some, but not all, of each stroke volume, and then contracting during diastole to facilitate peripheral run-off of the stored blood. The cushioning function thus supports diastolic blood flow to peripheral tissues.

Then the pressure pulse generated by ventricular contraction travels along the aorta as a wave (fig. 2). It is possible to calculate the velocity of this wave (i.e., pulse wave velocity, PWV) from the delay between two BP curves located at two different sites of the arterial tree. Of course, the distance between measuring sites should be known. An example is given in figure 3. Because a fundamental principle is that pulse waves travel faster in stiffer arteries, the measurement of PWV is considered the best surrogate to evaluate arterial stiffness (fig. 3). Aortic PWV determines how quickly a disturbance of the arterial wall is moved away from the heart (up to 2 m/s with exercise). It approximates 35 m/s in young persons at rest, but increases considerably with age. Given that

Fig. 2. The BP curve propagates along the arterial tree at a given velocity (PWV: see text). Note that, from central to peripheral arteries, SBP increases markedly while DBP is slightly reduced, and MAP (corresponding to the cross-sectional area under the BP curve) remains unmodified. With age, this amplification phenomenon, which is mainly due to wave reflections, tends to disappear [1-3].

Fig. 2. The BP curve propagates along the arterial tree at a given velocity (PWV: see text). Note that, from central to peripheral arteries, SBP increases markedly while DBP is slightly reduced, and MAP (corresponding to the cross-sectional area under the BP curve) remains unmodified. With age, this amplification phenomenon, which is mainly due to wave reflections, tends to disappear [1-3].

peripheral arteries are markedly stiffer than central arteries, an important limitation of PWV measurements is the presence of a large heterogeneity of the arterial wall at its different sites.

BP Propagation and Amplification [2]

When several simultaneous BP measurements are done at different points all along the aorta, it appears that the pressure wave changes shape as it travels down the aorta. Whereas the systolic blood pressure (SBP) actually increases with distance from the heart, the mean level of the arterial pressure (MAP) slightly falls (about 4 mm Hg) during the same course along the length of the aorta (fig. 2). Thus the amplitude of the pressure oscillation between systole and diastole, which is pulse pressure (PP), nearly doubles (fig. 2). The SBP and PP amplification along the vascular tree is a physiological finding, which approximates 14 mm Hg between the origin of the thoracic aorta and the brachial artery, and continues in the branches of the aorta out to the level of about the third generation of branches. Thereafter, both PP and MAP decrease rapidly to the levels found in the microcirculation, a territory in which a nearly steady flow is achieved (fig. 4).

Fig. 3. Non-invasive determination ofPWV between the carotid artery and the terminal aorta (i.e., the origin of femoral artery). The measured distance is L. If AT represents the time delay between the feet of the two waves, PWV equals L/AT. Distensibility may be then deduced from the Bramwell and Hill formula [1-3]. Automatic PWV measurements are widely used nowadays [1-3].

Fig. 3. Non-invasive determination ofPWV between the carotid artery and the terminal aorta (i.e., the origin of femoral artery). The measured distance is L. If AT represents the time delay between the feet of the two waves, PWV equals L/AT. Distensibility may be then deduced from the Bramwell and Hill formula [1-3]. Automatic PWV measurements are widely used nowadays [1-3].

Transition from the Macro- to the Microcirculation [2]

Whereas the macrocirculation is characterized by pulsatile flow as well as by the propagation of pressure wave, PWV and PP amplification, the microcirculation is influenced by steady flow, and therefore by Poiseuille's law. At the arteriolar level, the pressure gradient becomes proportional to the rate of flow, the viscosity of blood, and the length of the arteriolar tree, and mostly is inversely proportional to the fourth power of vascular diameter.

In order to optimize the capillary exchanges, a low hydrostatic pressure profile is physiologically achieved in the microvascular network (fig. 4). The general consensus is that the resulting BP decrease occurs predominantly in precapillary vessels ranging from 10 to 300 ^m [1-3]. Conversely, averyhigh vascular resistance (which represents, according to Poiseuille's law, the mechanical forces that are opposed to flow) builds up abruptly from larger to smaller arteries and capillaries, over a transitional short length of the path between arteries and veins, thus causing a steep decrease in MAP (fig. 4). At the same time, the PP amplitude decreases, resulting in almost completely steady flow through resistance vessels. However, a further contribution to opposition

Fig. 4. Transition from the macrocirculation (large arteries) to the microcirculation (arterioles-capillaries). The decrease in BP along the vascular bed is represented under normal BP conditions (a), during arterial hypertensive without vasomotor adaptation (b), and after adaptation to the arterioles resulting in enhanced peripheral resistance but normal capillary pressure (c). During the same traject, the pulsatility disappears [1-3].

Fig. 4. Transition from the macrocirculation (large arteries) to the microcirculation (arterioles-capillaries). The decrease in BP along the vascular bed is represented under normal BP conditions (a), during arterial hypertensive without vasomotor adaptation (b), and after adaptation to the arterioles resulting in enhanced peripheral resistance but normal capillary pressure (c). During the same traject, the pulsatility disappears [1-3].

to flow is also derived from the reflection of arterial pulsations that cannot enter the high resistance vessels and are summated with pressure waves approaching the area of high resistance [1, 2], This area of reflection, which is directly related to the number and geometrical properties of arteriolar bifurcations [1], contributes greatly to the hemodynamic profile of BP within large arteries (fig. 2).

Pulse Wave Morphology and Analysis (fig. 5)

If, in an individual, body length is 2 m at most and aortic PWV approximates 5 m/s, something must happen to the shape of the BP curve within the one beat if heart rate is 60/min. What happens is generation of wave reflections and their summation with the incident wave, as summarized in figure 5A and B. The incident wave passes away from the heart along the highly conductive arteries. There is a mismatch of impedance at the junction of a highly conductive artery and high resistance arterioles. So the wave cannot enter the arterioles and is repelled, traveling backward towards the heart. The morphology of any pulse wave results from the summation of incident (forward-traveling) and reflected (backward-traveling) pressure waves (fig. 5 ) . Reflected waves may be initiated from any discontinuity of the arterial or arteriolar wall, but are mainly issued from high resistance vessels [2]. Pulse wave propagation and

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