Fig. 14.1
Haemodynamic influences on pulse pressure and mean pressure. From; Koeppen BM, Stanton BA; Berne & Levy Physiology, Updated Edition, 6th Edition; Berne RM et al. Physiology. Philadelphia, PA: Copyright Elsevier (2010), with permission from Elsevier
Pulsatile—i.e. the pulse pressure (difference between systolic and diastolic blood pressure). The principal determinants of pulse pressure are the stroke volume and the stiffness of the large arteries.
Static or ‘steady-state’—represented by the mean arterial pressure. The determinants of the mean arterial pressure are cardiac output and peripheral vascular resistance:
(14.1)
Essential hypertension is characterised by changes in one or more of the haemodynamic determinants of blood pressure. Interestingly, which of these components is responsible for hypertension is strongly influenced by age. In adolescents and young adults (<30 years), the principal haemodynamic disturbance is an increased stroke volume. Peripheral vascular resistance is relatively normal, as is arterial stiffness. The result is that young people tend to present with an elevated pulse pressure—so-called isolated systolic hypertension (high systolic but normal or low diastolic pressure) (Fig. 14.2). Over time, cardiac output falls to normal or subnormal levels, and peripheral vascular resistance rises, probably due to remodelling of small resistance vessels. Consequently, pulse pressure is relatively normal, but mean pressure is elevated, and this gives rise to elevation in systolic and diastolic pressures—so-called ‘mixed’ systolic/diastolic hypertension (Fig. 14.2), which is by far the most common form of hypertension in middle-aged individuals.
Fig. 14.2
Pressure waveforms for typical examples of mixed hypertension and isolated systolic hypertension; compared to normotension. Reproduced with permission from; McEniery CM, Wilkinson IB, Avolio AP; Age, hypertension and arterial function; Clinical and Experimental Pharmacology and Physiology. 2007;34:665–671; reproduced with permission. © 2007 The Authors Journal compilation © 2007 Blackwell Publishing Asia Pty Ltd., with permission from John Wiley and Sons
In older adults (>50 years), isolated systolic hypertension is again the most common form of hypertension, but arterial stiffening is the principal haemodynamic disturbance, causing an exaggerated increase in pulse pressure as the large arteries can no longer effectively buffer the cyclical changes in blood pressure during each cardiac cycle. Indeed, this demonstrates the importance of normal arterial compliance. Table 14.1 summarises the relationship between haemodynamics and hypertension with age.
Table 14.1
summarises the relationship between haemodynamics and hypertension with age
Age | Principal haemodynamic disturbance | Predominant form of hypertension |
|---|---|---|
<30 years | Increased stroke volume | Isolated systolic hypertension |
30–50 years | Increased peripheral resistance | Mixed (systolic/diastolic) hypertension |
>50 years | Increased arterial stiffness | Isolated systolic hypertension |
It is important to understand that systolic pressure is not constant along the arterial tree. Moving from the aorta to the peripheral arteries, where we tend to measure blood pressure, systolic pressure rises by up to 30 mmHg due to increased vessel stiffness and wave reflections. In contrast, diastolic pressure falls by 1–2 mmHg. This difference between aortic and brachial pressure is important because the heart, brain and other major organs are exposed to aortic not brachial pressure, and certain drug therapies exert differential effects on peripheral and central pressure.
14.2 Ageing and Blood Pressure
With increasing age arteries get stiffer. This is illustrated in Fig. 14.3, and this leads to an increase in systolic central blood pressure as shown in Fig. 14.7. Published data on brachial pressure with age is given in Burt et al. (1995) for a USA population (Fig. 14.4). Herbert et al. (2014) present data on change in central pressure with age from data collected worldwide. Data on the change in the rate of hypertension with age for different parts of the world is provided by Kearney et al. (2005). They note lower overall rates (15–27 %) in Eastern and some developing countries. The highest rates were in established market economies (37 %), former socialist economies (37 %) and Latin America and the Caribbean (37 %). Wilkinson and McEniery (2012) noted that some populations have a much lower change of pressure with age identifying a rural community in China (Avolio et al. 1985), and a tribe in Cameroon living a hunter-gatherer lifestyle (Lemogoum et al. 2012) in this context. This leads to the idea that there is stiffening as a natural consequence of ageing and stiffening as a pathological process associated with disease (Wilkinson et al. 2012). This is illustrated in Fig. 14.5. The 2 processes are the following:
Fig. 14.3
Aortic PWV, measured between base of the neck and groin for all subjects (both male and female subjects) between ages 3 and 89 years. Individual values were determined as the average of 10 pairs of pulses simultaneously recorded with identical transcutaneous Doppler transducers. From; Avolio AP, Chen SG, Wang RP, Zhang CL, Li MF, O’Rourke MF; Effects of aging on changing arterial compliance and left ventricular load in a northern Chinese urban community. Circulation. 1983;68:50–58; with permission from Wolters Kluwer Health, Inc.
Fig. 14.4
Mean systolic and diastolic blood pressures by age and race/ethnicity for men and women, US population 18 years of age and older. From; Burt VL, Whelton P, Roccella EJ, Brown C, Cutler JA, Higgins M et al.; Prevalence of hypertension in the US population. Results from the Third National Health and Nutrition Examination Survey. 1988–1991. Hypertension. 1995;25:305-313; © 1995 American Heart Association, Inc., with permission from Wolters Kluwer Health, Inc.
Fig. 14.5
Schema demonstrating pathological versus biological vascular ageing. From; Wilkinson IB, McEniery CM. Arteriosclerosis: inevitable or self-inflicted? Hypertension. 2012;60:3–5; © 2012 American Heart Association, Inc., with permission from Wolters Kluwer Health, Inc.
Biological increase in stiffness with age. The repeated cyclic stress on the elastic fibres in the arterial wall leads to fibre fracture and loss of elasticity (O’Rourke 1990). Cyclic fatigue is commonly seen in engineering where repeated stretching and unstretching of materials many millions of times eventually lead to fracture of the material. In the human over a single decade, the elastic fibres in the artery wall will stretch and unstretch over 300 million times. This effect is also more marked at higher pressures. A measure of the degree of cyclic stretch fatigue is the product of age times pulse pressure times heartrate.
Pathological increase in stiffness with age. Diseases such as diabetes and aspects of Western lifestyle such as high salt intake, along with genetic predisposing factors, lead to biological changes in the vessel wall and increase in stiffness.
Biological and pathological factors form a vicious circle in which there continues to be increase in stiffness and pressure over time (Fig. 14.6) both of which contribute to the formation of atherosclerosis.
Fig. 14.6
The vicious circle of arteriosclerosis. Fatigue fracture of the elastic elements in the aorta leads to elevated systolic pressure and thus increased cyclic stress—setting up a vicious circle. Factors driving blood pressure elevation lead to increased systolic pressure, thereby accelerating the process, as do the factors driving arteriosclerosis. Ultimately, elevated systolic pressure and increased stiffness both lead to cardiovascular disease. From McEniery CM, Wilkinson IB. The pressures of ageing. Hypertension 2013;62:823–824. © 2013 American Heart Association, Inc., with permission from Wolters Kluwer Health, Inc.
14.3 Pressure and Stiffness
Blood pressure is inextricably linked to arterial stiffness, mainly stiffness of the aorta. This section will examine what happens to blood pressure as the stiffness of the aorta increases.
14.3.1 Role of PWV in Determining Pressure
It will be recalled from Chap. 4 that the blood pressure waveform (pressure–time) is a composite of the forward going pressure wave and the reverse going pressure wave. The pressure wave from the heart travels down the aorta and returns after being reflected from the distal arteriolar beds. The time at which the reverse going wave returns is determined by the pressure wave speed (the pulse wave velocity, PWV) in the aorta. The PWV is in turn determined by the stiffness, wall thickness and diameter of the aorta through the Moens–Korteweg equation described in Chap. 4 and reproduced below.
