3.3. Pulse wave velocity and autonomic regulation

3.3.1. Pulse wave velocity

The pressure pulse travels much faster than the blood itself, as was mentioned in chapter 3.1. PWV describes how quickly a blood pressure pulse travels from one point to another in the human body. The time difference between these two locations is known as the pulse transit time (PTT). PWV is typically measured between the carotid and the femoral artery. Atherosclerosis causes the arterial wall to become thicker and harder and narrows the arterial lumen (Ross 1999). The increased inflexibility of the arterial wall serves to increase PWV, because the energy of the blood pressure pulse cannot be stored in an inflexible wall. PWV can be used as an index of arterial distensibility (Asmar et al. 1995). In recent years, a number of papers have been published on the diagnosis of cardiovascular diseases and mortality risk prediction (Blacher et al. 1999, Laurent et al. 2001, van Popele et al. 2001, Safar et al. 1998). In terms of medical diagnosis, PWV is a highly interesting subject, because it provides an estimate of the condition of the cardiovascular system based on a large area of the human body.

Self-mixing interferometry has several advantages in PWV measurements. Firstly, it can also be used for pulse detection from underlying tissue. Secondly, the radial distensibility of the examined artery can be measured and thus it can be used to evaluate the arterial compliance according to the Bramwell-Hill equation.

Arterial elasticity (compliance) is determined as the ratio of change in volume to change in pressure, C = ΔV/ΔP. Alternatively volume can be replaced by the cross sectional area, ΔA (Pythoud et al. 1994). The elastic and geometric properties of the arterial tree also determine how fast a pressure pulse travels through the cardiovascular system. PWV can be expressed by the Bramwell-Hill equation (McDonald 1974)

Equation 28.

where ρ_b is the density of blood and A is the cross-sectional area of the arterial lumen in diastole. This relation enables the study of compliance by measuring the PWV. In addition, PWV can be formalised by the Moens-Korteweg equation (McDonald 1974)

Equation 29.

where E is the elastic modulus, h_v is the thickness of the arterial wall and r_vi is the internal radius of the artery.

3.3.2. Autonomic regulation

The human body is controlled by a host of regulation mechanisms, which, in turn, serve as major indicators of its condition. The actions of the mechanisms, particularly that of the autonomic nervous system, are reflected in rhythmical variations in the blood pressure shown in Fig. 13. The autonomic nervous system is closely connected with other regulatory systems, including the neuroendocrine and energy balance systems (Laitinen 2000). Malfunctions in autonomic cardiovascular regulation may result in cardiovascular diseases, including orthostatic intolerance, hypertension, coronary heart disease, cardiac dysrhythmia and heart failure (Bannister et al. 1992). Especially older people and diabetics show an increased mortality rate caused by these diseases (Tsuji et al. 1994, Ewing et al. 1980). The risk of sudden arrhythmic death is clearly increased in people with diminished vagal heart rate control after acute myocardial infarction (Hartikainen et al. 1996). The complex behaviour of the baroreflex system poses a problem owing to its strongly nonlinear components. So, to improve their understanding of the cardiovascular system, researchers use various mathematical models to describe it (Madwed et al. 1989, Ursino et al. 1994, Ursino 1999).

The cardiovascular regulation system comprises baroreflex regulation, whose main function is to maintain normal arterial pressure despite large alterations in physical stress. The central autonomic network controls baroreflex regulation via baroreceptors, which are mainly located in the aortic arch and the carotid sinus region. Baroreceptors measure the stretch caused by blood pressure against the arterial wall and pass their response to the centre of the autonomic network. As a result, the activity of the heart and blood vessels is either increased or decreased, depending on the response of the baroreceptors. Increased sympathetic outflow increases baroreflex regulation, whereas the exclusion of the sympathetic or parasympathetic outflow decreases it (Guyton & Hall 1998).

Other autonomic regulation mechanisms include thermoregulation and respiratory sinus arrhythmia (RSA), which, together with baroreflex regulation, affect heart rate variability. These three mechanisms can be detected from RR intervals. Thermoregulation (VLF component) operates at very low frequencies below 0.04 Hz, while baroreflex regulation is the low-frequency component (LF component), as it is located within the frequency range of 0.04 to 0.15 Hz. Finally, the frequency range between 0.15 and 0.4 Hz is known as the high-frequency component (HF-component). The effects of RSA can be found within this frequency band, depending on respiratory frequency. These spectral estimates are also recommendations of the Task Force of the European Society of Cardiology and the North American Society of Pacing and Electrophysiology (ESC/NASPE Task Force 1996). Table 2 summarises the spectral estimates of the different regulation mechanisms calculated from the RR interval.

Cardiovascular regulation mechanisms are normally studied by counting the RR intervals in the electrocardiogram (ECG). The rationale of the approach used in this thesis is that baroreflex-induced blood pressure changes in the artery affect the elastic properties of the arterial wall. The elastic properties of the wall, in turn, influence its movement. Thus, the effects of the baroreflex can be measured by measuring the movement of the arterial wall.