Effects of Autonomic Nervous System on the Pulse Transit Time-based Blood Pressure Estimation.

摘要

Cardiovascular diseases (CVDs) remain the number one cause of death worldwide. Amongst various risk factors, arterial blood pressure (BP), especially BP measured during nighttime, and BP variability are major indicators of cardiovascular morbidity and mortality.;Most of the state-of-the-art BP meters are designed with an inflatable cuff, which provide snapshots of BP and are uncomfortable during measurements. An alternative cuffless BP measurement approach is therefore studied in this work. The estimation principle is derived based on the fact that velocity of a pressure wave propagating along an artery, i.e., pulse wave velocity (PWV) is related to the pressure-dependent mechanical property of the artery. Thus, BP can be possibly estimated from PWV, or its reciprocal, pulse transit time (PTT), which can be conveniently acquired from electrocardiogram and photoplethysmogram without using an inflatable cuff.;The current PTT-based BP estimation was built on a model that assumes the artery to be a passive, thin-wall and homogeneous tube. However, arterial wall in reality exhibits a specific layered structure and consists of elastin, collagen fibers and smooth muscles. In fact, the PTT-BP relationship was found by many studies to be easily deteriorated by vasoconstriction/dilation, which reflects the vascular smooth muscle (VSM) activation level, i.e., VSM tone. In particular, innervating most blood vessels, the autonomic nervous system (ANS), primarily sympathetic nervous system, plays an important role in determining the arterial mechanical behavior thus PTT-BP relationship via regulating the VSM tone. It is therefore the aim of this thesis to investigate the effects of ANS on the PTT-based BP estimation.;Firstly, a constituent-based PTT-BP model was developed in the thesis, based on the micro-structurally motivated arterial mechanical model and Bramwell-Hill equation. Specifically, analytic PTT-BP relationship incorporating arterial structural and functional properties was deduced. Theoretical effects of various arterial properties on the relationship have been evaluated by simulation. The results revealed that PTT-BP curve will shift to the top right when VSM tone elevates, producing PTT-BP hysteresis.;Next, the mechanism of regulation of BP, PTT as well as heart rate (HR) by ANS was evaluated in 9 normotensive subjects in treadmill exercise by using time-frequency technique. Vagal withdrawal and subsequent sympathetic activity enhancement by exercise have been observed in only HR. In addition, the results indicate a frequency-dependent PTT-BP relationship.;Then we conducted water drinking experiments in a total of 32 healthy subjects to investigate the ANS controlled cardiovascular responses by the act of swallowing. Significant increment in HR and BP, and decrease in PTT were observed during drinking. On the other hand, considering the frequency-dependent nature of PTT-BP relationship, a novel method that estimates baroreflex sensitivity (BRS) from PTT based on the band-specified sequence technique has been proposed. The results showed high correlations between BRS estimated from BP and PTT. (gamma=0.90, 0.70 and 0.81 before, during and after drinking respectively).;Lastly, the effects of ANS mediated VSM tone on the PTT-BP relationship were validated in 46 subjects including 17 patients with CVDs in graded bicycle exercise stress test in supine position. The results demonstrated PTT-BP hysteresis as predicted by the simulation. Furthermore, two novel parameters, i.e., AreaN and DeltaSBP20 were proposed to evaluate the hysteresis phenomenon. Significant attenuation was observed in CVD patients with sympathetic overactivity. The two quantifications were proposed accordingly to be indices for assessing sympathetic function.;To conclude, this work addressed the effects of ANS on the PTT-BP relationship from both theoretical and experimental aspects. The work can help to improve the accuracy of PTT-based BP estimation and CVD control.