Pressure waveforms measured at different locations in the cardiovascular system present a very similar diastolic decay. Previous work has shown the cardiovascular system can be modelled as a Windkessel and wave system. This concept has been extended to any arbitrary location in the cardiovascular system. We suggest that it is possible to calculate a time-varying reservoir pressure P(t) and a distance- and time-varying wave pressure p(x, t) by fitting an exponential function to the diastolic decay of the measured pressure P; defining that the measured pressure P(x, t) = P(t)+p(x, t). Velocity waveforms U can also be separated into its reservoir, U , and wave, u,components as U(x, t) = U (x, t) + u(x, t).In this study we explore the implications of applying are servoir-wave separation and wave intensity analysis techniques to understand the haemodynamics of in-vivo, noninvasive measurements of P and U in the carotid arteries of normal human subjects. Wave intensity analysis reveals a particular wave pattern where reflections can be estimated easily, but foremost, it shows that reflections are a lot smaller than previously thought.We suggest through the use of this model that the heart is the main wave generator of the cardiovascular system. The arterial system instead of impeding the flow, it stores it and distributes it throughout the arteries towards the tissue during diastole. There are some wave reflections, mainly during systole,that contribute to the changes in the pressure and velocity waveforms, however, they are small and are more evident as the measurements get further away from the ascending aorta.The application of wave intensity analysis to non-invasively measured data can provide a good insight on the physiology and the local and global properties of the cardiovascular system in health and disease in the clinical setting. This study shows preliminary results and the potential of the technique for analysing non-invasive measures, and could be particularly useful to understand and quantify the effects of therapeutic drugs in the cardiovascular system.