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Although knowledge about the pulmonary circulation has advanced substantially, it often remains unclear why one patient behaves differently from another with what appears to be the same degree of pulmonary hypertension. Already in 1628 William Harvey understood the importance of the right ventricle (RV) and its interaction with the pulmonary circulation, emphasising the concept of a ‘unit’. However, over the next 400 years the appreciation of right ventricular-pulmonary arterial (RV-PA) coupling would be neglected and knowledge about RV pathophysiology in pulmonary hypertension lagged behind that of the pulmonary vasculature. It is now recognised that even if pulmonary arterial hypertension (PAH) specific therapies improve or reverse pulmonary vascular pathology, this only leads to clinical improvement if accompanied by a parallel increase in RV function. And yet, many PAH trials have focused only on pulmonary vascular resistance (PVR).
As the RV pushes blood through the pulmonary vasculature, PVR does not adequately account for RV afterload as it ignores the pulsatile nature of the cardiovascular system. The RV ejects blood against an arterial hydraulic load, which can be accurately described by PA input impedance as the relationship between pulsatile pressure and flow. To calculate PA impedance, pressure and flow waves generated by the RV are decomposed into mean values and a series of harmonic (sine) waves at multiples of the heart rate frequency. However, its measurement and quantification are somewhat difficult in vivo both in terms of acquisition and interpretation. Therefore, several simplified models of the arterial circulation have been proposed to characterise impedance more simply. One such a model is the three-element Windkessel …
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