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The fundamental physiological disturbance in pulmonary hypertension is an increase in right ventricular (RV) afterload, regardless of disease aetiology. Although a complete description of the arterial afterload can be constructed using complex impedance analysis in the frequency domain, more simple measures are required for clinical use. In general, there are two major factors which modulate the RV afterload, a steady component and a pulsatile component which are often represented by pulmonary vascular resistance (PVR) and pulmonary arterial compliance (PAC), respectively (figure 1). Furthermore, the pulmonary circulation is highly pulsatile and it is estimated that the pulsatile component of the pulmonary arterial load accounts for 25% of RV power, as compared with 10% in a systemic left ventricle–aorta coupled system.1 Thus, it stands to reason that assessment of PAC should be of both physiological and clinical relevance.
Right ventricular afterload consists of pulsatile and steady components which is represented by arterial compliance and resistance, respectively. In the pulmonary circulation, distal vessels may contribute more to total compliance compared with the systemic circulation. In the Windkessel model, RC time (multiple of compliance and resistance) relates to the time constant of diastolic pressure decay. Adapted from Chemla et al.4 PAP, pulmonary artery pressure.
At the systemic level, higher aortic stiffness or its inverse (compliance) is associated with an increased risk of …
Footnotes
Twitter @kearney_kate
Contributors KK and EML wrote and edited this manuscript.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Provenance and peer review Commissioned; internally peer reviewed.
Linked Articles
- Pulmonary vascular disease