Clinically, invasive measurement of pulmonary vascular flow and pressure provides the hemodynamic status of the pulmonary circulation with pulmonary arterial hypertension (PAH). Current diagnostics and therapeutics for PAH revolve around pulmonary vascular resistance (PVR), which is determined by the mean pressure divided by mean flow [1]. Though PVR correlates well with right ventricular (RV) afterload, failure of which is the primary determinant of mortality [2–4], PVR does not provide the complete measure of RV afterload since it neglects dynamic impedance effects [4, 5]. Although we have shown that impedance predicts clinical outcomes better than PVR alone, several key questions remain about the relationship between hemodynamics and impedance changes in pulmonary hypertension.

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