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Feasibility of Routine Pulmonary Arterial Impedance Measurements in Pulmonary Hypertension: Effects of Pharmacologic Interventions

Feasibility of Routine Pulmonary Arterial Impedance Measurements in Pulmonary Hypertension: Effects of Pharmacologic InterventionsHowever, PVR is known to be insufficient for the evaluation of all the forces that oppose RV ejection, which result from a dynamic interplay among resistance, elastance, and wave reflection. This information is contained in Ppa and flow waves, and can be quantified by a PVZ spectrum calculation. The method provides a measure of hydraulic load by a low-frequency impedance determination (Z1), and by an estimate of compliance and wave reflection using a high-frequency Zc determination, together with the measurement of Fmin and the frequency of phase angle zero crossing. An index of wave RF can be calculated from Z0 and Zc determinations.

In our PAH patients, the major change in the PVZ spectrum was an increase in Z0, or total PVR (that is PVR calculated as Ppa/Q), Z1 was markedly increased, indicating increased hydraulic load, and Zc, Fmin, F0 cross, and RF were increased as well, indicating important increases in arterial elastance and wave reflection. These results look comparable to those of the only reported PVZ determinations in eight patients and two patients, except for higher Z1 and Zc values, which appear to be related to more advanced disease, as assessed by Ppa, PVR, and cardiac output. Similar changes have been reported in patients with severe pulmonary hypertension secondary to mitral stenosis, or in those with advanced left heart failure. We could not consider a direct comparison between Swan-Ganz catheter-derived PVZ spectra and PVZ spectra obtained using high-fidelity, micromanometer-tipped technology because of the prohibitive cost related to single use imposed by the latest European Union regulations.
In our patients, both inhaled NO and IV epopro-stenol not only decreased PVR, but also shifted the entire PVZ spectrum to lower pressure/flow ratios. Both interventions are aimed at the small peripheral resistive arterioles. This is particularly true for NO diffusing from alveolar spaces to adjacent vascular structures, which is inactivated by avid uptake by hemoglobin as soon as it enters the bloodstream.