Key result
PaCO2 changes do not alter pulmonary arterial input impedance despite increasing PVR during hypercapnia.
Why the study?
The effects of changes in PaCO2 on pulmonary arterial input impedance and right ventricular load were not fully characterized.
In a goat model, changes in PaCO2 altered pulmonary vascular resistance and right ventricular work without significantly modifying pulmonary arterial input impedance.
Answers are grounded in this paper and cite their sources.
Goat model data on PaCO2 and impedance should not change practice; leaves open translation to human pulmonary hemodynamics.
Pulmonary arterial input impedance spectra were computed in goats in whom the appropriate pressure and flow transducers had been chronically implanted. In response to either hypocapnia or hypercapnia, under anesthesia (1% halothane in a 70% nitrous oxide--30% oxygen mixture) there were no significant modifications of impedance at zero frequency; no consistent or significant changes in the impedance moduli at frequencies between 2 and 14 Hz were observed; the position of the first impedance minimum or the subsequent maximum was not modified; however, pulmonary vascular resistance increased significantly with hypercapnia. Although the load opposing right ventricular ejection was not modified by variation of Paco2, right ventricular work was reduced in response to hypocapnia and augmented in response to hypercapnia.
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Foëx et al. (1975) studied this question. Changes in PaCO2 (hypocapnia or hypercapnia) was evaluated on Pulmonary arterial input impedance spectra and right ventricular work. Changes in PaCO2 did not significantly modify pulmonary arterial input impedance, although pulmonary vascular resistance increased with hypercapnia and right ventricular work varied with PaCO2.
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