title: Pulmonary vascular impedance and wave reflections in the hypoxic calf.
abstract: The alterations in pulsatile hemodynamics that occur during hypoxic pulmonary vasoconstriction have not been well characterized. Changes in oscillatory hemodynamics, however, may affect right ventricular-pulmonary vascular coupling and the dissipation of energy within the lung vasculature. To better define hypoxic pulsatile hemodynamics, we measured main pulmonary artery proximal and distal micromanometric pressures and ultrasonic flow in four open-chest calves during progressive hypoxia. Main pulmonary artery impedance and pressure transmission spectra were calculated using spectral analysis methods. Measured pressure and flow signals were separated in the time domain into forward and backward components. Hypoxia increased pulmonary blood pressure and resistance and produced multiple modifications in the impedance and pressure transmission spectra that indicated increased wave reflections and elasticity. The impedance and apparent phase velocity first-harmonic values were increased in amplitude, and the pressure transmission modulus plot showed an increased peak value. In addition, the impedance modulus plot demonstrated a rightward shift and increased oscillation in the mid- to high-frequency range. The time domain analysis also confirmed increased wave reflections and elasticity. Hypoxia produced large backward-traveling (reflected) pressure and flow waves. The initial portions of these waves arrived at the heart during systole, producing characteristic changes in the measured pressure and flow waveforms. With prolonged hypoxia, main pulmonary artery pulse wave velocity increased by 30%. Thus, hypoxia is associated with complex alterations in pulmonary artery elasticity and wave reflections that act to increase the oscillatory afterload of the right ventricle.
authors.affiliation: Veterans Affairs Medical Center, Denver 80220.
authors.forename: B D
authors.initials: BD
authors.lastname: Zuckerman
authors.forename: E C
authors.initials: EC
authors.lastname: Orton
authors.forename: L P
authors.initials: LP
authors.lastname: Latham
authors.forename: C C
authors.initials: CC
authors.lastname: Barbiere
authors.forename: K R
authors.initials: KR
authors.lastname: Stenmark
authors.forename: J T
authors.initials: JT
authors.lastname: Reeves
mesh_terms: D000818:Animals; D055592:Biophysical Phenomena; D001703:Biophysics; D001794:Blood Pressure / Q000502:physiology; D002417:Cattle; D006976:Hypertension, Pulmonary / Q000503:physiopathology; D000860:Hypoxia / Q000503:physiopathology*; D008297:Male; D011652:Pulmonary Circulation / Q000502:physiology*; D011673:Pulsatile Flow / Q000502:physiology; D014655:Vascular Resistance / Q000502:physiology; D014661:Vasoconstriction / Q000502:physiology