Key result
Viscoelasticity, rather than pure elasticity, is a key factor in interpreting terminal aortic impedance, with resonance frequency increasing from 2.4 to 10 Hz with increasing pressure.
Viscoelasticity, rather than pure elasticity, is a key factor in interpreting terminal aortic impedance and its relationship to resonance in the arterial circulation.
Emphasizes viscoelastic modeling for aortic impedance; leaves open human validation and clinical translation.
We used an inertance-viscoelastic windkessel model (IVW) to interpret aortic impedance patterns as seen in the terminal aortic circulation of the dog, and to explain evident oscillatory phenomena in flow measurements. This IVW model consists of an inertance, L, connected in series with a viscoelastic windkessel (VW) where the peripheral resistance, Rp, is connected in parallel with a Voigt cell (a resistor, Rd, in series with a capacitor, C) to account for viscoelasticity. Pressure and flow measurements were taken from the terminal aorta, just downstream of the origin of renal arteries, in three anaesthetised open-chest dogs, under a variety of haemodynamic conditions induced by administering a vasoconstrictor agent (methoxamine) and a vasodilator (sodium nitroprusside). Mean pressure ranged from 40 to 140 mm Hg. The resistance Rp was calculated as the ratio of mean pressure to mean flow. Parameters L, C and Rd were estimated by fitting measured to model predicted flow waves. We found that prominent oscillations observed in flow waves, from midsystole to diastole, are related to resonance that occurs at a frequency, f(o), where reactance of inertance of blood motion matches the reactance of arterial compliance. Estimates of f(o) increased from 2.4 to 10 Hz with increasing pressure and showed a correlation with values of static elastic moduli plotted against mean pressure of dogs' peripheral arteries previously reported by others. Viscous losses, Rd, of arterial wall motion limited the amplitude of resonance peak. We conclude that viscoelasticity, rather than pure elasticity, is a key issue to interpret terminal aortic impedance as it relates to resonance.
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Burattini et al. (1999) studied Terminal aortic circulation hemodynamics (n=3). Hemodynamic modulation (methoxamine and sodium nitroprusside) was evaluated on Resonance frequency (f(o)) and viscoelastic parameters. Viscoelasticity, rather than pure elasticity, is a key factor in interpreting terminal aortic impedance, with resonance frequency increasing from 2.4 to 10 Hz with increasing pressure.
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