The Japanese Journal of Thoracic Diseases
Pulmonary Vascular Input Impedance Analysis in Experimental Miliary Pulmonary Embolism
To elucidate the hemodynamic characteristics of acute pulmonary hypertension due to miliary embolism, pulmonary vascular input impedance was computed by means of Fourier analysis of individual pressure and flow wave in dogs. Seven healthy dogs weighting 8.5-17.5 (mean 11.8) kg were anesthetized with sodium pentobarbital (25mg/kg), and thoracotomy was performed at the left 5th intercostal space under artificial ventilation. A properly fitted electromagnetic flow transducer was placed around the
... ulmonary trunk and a micro-tip pressure transducer (pc-350) was set in the pulmonary artery near the flow transducer. A femoral vein was exposed, and doses of 0.3-0.6ml(50mg/ml) of lycopodium spore suspension was given repeatedly as needed. The degree of pulmonary circulatory disturbance was graded on the basis of the ratio of peak pulmonary arterial to peak aortic pressure. This ratio was used to assess relative pressure overload of the right ventricle, that is, in the control group less than 0.25, mild group 0.25-0.40, and moderate group greater than 0.40. Afour component lumped analog model for the pulmonary vascular bed, R1-L-C-R2, was employed, which consisted of a resistance R1 equal to the characteristic impedance in the proximal pulmonary aftery, a fluid inertia L combined in series, parallel combination of a peripheral resistance R2 and a lumped compliance C. These parameters of an analog model were calculated by the computer by the method of least squares from the pattern in pulmonary vascular impedance. In the mild and moderate group, pulmonary vascular input impedance was changed with an elevation of pulmonary areterial pressure compared with the control group. From the above-mentioned model simulation, R2 increased while C decreased markedly, according to the grade of pulmonary hypertension. The characteristic impedance, as estimated by averaging impedance spectrum at 7-11Hz, was unchanged. In this state, however, frequency at which the first input impedance showed minimum value shifted to a higher frequency. Considering this hemodynamic mechanism, in acute pulmonary hypertension due to miliary embolism, the peripheral resistance increased remarkably and the compliance of the proximal pulmonary artery decreased. It appeared that the proximal pulmonary artery responded to induced pulmonary hypertension with an increase of its radius and cross-sectional area. In conclusion, it is possible to estimate local alterations in the pulmonary vascular bed by means of pulmonary vascular impedance analysis in pulmonary hypertension and it is very reasonable that the energy output of the right heart is more precisely expressed in terms of pulmonary vascular input impedance than pulmonary vascular reslstance.