Pulmonary Vascular Impedance in the Dog
Pulmonary vascular hydraulic input impedance was measured in 13 anesthetized openchest dogs with normal sinus rhythm, and 2 dogs with surgically induced atrioventricular block, by means of electromagnetic flowmeters and strain gauge manometers of known frequency response. The linearity of the pulmonary bed was evaluated by measuring impedance while the heart rate, and hence the pulsatile input to the bed, was varied.
The pulmonary bed behaved as a quasilinear system, within the limits of accuracy of the methods employed and the range of frequencies tested. The use of input impedance, or oscillatory pressure/flow ratio, to describe some characteristics of the bed is therefore justifiable, and analogies with linear models like the simple transmission line are not unreasonable.
The characteristic input impedance averaged 3,094 dyne sec cm-5 kg, or about one-third the magnitude of the pulmonary vascular resistance, and was therefore a significant part of the total opposition that must be overcome in moving blood through the lungs. This impedance to pulsatile flow is not included in calculations of resistance from mean pressure and flow measurements.
The pattern of the impedance spectrum suggested that reflections originating from arteries 1.0 mm and less in diameter play a large role in determining input impedance and its variations with frequency. Pulmonary vasoconstriction by 5-hydroxytryptamine (serotonin) altered the impedance pattern in a manner consistent with increased wave reflection and displacement of the dominant reflecting sites to positions nearer the main pulmonary artery. Capillary compression by increased intra-alveolar pressure also increased reflection, but did not alter the sites of reflection significantly, providing further evidence that the normal impedance pattern and its modification by serotonin are both determined by the characteristics of the arterial part of the bed.
- Accepted October 9, 1964.
- © 1965 American Heart Association, Inc.