PULMONARY IMPEDANCE AND RIGHT VENTRICULAR-VASCULAR COUPLING IN ENDOTOXIN-SHOCK

Objective: We tested the hypothesis that right heart failure during en dotoxin shock may result from altered ventriculovascular coupling resp onsible for impeding power transfer to the pulmonary circulation Metho ds: The changes in vascular pulmonary input impedance and right ventri cular contractility produced by low-dose endotoxin infusion were studi ed in 6 intact anesthetized dogs. Results: Endotoxin insult resulted i n pulmonary hypertension (from 22 +/- 2 to 33 +/- 3 mmHg) associated w ith significant decreases in stroke volume (from 26.9 +/- 4 to 20.2 +/ - 3 mi) and right ventricular ejection fraction (from 41 +/- 3 to 32 /- 2%). The first minimum of input impedance spectrum and zero phase w ere shifted towards higher frequencies. Input resistance and character istic resistance were dramatically increased. The latter change contri buted to a significant increase in the pulsatile component of total ri ght ventricular power output from 13 to 21%, indicating a reduction in the hydraulic right ventricle power output delivered into the main pu lmonary artery. Overall changes in input pulmonary impedance were indi cative of increased afterload facing the right ventricle leading to de pressed performance. In contrast, right ventricular systolic elastance was simultaneously increased from 0.56 to 0.93 mmHg/ml indicating an increase in right heart contractility. Conclusion: These data suggest that pulmonary hypertension in the setting of experimental endotoxin s hock is accompanied by deleterious changes in the pulmonary impedance spectrum, which are responsible for a mismatch of increased contractil e state of the right ventricle to the varying hydraulic load ultimatel y leading to ventricular-vascular uncoupling. (C) 1998 Elsevier Scienc e B.V. All rights reserved.