Determination of left ventricular end-systolic pressure-volume relationships by the conductance (volume) catheter technique.

DA Kass, T Yamazaki, D Burkhoff, WL Maughan… - Circulation, 1986 - Am Heart Assoc
DA Kass, T Yamazaki, D Burkhoff, WL Maughan, K Sagawa
Circulation, 1986Am Heart Assoc
Using a multielectrode conductance catheter to estimate continuous left ventricular volume
we determined the end-systolic pressure-volume relationship (ESPVR) in situ in open-chest
anesthetized dogs. Dogs (n= 8) were studied in the control state and after pharmacologic
sympathectomy (hexamethonium) and surgical vagotomy both before and after the
administration of dobutamine. ESPVR was measured during brief (5 to 6 sec) preload
reduction by balloon occlusion of the inferior vena cava (IVCBO). The relationship was …
Using a multielectrode conductance catheter to estimate continuous left ventricular volume we determined the end-systolic pressure-volume relationship (ESPVR) in situ in open-chest anesthetized dogs. Dogs (n = 8) were studied in the control state and after pharmacologic sympathectomy (hexamethonium) and surgical vagotomy both before and after the administration of dobutamine. ESPVR was measured during brief (5 to 6 sec) preload reduction by balloon occlusion of the inferior vena cava (IVCBO). The relationship was highly reproducible. The slope (Ecs) and volume intercept (Vo) (mean +/- SD) in the control series were 5.8 +/- 3.6 mm Hg/ml and 6.5 +/- 12.5 ml, respectively. Upon release of the IVCBO (preload recovery), Ecs was 7.7 +/- 3.6 mm Hg/ml and Vo was 12.4 +/- 9.6 ml (p less than .01). Autonomic blockade produced a 50% reduction in Ecs and a concomitant decrease in Vo (p less than .01), and eliminated the difference between ESPVR generated by preload reduction (IVCBO) and preload recovery (IVCBO release). Subsequent dobutamine infusion increased Ecs to 6.1 +/- 3.5 mm Hg/ml and Vo to 4.1 +/- 6.9 ml, consistent with reported changes of the ESPVR with positive inotropic intervention. A small artifact of right ventricular filling was observed in the left ventricular volume catheter signal, but this did not appreciably alter the ESPVR. These results demonstrate the feasibility of the determination of ESPVR in situ by the conductance catheter and brief IVCBO and underline the importance of the use of rapid load changes to minimize reflex activation during the measurements.
Am Heart Assoc