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Cardiovascular Research 1983 17(2):113-121; doi:10.1093/cvr/17.2.113
© 1983 by European Society of Cardiology
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Copyright © 1983, European Society of Cardiology

Intravascular and extravascular pulmonary fluid volumes. III Response to sustained left atrial hypertension

ROBERT A SLUTSKY* and CHARLES B HIGGINS

From the Department of Radiology and Medicine (Cardiology), San Diego Veterans Administration Medical Center, and the University of California, San Diego, California

* Address for reprint requests: Robert A Slutsky, MD. San Diego VA Medical Center (114), 3350 La Jolla Village Drive, San Diego, California 92161, USA.

The response of intravascular (PBV) and extravascular (EVLW) pulmonary fluid volumes was examined using double indicator techniques (thermal-green dye) in five open-chest anaesthetised dogs during the production of sustained left atrial (LA) hypertension by LA balloon. Left atrial pressure was abruptly increased from 0.16±0.15 to 3.96±0.51 kPa (1.2±1.1 to 29.8±3.8 mmHg) (P<.001) and maintained at that level for 120 min.

Data were obtained prior to pressure elevation, immediately upon pressure elevation, and then every 30 min for a total of 2 h. PBV increased initially (209.7±78.2 to 377.5±92.1 cm3. P<0.01 but subsequently slowly declined (294.6±103.5 at 120 min P<0.05 vs peak value). Alternatively, EVLW increased slowly at first (260.6±77.9 to 291.3 ± 71.5 cm3), but more rapidly as time progressed (714.6±68.5 cm3 at 120 min P<.001 vs control or initial level). As EVLW rose and time passed after elevation of left atrial pressure, pulmonary vascular resistance (PVR) increased. In each animal, the relationship between the EVLW and PVR was linear (excluding the control point) with r values ≥0.91. With the initial increase in left atrial pressure, cardiac output (CO) declined (2.09±0.51 to 1.67±0.60 litre·min–1). As time passed, CO continued to decline in association with increases in EVLW and PVR.

Thus, we conclude that with sustained LA hypertension there ensues an early rise in PA followed by increases in EVLW. The rise in EVLW has a direct linear relationship with the subsequent elevation of PVR suggesting that accumulation of EVLW is at least in part responsible for the change in PVR occuring in response to pulmonary venous hypertension.


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