Apparent paradox ofneurohumoral axis inhibition after bodyfluid volumedepletion in patients withchronic congestive heart failure and waterretention

Background-Hypovolaemia stimulates thesympathoadrenal andreninsystems andwaterretention. Ithasbeenproposed thatincongestive heartfailure reduction ofcardiacoutputand anyassociated decrease inbloodpressure causeunderfilling ofthearterial compartment, which promotes andperpetuates neurohumoral activation andtheretention offluid. This studyexamined whether anintravascular volumedeficit accounts forpatterns that largely exceed thelimits ofahomoeostatic response, whicharesometimes seenin advanced congestive heartfailure. MethodsandResults-In 22patients with congestive heartfailure andwaterretentionthebodyfluid masswasreducedby ultraffitration and the neurohumoral reaction was monitored. A Diafilter, whichwaspartofan external venous circuit was regulated toproduce500 ml/hour ofultrafiltrate (mean(SD)3122 (1199) ml)until right atrial pressure was reducedto 50% ofbaseline. Haemodynamic variables, plasmareninactivity, noradrenaline, and aldosterone were measuredbefore andwithin 48hoursof ultrafiltration. After ultraflitration, whichproduceda 20% reduction of