Document Detail


Apparent paradox of neurohumoral axis inhibition after body fluid volume depletion in patients with chronic congestive heart failure and water retention.
MedLine Citation:
PMID:  7857735     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Hypovolaemia stimulates the sympathoadrenal and renin systems and water retention. It has been proposed that in congestive heart failure reduction of cardiac output and any associated decrease in blood pressure cause underfilling of the arterial compartment, which promotes and perpetuates neurohumoral activation and the retention of fluid. This study examined whether an intravascular volume deficit accounts for patterns that largely exceed the limits of a homoeostatic response, which are sometimes seen in advanced congestive heart failure. METHODS AND RESULTS: In 22 patients with congestive heart failure and water retention the body fluid mass was reduced by ultrafiltration and the neurohumoral reaction was monitored. A Diafilter, which was part of an external venous circuit was regulated to produce 500 ml/hour of ultrafiltrate (mean (SD) 3122 (1199) ml) until right atrial pressure was reduced to 50% of baseline. Haemodynamic variables, plasma renin activity, noradrenaline, and aldosterone were measured before and within 48 hours of ultrafiltration. After ultrafiltration, which produced a 20% reduction of plasma volume and a moderate decrease in cardiac output and blood pressure (consistent with a diminished degree of filling of the arterial compartment), there was an obvious decrease in noradrenaline, plasma renin activity, and aldosterone. In the next 48 hours plasma volume, cardiac output, and blood pressure recovered; the neurohumoral axis was depressed; and there was a striking enhancement of water and sodium excretion with resolution of the peripheral oedema and organ congestion. The neurohumoral changes and haemodynamic changes were not related. There were significant correlations between the neurohumoral changes and increase in urinary output and sodium excretion. CONCLUSIONS: In advanced congestive heart failure arterial underfilling was not the main mechanism for activating the neurohumoral axis and retaining fluid. Because a decrease in circulating hormones was associated with reabsorption of extravascular fluid it is likely that hypoperfusion and/or congestion of organs, such as the kidney and lung, reduce the clearance of circulating noradrenaline and help to keep plasma concentrations of renin and aldosterone raised. A positive feedback loop between fluid retention and plasma hormone concentrations may be responsible for progression of congestive heart failure.
Authors:
M D Guazzi; P Agostoni; B Perego; G Lauri; A Salvioni; F Giraldi; M Matturri; M Guazzi; G Marenzi
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  British heart journal     Volume:  72     ISSN:  0007-0769     ISO Abbreviation:  Br Heart J     Publication Date:  1994 Dec 
Date Detail:
Created Date:  1995-03-21     Completed Date:  1995-03-21     Revised Date:  2010-03-24    
Medline Journal Info:
Nlm Unique ID:  0370634     Medline TA:  Br Heart J     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  534-9     Citation Subset:  AIM; IM    
Affiliation:
Istituto di Cardiologia dell'Universit? degli Studi, Milan, Italy.
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MeSH Terms
Descriptor/Qualifier:
Aged
Aldosterone / blood
Body Fluids / metabolism*
Body Water / metabolism
Feedback
Female
Follow-Up Studies
Heart Failure / metabolism*,  physiopathology
Hematocrit
Hemofiltration*
Humans
Kidney / metabolism
Male
Middle Aged
Neurotransmitter Agents / metabolism*
Norepinephrine / blood
Plasma Volume
Renin / blood
Sodium / metabolism
Stroke Volume
Chemical
Reg. No./Substance:
0/Neurotransmitter Agents; 51-41-2/Norepinephrine; 52-39-1/Aldosterone; 7440-23-5/Sodium; EC 3.4.23.15/Renin
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