The regulation and measurement of plasma volume in heart failure
Paul R. Kalra, MA, MRCP*,*,
Constantinos Anagnostopoulos, MD, PhD, FESC ,
Aidan P. Bolger, BSc, MRCP*,
Andrew J. S. Coats, DM, FACC* and
Stefan D. Anker, MD, PhD*
* Clinical Cardiology, National Heart and Lung Institute, London, United Kingdom
Department of Nuclear Medicine, Royal Brompton Hospital, London, United Kingdom
Department of Cardiology, Franz-Volhard-Klinik (Charité, Campus Berlin-Buch) at Max Delbrück Centrum for Molecular Medicine, Berlin, Germany
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Figure 1 A summary of neurohormonal mechanisms involved in sodium and water (and hence plasma volume) homeostasis. Although the figure separates the sodium and water retaining systems and the opposing natriuretic and diuretic systems, considerable interaction between the individual components occurs. ANP = atrial natriuretic peptide; BNP = brain natriuretic peptide; NO = nitric oxide; PG = vasodilatory prostaglandins.
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Figure 2 Amalgamated data on plasma volume measurements from the studies by Anand et al. (4) and Feigenbaum et al. (42), as assessed by human serum albumin labeled with radioactive iodine and Evans blue dye dilution method, respectively. Plasma volume was similar in both groups of control subjects. There is, however, a marked difference in plasma volume when comparing stable, well-treated patients with chronic heart failure (CHF) and untreated edematous patients in the two studies. This may reflect an increase in plasma volume in the order of 70% during an episode of decompensated heart failure. White bar = control subjects (4); black bar = edematous patients with CHF (4); dotted bar = control subjects (42); diagonal bar = treated patients with CHF (42).
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