European Journal of Heart Failure (2024) POSITION PAPER
doi:10.1002/ejhf.3244
Dietary sodium and fluid intake in heart
failure. A clinical consensus statement of the
Heart Failure Association of the ESC
Wilfried Mullens1,2*, Kevin Damman3, Sebastiaan Dhont1,2, Debasish Banerjee4,
Antoni Bayes-Genis5, Antonio Cannata6, Ovidiu Chioncel7, Maja Cikes8,
Justin Ezekowitz9, Andreas J. Flammer10, Pieter Martens11,1, Alexandre Mebazaa12,
Robert J. Mentz13, Òscar Miró14, Brenda Moura15, Julio Nunez16,
Jozine M. Ter Maaten3, Jeffrey Testani17, Roland van Kimmenade18,
Frederik H. Verbrugge19,20, Marco Metra21, Giuseppe M.C. Rosano22,23,
and Gerasimos Filippatos24*
1 Department of Cardiology, Ziekenhuis Oost-Limburg A.V, Genk, Belgium; 2 Hasselt University, Hasselt, Belgium; 3 University of Groningen, Department of Cardiology, University
Medical Centre Groningen, Groningen, The Netherlands; 4 Renal and Transplantation Unit, St George’s University Hospitals National Health Service Foundation Trust, London,
UK; 5 Heart Institute, Hospital Universitari Germans Trias i Pujol, Universitat Autònoma de Barcelona, CIBERCV, Barcelona, Spain; 6 School of Cardiovascular Medicine and
Sciences, King’s College London, London, UK; 7 Emergency Institute for Cardiovascular Diseases, University of Medicine Carol Davila, Bucharest, Romania; 8 Department of
Cardiovascular Diseases, University of Zagreb School of Medicine & University Hospital Center Zagreb, Zagreb, Croatia; 9 Division of Cardiology, Department of Medicine,
University of Alberta, Edmonton, Alberta, Canada; Canadian VIGOUR Centre, University of Alberta, Edmonton, AB, Canada; 10 Department of Cardiology, University Heart
Center, University Hospital Zurich, Zurich, Switzerland; 11 Department of Cardiovascular Medicine, Heart Vascular and Thoracic Institute, Cleveland Clinic, Cleveland, OH, USA;
12 Université de Paris, MASCOT, INSERM, Paris, France; 13 Duke Clinical Research Institute, Durham, NC, USA; 14 Department of Emergency, Hospital Clínic, ‘Processes and
Pathologies, Emergencies Research Group’ IDIBAPS, University of Barcelona, Barcelona, Spain; 15 Hospital das Forças Armadas and Cintesis - Faculdade de Medicina da
Universidade do Porto, Porto, Portugal; 16 Cardiology Department and Heart Failure Unit, Hospital Clínico Universitario de Valencia, University of Valencia, INCLIVA, Valencia,
Spain; 17 Section of Cardiovascular Medicine, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT, USA; 18 Department of Cardiology, Radboud
University Medical Center, Nijmegen, The Netherlands; 19 Centre for Cardiovascular Diseases, University Hospital Brussels, Jette, Belgium; 20 Faculty of Medicine and Pharmacy,
Vrije Universiteit Brussel, Jette, Belgium; 21 Cardiology, ASST Spedali Civili, and Department of Medical and Surgical Specialties, Radiological Sciences and Public Health, University
of Brescia, Brescia, Italy; 22 Cardiology Clinical Academic Group, Molecular and Clinical Research Institute, St Georges University of London, London, UK; 23 Cardiology,
San Raffaele Cassino, Rome, Italy; and 24 Department of Cardiology, Attikon University Hospital, Athens, Greece
Received 29 February 2024; revised 27 March 2024; accepted 3 April 2024
Sodium and fluid restriction has traditionally been advocated in patients with heart failure (HF) due to their sodium and water avid state.
However, most evidence regarding the altered sodium handling, fluid homeostasis and congestion-related signs and symptoms in patients with
HF originates from untreated patient cohorts and physiological investigations. Recent data challenge the beneficial role of dietary sodium and
fluid restriction in HF. Consequently, the European Society of Cardiology HF guidelines have gradually downgraded these recommendations
over time, now advising for the limitation of salt intake to no more than 5 g/day in patients with HF, while contemplating fluid restriction of
1.5–2 L/day only in selected patients. Therefore, the objective of this clinical consensus statement is to provide advice on fluid and sodium
intake in patients with acute and chronic HF, based on contemporary evidence and expert opinion.
..........................................................................................................
Keywords Heart failure • Sodium • Fluid
*Corresponding authors. Dr Wilfried Mullens, Ziekenhuis Oost-Limburg - Genk, Belgium and Hasselt University, Belgium. Email: wilfried.mullens@zol.be
Dr Gerasimos Filippatos, Department of Cardiology, Attikon University Hospital, Athens, Greece. Email: gfilippatos@gmail.com
© 2024 European Society of Cardiology.
, 18790844, 0, Downloaded from https://onlinelibrary.wiley.com/doi/10.1002/ejhf.3244 by Cochrane Saudi Arabia, Wiley Online Library on [14/05/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
2 W. Mullens et al.
Introduction as an integral part of the digestive process.12 Interestingly, oral
........................................................................................................................................................................
ingestion accounts for only ∼1.5–2 L of water and ∼4 g of Na+ .
Patient education and self-care play a pivotal role in the man- Within an evolutionary framework, humans have adapted to limited
agement of heart failure (HF).1 The 2021 European Society of Na+ availability by developing a highly efficient GI system, respon-
Cardiology (ESC) HF guidelines recommend avoiding excessive sible for the (re)absorption of nearly all available Na+ and water.11
salt intake (>5 g/day) in all patients with HF, irrespective of ejec- The absorption of the majority of nutrients, Na+ included, occurs
tion fraction.2 Additionally, for patients with severe or advanced within the small intestines through different pathways, regulated
HF, restricted fluid intake (<1.5–2 L/day) may be considered to by signal transduction processes affected by neural, paracrine, and
alleviate symptoms.2 These recommendations derive from the endocrine factors.12–14 Serum levels of Na+ and serum osmolal-
pathophysiological changes in the sympathetic nervous system, the ity begin to increase within ∼30 min after oral ingestion.15 This
renin–angiotensin–aldosterone system (RAAS), the vasopressin highly efficient process can in part be attributed to the intricate
axis, and vasodilatory/natriuretic pathways in patients with HF. microstructure of the intestinal villi, which form a plexus, repre-
Collectively, these maladaptive responses to the initial cardiac senting an optimal architectural arrangement for absorption16,17
event or disorder result in increased sodium (Na+ ) and water (Figure 2). Key Na+ transporters at the brush border include
avidity.3 It is important to note that these recommendations are members of the sodium/hydrogen exchange (NHE) family, notably
based on expert consensus and have not been supported by NHE3, as well as the sodium–glucose cotransporter 1 (SGLT1).
adequately powered randomized clinical trials. Moreover, obser- Meanwhile, the distal part of the colon contains epithelial Na+
vational studies indicate that patient adherence to Na+ and fluid channels (ENaC) responsive to mineralocorticoids.18 The individ-
restriction is generally suboptimal, as these restrictions have been ual contribution of the specific Na+ channels to overall Na+ uptake
associated with a poor quality of life as well as elevated plasma can differ in the post-prandial phase (when other nutrients are
renin activity.4–7 Recent data suggest that a more lenient approach available) versus the inter-prandial phase. Water follows passively
to fluid and Na+ intake may not be detrimental, while stringent driven by osmosis.19
restrictions may be harmful in certain conditions.
Circulatory volume
Normal physiology of sodium and Water or fluid homeostasis within the human body is controlled
fluid handling through two principal mechanisms. Initially, the hypothalamic thirst
centre, which promptly triggers the release of vasopressin from
Salt, sodium and fluids the pituitary gland in response to an increase in serum osmolality
Sodium is an essential trace element with a central role in a (carefully sensed by osmoreceptors) and/or a more prominent
wide array of physiological processes within living organisms. decrease in blood pressure (monitored by baroreceptors). Sub-
Approximately 30% of the body’s Na+ content, which amounts to sequently, the RAAS operates to preserve a constant effective
∼92 g, is sequestered within the bone as Na+ apatite and is not circulatory volume, predominantly through the modulation of
fully exchangeable. A further 10% resides within the intracellular Na+ levels. These regulatory processes are vital for preserv-
compartment, while the remaining 60% is dispersed within the ing the stability of the body’s internal environment, responding
extracellular fluid, which includes the plasma and interstitial fluid8,9 quickly to physiological changes to ensure cellular and systemic
(Figure 1). Therefore, Na+ is the dominant extracellular electrolyte equilibrium.
and largely determines serum osmolality and consequently, extra- An increase in serum osmolality by even a small margin, mea-
cellular volume.9 Figure 1 illustrates the Na+ and fluid distribution sured in milliosmoles per L, prompts the kidneys to conserve free
within the human body, a process which is tightly regulated in water. This response is crucial due to the brain’s sensitivity to
response to water and salt intake and aerobic, metabolic water osmotic fluctuations. Notably, the body expels water at a faster
production, as well as (mal)adaptive responses to physiological and rate compared to Na+ . This is because Na+ excretion involves
pathological circumstances. additional physiological processes, as depicted in Figure 3, which
Salt, or sodium chloride (NaCl), constitutes the main dietary outlines the sequence of events following the consumption of 1 L
source of Na+ . The average intake in Western nations is ∼4 g/day, of NaCl 0.9%.20
equivalent to a salt intake of 10 g with 1 g of Na+ corresponding to Splanchnic veins ordinarily store approximately 25% of the total
2.54 g of salt.10,11 To determine the quantity of Na+ in a given mass blood volume, which is essential for maintaining and adapting car-
of salt, it is essential to take into account the atomic mass units diac preload, influenced by neurohormonal pathways (given their
involved in the compound. The calculation involves multiplying the high density of α1 and α2 receptors).21,22 Part of the GI absorbed
total mass of NaCl in grams by the Na+ fraction, which is ∼0.40, serum Na+ and fluids eventually drain from the capillaries into
in order to obtain the Na+ content in grams. the tissues and interstitium, determined by the intricate balance
of oncotic and hydrostatic pressures according to the Starling
principle.23 It has been hypothesized that part of total body Na+ is
Gastrointestinal absorption eventually bound to the negative electrostatic glycosaminoglycan
On a daily basis, the gastrointestinal (GI) tract effectively regulates (GAG) networks in the gel-like interstitium mostly in the skin,
roughly 9 L of fluids and 18 g of Na+ , primarily through secretion bone and cartilage which may acts as a storage reservoir.9 These
© 2024 European Society of Cardiology.
