Water and electrolyte homeostasis during decongestion in heart failure

In heart failure, sodium retention generally occurs out of proportion to water retention and may occur disproportionate to chloride retention, requiring excretion of other cations (i.e. potassium, magnesium, and hydrogen). Renal homeostatic mechanisms keep chloride levels in balance, making it the primary regulator of intravascular tonicity. Excess total body sodium stores and potassium depletion increase the vulnerability to dehydration, especially in the intracellular compartment. With decompensation, extracellular volume expansion with sodium and chloride overload occurs, further enhancing potassium losses. While diuretics are vital to treat fluid overload, they derange important electrolyte and water balances. Diuretic therapies in heart failure produce disproportionate electrolyte‐free water excretion, further exacerbate potassium depletion, and cause chloride losses disproportionate to natriuresis. This can be mitigated by allowing liberal electrolyte‐free water intake, providing aggressive potassium and chloride supplementation, and using upfront proximal diuretics to preserve the chloride balance.