SALT AND WATER BALANCE IN CONGESTIVE HEART FAILURE
Authors: Dyckner Thomas , Wester Per‐Olov 
Published: August 2010

Abstract The majority of symptoms related to congestive heart failure (CHF) can be derived from the excessive accumulation of fluid in the body. The retention of fluid is the result of the activation of a complex system of compensatory mechanisms working on the kidneys and altering the hemodynamic situation in the body. The compensatory mechanisms are essentially the same as those activated in acute blood loss. The common denominator for CHF and acute blood loss is a decrease of the effective arterial blood volume (EABV), a parameter defined as blood volume in relation to vascular capacity.

In the early stages of CHF there is an increased sympathoadrenergic tone, leading to a peripheral vasoconstriction and a decrease of blood flow to the kidneys. Due to a preferential constriction of the efferent arterioles, the filtration fraction is increased and the glomerular filtration rate remains unchanged. However, there is an increased colloid osmotic pressure and a decreased intravascular hydrostatic pressure in the peritubular capillaries. These alterations result in an increased reabsorption of sodium and water in the kidneys. Furthermore, the blood flow in the kidneys is rerouted from the cortical to the juxtamedullary nephrons, which have larger glomeruli and longer loops of Henle. This will further increase the retention of salt and water.

The renin‐angiotensin‐aldosterone (R‐A‐A) system is also activated due to the decrease of EABV. Angiotensin II exerts about the same effects as norepinephrine–vasoconstriction, rerouting of blood within the kidney and preferential vasoconstriction of the efferent arterioles–all changes contributing to the retention of salt and water. Angiotensin II also increases the aldosterone levels. Aldosterone is one of the main factors in the evolution of edema. This hormone increases the absorption of sodium from the distal tubules in exchange for hydrogen and potassium. In the early stages of CHF these mechanisms seem adequate and often succeed in helping the damaged myocardium to keep the EABV within tolerable limits. This is accomplished at the price of an increased extracellular volume and a raised total body sodium content.

If the mechanisms succeed, there is a deactivation of the compensatory mechanisms, the hormone levels returning to about normal, since there is no “error signal”. Later on, when the myocardial inadequacy has progressed, the compensatory mechanisms are once again recruited, and excessively so, since the “error signal” persists due to the inability of the diseased myocardium to respond. There is a decreased baroreceptor sensitivity, promoting the release of arginine vasopressin (AVP). The secretion of AVP leads to further accumulation of fluid and to a potentiation of the vasoconstrictor effects of norepinephrine and angiotensin II. At this stage the effect of the compensatory mechanisms seems rather negative to the organism, resulting in a further burden for the already weakened myocardium. The outcome is an excessive retention of sodium and water and the development of massive edemas.