Chapter 2 Water, sodium and potassium
Water and sodium homoeostasis
Water and ECF osmolality
Other stimuli affecting vasopressin secretion (Fig. 2.5) include angiotensin II, arterial and venous baroreceptors and volume receptors (which sense blood pressure and volume, respectively). Hypovolaemia and hypotension increase the slope of the vasopressin response to an increase in osmolality (see Fig. 2.4A) and lower the threshold osmolality for vasopressin secretion. The vasopressin response to a fall in blood pressure is exponential: it is relatively small with small decreases in plasma volume, but greater falls cause a massive increase in vasopressin secretion (se Fig. 2.4B). Osmolar controls are overridden, so that ECF volume is defended (by stimulating water retention) at the expense of a decrease in osmolality.
Sodium and ECF volume
Natriuretic peptide hormones also have a role in controlling sodium excretion. Atrial natriuretic peptide (ANP) is a 28 amino acid peptide, one of a family of similar peptides, secreted by the cardiac atria in response to atrial stretch following a rise in atrial pressure (e.g. due to ECF volume expansion). ANP acts both directly by inhibiting distal tubular sodium reabsorption and through decreasing renin (and hence aldosterone) secretion. It also antagonizes the pressor effects of norepinephrine (noradrenaline) and angiotensin II (and thus tends to increase GFR) and has a systemic vasodilatory effect. It appears to provide ‘fine tuning’ of sodium homoeostasis but is probably more important in pathological states than physiologically. Two other structurally similar peptides have been identified: one (brain natriuretic peptide, BNP) is secreted by the cardiac ventricles in response to ventricular stretching and has similar properties to ANP; the other (C-type natriuretic peptide, CNP) is present in high concentrations in vascular endothelium and is a vasodilator. Measurement of BNP is of value in the management of patients with suspected cardiac failure (see Chapter 14). Increased secretion of natriuretic peptides has been postulated to be at least in part responsible for the natriuresis seen in cerebral salt-wasting (see p. 27).
Water and sodium depletion
Sodium depletion
Sodium depletion is seldom due to inadequate oral intake alone, but sometimes inadequate parenteral input is responsible. More often, it is a consequence of excessive sodium loss (Fig. 2.10). Sodium can be lost from the body either isotonically (e.g. in plasma) or hypotonically (e.g. in sweat or dilute urine). In each case, there will be a decrease in ECF volume (see Fig. 2.8), but this will be less if the fluid lost is hypotonic than if it is isotonic, as some of the water loss will be shared with the ICF. The clinical features of sodium depletion (see Fig. 2.10) are primarily a result of the decrease in ECF volume.
The decrease in GFR may lead to pre-renal uraemia (see Case history 4.1). In contrast to the effects of pure water depletion, plasma protein concentration and the haematocrit are usually clearly increased in sodium depletion, unless this is a result of the loss of plasma or blood. Furthermore, because the fluid loss is borne mainly by the ECF, signs of a reduced ECF volume are usually present, and there is a greater risk of peripheral circulatory failure than in water depletion. The features of sodium and water depletion are compared in Figure 2.11.

Figure 2.11 Clinical and laboratory findings in sodium and water depletion. *Unless due to loss of blood.
Water and sodium excess
Water excess
The clinical features of water overload (see Fig. 2.13) are related to cerebral overhydration; their incidence and severity depend upon the extent of the water excess and its time course. Thus, a patient with a plasma sodium concentration of 120 mmol/L, in whom water retention has occurred gradually over several days, may be asymptomatic, while one in whom this is an acute phenomenon may show signs of severe water intoxication. In the short term, the effects of hypotonicity are mitigated to some extent by a movement of ions out of cerebral glial cells; more chronically (days), a decrease in intracellular organic ‘osmolytes’ further reduces intracellular water content (see Fig 2.9A). As is the case with water depletion, this adaptation necessitates a cautious approach to treatment, particularly in chronic water overload. The management of water overload is discussed together with that of hyponatraemia on p. 28.
Sodium excess
Sodium excess can result from increased intake or decreased excretion. The clinical features are related primarily to expansion of ECF volume (Fig. 2.14). When related to excessive intake (e.g. the inappropriate use of hypertonic saline), a rapid shift of water from the intracellular compartment may also cause cerebral dehydration. When sodium overload is due to excessive intake, hypernatraemia is usual (see Case history 2.5).
Laboratory assessment of water and sodium status
• patients with dehydration or excessive fluid loss, as a guide to appropriate replacement
• patients on parenteral fluid replacement who are unable to indicate or respond to thirst (e.g. the comatose, infants and the elderly)
• patients with unexplained confusion, abnormal behaviour or signs of CNS irritability.
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