Water, electrolytes and acid–base balance

Chapter 13 Water, electrolytes and acid–base balance

Distribution and composition of body water

In normal, healthy people, the total body water constitutes 50–60% of lean bodyweight in men and 45–50% in women. In a healthy 70 kg male, total body water is approximately 42 L. This is contained in three major compartments:

In addition, small amounts of water are contained in bone, dense connective tissue, and epithelial secretions, such as the digestive secretions and cerebrospinal fluid.

The intracellular and interstitial fluids are separated by the cell membrane; the interstitial fluid and plasma are separated by the capillary wall (Fig. 13.1). In the absence of solute, water molecules move randomly and in equal numbers in either direction across a semi-permeable membrane. However, if solutes are added to one side of the membrane, the intermolecular cohesive forces reduce the activity of the water molecules. As a result, water tends to stay in the solute-containing compartment because there is less free diffusion across the membrane. This ability to hold water in the compartment can be measured as the osmotic pressure.

Osmotic pressure

Osmotic pressure is the primary determinant of the distribution of water among the three major compartments. The concentrations of the major solutes in the compartments differ, each having one solute that is primarily limited to that compartment and therefore determines its osmotic pressure:

Regulation of the plasma volume is somewhat more complicated because of the tendency of the plasma proteins to hold water in the vascular space by an oncotic effect which is, in part, counterbalanced by the hydrostatic pressure in the capillaries that is generated by cardiac contraction (Fig. 13.1). The composition of intracellular and extracellular fluids is shown in Table 13.1.

A characteristic of an osmotically active solute is that it cannot freely leave its compartment. The capillary wall, for example, is relatively impermeable to plasma proteins, and the cell membrane is ‘impermeable’ to Na+ and K+ because the Na+/K+-ATPase pump largely restricts Na+ to the extracellular fluid and K+ to the intracellular fluid. By contrast, Na+ freely crosses the capillary wall and achieves similar concentrations in the interstitium and plasma; as a result, it does not contribute to fluid distribution between these compartments. Similarly, urea crosses both the capillary wall and the cell membrane and is osmotically inactive. Thus, the retention of urea in renal failure does not alter the distribution of the total body water.

A conclusion from these observations is that body Na+ stores are the primary determinant of the extracellular fluid volume. Thus, the extracellular volume – and therefore tissue perfusion – are maintained by appropriate alterations in Na+ excretion. For example, if Na+ intake is increased, the extra Na+ will initially be added to the extracellular fluid. The associated increase in extracellular osmolality will cause water to move out of the cells, leading to extracellular volume expansion. Balance is restored by excretion of the excess Na+ in the urine.

Regulation of extracellular volume (Fig. 13.3)

The extracellular volume is determined by the sodium concentration. The regulation of extracellular volume is dependent upon a tight control of sodium balance, which is exerted by normal kidneys. Renal Na+ excretion varies directly with the effective circulating volume. In a 70 kg man:

The unifying hypothesis of extracellular volume regulation in health and disease proposed by Schrier states that the fullness of the arterial vascular compartment – or the so-called effective arterial blood volume (EABV) – is the primary determinant of renal sodium and water excretion. Thus effective arterial blood volume constitutes effective circulatory volume for the purposes of body fluid homeostasis.

The fullness of the arterial compartment depends upon a normal ratio between cardiac output and peripheral arterial resistance. Thus, diminished EABV is initiated by a fall in cardiac output or a fall in peripheral arterial resistance (an increase in the holding capacity of the arterial vascular tree). When the EABV is expanded, the urinary Na+ excretion is increased and can exceed 100 mmol/L. By contrast, the urine can be rendered virtually free of Na+ in the presence of EABV depletion and normal renal function.

These changes in Na+ excretion can result from alterations both in the filtered load, determined primarily by the glomerular filtration rate (GFR), and in tubular reabsorption, which is affected by multiple factors. In general, it is changes in tubular reabsorption that constitute the main adaptive response to fluctuations in the effective circulating volume. How this occurs can be appreciated from Table 13.2 and Figure 13.4 and Figure 12.2 (see p. 563), which depicts the sites and determinants of segmental Na+ reabsorption. Although the loop of Henle and distal tubules make a major overall contribution to net Na+ handling, transport in these segments primarily varies with the amount of Na+ delivered; that is, reabsorption is flow-dependent. In comparison, the neurohumoral regulation of Na+ reabsorption according to body needs occurs primarily in the proximal tubules and collecting ducts.

Neurohumoral regulation of extracellular volume

This is mediated by volume receptors that sense changes in the EABV rather than alterations in the sodium concentration. These receptors are distributed in both the renal and cardiovascular tissues.

High-pressure arterial receptors (carotid, aortic arch, juxtaglomerular apparatus) predominate over low-pressure volume receptors in volume control in mammals. The low-pressure volume receptors are distributed in thoracic tissues (cardiac atria, right ventricle, thoracic veins, pulmonary vessels) and their role in the volume regulatory system is marginal.

Aldosterone and possibly ANP are responsible for day-to-day variations in Na+ excretion, by their respective ability to augment and diminish Na+ reabsorption in the collecting ducts.

A salt load, for example, leads to an increase in the effective circulatory and extracellular volume, raising both renal perfusion pressure, and atrial and arterial filling pressure. The increase in the renal perfusion pressure reduces the secretion of renin, and subsequently that of angiotensin II and aldosterone (see Fig. 12.5), whereas the rise in atrial and arterial filling pressure increases the release of ANP. These factors combine to reduce Na+ reabsorption in the collecting duct, thereby promoting excretion of excess Na+.

By contrast, in patients on a low Na+ intake or in those who become volume-depleted as a result of vomiting and diarrhoea, the ensuing decrease in effective volume enhances the activity of the renin-angiotensin-aldosterone system and reduces the secretion of ANP. The net effect is enhanced Na+ reabsorption in the collecting ducts, leading to a fall in Na+ excretion. This increases the extracellular volume towards normal.

With more marked hypovolaemia, a decrease in GFR leads to an increase in proximal and thin ascending limb Na+ reabsorption which contributes to Na+ retention. This is brought about by enhanced sympathetic activity acting directly on the kidneys and indirectly by stimulating the secretion of renin/angiotensin II (see Fig. 13.3b) and non-osmotic release of antidiuretic hormone (ADH), also called vasopressin. The pressure natriuresis phenomenon may be the final defence against changes in the effective circulating volume. Marked persistent hypovolaemia leads to systemic hypotension and increased salt and water absorption in the proximal tubules and ascending limb of Henle. This process is partly mediated by changes in renal interstitial hydrostatic pressure and local prostaglandin and nitric oxide production.

Mechanism of impaired escape from actions of aldosterone and resistance to ANP

Not only is the activity of the renin-angiotensin-aldosterone system increased in oedematous conditions such as cardiac failure, hepatic cirrhosis and hypoalbuminaemia, but also the action of aldosterone is more persistent than in normal subjects and patients with Conn’s syndrome, who have increased aldosterone secretion (see p. 989).

In normal subjects, high doses of mineralocorticoids initially increase renal sodium retention so that the extracellular volume is increased by 1.5–2 L. However, renal sodium retention then ceases, sodium balance is re-established, and there is no detectable oedema. This escape from mineralocorticoid-mediated sodium retention explains why oedema is not a characteristic feature of primary hyperaldosteronism (Conn’s syndrome). The escape is dependent on an increase in delivery of sodium to the site of action of aldosterone in the collecting ducts. The increased distal sodium delivery is achieved by high extracellular volume-mediated arterial overfilling. This suppresses sympathetic activity and angiotensin II generation, and increases cardiac release of ANP with resultant increase in renal perfusion pressure and GFR. The net result of these events is reduced sodium absorption in the proximal tubules and increased distal sodium delivery which overwhelms the sodium-retaining actions of aldosterone.

In patients with the above oedematous conditions, e.g. heart failure, escape from the sodium-retaining actions of aldosterone does not occur and therefore they continue to retain sodium in response to aldosterone. Accordingly they have substantial natriuresis when given spironolactone, which blocks mineralocorticoid receptors. Alpha-adrenergic stimulation and elevated angiotensin II increase sodium transport in the proximal tubule, and reduced renal perfusion and GFR further increases sodium absorption from the proximal tubules by presenting less sodium and water in the tubular fluid. Sodium delivery to the distal portion of the nephron, and thus the collecting duct, is reduced. Similarly, increased cardiac ANP release in these conditions requires optimum sodium concentration at the site of its action in the collecting duct for its desired natriuretic effects. Decreased sodium delivery to the collecting duct is therefore the most likely explanation for the persistent aldosterone-mediated sodium retention, absence of escape phenomenon and resistance to natriuretic peptides in these patients (Fig. 13.3b).

Regulation of water excretion

Body water homeostasis is affected by thirst and the urine concentrating and diluting functions of the kidney. These in turn are controlled by intracellular osmoreceptors, principally in the hypothalamus, to some extent by volume receptors in capacitance vessels close to the heart, and via the renin-angiotensin system. Of these, the major and best-understood control is via osmoreceptors. Changes in the plasma Na+ concentration and osmolality are sensed by osmoreceptors that influence both thirst and the release of ADH (vasopressin) from the supraoptic and paraventricular nuclei of the anterior hypothalamus.

ADH plays a central role in urinary concentration by increasing the water permeability of the normally impermeable cortical and medullary collecting ducts. There are three major G-protein coupled receptors for vasopressin (ADH):

Activation of the V1A receptors induces vasoconstriction while V1B receptors appear to mediate the effect of ADH on the pituitary, facilitating the release of ACTH. The V2 receptors mediate the antidiuretic response as well as other functions.

The ability of ADH to increase the urine osmolality is related indirectly to transport in the ascending limb of the loop of Henle, which reabsorbs NaCl without water. This process, which is the primary step in the countercurrent mechanism, has two effects: it makes the tubular fluid dilute and the medullary interstitium concentrated. In the absence of ADH, little water is reabsorbed in the collecting ducts, and a dilute urine is excreted. By contrast, the presence of ADH promotes water reabsorption in the collecting ducts down the favourable osmotic gradient between the tubular fluid and the more concentrated interstitium. As a result, there is an increase in urine osmolality and a decrease in urine volume.

The cortical collecting duct has two cell types (see also p. 597) with very different functions:

The ADH-induced increase in collecting duct water permeability occurs primarily in the principal cells. ADH acts on V2 (vasopressin) receptors located on the basolateral surface of principal cells, resulting in the activation of adenyl cyclase. This leads to protein kinase activation and to preformed cytoplasmic vesicles that contain unique water channels (called aquaporins) moving to and then being inserted into the luminal membrane. Four renal aquaporins have been well characterized and are localized in different areas of the cells of the collecting duct. The water channels span the luminal membrane and permit water movement into the cells down a favourable osmotic gradient (Fig. 13.5). This water is then rapidly returned to the systemic circulation across the basolateral membrane. When the ADH effect has worn off, the water channels aggregate within clathrin-coated pits, from which they are removed from the luminal membrane by endocytosis and returned to the cytoplasm. A defect in any step in this pathway, such as in attachment of ADH to its receptor or the function of the water channel, can cause resistance to the action of ADH and an increase in urine output. This disorder is called nephrogenic diabetes insipidus.

Plasma osmolality

In addition to influencing the rate of water excretion, ADH plays a central role in osmoregulation because its releaseis directly affected by the plasma osmolality. At a plasma osmolality of <275 mosmol/kg, which usually represents a plasma Na+ concentration of <135–137 mmol/L, there is essentially no circulating ADH. As the plasma osmolality rises above this threshold, however, the secretion of ADH increases progressively.

Two simple examples will illustrate the basic mechanisms of osmoregulation, which is so efficient that the plasma Na+ concentration is normally maintained within 1–2% of its baseline value.

Osmoregulation versus volume regulation

A common misconception is that regulation of the plasma Na+ concentration is closely correlated with the regulation of Na+ excretion. However, it is related to volume regulation, which has different sensors and effectors (volume receptors) from those involved in water balance and osmoregulation (osmoreceptors).

The roles of these two pathways should be considered separately when evaluating patients.

In some cases, both volume and osmolality are altered and both pathways are activated. For example, if a person with normal renal function eats salted potato chips and peanuts without drinking any water, the excess Na+ will increase the plasma osmolality, leading to osmotic water movement out of the cells and increased extracellular volume. The rise in osmolality will stimulate both ADH release and thirst (the main reason why many restaurants and bars supply free salted foods), whereas the hypervolaemia will enhance the secretion of ANP and suppress that of aldosterone. The net effect is increased excretion of Na+ without water.

This principle of separate volume and osmoregulatory pathways is also evident in the syndrome of inappropriate ADH secretion (SIADH). Patients with SIADH (see p. 993) have impaired water excretion and hyponatraemia (dilutional) caused by the persistent presence of ADH. However, the release of ANP and aldosterone is not impaired and, thus, Na+ handling remains intact. These findings have implications for the correction of the hyponatraemia in this setting which initially requires restriction of water intake.

ADH is also secreted by non-osmotic stimuli such as stress (e.g. surgery, trauma), markedly reduced effective circulatory volume (e.g. cardiac failure, hepatic cirrhosis), psychiatric disturbance and nausea, irrespective of plasma osmolality. This is mediated by the effects of sympathetic overactivity on supraoptic and paraventricular nuclei. In addition to water retention, ADH release in these conditions promotes vasoconstriction owing to the activation of V1A (vasopressin) receptors distributed in the vascular smooth muscle cells.

Increased extracellular volume

Increased extracellular volume occurs in numerous disease states. The physical signs depend on the distribution of excess volume and on whether the increase is local or systemic. According to Starling principles, distribution depends on:

Depending on these factors, fluid accumulation may result in expansion of interstitial volume, blood volume or both.


Extracellular volume expansion is due to sodium chloride retention. Increased oral salt intake does not normally cause volume expansion because of rapid homeostatic mechanisms which increase salt excretion. However, a rapid intravenous infusion of a large volume of saline will cause volume expansion. Most causes of extracellular volume expansion are associated with renal sodium chloride retention.

Nephrotic syndrome

Interstitial oedema is a common clinical finding with hypoalbuminaemia, particularly in the nephrotic syndrome. Expansion of the interstitial compartment is secondary to the accumulation of sodium in the extracellular compartment. This is due to an imbalance between oral (or parenteral) sodium intake and urinary sodium output, as well as alterations of fluid transfer across capillary walls. The intrarenal site of sodium retention is the cortical collecting duct (CCD) where Na+/K+-ATPase expression and activity are increased threefold along the basolateral surface (Fig. 13.4). In addition, amiloride-sensitive epithelial sodium channel activity is also increased in the CCD. The renal sodium retention should normally be counterbalanced by increased secretion of sodium in the inner medullary collecting duct, brought about by the release of ANP. This regulatory pathway is altered in patients with nephrotic syndrome by enhanced kidney specific catabolism of cyclic GMP (the second messenger for ANP) following phosphodiesterase activation.

Oedema generation was classically attributed to the decrease in the plasma oncotic pressure and the subsequent increase in the transcapillary oncotic gradient. However, the oncotic pressure and transcapillary oncotic gradient remain unchanged and the transcapillary hydrostatic pressure gradient is not altered. Conversely, capillary hydraulic conductivity (a measure of permeability) is increased. This is determined by intercellular macromolecular complexes between the endothelial cells consisting of tight junctions (made of occludins, claudins and ZO proteins) and adherens junctions (made of cadherin, catenins and actin cytoskeleton). Elevated TNF-α levels in nephrotic syndrome activate protein kinase C, which changes phosphorylation of occludin and capillary permeability. In addition, increased circulating ANP can increase capillary hydraulic conductivity by altering the permeability of intercellular junctional complexes. Furthermore, reduction in effective circulatory volume and the consequent fall in cardiac output and arterial filling can lead to a chain of events as in cardiac failure and cirrhosis (see above and Fig. 13.3). These factors result in extracellular volume expansion and oedema formation.

Sodium retention

A decreased GFR decreases the renal capacity to excrete sodium. This may be acute, as in the acute nephritic syndrome (see p. 582), or may occur as part of the presentation of chronic kidney disease. In end-stage renal failure, extracellular volume is controlled by the balance between salt intake and its removal by dialysis.

Numerous drugs cause renal sodium retention, particularly in patients whose renal function is already impaired:

Substantial amounts of sodium and water may accumulate in the body without clinically obvious oedema or evidence of raised venous pressure. In particular, several litres may accumulate in the pleural space or as ascites; these spaces are then referred to as ‘third spaces’. Bone may also act as a ‘sink’ for sodium and water.


The underlying cause should be treated where possible. Heart failure, for example, should be treated, and offending drugs such as NSAIDs withdrawn.

Sodium restriction has only a limited role, but is useful in patients who are resistant to diuretics. Sodium intake can easily be reduced to approximately 100 mmol (2 g) daily; reductions below this are often difficult to achieve without affecting the palatability of food.

Manoeuvres that increase venous return (e.g. strict bed rest or water immersion) stimulate salt and water excretion by effects on cardiac output and ANP release, but they are seldom of practical value.

The mainstay of treatment is the use of diuretic agents, which increase sodium, chloride and water excretion in the kidney (Table 13.3). These agents act by interfering with membrane ion pumps which are present on numerous cell types; they mostly achieve specificity for the kidney by being secreted into the proximal tubule, resulting in much higher concentrations in the tubular fluid than in other parts of the body.

Clinical use of diuretics

Loop diuretics

These potent diuretics are useful in the treatment of any cause of systemic extracellular volume overload. They stimulate excretion of both sodium chloride and water by blocking the sodium-potassium-2-chloride (NKCC2) channel in the thick ascending limb of Henle (Fig. 13.6) and are useful in stimulating water excretion in states of relative water overload. They also act by causing increased venous capacitance, resulting in rapid clinical improvement in patients with left ventricular failure, preceding the diuresis. Unwanted effects include:


Figure 13.6 Transport mechanisms in the thick ascending limb of the loop of Henle. Sodium chloride is reabsorbed in the thick ascending limb by the bumetanide-sensitive sodium-potassium-2-chloride cotransporter (NKCC2). The electroneutral transporter is driven by the low intracellular sodium and chloride concentrations generated by the Na+/K+-ATPase and the kidney-specific basolateral chloride channel (ClC-Kb). The availability of luminal potassium is rate-limiting for NKCC2, and recycling of potassium through the ATP-regulated potassium channel (ROMK – renal outer medulla K+ channel) ensures the efficient functioning of the NKCC2 and generates a lumen-positive transepithelial potential. Genetic studies have identified putative loss of function mutations in the genes encoding NKCC2 1, ROMK 2, ClC-Kb 3, and barttin 4 in subgroups of patients with Bartter’s syndrome. In contrast to the normal condition, loss of function of NKCC2 impairs reabsorption of sodium and potassium. Inactivation of the basolateral ClC-Kb and barttin reduces transcellular reabsorption of chloride. Loss of function of any of these will reduce the transepithelial potential and thus decrease the driving force for the paracellular reabsorption of cations (K+, Mg2+, Ca2+ and Na+). Paracellin-1 is necessary for the paracellular transport of Ca2+ and Mg2+. In most patients with Bartter’s syndrome, urinary calcium excretion is increased. Hypercalcaemia or increased activation of calcium-sensing receptor inactivates ROMK and causes Bartter’s syndrome. Ka and Kb, kidney-specific basolateral chloride channel. ROMK, renal outer medullary potassium channel.

There is little to choose between the drugs in this class. Bumetanide has a better oral bioavailability than furosemide, particularly in patients with severe peripheral oedema, and has more beneficial effects than furosemide on venous capacitance in left ventricular failure.

Thiazide diuretics (see p. 719)

These are less potent than loop diuretics. They act by blocking a sodium chloride channel in the distal convoluted tubule (Fig. 13.7). They cause relatively more urate retention, glucose intolerance and hypokalaemia than loop diuretics. They interfere with water excretion and may cause hyponatraemia, particularly if combined with amiloride or triamterene. This effect is clinically useful in diabetes insipidus. Thiazides reduce peripheral vascular resistance by mechanisms that are not completely understood but do not appear to depend on their diuretic action, and are widely used in the treatment of essential hypertension. They are also used extensively in mild to moderate cardiac failure. Thiazides reduce calcium excretion. This effect is useful in patients with idiopathic hypercalciuria, but may cause hypercalcaemia. Numerous agents are available, with varying half-lives but little else to choose between them. Metolazone is not dependent for its action on glomerular filtration, and therefore retains its potency in renal impairment.

Resistance to diuretics

Resistance may occur as a result of:

Management. Intravenous administration of diuretics may establish a diuresis. High doses of loop diuretics are required to achieve adequate concentrations in the tubule if GFR is depressed. However, the daily dose of furosemide must be limited to a maximum of 2 g for an adult, because of ototoxicity. Intravenous albumin solutions restore plasma oncotic pressure temporarily in the nephrotic syndrome and allow mobilization of oedema but do not increase the natriuretic effect of loop diuretics.

Combinations of various classes of diuretics are extremely helpful in patients with resistant oedema. A loop diuretic plus a thiazide inhibit two major sites of sodium reabsorption; this effect may be further potentiated by addition of a potassium-sparing agent. Metolazone in combination with a loop diuretic is particularly useful in refractory congestive cardiac failure, because its action is less dependent on glomerular filtration. However, this potent combination can cause severe electrolyte imbalance. Both aminophylline and dopamine increase renal blood flow and may be useful in refractory cardiogenic sodium retention. In addition, theophyllines, by inhibiting phosphodiesterase activity in the inner medullary collecting duct, prolong the action of cyclic GMP (a second messenger of ANP).

Decreased extracellular volume

Deficiency of sodium and water causes shrinkage both of the interstitial space and of the blood volume and may have profound effects on organ function.

Clinical features

Symptoms. Thirst, muscle cramps, nausea and vomiting, and postural dizziness occur. Severe depletion of circulating volume causes hypotension and impairs cerebral perfusion, causing confusion and eventual coma.

Signs can be divided into those due to loss of interstitial fluid and those due to loss of circulating volume.

Loss of more than this causes the following:


The overriding principle is to replace what is missing.

Loss of water and electrolytes

Loss of water and electrolytes, as occurs with vomiting, diarrhoea, or excessive renal losses, should be treated by replacement of the loss. If possible, this should be with oral water and sodium salts. These are available as slow sodium (600 mg, approximately 10 mmol each of Na+ and Cl per tablet), the usual dose of which is 6–12 tablets/day with 2–3 L of water. It is used in mild or chronic salt and water depletion, such as that associated with renal salt wasting.

Sodium bicarbonate (500 mg, 6 mmol each of Na+ and HCO3 per tablet) is used in doses of 6–12 tablets/day with 2–3 L of water. This is used in milder chronic sodium depletion with acidosis (e.g. chronic kidney disease, post-obstructive renal failure, renal tubular acidosis). Sodium bicarbonate is less effective than sodium chloride in causing positive sodium balance. Oral rehydration solutions are described in Box 4.10.

Intravenous fluids are sometimes required (Table 13.6). Rapid infusion (e.g. 1000 mL per hour or even faster) is necessary if there is hypotension and evidence of impaired organ perfusion (e.g. oliguria, confusion); in these situations, plasma expanders (colloids) are often used in the first instance to restore an adequate circulating volume (see p. 887). Repeated clinical assessments are vital in this situation, usually complemented by frequent measurements of central venous pressure (see p. 872, for the management of shock). Severe hypovolaemia induces venoconstriction, which maintains venous return; over-rapid correction does not give time for this to reverse, resulting in signs of circulatory overload (e.g. pulmonary oedema) even if a total body extracellular fluid (ECF) deficit remains. In less severe ECF depletion (such as in a patient with postural hypotension complicating acute tubular necrosis), the fluid should be replaced at a rate of 1000 mL every 4–6 h, again with repeated clinical assessment. If all that is required is avoidance of fluid depletion during surgery, 1–2 L can be given over 24 h, remembering that surgery is a stimulus to sodium and water retention and that over-replacement may be as dangerous as under-replacement. Regular monitoring by fluid balance charts, bodyweight and plasma biochemistry is mandatory.

Disorders of sodium concentration

These are best thought of as disorders of body water content. As discussed above, sodium content is regulated by volume receptors; water content is adjusted to maintain, in health, a normal osmolality and (in the absence of abnormal osmotically active solutes) a normal sodium concentration. Disturbances of sodium concentration are caused by disturbances of water balance.


Hyponatraemia (Na <135 mmol/L) is a common biochemical abnormality. The causes depend on the associated changes in extracellular volume:

Table 13.7 Causes of hyponatraemia with decreased extracellular volume (hypovolaemia)

Extrarenal (urinary sodium <20 mmol/L) Kidney (urinary sodium >20 mmol/L)

Table 13.8 Causes of hyponatraemia with normal extracellular volume (euvolaemia)

Table 13.9 Causes of hyponatraemia with increased extracellular volume (hypervolaemia)

Heart failure

Oliguric kidney injury

Liver failure


Rarely, hyponatraemia may be a ‘pseudo-hyponatraemia’. This occurs in hyperlipidaemia (either high cholesterol or high triglyceride) or hyperproteinaemia where there is a spuriously low measured sodium concentration, the sodium being confined to the aqueous phase but having its concentration expressed in terms of the total volume of plasma. In this situation, plasma osmolality is normal and therefore treatment of ‘hyponatraemia’ is unnecessary. Note: Artefactual ‘hyponatraemia’, caused by taking blood from the limb into which fluid of low sodium concentration is being infused, should be excluded.

Hyponatraemia with hypovolaemia

This is due to salt loss in excess of water loss; the causes are listed in Table 13.7. In this situation, ADH secretion is initially suppressed (via the hypothalamic osmoreceptors); but as fluid volume is lost, volume receptors override the osmoreceptors and stimulate both thirst and the release of ADH. This is an attempt by the body to defend circulating volume at the expense of osmolality.

With extrarenal losses and normal kidneys, the urinary excretion of sodium falls in response to the volume depletion, as does water excretion, leading to concentrated urine containing <10 mmol/L of sodium. However, in salt-wasting kidney disease, renal compensation cannot occur and the only physiological protection is increased water intake in response to thirst.

Mar 31, 2017 | Posted by in GENERAL & FAMILY MEDICINE | Comments Off on Water, electrolytes and acid–base balance
Premium Wordpress Themes by UFO Themes
%d bloggers like this: