• Assess volume status (p. 368). Hyponatraemia with a normal, decreased or increased extracellular volume has different causes and different therapy (Fig. 11.2).

Fig. 11.2 Diagnosis and causes of hyponatraemia.

•Treating hyponatraemia with encephalopathy, see Chapter 20, Emergencies in medicine, p. 711

• A serum Na⁺ rise of 5 mmol/L will almost always control seizures.

• Transfer to the HDU and ensure regular clinical review.

• Document neurology regularly.

• Repeat Na⁺ after 2 hours and then 4-hourly.

• If acute: aim to increase Na⁺ by 2 mmol/L/hour or until asymptomatic.

• If chronic: aim to increase Na⁺ by 0.5 mmol/L/hour or until asymptomatic.

• Never correct by > 10 mmol/L/24 hours. CPM often takes a few days to develop; it causes a spastic para-/quadriparesis and mental disturbances, and can lead to death. MRI is useful in diagnosis.

• Calculation:

• For practical purposes total body water can be calculated as 50% of weight in kg.

• 3% NaCl (hypertonic saline) contains 1 mmol NaCl per 2 mL (513 mmol in 1 L). Acute and chronic hyponatraemia require different hourly correction rates (see above)

For example, a 50 kg woman has a serum sodium of 115 mmol/L. She requires 10 mmol to correct to 125 mmol/L. Thus, 10 × half of the body (i.e. 25) = 250. Thus, she requires 250 mmol of 3% NaCl, which is 500 mL. This should be given slowly over 4–6 hours via a central vein.

Hyponatraemia with a decreased extracellular volume

A decreased volume stimulates thirst and vasopressin release, which in turn inhibits water excretion. Losses from the kidney occur in tubulointerstitial disease, the recovery phase of acute tubular necrosis, unilateral renal artery stenosis, excessive use of diuretics, adrenocortical insufficiency and osmotic diuresis (e.g. hyperglycaemia, severe uraemia). Losses from the gastrointestinal tract are due to vomiting, diarrhoea, naso-gastric suction and haemorrhage (Table 11.2). Losses can also occur from the skin (burns), pericarditis and peritonitis.

• Management. The underlying diagnosis is usually apparent. Urinary Na⁺ will be very low (< 10 mmol/L) unless the sodium loss is renal in origin. Replace salt and water with oral rehydration fluid (p. 59) or IV 0.9% NaCl. If the patient is encephalopathic (depressed level of consciousness, fitting), hypertonic 3% sodium chloride is given slowly as above.

Table 11.2 Average concentrations and potential daily losses of water and electrolytes from the gut

Hyponatraemia with an increased extracellular volume

In this situation there is evidence of volume overload with a decreased circulatory volume, e.g. oedema. This leads to a reduced glomerular filtration rate with avid reabsorption of sodium from the proximal tubule. This in turn leads to a reduced delivery of chloride to the diluting ascending loop of Henle. There is thus an inability to excrete dilute urine.

• Causes include heart failure, liver cirrhosis and the nephrotic syndrome, in which there is evidence of fluid overload that exceeds the increase in sodium so that a dilutional hyponatraemia occurs.

• Management

• Fluid is restricted to < 1 L intake per day.

• A loop diuretic such as furosemide 20–40 mg IV 8-hourly leads to a diuresis of water in excess of salt.

• In encephalopathy (depressed level of consciousness, fitting), hypertonic 3% sodium chloride is given slowly as above.

• V₂ antagonists, e.g. tolvaptan, are now being used.

Hypernatraemia

Defined as a serum Na⁺ > 145 mmol/L, hypernatraemia is almost always due to a water deficit. As osmolality increases, water leaves cells, including the cells in the brain. The brain compensates over time by retaining organic solutes, increasing cellular tonicity and so reducing water loss into the hyperosmolar ECF. Sudden correction may lead to a rapid gain of water with intracranial expansion of the brain and tentorial herniation. Symptoms and signs include thirst, weakness and confusion progressing to coma and fits.

Causes

Water deficit is due to the following:

• Renal water loss as seen in diabetes insipidus (DI), either pituitary (failure of ADH secretion) or nephrogenic (failure of response to ADH), or due to an osmotic diuresis.

• Pituitary DI occurs from pituitary tumours, infections, infiltration, post-surgical, post-radiotherapy, trauma or vascular causes.

• Nephrogenic DI is due to renal tubular acidosis, hypokalaemia, hypercalciuria, drugs — lithium or glibenclamide (glyburide) — or sickle cell disease. Osmotic diuresis is seen with a diabetic hyperosmolar state.

• Non-renal water loss as seen in diarrhoea and also with increased insensible losses through the skin or lungs.

• Excessive administration of sodium when hypertonic sodium solutions are used (e.g. 8.4% sodium bicarbonate after cardiac arrest), excess of 0.9% saline, particularly if accompanied by renal loss (diabetic ketoacidosis) or ingestion of drugs with high sodium content, e.g. piperacillin.

Hypernatraemia is accompanied by increased plasma osmolality, which is a potent stimulus to thirst, and hypernatraemia does not occur unless thirst is impaired or water unavailable.

Investigations

• Simultaneous urine and plasma osmolality and sodium measurement is carried out.

• A water deprivation test is used in DI; the administration of desmopressin will correct pituitary DI but not nephrogenic DI.

Management

Always treat underlying cause.

• Acute hypernatraemia (< 24 hours’ duration, usually due to hypertonic IV solutions) is safe to correct quickly. Aim to lower the Na⁺ by 1 mmol/L/hour, checking Na⁺ after 2 hours then 4-hourly, and re-assess your patient regularly.

• Chronic hypernatraemia (> 24 hours) should be corrected slowly to avoid cerebral oedema.

• Fully assess and document neurological status.

• Aim to lower Na⁺ by not more than 1 mmol/L every 2 hours, or < 10 mmol/L/day; correct 50% of the water deficit in the first 12–24 hours and the remaining water deficit over next 24–48 hours.

• Check serum Na⁺ after 2 hours then 4-hourly.

• Calculate water deficit (include ongoing losses!).

• Calculate TBW (p. 368):

So, in a 50 kg female with a serum Na⁺ of 155 mmol/L:

Include ongoing losses in the deficit (allow 1 L insensible losses/day).

• The fall in N⁺ per litre of correction fluid = ([Na⁺] in fluid − plasma [Na⁺])/TBW + 1. Administer an appropriate volume of replacement fluid for the desired drop in [Na⁺] per hour/day. Replacement fluid is either 0.18% saline with 4% glucose or 5% glucose alone. K⁺ must be added as required.

Potassium

Most of the total body K⁺ (about 3500 mmol) is intracellular, with only 2% (or 70 mmol) in the extracellular space. Total body K⁺ is kept in strict balance; dietary intake amounts to about 100 mmol/day, with 90 mmol/day lost in the urine (and the rest in stool). This gives a normal range for serum K⁺ of 3.5–5.5 mmol/L; this is, however, a poor indicator of total body potassium.

Abrupt changes in K⁺ can be life-threatening, so a number of compensatory mechanisms exist to maintain serum K⁺ within the normal range.

• Extracellular K⁺ can be ‘shifted’ rapidly into or out of cells. Trans-membrane Na⁺/K⁺-ATPases pump K⁺ into cells (and Na⁺ out) under the influence of insulin or β₂ receptor stimulation by catecholamines. By moving K⁺ into cells, transient hyperkalaemia can be accommodated, even though total body K⁺ is unchanged.

• Total body K⁺ is controlled by modifying urinary losses (which can vary from < 10 mmol/day to > 200 mmol/day).

• Fine control of urinary K⁺ secretion is regulated mainly by aldosterone (but also by high tubular sodium delivery and pH). Aldosterone acts in the distal nephron to promote Na⁺ retention and K⁺ losses (hyperkalaemia stimulates aldosterone release). With a well-maintained urine output, renal K⁺ losses can be profound, correcting a raised total body K⁺ within days. The kidney is less efficient in response to hypokalaemia; although aldosterone secretion is suppressed, hypovolaemia will override this mechanism (to conserve Na⁺).

History and examination

These may suggest an underlying cause. Always take a full drug history and review the drug chart.

Investigations

Repeat any abnormal serum K⁺. Check Na⁺, renal function, bicarbonate, glucose, serum Mg²⁺, urinary K⁺ and thyroid function if hypokalaemic. Do an ECG to exclude cardiac toxicity. Monitor urine output and re-measure serum K⁺ repeatedly to assess response to therapy.

Hyperkalaemia

Always exclude spurious hyperkalaemia — usually due to haemolysis after phlebotomy, particularly with abnormal cells. Hyperkalaemia is a relative state; patients with longstanding renal impairment can tolerate K⁺ of up to 7 mmol/L, while those accustomed to low–normal K⁺ may develop dangerous arrhythmias if K⁺ is about 6.0. It is never safe to ignore a K⁺ > 6.5 mmol/L.

Causes

Causes of hyperkalaemia are decreased excretion due to renal failure and drugs, e.g. amiloride, triamterene, spironolactone, NSAIDs, ACE inhibitors and ciclosporin, increased release of K⁺ from cells, diabetic ketoacidosis, rhabdomyolysis, digoxin poisoning, tumour lysis and increased extraneous load of oral potassium chloride, salt substitutes or transfusion of stored blood.

Clinical features

Cardiotoxicity is the most serious effect and an ECG is performed. Muscle weakness occurs due to partial depolarization of the cell membrane impairing membrane excitability. This produces weakness and a flaccid paralysis. Respiratory muscle involvement can cause hypoventilation and metabolic acidosis occurs due to impaired acid excretion, as hyperkalaemia inhibits both the synthesis of ammonia in the proximal convoluted tubule and reabsorption in the loop of Henle.

Management (See Emergencies in medicine p. 711)

• Re-check K⁺ and stop all K⁺-sparing drugs.

• Check the ECG for electrical signs of hyperkalaemia; tall, tented T waves progress to P wave loss and a prolonged PR interval, then widening of the QRS complex to ventricular fibrillation (Fig. 11.3).

• Protect the heart: calcium (10 mL 10% calcium gluconate or 5 mL 10% calcium chloride) given as a slow IV bolus over 5 minutes usually normalizes cardiac membrane excitability, preventing or reversing arrhythmias. Its effect only lasts 15 minutes but the dose can be repeated.

• Shift K⁺ into cells: 10 U short-acting insulin in 50 mL of 50% glucose will activate trans-membrane Na⁺/K⁺-ATPase, lowering serum K⁺ by 1 mmol/L for about 4 hours. This can be repeated, if need be. Monitor capillary blood glucose.

• Encourage a good urine output if possible (often not if underlying kidney disease): keep well hydrated with 0.9% saline, and give furosemide 20–40 mg oral/IV as a potassium-wasting diuretic. Aim for urine output > 2 L/day.

• Other agents

Fig. 11.3 Progressive ECG changes with increasing hyperkalaemia.

• β₂ agonists such as salbutamol will also pump K⁺ into cells (by activating trans-membrane Na⁺/K⁺-ATPase), but are not additive to insulin and glucose; they may provoke cardiac instability and arrhythmias.

• Sodium bicarbonate corrects acidosis, with the net effect of driving K⁺ into cells. This may help in severe acidosis (pH < 7.2), but causes hypocalcaemia (in turn arrhythmogenic) and gives a large salt load.

• K⁺-binding resins exchange luminal K⁺ for resin-bound calcium in the gut. They are slow to have an action (24 hours) and cause constipation (limiting a route of K⁺ excretion).

• Haemodialysis will rapidly control resistant hyperkalaemia within 20–30 minutes.

Hypokalaemia

Causes

• Increased renal excretion is the commonest cause of hypokalaemia, usually due to the use of diuretics, both thiazides and loop diuretics. Increased aldosterone secretion, either primary (Conn’s syndrome) or secondary to ECF depletion, cardiac failure, hepatic cirrhosis or the nephrotic syndrome, causes increased sodium reabsorption in the collecting ducts and K⁺ loss. Type 1 distal renal tubular acidosis and, in the diuretic phase following renal damage or obstruction, hypokalaemia occur.

• Reduced intake, particularly if associated with vomiting or severe diarrhoea, with loss of potassium via the gastrointestinal tract, causes hypokalaemia.

• Redistribution into cells decreases serum K⁺ without affecting total body K⁺. This occurs with insulin therapy for ketoacidosis or following β-adrenergic stimulus.

Clinical features

Hypokalaemia of > 3 mmol/L is usually well tolerated. Symptoms, predominantly apathy, myalgia and weakness, are all due to a neuromuscular disturbance. It can progress to life-threatening cardiac arrhythmias if K⁺ < 2.5 mmol/L. Eventually an areflexic paralysis may also occur. A spot urinary K⁺ will rapidly differentiate renal losses from extra-renal losses (when urinary K⁺ < 20 mmol/L). Patients prescribed digoxin or other anti-arrhythmics are at particular risk of arrhythmias from hypokalaemia.

Diagnosis

The causes of hypokalaemia can usually be found in the history but urine K⁺ is helpful, as well as an assessment of acid–base balance.

Management of asymptomatic or mild hypokalaemia (K > 2.5 mmol/L)

• Stop diuretics if prescribed, or change to a potassium-sparing diuretic.

• Start oral potassium chloride (KCl) supplements as 1–3 g 3 times daily (limited by gastrointestinal tolerability). It is always safer to give orally than intravenously, which is only used in severe hypokalaemia.

• Re-check K⁺ within 1 week, and more frequently if renal impairment is present.

Management of symptomatic or life-threatening hypokalaemia (K < 2.5 mmol/L)

• Check the ECG for electrical signs of hypokalaemia (Fig. 11.3): small T waves, the presence of a U wave (after the T wave) and an increasing PR interval (poor correlation with serum K⁺ levels).

• Check magnesium, and if low, correct (p. 379).

• Add 20–40 mmol KCl to 1 L 0.9% saline and infuse at 20 mmol KCl/hour.

Magnesium

Magnesium contributes to all energy (ATP)-requiring reactions, as well as cell membrane function, nerve conduction and muscle contraction. Plasma Mg²⁺ is tightly controlled by the kidney (modifying urinary losses) within a normal range of 0.75–1.1 mmol/L (1.5–2.2 mEq/L).

History and examination

These may suggest an underlying cause. Always take a full drug history and review the drug chart. Check K⁺, Ca²⁺, Na⁺ and renal function. Obtain an ECG to exclude cardiac toxicity.

Hypomagnesaemia

This is common in undernourished hospitalized patients. Hypomagnesaemia presents with the symptoms of hypokalaemia and hypocalcaemia, both of which occur as a result of a low plasma Mg²⁺.

Clinical features

Irritability, tremor, ataxia, hyper-reflexia, confusion and fits may be present.

Causes

Causes are decreased absorption; increased renal excretion, e.g. drugs (diuretics); and gut losses, e.g. excessive purgation, diarrhoea, prolonged naso-gastric suction or acute pancreatitis.

Management

Withdraw any causal agents. ECG evidence of hypomagnesaemia includes prolonged PR interval, broad flattened T waves and a widening QRS complex leading to fatal ventricular arrhythmias. Oral magnesium is poorly absorbed and tolerated. Even mild hypomagnesaemia (> 0.4 mmol/L) should be treated with IV magnesium sulphate (20–60 mmol/day in 0.9% saline). Acute or severe hypomagnesaemia is associated with torsades de pointes (p. 409). Give 2–4 mL 50% magnesium sulphate as a bolus.

Hypermagnesaemia

Hypermagnesaemia only usually occurs in patients with impaired renal function (unable to excrete Mg²⁺) given magnesium (usually as an enema). It presents as neuromuscular depression (depressed reflexes, respiratory weakness and bradyarrhythmias).

Management

Discontinuing Mg²⁺ (if urine output is well maintained) will usually safely lower levels. Giving 10 mL 10% calcium gluconate antagonizes magnesium’s cardiotoxic effect. Haemodialysis rapidly corrects severe hypermagnesaemic toxicity.

Phosphate

Phosphate is essential to almost all biochemical systems, and its control is closely linked to that of calcium. Active vitamin D₃ increases dietary phosphorus absorption, with most (80%) total body phosphate (the inorganic fraction of phosphorus) found in the skeleton. Sodium–phosphate co-transporters in the kidney retain phosphate (depending on oral phosphorus intake) for a normal plasma range of 0.8–1.4 mmol/L (3.0–4.5 mg/dL) (higher in children). Parathyroid hormone and phosphatonins inhibit renal reabsorption to encourage phosphate wasting in response to a rising plasma phosphate.

Check Ca²⁺, Na⁺, K⁺, renal function and bicarbonate, glucose and parathormone levels.

Hypophosphataemia

Phosphate depletion is common in the critically ill, often presenting with symptoms as limited reserves are redistributed to provide energy or synthesize protein in response to treatment. Acutely, symptoms include respiratory and proximal muscle weakness, ileus and cardiac depression. Spontaneous muscle breakdown and acute confusion may follow. Prolonged hypophosphataemia leads to osteomalacia.

Causes

Causes include decreased intake and intestinal absorption, e.g. dietary factors, vomiting, malabsorption and alcohol withdrawal. Renal losses occur with renal tubular defects and with diarrhoea. Redistribution into cells (similar to K⁺) is probably the major cause in hospital and is seen in the treatment of diabetic ketoacidosis, in refeeding after malnutrition and in respiratory alkalosis. It is also seen after parathyroidectomy.

Management

• Mild hypophosphataemia (> 0.5 mmol/L) rarely needs treating. Generally, increase dietary phosphorus (or phosphate in total parenteral nutrition (TPN)). Oral phosphate supplements are poorly tolerated (diarrhoea) but may be useful in chronic depletion.

• Symptomatic hypophosphataemia should be treated with IV phosphate at no more than 9 mmol/12 hours in TPN or 5% glucose.

• Phosphate infusion may precipitate hypocalcaemia — check Ca²⁺ repeatedly.

Hyperphosphataemia

Chronic hyperphosphataemia leads to vascular and soft tissue calcification, as the [calcium × phosphate] product exceeds the limit of solubility.

Causes

The cause is usually renal failure but hyperphosphataemia is also seen in hypoparathyroidism, tumour lysis syndrome and rhabdomyolysis, or after excess phosphate administration.

Management

• Acute hyperphosphataemia rarely needs treating (rhabdomyolysis, tumour lysis).

• Chronic hyperphosphataemia is almost always associated with renal impairment. Limit the dietary phosphorus intake, and use oral phosphate binders (e.g. calcium carbonate 0.5–1 g 3 times daily) with meals to limit phosphorus absorption.

Acid–base disorders

The concentration of hydrogen ions [H⁺] is tightly regulated in all body compartments. In extracellular fluid (including blood), the normal pH range is 7.38–7.42 (pH = negative log of [H⁺]). To maintain pH within this narrow range, buffering systems work in concert with the lungs and kidneys to minimize sudden changes in [H⁺].

Physiological buffers

• Bicarbonate (HCO₃⁻) H⁺ + HCO₃ ↔ H₂CO₃

CO₂ + H₂O

• Bone salts (calcium carbonate and calcium phosphate)

• Blood proteins (haemoglobin).

Normal dietary acid intake is about 70 mmol/day. Any acid load is rapidly buffered by bicarbonate (normal serum range 22–26 mmol/L). As the bicarbonate buffering system does not reduce the total acid load, the kidney excretes H⁺ to maintain homeostasis. To achieve this, bicarbonate must be and is efficiently reabsorbed in the proximal tubule, with acid excretion occurring in the collecting duct. Under the influence of aldosterone, Na⁺ is reabsorbed, leaving the tubular lumen increasingly electro-negative. To maintain electrical neutrality, H⁺ (and K⁺) is secreted into the lumen. H⁺ is rapidly buffered in the urinary space by titratable acids (H⁺ incorporated to form phosphoric or sulphuric acid) or ammonia (to form NH₄⁺), and passed out as acidified urine (pH < 5 in the face of acidosis).

Diagnostic tests

• Arterial blood gases. Acid–base disorders are grouped as metabolic, respiratory or mixed in nature, depending on the principal contributor to the derangement (Fig. 11.4 and Table 11.3).

• Metabolic acidosis is due to either bicarbonate loss or the accumulation of acid. Hyperventilation leads to a primary decrease in plasma bicarbonate and a compensatory fall in PCO₂.

• Metabolic alkalosis is due to hydrogen iron loss or bicarbonate gain, leading to an increase in plasma bicarbonate. There is a compensatory rise in PCO₂.

• Respiratory acidosis is caused by retention of CO₂ with a rise in PCO₂ and [H⁺], partly compensated by a rise in bicarbonate.

• Respiratory alkalosis is caused by hyperventilation, with a fall in PCO₂ or metabolic acidosis.

• Plasma anion gap (AG). Measurement is helpful in the diagnosis of metabolic acidosis. It is calculated by subtracting measured cations from anions:

Fig. 11.4 The Flenley acid–base nomogram.

Table 11.3 Changes in arterial blood gases, pH and bicarbonate

This should be corrected for hypoalbuminaemia by adding 0.25 × (44 − serum albumin). In AG each 1 g/L of albumin has a negative charge of 0.2 − 0.28 mmol/L. A high AG is seen in renal failure (increase of sulphate and phosphate) or an accumulation of organic acids, e.g. lactate, ketones. A low AG occurs, e.g. in hypoalbuminaemia and hyperlipidaemia.

• Urinary anion gap (UAG). Measurement is useful in distinguishing a renal tubular acidosis from an extra-renal bicarbonate loss such as in diarrhoea. Again, it is the difference between the major measured anions and cations:

In diarrhoea, urinary ammonium chloride (NH₄Cl) is high, giving a negative UAG. A positive (or zero) UAG is seen in renal disease and distal renal tubular acidosis (low urinary NH₄ production).

Metabolic acidosis (Fig. 11.4) is defined as a fall in systemic pH to < 7.35 with a primary decrease in plasma bicarbonate. It may be caused by excess generation or retention of acid, or by increased bicarbonate losses.

Metabolic acidosis is often associated with serious underlying disease, and history and examination should be directed toward a global patient assessment, with particular attention to haemodynamic stability and excluding sepsis.

If the systemic pH falls < 7.2, acidaemia leads to impaired cardiac contractility, vasodilatation, resistance to catecholamines and ineffective oxygen delivery. This reflects the severity of the associated insult.

• Check Na⁺, K⁺, Ca²⁺, glucose and renal function. Obtain a venous or arterial blood gas.

• Measure the AG.

• If normal AG: urinary pH, ketones and electrolytes are helpful.

• If high AG: blood lactate, toxicology screen, urine for oxalate crystals (found with ethylene glycol poisoning) are measured.

Metabolic acidosis with normal AG

• Causes. Metabolic acidosis with a normal AG is caused by increased gastrointestinal bicarbonate losses, e.g. diarrhoea, ileostomy, and increased renal bicarbonate loss. This occurs in proximal (type II) renal tubular acidosis, hypoparathyroidism, tubular damage due to drugs and with acetazolamide. Increased renal hydrogen ion secretion occurs in type I and type IV renal tubular acidosis. Increased hydrochloride production occurs rarely with ammonium chloride ingestion and increased catabolism of lysine and arginine. In all these conditions plasma bicarbonate decreases. It is replaced by chloride to maintain electroneutrality. These conditions are sometimes referred to collectively as ‘hyperchloraemic acidosis’.

•Management

• If possible, correct the underlying cause.

• Chronic mild acidosis should be treated with bicarbonate replacement therapy to prevent long-term osteomalacia, muscle wasting and anorexia. Use oral NaHCO₃ as 1.5–4.5 g in 3 divided doses.

• Severe acidosis (pH < 7.2) in an unwell patient may require IV NaHCO₃ if there is real concern that acidaemia may be affecting cardiac performance; 200–500 mL 1.26% should be given over 1–4 hours. Always be aware of the Na⁺ load. Ventilation needs to be increased to remove the CO₂ generated.

Metabolic acidosis with high AG

Causes

• Chronic kidney disease is a frequent cause of chronic acidosis, caused by failure to excrete the fixed acid load of sulphate, phosphate and organic ions. Acidosis also occurs when functioning nephrons decrease, so there is an inability to excrete ammonia and hydrogen ions in the urine. Tubular disease may cause bicarbonate wasting.

• Diabetic ketoacidosis causes a high anion gap acidosis with the accumulation of organic acids, aceto-acetic acid and hydroxybutyric acid, owing to their increased production and decreased peripheral utilization (p. 608).

• Lactic acidosis occurs when there is increased production because of abnormal cellular respiration, either due to lack of oxygen in the tissues (type A) or a metabolic abnormality such as may be induced by a drug (type B). The most common cause in clinical practice is type A lactic acidosis, occurring in septic or cardiogenic shock.

Metabolic acidosis commonly occurs, e.g. in cholera, when there is an expected normal AG acidosis owing to massive gastrointestinal losses of bicarbonate but the AG is often increased owing to renal failure and lactic acidosis as a result of hypovolaemia.

Clinical features. There is stimulation of respiration, leading to air hunger or Kussmaul respiration. Acidosis increases delivery of oxygen to the tissues by shifting the oxyhaemoglobin dissociation curve to the right but it also leads to inhibition of 2,3DPG production, which returns the curve towards normal. Cardiovascular dysfunction is common, as acidosis is negatively ionotropic. Severe acidosis is often associated with confusion and fits.

•Management

• Always treat the underlying cause, rather than the acidosis.

• The use of NaHCO₃ is highly controversial; theoretically, rapidly raising the pH may worsen the accompanying intracellular acidosis, decrease plasma ionized calcium (which itself impairs cardiac contractility) and abolish protective conditioning that acidosis may confer against hypoxia.

• Correction is only rarely required (if systemic pH < 6.9 in patients with poor cardiac performance); use 1.26% or 1.4% NaHCO₃. Aim for a pH > 7.1 or a plasma bicarbonate > 10 mmol/L, then review.

• The occasional use of 8.4% NaHCO₃ should be reserved for the management of patients in cardiac arrest.

Metabolic alkalosis

The retention of bicarbonate or loss of H⁺ leads to a metabolic alkalosis (Fig. 11.4), usually due to primary chloride or potassium depletion. Any significant loss of Cl⁻ (vomiting, diuretics) will lead to HCO₃⁻ retention to maintain electrical neutrality. Any cause of secondary hyperaldosteronism (e.g. hypovolaemia) will lead to Na⁺ retention, and potassium and H⁺ depletion. Hypoventilation may buffer an evolving alkalosis to a degree, and modest elevations of PCO₂ are usual.