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Unlike sodium, potassium is mainly an intracellular ion and the small quantities measurable in the serum and extracellular fluid represent only a fraction of the total body potassium. However, the exact value of the serum potassium is important as cardiac arrhythmias can occur at values outside of the normal range. The intracellular potassium acts as a large buffer to maintain the serum value within its normal narrow range. Thus hypokalaemia is usually only manifest after significant total body depletion has occurred. Similarly, hyperkalaemia represents significant total body overload, beyond the ability of the kidney to compensate. The exception to both these statements is the situation in which the cell wall pumping mechanism is breached. A breakdown of the causes of hyper- and hypokalaemia is given in Table B.6.

Table B.6. Causes of hypo- and hyperkalemia




Renal failure



Volume depletion

Adrenal insufficiency

Primary hyperaldosteronism

Cell lysis

Diuretic abuse

Excessive potassium intake


Hypokalaemia is rarely a great emergency. It is usually the result of excessive potassium losses from acute diarrhoeal illnesses. As total body depletion will have occurred, large amounts are required to return the serum potassium to normal. The fastest way of giving this is with oral supplementation. In cases where this is unlikely to be tolerated, IV supplements are required. However, strong potassium solutions are highly irritant and can precipitate arrhythmias, thus the concentration of potassium in IV solutions ought not to exceed 80mmol/l when given centrally except on intensive care units. Fortunately this is not usually a problem as renal conservation of potassium aids restoration of normal serum levels.

Patients who are alkalotic, hyperglycaemic (but not diabetic), or are receiving insulin from exogenous sources will have high intracellular potassium stores. Thus hypokalaemia in these cases is the result of a redistribution of potassium rather than potassium deficiency and treatment of the underlying causes is indicated.

Hyperaldosteronism is a cause of hypokalaemic alkalosis. Patients with this condition will have salt and water retention and will be hypertensive on presentation. Secondary hyperaldosteronism is the body's natural response to hypovolaemia and salt deficiency and is thus a common cause of hypokalaemic alkalosis. As there is primary salt and water deficiency the patient is not usually hypertensive. The most common causes are diarrhoeal illness and salt-losing conditions such as cystic fibrosis. External loss of fluid from intestinal ostomies or drains are other causes. Although potassium replacement is required in this condition the main thrust of therapy has to be with salt and water replacement to re-expand the circulation and cut down on aldosterone production.


Hyperkalaemia is a dangerous condition. Although the normal range extends up to 5-5 mmol/l it is rare to get arrhythmias below 7-5 mmol/l. The most common cause of hyperkalaemia is renal failure - either acute or chronic. Hyperkalaemia can also result from potassium overload, loss of potassium from cells due to acidosis or cell lysis, hypoaldosteronism and hypoadrenalism.

The immediate treatment of hyperkalaemia is shown schematically in Figure B.2. If there is no immediate threat to the patient's life because of an arrhythmia then a logical sequence of investigation and treatment can be followed. Beta-2 stimulants, such as salbutamol, are the immediate treatment of choice. They act by stimulating the cell wall pumping mechanism and promoting cellular potassium uptake. They are best administered by nebuliser. The dose to be given is shown in Table B.8. The serum potassium will fall by about 1 mmol/l with these dosages.

Salbutamol Potassium Mechanism

Figure B.2. Algorithm for the management of hyperkalaemia

Table B.B. Salbutamol dose by age

Age (years)

Salbutamol dose (mg)







Sodium bicarbonate is also effective at rapidly promoting intracellular potassium uptake. The effect is much greater in the acidotic patient (in whom the hyperkalaemia is likely to be secondary to movement of potassium out of the cells). The dosage is the same as that used for treating acidosis and 2-5ml/kg of 8-4% NaHCO3 is usually effective. It is mandatory to also check the serum calcium, since particularly in patients with profound sepsis or renal failure, hyperkalaemia can be accompanied by marked hypocalcaemia. The use of bicarbonate in these situations can provoke a crisis by lowering the ionised calcium fraction, precipitating tetany, convulsions or hypotension and arrhythmias.

Insulin and dextrose are the classic treatment for hyperkalaemia. They are not, however, without risks. It is very easy to precipitate hypoglycaemia if monitoring is not adequate. Large volumes of fluid are often used as a medium for the dextrose and, particularly in the patient with renal failure, hypervolaemia and dilutional hyponatraemia can then be a problem. Many patients are quite capable of significantly increasing endogenous insulin production in response to a glucose load and this endogenous insulin is just as capable of promoting intracellular potassium uptake. It thus makes sense to start treatment with just an intravenous glucose load and then to add insulin as the blood sugar rises. The initial dosage of glucose ought to be 0-5/kg/hour, i.e. 2-5 ml/kg/hour of 20% dextrose. Once the blood sugar is above 10 mmol/l, insulin can be added if the potassium is not falling.The dosage of insulin is initially half that used in diabetic ketoacidosis, i.e. 0-05 units/kg/hour.This can then be titrated according to the blood sugar.

The above treatments are the fastest means of securing a fall in the serum potassium but all work through a redistribution of the potassium into cells. Thus the problem is merely delayed rather than treated in the patient with potassium overload. The only ways of removing potassium from the body are with dialysis or ion exchange resins such as calcium resonium. If it is anticipated that the problem of hyperkalaemia is going to persist then the use of these treatments ought not to be delayed. Dialysis can only be started when the patient is in an appropriate environment. Ion exchange resins can be used at the outset. The dosage of calcium resonium is 1 g/kg as an initial dose either orally or rectally, followed by 1 g/kg/day in divided doses.

In an emergency situation where there is an arrhythmia (heart block or ventricular arrhythmia) the treatment of choice is intravenous calcium. This will stabilise the myocardium but will have no effect on the serum potassium. Thus the treatments discussed above will still be necessary.The dosage is 0-5 ml/kg of 10% Ca gluconate (i.e. 0-1 mmol/kg Ca). This dose can be repeated twice. With a very high potassium, more than one treatment can be used simultaneously.

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