11 Serum potassium concentration is normally kept within a tight range (3.5–5.3 mmol/L). Potassium intake is variable (30–100 mmol/day in the UK) and potassium losses (through the kidneys) usually mirror intake. The two most important factors that determine potassium excretion are the glomerular filtration rate and the plasma potassium concentration. A small amount (~5 mmol/day) is lost in the gut. Potassium balance can be disturbed if any of these fluxes is altered (Fig 11.1). An additional factor often implicated in hyperkalaemia and hypokalaemia is redistribution of potassium. Nearly all of the total body potassium (98%) is inside cells. If, for example, there is significant tissue damage, the contents of cells, including potassium, leak out into the extracellular compartment, causing potentially dangerous increases in serum potassium (see below). Hyperkalaemia is one of the commonest electrolyte emergencies encountered in clinical practice. If severe (>7.0 mmol/L), it is immediately life-threatening and must be dealt with as an absolute priority; cardiac arrest may be the first manifestation. ECG changes seen in hyperkalaemia (Fig 11.2) include the classic tall ‘tented’ T-waves and widening of the QRS complex, reflecting altered myocardial contractility. Other symptoms include muscle weakness and paraesthesiae, again reflecting involvement of nerves and muscles. Fig 11.2 Typical ECG changes associated with hyperkalaemia. (a) Normal ECG (lead II). (b) Patient with hyperkalaemia: note peaked T-wave and widening of the QRS complex. Hyperkalaemia can be categorized as due to increased intake, redistribution or decreased excretion. In practice, virtually all patients with hyperkalaemia will have a reduced GFR.
Hyperkalaemia
Serum potassium and potassium balance
Hyperkalaemia
Decreased excretion
Renal failure. The kidneys may not be able to excrete a potassium load when the glomerular filtration rate is very low, and hyperkalaemia is a central feature of reduced glomerular function. It is exacerbated by the associated metabolic acidosis, due to the accumulation of organic ions that would normally be excreted.
Hypoaldosteronism. Aldosterone stimulates sodium reabsorption in the renal tubules at the expense of potassium and hydrogen (see p. 15
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Hyperkalaemia
