80. Disorders of potassium balance. Hypo- and hyperkalaemia

Last updated on May 25, 2019 at 19:16

Potassium in the body

98% of all potassium in the body is intracellular. In the intracellular space is the concentration 140 – 160 mM, while in the extracellular space is it just 3.5 – 5.5 mM.

The serum potassium level depends in two things:

  • The internal potassium balance, the balance between the intracellular and extracellular compartments
  • The external potassium balance, the balance between potassium intake and potassium loss
The internal potassium balance

The internal balance depends on 6 things:

  • pH
  • Tonicity of the extracellular space
  • Insulin
  • Catecholamines
  • Mineralocorticoids
  • Physical activity

pH: Cells have the possibility to excrete K+ in exchange for H+ and visa versa. If the extracellular H+ concentration is low (alkalosis) will H+ be pumped out of cells while K+ will be pumped into cells. If the extracellular H+ level is high (acidosis) will H+ be pumped into cells while K+ will be pumped out. Acidosis can therefore cause hyperkalaemia while alkalosis can cause hypokalaemia.

Tonicity: When the extracellular space is hypertonic (due to increased sodium or glucose concentration for example) will water flow out of cells and into the EC space. Because the K+ level inside the cell doesn’t change will the K+ concentration increase, as the cells have lost water. This concentration increase causes K+ to flow out of the cell, potentially causing hyperkalaemia.

Insulin enhances Na+/K+ ATPase activity, causing K+ to enter the cells. In fact, when there is a hyperkalaemia that should be quickly normalized it is common to give insulin and glucose simultaneously. This doesn’t really fix the elevated K+ level in the body though, it just “hides” the potassium inside cells.

Catecholamines also enhances Na+/K+ ATPase activity, via β2-receptors. α-receptors decrease the activity.

Mineralocorticoids contribute to the balance. I don’t know how (book doesn’t explain). Probably not too important.

Physical activity causes K+ outflow from muscle cells.

The external potassium balance

The daily intake of food is ca 40 – 120 mmol K+. This extra potassium reaches the extracellular space and not the cells in normal cases. 90% of the lost potassium is excreted by the kidneys, the remaining through the GI tract.

The external balance depends on 5 things:

  • K+ intake
  • Mineralocorticoids
  • Filtration
  • pH
  • GI excretion

K+ intake is counter-regulated by kidney and GI excretion, so even a high potassium intake isn’t dangerous (unless it’s intravenous). In end-stage renal failure, when the GFR < 5 mL/min can even a few bananas cause severe hyperkalaemia.

Mineralocorticoids play a much larger role in the external balance than the internal. Aldosterone and some of its weaker precursors enhance Na+/K+ and Na+/H+ exchange in the distal tubules and collecting duct. This causes K+ and H+ loss.

The GFR determines how much K+ is filtered. When it’s increased will more water and sodium reach the distal tubules, which increases Na+/K+ exchange, causing sodium to be reabsorbed and more potassium to be excreted. Increased flow rate, such as in osmotic diuresis, inhibits K+ reabsorption. Increased level of anions in the filtrate, like bicarbonate, increases K+ excretion because of electroneutrality.

pH also influences the potassium excretion. Renal K+ excretion decreases in acidosis and increases in alkalosis.

GI excretion only accounts for 10% of potassium loss in healthy people, but in severe renal failure may this number go up to 50% to compensate for the failing kidneys.

Hypokalaemia

Most important causes:

  • Metabolic alkalosis
  • Cushing syndrome
  • Insulin treatment
  • β2-receptor agonist
  • Osmotic diuresis
  • Increased mineralocorticoid activity
  • Extreme sweating
  • Diarrhoea
  • Diuretics
  • Renal tubular acidosis I
  • Renal tubular acidosis II

Consequences of hypokalaemia:

  • Development of metabolic alkalosis
  • Hyperpolarized membranes (membrane potential becomes more negative)
    • Muscle weakness
    • Arrhythmias
  • Polyuria (hypokalaemia causes nephrogenic diabetes insipidus where the kidney responds less to ADH)
Hyperkalaemia

Causes:

  • Metabolic acidosis
  • Chronic renal failure
  • Diabetes mellitus type 1
  • Mass cell destruction (tumor treatment, haemolytic anaemia)
  • Hypoaldosteronism
  • Renal tubular acidosis IV
  • Drugs that inhibit aldosterone or RAAS

Consequences:

  • Hypopolarized membranes (more positive membrane potential)
  • Arrhythmias
  • Muscle weakness
  • Respiratory depression

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79. Respiratory acidosis and alkalosis. Causes, compensation, consequences

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81. States of decreased extracellular volume, and their consequences

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