Describe the function, distribution, regulation and physiological importance of
sodium, chloride,potassium, magnesium, calcium and phosphateions.
Function and Dysfunction
Potassium is important for:
- Regulation of intracellular pH
- Control of intracellular volume
- DNA and protein synthesis
- Enzymatic function
- Resting membrane potential
The resting membrane potential is determined by the ratio of intracellular:extracellular potassium, as per the Nernst equation:
- Small changes in extracellular ion concentration produce large changes in voltage
This has significant effect on excitable tissues.
- Rapid changes in potassium concentration cause symptoms at lower levels than chronic changes
Symptoms are related to the change in action potential generation.
Ventricular Action Potential in Hyperkalaemia:
- The resting membrane potential to become less negative
As per the Nernst equation.
- This results in the resting membrane potential being closer to the threshold potential, increasing irritability
- Several symptoms, including:
- ECG findings are those of prolonged depolarisation and rapid repolarisation:
|Serum [K+] (mmol/L)||ECG Findings|
|5.5-6.5||Tall tented T waves|
|6.5-7.5||Loss of P wave, lengthening PR interval|
- Causes the resting membrane potential to become more-negative
This makes it more difficult for a stimulus to reach the threshold potential, and therefore it is harder to generate and propagate action potential.
- ECG findings are those of rapid depolarisation and prolonged repolarisation, and include:
- Prolonged PR
- Long QT
- Flat T waves or TWI
- U waves
- ST depression
- Severe hypokalaemia may result in:
- Frequent supraventricular and ventricular ectopics
- Supraventricular arrhythmias
- Ventricular arrhythmias
Serum potassium is dependent on intake, sequestration, and elimination.
Dietary intake may be highly variable. Potassium is completely absorbed from the upper GI tract.
Several factors affect potassium sequestration:
- Insulin and β2-agonism results in increase activity of the Na+-K+ ATPase pump, shifting potassium into cells following a meal and during exercise
- Acidosis causes an extracellular shift of potassium, as hydrogen ions are exchanged for potassium ions
The reverse occurs in alkalosis.
- Cell lysis may release a large amount of potassium into circulation and cause significant hyperkalaemia if a large number of cells are destroyed
- Aldosterone increases uptake of potassium into cells
Elimination of potassium occurs via the kidneys, and is dependent on production of large volumes of glomerular filtrate and secretion by the distal convoluted tubule and collecting duct.
In normal conditions:
- The PCT and ascending limb reabsorb the majority of absorbed potassium
This is essentially fixed.
- PCT absorbs ~55%
- Ascending limb absorbs ~30%
- The principal cells of the DCT and collecting duct secrete potassium
Altering potassium secretion is the main method by which the kidney regulates serum potassium.
- The collecting duct has a much greater role than the DCT
- With normal dietary intake, more potassium is secreted than reabsorbed
This changes in conditions of potassium depletion.
Control of Tubular Secretion
Tubular potassium secretion is mainly a function of:
- Plasma [K+]
Increased plasma [K+] stimulates the Na+-K+ ATPase pump in the principal cells, and also stimulates aldosterone release from the adrenal cortex.
- Tubular flow rate
Movement of potassium out of principal cells occurs down a passive concentration gradient. Increasing tubular flow rate increases the concentration gradient for potassium
Aldosterone increases production of the Na+-K+ ATPase pump, which increases potassium secretion and uptake into cells.
Minor contributors include:
- Sodium and water content
- High sodium content inhibits aldosterone release, reducing potassium elimination
- High water content inhibits ADH excretion and reduces secretion of potassium, however high water content also increases flow through the renal tubule, which indirectly increases tubular secretion of potassium.
Alkalosis increases elimination of potassium as the Na+-K+ ATPase pump is stimulated by low H+ ion concentration.
- Kam P, Power I. Principles of Physiology for the Anaesthetist. 3rd Ed. Hodder Education. 2012.
- Hall, JE, and Guyton AC. Guyton and Hall Textbook of Medical Physiology. 11th Edition. Philadelphia, PA: Saunders Elsevier. 2011.
- Nickson,C. Hyperkalaemia. Life in the Fast Lane.
- Parham WA, Mehdirad AA, Biermann KM, Fredman CS. Hyperkalemia Revisited. Texas Heart Institute Journal. 2006;33(1):40-47.