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Pathophysiology · Chapter 12. Electrolyte Balance Disorders

Hyperkalemia

*Hyperkalaemia*

Hyperkalemia is a common form of electrolyte metabolism disorder in which the serum potassium concentration exceeds 5.5 mmol/L. This condition poses a serious threat to life because it disrupts electrophysiological processes in excitable tissues and can lead to fatal cardiac events.

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Diagnostic criteriaSerum potassium levels rise above the normal threshold of 5.5 mmol/L.
Cardiac riskAt potassium concentrations exceeding 10 mEq/L (or 13 mmol/L), cardiac arrest in diastole may occur.
Renal reserveNormally, healthy kidneys are capable of excreting up to 1,000 mEq of potassium per day.
Effect of acidosisA 0.1-unit decrease in blood pH increases plasma potassium concentration by 0.6 mEq/L.
4 min readFor medical studentsUpdated 09/24/2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesReviewed by medical editor: Aulov A. A., general practitioner · 09/24/2026

Main causes (etiology)

There are three main groups of factors leading to the development of hyperkalemia:

  • Decreased renal excretion. Healthy kidneys excrete an amount of potassium significantly exceeding daily intake. However, in renal tissue damage, hyperkalemia occurs even with normal or reduced intake of this ion. Another cause is hypoaldosteronism (associated with adrenal insufficiency or reduced sensitivity of the tubular epithelium in amyloidosis, renal failure, and interstitial lesions). A defect in $Na^+$ ion reabsorption occurs in the distal tubules, which disrupts the coupled excretion of $K^+$.
  • Redistribution from cells to the blood. Observed during massive cell damage and destruction: erythrocyte hemolysis, burns, crush injuries, ischemia, necrosis, and crush syndrome. Additionally, potassium efflux is stimulated by hypoinsulinemia (due to enhanced glycogenolysis and proteolysis) and intracellular acidosis, during which $K^+$ ions leave the cell and $Cl^-$ ions enter it.
  • Excessive intake into the body. Acute or chronic dietary hyperkalemia is extremely rare, as undamaged kidneys effectively eliminate the excess.

Clinical manifestations

The symptoms of hyperkalemia are entirely due to the disruption of membrane potential (MP) formation, action potential (AP), and excitation transmission at neuromuscular synapses.

Neuromuscular disorders Patients complain of muscle pain and severe weakness. Objective examination reveals muscle hypotonia, hyporeflexia, and in severe cases, muscle paralysis. In internal organs, a characteristic visceral manifestation is intestinal atony.

Cardiovascular system disorders The most important clinical sign is a progressive drop in cardiomyocyte excitability and a significant increase in the cholinergic properties of the heart. This leads to bradycardia and severe arrhythmias. Atrioventricular and intraventricular blocks develop. At potassium levels of 8–10 mmol/L, complete impulse conduction block is possible, and at values above 10 mEq/L, cardiac arrest in diastole occurs.

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Methods for treating hyperkalemia

Emergency therapy includes three main directions:

  1. Elimination of the cause. Removal of the primary etiological factor that triggered the electrolyte metabolism disorder.
  2. Activation of redistribution. Stimulation of $K^+$ transport from the extracellular fluid back into cells. For this purpose, intravenous administration of calcium chloride solution, sodium bicarbonate (potentiates intracellular potassium transport), or a combination of dextrose (glucose) with insulin is used. Insulin stimulates the co-transport of glucose and potassium into cells, which relatively quickly reduces hyperkalemia and cardiotoxicity.
  3. Stimulation of excess excretion. Hemodialysis is used (reduces potassium content by half in 3–4 hours), along with diuretics (e.g., furosemide) and aldosterone preparations (desoxycorticosterone acetate, trimethylacetate). High efficacy is demonstrated by cation-exchange resins (sodium polystyrene sulfonate). Entering the intestine, where the potassium concentration is 2–4 times higher than in the blood, they bind and remove 60–100 mmol of the macroelement within the first 4–6 hours.

Briefly: answers to topical questions

What characteristic ECG changes occur in hyperkalemia?

Specific ECG changes in hyperkalemia affect waveform shapes and time intervals, progressing as potassium concentration increases.

Changes include:

  • T wave — becomes tall, narrow, pointed, and symmetrical (peaked).
  • QT interval — shortens.
  • PR interval — lengthens.
  • P wave — widens and subsequently disappears.
  • QRS complex — widens.

At a $K^+$ concentration of 8–9 mmol/L, the QRS complex merges with the T wave, giving the QRST complex a sinusoidal appearance. At levels above 9 mmol/L, atrioventricular block, ventricular tachycardia, or ventricular fibrillation develop.

How to memorize

To remember the medications administered intravenously for potassium redistribution into cells, use the acronym BIK: Bicarbonate (sodium), Insulin with Glucose, Kalium (calcium) chloride.

Class and exam questions

Why does intracellular acidosis increase blood potassium levels?

In acidosis, a compensatory ion exchange occurs: hydrogen ions move inside cells, while potassium ions pass into the extracellular fluid and blood. Simultaneously, the inward transport of chlorides is stimulated.

How does hypoinsulinemia affect potassium metabolism?

Insulin deficiency leads to enhanced glycogenolysis and proteolysis in tissues. The breakdown of these intracellular structures is accompanied by the release of a large amount of potassium into the bloodstream.

Why does excess dietary potassium rarely cause hyperkalemia in healthy individuals?

Healthy kidneys have a massive excretion reserve. Normally, they are capable of excreting up to 1,000 mEq of potassium per day, which significantly exceeds its typical dietary intake.

What is the mechanism of action of cation-exchange resins in the treatment of hyperkalemia?

Drugs (e.g., sodium polystyrene sulfonate) act in the intestinal lumen. Since the potassium content in intestinal juice is 2–4 times higher than in blood serum, the resins effectively bind and excrete it from the body.

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What else to study on this topic

  • Electrophysiology of excitable tissues: formation of membrane potential and action potential
  • Pathogenesis of crush syndrome (prolonged crush syndrome) and its systemic consequences
  • The role of aldosterone in regulating sodium reabsorption and potassium secretion in the distal renal tubules
  • Mechanisms of intracellular acidosis development and its effect on electrolyte balance
  • Effect of hyperkalemia on the cholinergic properties of the myocardium

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Other topics in section "Chapter 12. Electrolyte Balance Disorders"

HypernatremiaHyponatremiaChlorine metabolism disordersHypokalemiaHypercalcemiaHypocalcemiaHyperphosphatemiaHypophosphatemiaHypermagnesemiaHypomagnesemia
Entire section «Chapter 12. Ion Metabolism Disorders»

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