Why does hyperkalemia cause muscle weakness?

Written by Luo Han Ying
Endocrinology
Updated on May 07, 2025
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The muscles that govern movement in our body are striated muscles, and each muscle cell in striated muscles has many receptors, which we can think of as a signal receiving and transmitting station. When we need to move, the brain nerves will send a signal to this station, which then controls muscle movement. A very important ion in muscle movement is the calcium ion. There is a receptor for calcium ions on our muscle cells, and it is related to the concentration of blood potassium. When the concentration of blood potassium is too low, a condition known as hypokalemia, or too high, known as hyperkalemia, the calcium ion receptor will be inhibited. At this point, our muscles will exhibit symptoms of muscle weakness.

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Written by Wei Shi Liang
Intensive Care Unit
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Treatment of Hyperkalemia with Drugs

Hyperkalemia primarily affects the conduction of the heart and muscle nerves, with typical clinical manifestations including severe bradycardia, atrioventricular block, and even sinus arrest. Once hyperkalemia occurs clinically, immediate treatment should be administered. The first approach to treatment is promoting the excretion of potassium, using furosemide or other diuretics to increase renal potassium excretion, and taking a small dose of sodium polystyrene sulfonate orally to eliminate potassium. For life-threatening severe hyperkalemia, if serum potassium is greater than 6.5 mmol/L, hemodialysis treatment is necessary. The second aspect involves shifting potassium into cells, using calcium to alter cell excitability, which can protect the heart from the damage to the conduction system caused by hyperkalemia. Additionally, using glucose with insulin and administering sodium bicarbonate can be effective. It is important to note that all the above medications should be used under the guidance of a doctor.

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Written by Wei Shi Liang
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The difference between hyperkalemia and hypokalemia.

Hypokalemia refers to a serum potassium concentration lower than 3.5mmol/L, and its clinical manifestations are diverse. The most life-threatening symptoms involve the cardiac conduction system and the neuromuscular system. Mild hypokalemia shows on an electrocardiogram as flattened T waves and the appearance of U waves, while severe hypokalemia can lead to fatal arrhythmias, such as torsades de pointes and ventricular fibrillation. In terms of the neuromuscular system, the most prominent symptom of hypokalemia is the loss of tone in smooth muscles and flaccid paralysis in skeletal muscles, which, when involving respiratory muscles, can lead to respiratory failure. Hyperkalemia, on the other hand, refers to a serum potassium concentration exceeding 5.5mmol/L, mainly presenting clinical symptoms in cardiac and neuromuscular conduction. Severe cases can cause bradycardia, atrioventricular conduction block, and even sinus arrest. Mild hyperkalemia, with levels between 5.5 to 6.0mmol/L, shows on an electrocardiogram as peaked T waves. As hyperkalemia continues to increase, it can lead to lengthening of the PR interval or disappearance of the P wave, QRS widening, and eventually cardiac arrest. Regarding the neuromuscular system, the clinical manifestations of hyperkalemia are very similar to those of hypokalemia, including weakness and paralysis of skeletal and smooth muscles.

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Written by Wei Shi Liang
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What are the symptoms of hyperkalemia?

The effects of hyperkalemia on the body mainly include the following aspects: First, the impact on muscle tissue: mild hyperkalemia can cause slight tremors in muscles. If the potassium levels continue to rise, this can lead to decreased neuromuscular excitability, resulting in limbs becoming weak and flaccid, and even leading to delayed paralysis. Second, the impact on the cardiac system: it can cause a decrease in myocardial excitability, conductibility, and automaticity. The electrocardiogram shows a depressed P wave, widened QRS complex, shortened QT interval, and peaked T waves. Third, hyperkalemia affects acid-base balance and can lead to metabolic acidosis during hyperkalemia.

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Written by Gan Jun
Endocrinology
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What are the changes in urine output in hyperkalemia?

When patients experience hyperkalemia, urine output generally decreases, leading to reduced potassium excretion by the kidneys, typically accompanied by abnormal kidney function. Thus, as long as kidney function is normal and daily urine output exceeds 500 milliliters, hyperkalemia is usually rare. Some causes of reduced renal potassium excretion include decreased glomerular filtration rates and reduced potassium secretion by the renal tubules, commonly seen in acute and chronic renal failure, adrenal cortex insufficiency, low renin, low aldosterone blood conditions, renal tubular acidosis, and long-term use of diuretics, especially potassium-sparing diuretics. Additionally, β-adrenergic tissue agents and angiotensin-converting enzyme inhibitors can cause drug-induced hyperkalemia, leading to abnormal kidney function and, consequently, decreased potassium excretion by the kidneys, ultimately resulting in reduced urine output.

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Written by Wei Shi Liang
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Hyperkalemia can be seen in which diseases?

Hyperkalemia is a condition where the serum potassium concentration exceeds 5.5 millimoles per liter. Common causes include excessive intake of potassium, such as high-dose potassium penicillin intravenous infusion, ingestion of potassium-containing medications, or transfusion of large amounts of stored blood, all of which can lead to hyperkalemia. Additionally, patients with renal failure who experience oliguria or anuria may have reduced potassium excretion. In such cases, inappropriate potassium supplementation or the use of potassium-sparing diuretics can lead to severe hyperkalemia. Lastly, the movement of potassium from inside the cells—during metabolic acidosis and respiratory acidosis—causes ion exchange, leading to hydrogen ions entering the cells while potassium ions leak out, resulting in hyperkalemia.