Does hyperkalemia cause a fast or slow heart rate?

Written by Wei Shi Liang
Intensive Care Unit
Updated on March 09, 2025
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Hyperkalemia often causes a slowed heart rate and is associated with various arrhythmias. When serum potassium is between 6.6 to 8.0 mmol/L, tented T-waves may be observed. When serum potassium levels rise rapidly, it can lead to ventricular tachycardia or even ventricular fibrillation. On the other hand, a slow increase in serum potassium can cause conduction blocks, and in severe cases, may lead to cardiac arrest. These are the heart rate changes caused by hyperkalemia, which typically result in a slower heart rate.

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Written by Wei Shi Liang
Intensive Care Unit
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Clinical manifestations of hyperkalemia

The clinical manifestations of hyperkalemia mainly affect the cardiovascular system, often presenting with slowed heart rate and various arrhythmias. When the blood potassium level is between 6.6 and 8.0 mmol/L, a tent-shaped T-wave can be observed. Rapid increases in blood potassium can lead to ventricular tachycardia, and even ventricular fibrillation. A gradual increase in blood potassium can cause conduction blocks, and in severe cases, cardiac arrest. Sudden death in severe hyperkalemia is mainly due to ventricular fibrillation and cardiac arrest. The second aspect is symptoms related to the neuromuscular system. As the concentration of potassium ions in the extracellular fluid increases, the resting membrane potential drops, leading to muscle weakness and even paralysis, typically more pronounced in the lower limbs and extending upward along the trunk. In severe cases, some patients may experience difficulty in swallowing and breathing difficulties. Symptoms involving the central nervous system mainly include restlessness, confusion, and fainting.

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Written by Wei Shi Liang
Intensive Care Unit
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Is hyperkalemia acidosis?

Hyperkalemia is not acidosis, but during acidosis, the hydrogen ions of the gastric fluid within cells enter the cells, causing the potassium ions inside the cells to move to the extracellular fluid, resulting in hyperkalemia. Clinically, it is commonly seen in organic acidosis, lactic acidosis, diabetic ketoacidosis, and acute renal failure causing acidosis. Once hyperkalemia occurs and is diagnosed, immediate treatment should be administered. First, the primary disease should be treated; next, serum potassium should be reduced. In particularly severe cases, bedside hemofiltration can be administered, and the cardiotoxic effects of hyperkalemia should be mitigated.

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Endocrinology
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Causes of hyperkalemia

The causes of hyperkalemia may include: First, excessive intake, such as consuming too much high-potassium food, medications with high potassium content, including some traditional Chinese medicines, potassium penicillin, stored blood, and excessive potassium supplementation. Second, it could be due to decreased potassium excretion by the kidneys. When renal insufficiency, acute or chronic renal failure occurs, it is often accompanied by severe hyperkalemia. Third, there is also decreased potassium secretion by renal tubules. When there is a deficiency of corticosteroids, there can be degenerative, asymptomatic hyperkalemia. Hyperkalemia can also occur when renal tubules are insensitive to aldosterone. Fourth, medications that reduce potassium excretion, such as the use of potassium-sparing diuretics, angiotensin-converting enzyme inhibitors, other nonsteroidal anti-inflammatory drugs, cyclosporine, etc., can also cause hyperkalemia. Fifth, the shift of potassium from inside the cells to the extracellular fluid, which can be caused by tissue damage, hypoxia, or the use of certain medications, leading to hyperkalemia.

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Written by Wei Shi Liang
Intensive Care Unit
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Common causes of hyperkalemia

Hyperkalemia is caused by increased intake or decreased excretion, or by the transfer of potassium ions from inside the cells to the outside. Increased intake generally does not cause hyperkalemia in individuals with normal kidney function, unless potassium is supplemented intravenously in excessive amounts or too quickly. Moreover, decreased excretion is a major cause of hyperkalemia, typically seen in renal failure, deficiency of adrenocortical hormones, and primary renal tubular disorders in potassium secretion. Additionally, a large transfer of potassium ions from inside the cells to the outside can occur in conditions such as massive cell breakdown, acidosis, tissue hypoxia, periodic paralysis, and insulin deficiency.

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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.