What are the causes of hyperkalemia?

Written by Wei Shi Liang
Intensive Care Unit
Updated on September 05, 2024
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Hyperkalemia, with blood potassium levels greater than 5.5 mmol/L, commonly occurs due to decreased potassium excretion or abnormal potassium transport within cells, as well as other reasons such as excessive intake. Decreased potassium excretion can commonly be due to renal failure, the use of potassium-sparing diuretics, renal tubular acidosis, and reduced secretion of corticosteroid aldosterone. Abnormal potassium transport includes conditions such as acidosis, rhabdomyolysis, extensive burns, severe trauma, intestinal necrosis, and peritoneal bleeding, among other diseases. Excessive potassium intake can be due to sample hemolysis or an elevation in white blood cells, both of which can lead to hyperkalemia. Therefore, it is crucial to be vigilant in clinical settings and address the condition promptly and appropriately.

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Written by Wei Shi Liang
Intensive Care Unit
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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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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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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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The effect of hyperkalemia on the myocardium

The primary mechanism by which hyperkalemia causes arrhythmias is due to dysfunction of myocardial conduction, which is also related to various other factors such as other myocardial lesions, failure, and ionic states. The main impact on the myocardium is on its excitability; myocardial excitability can decrease or even disappear, and its conductivity is also affected, causing a reduction in conductivity. The effect on myocardial automaticity is a decrease in automaticity. Electrocardiographically, there are manifestations such as a low P wave, prolonged PR interval, and widened QRS complex without disappearance; these are some of the presentations of hyperkalemia.

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Principles of treatment for hyperkalemia

First, to counteract the cardiac inhibitory effects of potassium, calcium salts can be injected, and sodium bicarbonate can be used to alkalinize the blood. Then, an infusion of hypertonic glucose and insulin can be administered to promote the internal movement of potassium ions. Secondly, to promote the excretion of potassium, diuretics can be used. The second method involves the use of cation exchange resins and sorbitol. The third method employs dialysis therapy, which can include both hemodialysis and peritoneal dialysis. The fourth method is to reduce the sources of potassium, stop a high potassium diet or the use of potassium-containing drugs. In cases of severe hyperkalemia, where there is a life-threatening emergency, urgent measures should be taken, primarily the intravenous administration of calcium ion antagonists to counteract the cardiac toxicity of potassium. In cases of severe arrhythmias or even cardiac arrest, emergency installation of a pacemaker or defibrillation can be carried out, and respiratory muscle paralysis may require ventilatory support. (Medication use should be under the guidance of a doctor)