Common causes of hyperkalemia

Written by Wei Shi Liang
Intensive Care Unit
Updated on September 09, 2024
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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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Endocrinology
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What are the causes of hyperkalemia?

The first reason is the excessive intake or administration of potassium, which can lead to hyperkalemia. For example, consuming foods that are very rich in potassium, or intravenously infusing solutions containing potassium. Additionally, the use of potassium salts of penicillin can also cause hyperkalemia, as well as the transfusion of stored blood, which can easily lead to hyperkalemia. Besides excessive intake and administration of potassium, diseases related to reduced excretion can also cause hyperkalemia, such as the most common instances during acute or chronic renal failure, where patients are prone to hyperkalemia. Furthermore, patients with reduced adrenal cortex function, such as aldosterone deficiency or Addison's disease, are also prone to hyperkalemia. Additionally, the use of diuretics that inhibit potassium excretion, notably spironolactone—a potassium-sparing diuretic—can also cause an increase in blood potassium levels. Another reason is a change in potassium distribution, such as when potassium moves from inside the cells to the outside, which can easily lead to hyperkalemia. This is common in cases of tissue damage, such as muscle contusion, or electrical burns, and tissue hypoxia, which also can easily lead to a change in potassium distribution, causing an increase in extracellular potassium. If hemolysis occurs in a test tube, such as if the venipuncture takes too long, or in conditions like leukocytosis or severe shaking of the blood sample, these might also lead to hyperkalemia. (The use of medications should be under the guidance of a doctor.)

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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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Hyperkalemia

Typically, when serum potassium exceeds 5.5 mmol/L, it is referred to as hyperkalemia. However, an increase in serum potassium does not necessarily reflect an overall increase in body potassium; serum potassium can also rise when there is a deficiency of total body potassium. Therefore, in clinical practice, serum potassium is evaluated in conjunction with an electrocardiogram and medical history to determine if a patient has hyperkalemia. Hyperkalemia is an important emergency in internal medicine and can often lead to sudden cardiac arrest. It should be identified and prevented early.

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The effects of hyperkalemia on the body

Hyperkalemia affects the body mainly in three aspects. Firstly, hyperkalemia impacts muscle tissues, clinically manifesting as symptoms such as muscle tremors. Secondly, the effect of hyperkalemia on the heart primarily manifests as decreased excitability, conductivity, and automaticity of the myocardium. It affects electrocardiograms, characterized by a depressed P wave, widened QS wave, reduced R wave, and elevated T wave. Thirdly, hyperkalemia affects acid-base balance; during hyperkalemia, potassium efflux from cells can lead to metabolic acidosis, resulting in alkaline urine.

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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.