The difference between hyperkalemia and hypokalemia.

Written by Wei Shi Liang
Intensive Care Unit
Updated on September 05, 2024
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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
Intensive Care Unit
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What are the causes of hyperkalemia?

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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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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Written by Zhao Xin Lan
Endocrinology
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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)

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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 Wang Li Bing
Intensive Care Medicine Department
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Why is calcium used for hyperkalemia?

Hyperkalemia can increase the excitability of myocardial cells, leading to various malignant arrhythmias and even sudden death. Immediate treatment is necessary after hyperkalemia occurs. Clinically, it can be treated by hemodialysis or conservatively with medication. Why use calcium preparations for hyperkalemia? Because after using calcium preparations, the excitability of myocardial cells can be stabilized, effectively maintaining stable heart rates in patients and preventing sudden death due to malignant arrhythmias.