What are the symptoms of hyperkalemia?

Written by Wei Shi Liang
Intensive Care Unit
Updated on September 23, 2024
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Mild hyperkalemia can affect muscle tissues, causing mild muscle tremors, while severe hyperkalemia may reduce the excitability of neuromuscular functions, leading to weakness and even flaccid paralysis in the limbs. Hyperkalemia can also impact the heart, mainly resulting in decreased myocardial excitability, decreased myocardial conductivity, and decreased myocardial automaticity. The effects on the electrocardiogram (ECG) primarily manifest as low and widened P waves, widened QS complexes, decreased R waves, and elevated T waves. Regarding myocardial contractility, hyperkalemia mainly causes a decrease in contractility and can lead to metabolic acidosis.

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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
Intensive Care Unit
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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 Wei Shi Liang
Intensive Care Unit
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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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Written by Gan Jun
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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 Zhao Xin Lan
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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)