Treatment methods for hyperkalemia

Written by Wang Li Bing
Intensive Care Medicine Department
Updated on September 30, 2024
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In clinical practice, a blood potassium level greater than 5.5 millimoles per liter is referred to as hyperkalemia. Once hyperkalemia occurs, it must be actively managed: the first step is to stop using medications that increase blood potassium, such as sustained-release potassium chloride, potassium-sparing diuretics like spironolactone, and ACE inhibitors; the second step is to use calcium supplements to counteract the toxic effects of high potassium on the heart; the third step is to use hypertonic glucose with insulin and sodium bicarbonate to correct acidosis and promote the movement of potassium into the cells; the fourth step is to use the diuretic furosemide to help reduce blood potassium. If drug treatment is ineffective, bedside hemodialysis may be employed. (Use of the above medications should be 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?

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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Can hyperkalemia be cured?

Hyperkalemia is treatable. The first cause of hyperkalemia is an excess of potassium, mainly seen in reduced renal excretion and excessive potassium intake, such as the infusion of a large volume of stored blood. In this case, diuretics can be used to increase the excretion of potassium. For cases of excessive potassium intake and excessive transfusion of stored blood, treatment options include diuresis and the use of glucose with insulin to lower potassium levels, or even treatment with sodium bicarbonate. In cases of shift hyperkalemia, primarily seen in hemolysis and septic shock, dialysis can be used to reduce hyperkalemia while simultaneously treating the underlying disease. The third type is concentration hyperkalemia and severe hemorrhagic shock, which causes a reduction in blood volume leading to blood concentration and relative hyperkalemia. Treatment of the primary disease first is advisable, and typically, the high blood potassium can self-correct after the primary disease is cured. There is also a condition known as pseudohyperkalemia, for example, prolonged storage of drawn blood can cause hemolysis within the tube, poor venipuncture technique, thrombocytosis, and leukocytosis can all lead to pseudo-hyperkalemia. In these cases, re-drawing blood multiple times to verify the potassium levels can address this issue. Therefore, hyperkalemia is treatable.

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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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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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What kind of urine occurs with hyperkalemia?

Primary hyperkalemia often coincides with metabolic acidosis, and in hyperkalemia-induced metabolic acidosis, paradoxical alkaline urine can occur. Once hyperkalemia occurs, it primarily affects the conduction of the heart and neuromuscular system. Typical clinical manifestations include severe bradycardia, atrioventricular conduction block, and even sinus arrest. In mild hyperkalemia, the electrocardiogram shows peaked T-waves; as potassium levels continue to rise, the PR interval prolongs, T-waves disappear, QRS complex widens, and ultimately, cardiac arrest occurs. Immediate treatment should be administered upon diagnosis to promote the excretion of potassium, maximizing the renal excretion capacity with diuretics. If drug-induced potassium excretion does not normalize levels and serum potassium exceeds 6.5 mmol/L, hemodialysis may be necessary. Additionally, some drugs can be used to shift potassium into the cells and protect cardiac function. (The use of any medication should be under the guidance of a doctor.)