Why does hyperkalemia cause acidosis?

Written by Wei Shi Liang
Intensive Care Unit
Updated on September 25, 2024
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The concentration of potassium ions in serum is 3.5 to 5.5 millimoles per liter, and concentrations above 5.5 millimoles per liter are considered hyperkalemia. In the state of hyperkalemia, potassium ions in the extracellular fluid move into the intracellular fluid, while hydrogen ions in the intracellular fluid move to the extracellular fluid. At this time, through a compensatory mechanism, there is an increase in hydrogen ions in the extracellular fluid, significantly higher than normal levels, resulting in acidosis. Therefore, hyperkalemia often accompanies metabolic acidosis, which in turn affects the renal tubular epithelial cells, causing an abnormal alkaline urine. This is the main reason why hyperkalemia leads to acidosis.

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How is hyperkalemia treated?

For hyperkalemia, commonly used clinical treatments include firstly diuretics, which increase the excretion of potassium, thus increasing its discharge from the body. Additionally, hypertonic glucose with insulin is used intravenously to facilitate the movement of potassium from outside to inside the cells. Sodium bicarbonate can also be used to correct acidosis, which can likewise reduce blood potassium levels. When hyperkalemia causes ventricular arrhythmias, calcium injections should be administered immediately to counteract the cardiac toxicity of high potassium. If these treatments do not result in significant effects and the condition is critical, emergency hemodialysis or peritoneal dialysis can be performed to lower blood potassium levels. (Medication should be administered under the guidance of a doctor.)

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Clinical manifestations of hyperkalemia

The clinical manifestations of hyperkalemia are not specific. Early symptoms often include numbness in the limbs, sensory abnormalities, extreme fatigue, and muscle pain. In severe cases, there can be difficulties in swallowing, speaking, and breathing, paralysis of the limbs, and tendon reflexes may disappear. The central nervous system may show signs of restlessness, fainting, and confusion. Some may experience a slow heart rate, ventricular fibrillation, and in the most severe cases, it can lead to cardiac arrest. Other symptoms may include nausea, vomiting, diarrhea, and other gastrointestinal symptoms.

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The impact of hyperkalemia on the heart

The effects of hyperkalemia on the heart mainly manifest in the following ways: First, it affects the excitability of the myocardium, as hyperkalemia can cause reduced or even absent myocardial excitability; second, it impacts myocardial conductivity. In hyperkalemia, due to the reduced resting potential, the amplitude and speed of the action potential's phase zero decrease, leading to slowed excitability spread and reduced conductivity; third, it influences the automaticity of the myocardium. In hyperkalemia, due to slowed automatic depolarization, the automaticity is reduced. Additionally, hyperkalemia produces characteristic changes in the electrocardiogram, such as depression or disappearance of the P wave, prolongation of the PR interval, widening of the S wave, and narrowing and peaking of the T wave, which are the main changes in the electrocardiogram due to hyperkalemia.

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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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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.)