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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Written by Wei Shi Liang
Intensive Care Unit
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Common causes of hyperkalemia

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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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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Why does hyperkalemia cause acidosis?

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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Written by Wei Shi Liang
Intensive Care Unit
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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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How is hyperkalemia treated?

Hyperkalemia must be handled immediately after it occurs, otherwise it can cause malignant arrhythmias and even endanger life. The first step is to stop potassium supplements, such as potassium chloride sustained-release tablets; the second step is to stop potassium-sparing diuretics, such as spironolactone and other drugs. We can administer calcium intravenously to antagonize the toxic effects of high potassium on the heart. Additionally, we can use high glucose with insulin and intravenously drip sodium bicarbonate, which can promote the movement of potassium into cells. We can also use diuretics to excrete potassium through urine. If the treatment effect is poor after medication, we can use bedside hemodialysis to reduce blood potassium.