The role of calcium agents in hyperkalemia

Written by Wei Shi Liang
Intensive Care Unit
Updated on September 07, 2024
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Change the excitability of autonomic cells to protect the heart. Hyperkalemia mainly affects the conduction of the heart and neuromuscular system. Typical clinical manifestations include severe bradycardia, atrioventricular block, and even sinus arrest. By using calcium agents to change the excitability of autonomic cells, we can protect the heart from the damage to the conduction system caused by hyperkalemia. This allows the potassium ions to move from outside the cell to inside the cell. While protecting the myocardium, it is also necessary to use some medications to lower blood potassium. If the blood potassium is particularly high, dialysis or continuous bedside blood filtration can be used to reduce the blood potassium to a normal range.

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Written by Chen Li Ping
Endocrinology
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The Impact of Hyperkalemia on the Heart

Typically, when serum potassium exceeds 5.5 mmol/L, it is referred to as hyperkalemia. The manifestations of hyperkalemia on the cardiovascular system usually include bradycardia and arrhythmias, but generally do not lead to congestive heart failure. Sometimes, there may be cardiac enlargement and diminished heart sounds, with characteristic changes on an electrocardiogram. Finally, when serum potassium reaches 12 mmol/L, some parts of the myocardium may be excited and recover, while others have not yet depolarized, making it very easy to cause tachycardia, flutter, ventricular fibrillation, and even cardiac arrest, leading to death. Therefore, hyperkalemia is also a major cause of sudden cardiac death. Some patients with hyperkalemia may only exhibit arrhythmias and show no neuromuscular symptoms before death, thus a rapid diagnosis is crucial. The severity of hyperkalemia is generally assessed by both the measured serum potassium concentration and changes in the electrocardiogram.

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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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Written by Wei Shi Liang
Intensive Care Unit
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The difference between hyperkalemia and hypokalemia

Potassium ions are one of the essential electrolytes necessary for human life. Their physiological functions include maintaining cell metabolism, regulating osmotic pressure and acid-base balance, and preserving cell emergency functions, among others. The normal concentration of serum potassium is between 3.5 and 5.5 millimoles per liter. If it falls below 3.5 millimoles per liter, it is categorized as hypokalemia. If it exceeds 5.5 millimoles per liter, it is categorized as hyperkalemia. Common causes of hypokalemia include insufficient potassium intake, excessive potassium excretion, and the shifting of potassium from outside to inside the cells. The main causes of hyperkalemia include increased intake or reduced excretion of potassium, as well as substantial movement of potassium from inside the cells to the outside. Whenever hyperkalemia or hypokalemia occurs, it should be actively managed.

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Written by Wang Li Bing
Intensive Care Medicine Department
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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.

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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.