The Impact of Hyperkalemia on the Heart

Written by Chen Li Ping
Endocrinology
Updated on October 20, 2024
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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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Mild hyperkalemia clinical manifestations

When blood potassium exceeds 5.5 millimoles per liter, it is referred to as hyperkalemia. Clinically, mild manifestations of hyperkalemia commonly involve the cardiovascular system, including bradycardia, audible enlargement of the heart, and weakened heart sounds. The electrocardiogram may show a shortened QT interval and peaked T waves. Symptoms related to the neuromuscular system include numbness in the lips and limbs, muscle soreness, and, in severe cases, paralysis of the respiratory muscles, which can lead to suffocation. All cases of hyperkalemia present various degrees of metabolic acidosis or azotemia, among other symptoms.

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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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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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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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Common Causes of Hyperkalemia

Hyperkalemia is when the serum potassium concentration exceeds 5.5 millimoles per liter. Common causes include excessive potassium intake and large doses of potassium salts, which can lead to hyperkalemia, as well as the use of stored blood. Another cause is reduced potassium excretion; in patients with renal insufficiency, reduced urine output or anuria leads to decreased renal potassium excretion. If potassium supplementation is inappropriate at this time, or if potassium-sparing diuretics are used, severe hyperkalemia can occur. Another scenario is the leakage of intracellular potassium during respiratory and metabolic acidosis, where sodium ion exchange occurs in cells, hydrogen ions enter the cells, and potassium ions leak out to the extracellular space, which can lead to increased blood potassium. These are the common causes of hyperkalemia.