The impact of hyperkalemia on the heart

Written by Wei Shi Liang
Intensive Care Unit
Updated on December 15, 2024
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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 should not be eaten with hyperkalemia?

Potassium is an important element in human blood. Typically, the electrolytes we measure in blood tests include sodium, potassium, chloride, and calcium. Both low and high levels of potassium can have adverse effects on the body, especially hyperkalemia, which can cause sudden cardiac arrest and is considered dangerous in clinical settings. Patients with normal kidney function are less likely to develop hyperkalemia, which is more commonly seen in those who may have consumed Chinese herbal medicines containing high amounts of potassium for a long time. In patients with renal insufficiency, due to impaired kidney excretory function, hyperkalemia occurs more easily. Patients with hyperkalemia should generally avoid ACE inhibitors and ARB medications. For example, drugs like ACE inhibitors and spironolactone can further exacerbate hyperkalemia, so these types of medications are definitely not advisable. (The use of medications should be under the guidance of a professional doctor.)

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Written by Wei Shi Liang
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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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What should be noted in the diet for hyperkalemia?

In cases of hyperkalemia, it is important to avoid eating foods high in potassium, such as corn, lettuce, carp, eel, lamb, beef, pork, as well as dates, bananas, and others. These foods are rich in potassium and should be consumed less or not at all. Additionally, a diet high in sugar and fat should be provided, or some intravenous nutrition may be used, to ensure sufficient caloric intake and prevent the release of potassium from metabolic breakdown, which could lead to an increase in blood potassium levels. Also, it is important to avoid certain medications high in potassium, such as traditional Chinese medicines. (Medication use should be under the guidance of a professional doctor.)

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What are the causes of hyperkalemia?

The first reason is the excessive intake or administration of potassium, which can lead to hyperkalemia. For example, consuming foods that are very rich in potassium, or intravenously infusing solutions containing potassium. Additionally, the use of potassium salts of penicillin can also cause hyperkalemia, as well as the transfusion of stored blood, which can easily lead to hyperkalemia. Besides excessive intake and administration of potassium, diseases related to reduced excretion can also cause hyperkalemia, such as the most common instances during acute or chronic renal failure, where patients are prone to hyperkalemia. Furthermore, patients with reduced adrenal cortex function, such as aldosterone deficiency or Addison's disease, are also prone to hyperkalemia. Additionally, the use of diuretics that inhibit potassium excretion, notably spironolactone—a potassium-sparing diuretic—can also cause an increase in blood potassium levels. Another reason is a change in potassium distribution, such as when potassium moves from inside the cells to the outside, which can easily lead to hyperkalemia. This is common in cases of tissue damage, such as muscle contusion, or electrical burns, and tissue hypoxia, which also can easily lead to a change in potassium distribution, causing an increase in extracellular potassium. If hemolysis occurs in a test tube, such as if the venipuncture takes too long, or in conditions like leukocytosis or severe shaking of the blood sample, these might also lead to hyperkalemia. (The use of medications should be under the guidance of a doctor.)

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What are the changes in urine output in hyperkalemia?

When patients experience hyperkalemia, urine output generally decreases, leading to reduced potassium excretion by the kidneys, typically accompanied by abnormal kidney function. Thus, as long as kidney function is normal and daily urine output exceeds 500 milliliters, hyperkalemia is usually rare. Some causes of reduced renal potassium excretion include decreased glomerular filtration rates and reduced potassium secretion by the renal tubules, commonly seen in acute and chronic renal failure, adrenal cortex insufficiency, low renin, low aldosterone blood conditions, renal tubular acidosis, and long-term use of diuretics, especially potassium-sparing diuretics. Additionally, β-adrenergic tissue agents and angiotensin-converting enzyme inhibitors can cause drug-induced hyperkalemia, leading to abnormal kidney function and, consequently, decreased potassium excretion by the kidneys, ultimately resulting in reduced urine output.