Subscribe
Hyperkalemia
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.
Treatment methods for hyperkalemia
In clinical practice, a blood potassium level greater than 5.5 millimoles per liter is referred to as hyperkalemia. Once hyperkalemia occurs, it must be actively managed: the first step is to stop using medications that increase blood potassium, such as sustained-release potassium chloride, potassium-sparing diuretics like spironolactone, and ACE inhibitors; the second step is to use calcium supplements to counteract the toxic effects of high potassium on the heart; the third step is to use hypertonic glucose with insulin and sodium bicarbonate to correct acidosis and promote the movement of potassium into the cells; the fourth step is to use the diuretic furosemide to help reduce blood potassium. If drug treatment is ineffective, bedside hemodialysis may be employed. (Use of the above medications should be under the guidance of a doctor.)
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.
Is hyperkalemia acidosis?
Hyperkalemia is not acidosis, but during acidosis, the hydrogen ions of the gastric fluid within cells enter the cells, causing the potassium ions inside the cells to move to the extracellular fluid, resulting in hyperkalemia. Clinically, it is commonly seen in organic acidosis, lactic acidosis, diabetic ketoacidosis, and acute renal failure causing acidosis. Once hyperkalemia occurs and is diagnosed, immediate treatment should be administered. First, the primary disease should be treated; next, serum potassium should be reduced. In particularly severe cases, bedside hemofiltration can be administered, and the cardiotoxic effects of hyperkalemia should be mitigated.
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.
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.
Why is calcium used for hyperkalemia?
Hyperkalemia can increase the excitability of myocardial cells, leading to various malignant arrhythmias and even sudden death. Immediate treatment is necessary after hyperkalemia occurs. Clinically, it can be treated by hemodialysis or conservatively with medication. Why use calcium preparations for hyperkalemia? Because after using calcium preparations, the excitability of myocardial cells can be stabilized, effectively maintaining stable heart rates in patients and preventing sudden death due to malignant arrhythmias.
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.
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.)
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.