Subscribe
Hyperkalemia
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.
Common symptoms of hypokalemia and hyperkalemia
The common symptoms of hyperkalemia and hypokalemia, mainly seen in severe cases of high or low potassium, manifest as neurological and muscular symptoms as well as circulatory system symptoms, which are fairly similar in both conditions. If the blood potassium is particularly low, less than 2.0 mmol per liter, it can lead to reduced or absent reflexes. In severe cases, this may progress to paralysis of the respiratory muscles, causing respiratory pump failure. For hyperkalemia, particularly severe cases may also present with swallowing difficulties and respiratory distress. These central nervous system issues can lead to confusion and fainting. Another similar issue is the impact on the circulatory system; severe hypokalemia can cause ventricular tachycardia and even ventricular fibrillation, leading to death. In hyperkalemia, the impact on the cardiovascular system primarily causes malignant tachycardia and can also result in ventricular fibrillation. The main cause of sudden death in hyperkalemia is ventricular fibrillation and cardiac arrest, demonstrating that severe hyperkalemia and hypokalemia similarly cause significant arrhythmic conditions in the heart.
The role of calcium agents in hyperkalemia
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.
What are the causes of hyperkalemia?
Hyperkalemia, with blood potassium levels greater than 5.5 mmol/L, commonly occurs due to decreased potassium excretion or abnormal potassium transport within cells, as well as other reasons such as excessive intake. Decreased potassium excretion can commonly be due to renal failure, the use of potassium-sparing diuretics, renal tubular acidosis, and reduced secretion of corticosteroid aldosterone. Abnormal potassium transport includes conditions such as acidosis, rhabdomyolysis, extensive burns, severe trauma, intestinal necrosis, and peritoneal bleeding, among other diseases. Excessive potassium intake can be due to sample hemolysis or an elevation in white blood cells, both of which can lead to hyperkalemia. Therefore, it is crucial to be vigilant in clinical settings and address the condition promptly and appropriately.
The difference between hyperkalemia and hypokalemia.
Hypokalemia refers to a serum potassium concentration lower than 3.5mmol/L, and its clinical manifestations are diverse. The most life-threatening symptoms involve the cardiac conduction system and the neuromuscular system. Mild hypokalemia shows on an electrocardiogram as flattened T waves and the appearance of U waves, while severe hypokalemia can lead to fatal arrhythmias, such as torsades de pointes and ventricular fibrillation. In terms of the neuromuscular system, the most prominent symptom of hypokalemia is the loss of tone in smooth muscles and flaccid paralysis in skeletal muscles, which, when involving respiratory muscles, can lead to respiratory failure. Hyperkalemia, on the other hand, refers to a serum potassium concentration exceeding 5.5mmol/L, mainly presenting clinical symptoms in cardiac and neuromuscular conduction. Severe cases can cause bradycardia, atrioventricular conduction block, and even sinus arrest. Mild hyperkalemia, with levels between 5.5 to 6.0mmol/L, shows on an electrocardiogram as peaked T waves. As hyperkalemia continues to increase, it can lead to lengthening of the PR interval or disappearance of the P wave, QRS widening, and eventually cardiac arrest. Regarding the neuromuscular system, the clinical manifestations of hyperkalemia are very similar to those of hypokalemia, including weakness and paralysis of skeletal and smooth muscles.