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Hyperkalemia
Can hyperkalemia be cured?
The main focus is on the cause of hyperkalemia. If hyperkalemia is due to consuming foods rich in potassium, administration of potassium-containing solutions, transfusion of stored blood, use of potassium-sparing diuretics like spironolactone, or prolonged venipuncture causing severe shaking of the blood sample during transport, addressing these causes can prevent the occurrence of hyperkalemia. If hyperkalemia is caused by certain diseases, such as renal failure or adrenal insufficiency, active treatment of the underlying disease is required. If the renal failure is acute, recovery of kidney function might prevent the recurrence of hyperkalemia. However, if there is chronic renal insufficiency, there tends to be a higher recurrence rate of hyperkalemia. Therefore, whether hyperkalemia can be cured largely depends on identifying the underlying cause.
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.
Principles of treatment for hyperkalemia
First, to counteract the cardiac inhibitory effects of potassium, calcium salts can be injected, and sodium bicarbonate can be used to alkalinize the blood. Then, an infusion of hypertonic glucose and insulin can be administered to promote the internal movement of potassium ions. Secondly, to promote the excretion of potassium, diuretics can be used. The second method involves the use of cation exchange resins and sorbitol. The third method employs dialysis therapy, which can include both hemodialysis and peritoneal dialysis. The fourth method is to reduce the sources of potassium, stop a high potassium diet or the use of potassium-containing drugs. In cases of severe hyperkalemia, where there is a life-threatening emergency, urgent measures should be taken, primarily the intravenous administration of calcium ion antagonists to counteract the cardiac toxicity of potassium. In cases of severe arrhythmias or even cardiac arrest, emergency installation of a pacemaker or defibrillation can be carried out, and respiratory muscle paralysis may require ventilatory support. (Medication use should be under the guidance of a doctor)
Hyperkalemia
Typically, when serum potassium exceeds 5.5 mmol/L, it is referred to as hyperkalemia. However, an increase in serum potassium does not necessarily reflect an overall increase in body potassium; serum potassium can also rise when there is a deficiency of total body potassium. Therefore, in clinical practice, serum potassium is evaluated in conjunction with an electrocardiogram and medical history to determine if a patient has hyperkalemia. Hyperkalemia is an important emergency in internal medicine and can often lead to sudden cardiac arrest. It should be identified and prevented early.
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.
Clinical manifestations of hyperkalemia
The clinical manifestations of hyperkalemia are not specific. Early symptoms often include numbness in the limbs, sensory abnormalities, extreme fatigue, and muscle pain. In severe cases, there can be difficulties in swallowing, speaking, and breathing, paralysis of the limbs, and tendon reflexes may disappear. The central nervous system may show signs of restlessness, fainting, and confusion. Some may experience a slow heart rate, ventricular fibrillation, and in the most severe cases, it can lead to cardiac arrest. Other symptoms may include nausea, vomiting, diarrhea, and other gastrointestinal symptoms.
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.