Effects Of High Potassium Levels In The Human Body – Professor of Internal Medicine, Department of Clinical Research, Division of Diabetes and Obesity Research, Cedars-Sinai Medical Center, Los Angeles, CA

Hyperkalemia is caused by the movement of Potassium out of the cells or the production of negative potassium. Cell migration increases plasma potassium concentration, but decreased potassium uptake leads to persistent hyperkalemia. Impaired renal calcium absorption is due to decreased sodium delivery to the distal nephron, decreased mineralocorticoid levels, or dysfunction or damage to the cortical collecting duct. Sometimes, all three of these problems are present. High intake of potassium can cause hyperkalemia but usually in the case of kidney failure. We discuss the clinical manifestations of hyperkalemia and present an approach to diagnosis and treatment.

Effects Of High Potassium Levels In The Human Body

Hyperkalemia is common in patients with heart disease. Its consequences can be serious and life-threatening, and its management and prevention require a multifaceted approach aimed at reducing the consumption of high-calcium foods, adjusting medications that cause hyperkalemia, and adding drugs to reduce the concentration of plasma calcium. In this way, patients with high blood pressure can get the cardiovascular benefits of drugs that block the renin-angiotensin-aldosterone system without developing hyperkalemia.

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The body of a typical 70-kg person contains 3, 500 mmol of potassium, 98% of which is in the intracellular space; the remaining 2% is in the extracellular space. This large intracellular-to-extracellular gradient determines cell voltage and explains why disturbances in plasma potassium can lead to manifestations in sensitive tissues such as the heart and nervous system.

The most important factors for the distribution of potassium between the intracellular and extracellular space are insulin and beta-adrenergic receptor stimulation.

Maintaining the body’s potassium content is the main function of the kidneys, with a small contribution from the gastrointestinal tract.

A normal kidney can produce too much potassium, and hyperkalemia may go undetected in the absence of kidney disease. This great strength has evolved to handle the Paleolithic man’s diet, which contained 4 times more potassium than modern diets.

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In the early days of agriculture, potassium consumption decreased as sodium consumption increased. A popular theory suggests that this imbalance between the diet of today and the nutritional requirements encoded in the genome during evolution can lead to chronic diseases such as hypertension, stroke, kidney, and bone disease.

The causes of hyperkalemia are summarized in Table 1. The movement of potassium from cells to the extracellular space is a cause of central hyperkalemia, but chronic hyperkalemia indicates impaired excretion. renal potassium. The following information is a guide to the approach to the hyperkalemic patient.

Pseudohyperkalemia, an art of measurement, occurs due to the mechanical release of potassium from cells during phlebotomy and sample processing.

This diagnosis is made when the serum potassium concentration exceeds the plasma potassium concentration by more than 0.5 mmol/L, and should be considered when hyperkalemia occurs in the absence of a clinical risk factor. Hand pinching, use of a tourniquet, or use of small needles during phlebotomy can cause pseudohyperkalemia.

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Meaning of pseudohyperkalemia. Since serum is the liquid part of blood that remains after coagulation, the release of potassium from cells that are injured during the process of coagulation can increase Potassium Levels. in the serum. Plasma is the blood-free portion of blood that has been treated with anticoagulants; no cells are injured and release potassium. Therefore, the serum potassium level will be higher than that in the plasma.

Reverse pseudohyperkalemia, in contrast, occurs when the plasma potassium level is falsely elevated but the serum value is normal. This condition has been described in hematologic diseases characterized by leukocytosis expressed in malignant cells that are capable of lysis and low mechanical stress due to increased weakness or changes in sodium-potassium ATPase pump action.

An increase in plasma calcium and a decrease in plasma calcium may increase the ability of calcium chelation and potassium release in a sample tube stained with the anticoagulant ethylenediaminetetraacetic acid.

Excess potassium intake may cause hyperkalemia in patients with reduced renal function or adrenal disease.

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Foods rich in potassium include bananas (a medium-sized banana contains 451 mg or 12 mmol of potassium) and potatoes (844 mg or 22 mmol in large baked potatoes with skin). Other potassium-rich foods include watermelon, citrus juices, and avocados. The least common dietary sources are raw coconut water (magnesium concentration 44.3 mmol/L) and noni juice (56 mmol/L).

Salt substitutes, recommended to cancer and chronic cancer patients, can be hidden sources of dietary potassium.

Clay ingestion is a possible cause of dyskalemia. Eating junk food can cause hypokalemia due to the binding of potassium in the gastrointestinal tract. Red mud or river mud, on the other hand, is enriched with potassium (100 mmol of potassium in 100 g of mud) and can lead to hyperkalemia. patients with chronic cancer.

Eating hot game heads. Some chew and eat the heads of the burned competition, a disease known as cautopyreiophagia. In one case reported,

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This action is an additional 80 mmol of potassium intake per day in the hypotensive patient, resulting in a plasma potassium concentration of 8 mmol/L.

Acute hyperkalemia results from redistribution of cellular potassium. A transfer of more than 2% of the body’s potassium from the intracellular to the extracellular space can double the plasma potassium concentration.

Tissue injury. Hyperkalemia often occurs in diseases that cause tissue damage such as rhabdomyolysis, trauma, severe hemolysis, and cancer.

Insulin deficiency. Insulin and catecholamines are important regulators of potassium distribution in the body. After a meal, the release of insulin not only determines the concentration of plasma glucose, but also potassium enters the cells until the kidneys have time to produce it. weight potassium food and restore the potassium content in the whole body.

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Exercise, beta-blockers. During exercise, potassium is released from skeletal muscle cells and accumulates in the interstitial compartment, where it exerts a vasodilatory effect. A concomitant increase in circulating catecholamines regulates this release by promoting cellular potassium uptake through beta-adrenergic receptor stimulation.

Metabolic acidosis can release (ie move) potassium from cells, but this effect depends on the type of acid. Hyperchloremic acid is usually aniongap acidosis (mineral acidosis) and this effect usually occurs due to the imbalance of the cell membrane with chloride anion. As hydrogen ions move into the cell due to the accumulation of ammonia and hydrogen peroxide, the electrolyte imbalance is maintained by the release of potassium.

In contrast, carbonic acid (such as lactic, betahydroxybutyric, or methylmalonic acid) does not cause potassium movement, as most carbonic anions cross the cell membrane with hydrogen. Lactic acid usually affects the movement of potassium, but it is caused by the loss of cell integrity due to cell ischemia. Hyperkalemia is usually present in patients with diabetic ketoacidosis due to insulin deficiency and hypertonicity, not the underlying carbon dioxide.

Hypertonic conditions can create hyperkalemia due to cell movement. For example, hyperglycemia, such as diabetic ketoacidosis, draws water from the intracellular into the extracellular compartment, thereby increasing intracellular potassium and creating a more favorable gradient for the flow of potassium through membrane channels. This effect also occurs in neurosurgical patients who are given large amounts of hypertonic mannitol. Repeated doses of immunoglobulin lead to extracellular accumulation of sorbitol, maltose, or sucrose, because these sugars are added to preparations to inhibit immunoglobulin synthesis.

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Chronic hyperkalemia is more related to decreased renal potassium transport than cellular turnover. In most cases, the doctor can distinguish between cell migration and renal failure based on available clinical data.

The transtubular potassium gradient has been used to determine if there is a disturbance in renal potassium excretion and to assess renal potassium management.

This calculation is based on the assumption that only water is collected before core collection and not the solution. We have long since found this idea to be wrong; a large amount of urea is returned each day to the lower medullary collecting duct due to urea recycling.

One situation in which the transtubular potassium gradient may be used is to determine whether hyperkalemia is the result of low aldosterone levels rather than aldosterone resistance. One can compare the trans-tubular potassium gradient before and after a physiologic dose (0.05 mg) of 9-alpha fludro-cortisone. An increase of more than 6 in a 4-hour period suggests aldosterone deficiency, while smaller changes indicate aldosterone inhibition.

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24-hour potassium excretion, urinary potassium-creatinine ratio. A better way to assess renal potassium management is to measure the amount of potassium in a 24-hour urine collection or to determine the urine potassium ratio with a laboratory. A 24-hour potassium depletion of less than 15 mmol or a potassium-creatinine ratio of less than 1 indicates an extrarenal cause of hypokalemia. A ratio greater than 20 would be an appropriate renal response to hyperkalemia.

One or more of 3 diseases should be considered in a hyperkalemic patient with impaired potassium absorption:

Under normal conditions, potassium is freely filtered across the glomerulus, and then most of it is collected in the proximal tubule and thick ascending limb. Calcium begins to be produced in the bronchial tubes and

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