Discover the Side effects of too much potassium in the blood.
Higher than normal potassium levels in the blood could be a sign of kidney disease, for example.
Normally, the potassium concentration in the blood should be between 3.6 and 5 mmol / L.
Doctors often prescribe dosages of the main electrolytes (chemical elements that carry an electric charge) in plasma (sodium, potassium, chlorine, bicarbonate) in patients with hypertension or with heart or kidney disease.
Plasma is the liquid that carries the various cells in the blood.
Knowing the plasma concentrations of these substances is essential because they play a major role in water transfers between the different water compartments, the regulation of the pH (acidity index) of the plasma, and the transmission of water. nerve impulses.
The concentration of potassium in the blood plasma is normally between 3.6 and 5 mmol / L (130-200 mg / L).
The distribution of potassium in the body is very unequal since its concentration in the cells varies from 90 to 150 mmol / l.
Food provides approximately 60 to 120 mmol of potassium per day in an adult. The foods highest in potassium are fruits, vegetables, and chocolate.
Almost all of the potassium ingested is absorbed in the digestive tract and is found in the urine in an amount equivalent to that absorbed in the intestine.
The main physiological role of potassium, which carries a positive charge, is to generate the membrane potential which is the difference in electrical charge on either side of the cell membrane, the interior of the cell being electronegative concerning outside.
The severity of hyperkalemia (increased potassium concentration in the plasma) arises from the disturbance it causes, the membrane potential in the heart cells, and the resulting rhythm disturbances.
In routine clinical practice, potassium is measured in plasma and urine.
It is essential that the blood sample is not hemolyzed, which would distort the result by passing potassium from the red blood cells into the plasma.
Hyperkalaemia results either from a defect in renal excretion of potassium or from an increased passage of cellular potassium into the extracellular compartment.
Hyperkalaemia of renal origin occurs in renal failure or, in healthy kidneys, if the secretion of aldosterone, a hormone that controls the transport of sodium and potassium in the distal part of the nephron (structural and functional unit of the kidney which has about 1,000,000 nephrons), is insufficient.
Acute or chronic renal failure is the main cause of hyperkalemia and the only cause of high hyperkalemia.
In the first case, it can be aggravated by tissue destruction, as seen in muscle crush syndrome common in natural disasters, eg earthquakes.
In the second case, it appears at the end of the disease, i.e. when the number of functional nephrons becomes insufficient and is favored by acidosis (decrease in pH, i.e. increase in l plasma acidity) with which it often coexists.
It can also occur accidentally when a dietary excess of potassium has been ingested or when potassium-sparing diuretics have been inadvertently prescribed.
Hyperkalaemia due to insufficient secretion of aldosterone is observed in slow adrenal cortical insufficiency also called Addison’s disease.
Hyperkalaemia is associated with hypokalemia (decrease in the amount of potassium excreted in the urine), hyponatremia (decrease in sodium concentration in plasma), and increased plasma renin (the enzyme causing the process leading to the production of angiotensin II, a hypertensive hormone).
Finally, hyperkalemia of renal origin can follow the taking of drugs, mainly those which block the action of aldosterone, those which inhibit the reabsorption of sodium by the epithelial sodium channel of the distal nephron and, therefore, also inhibit the passage of potassium in the urine and all those which decrease the secretion of aldosterones, such as ACE inhibitors or angiotensin II receptor antagonists. In all of these cases, hyperkalemia is associated with hypokalemia.
The second major cause of hyperkalemia is the increased passage of potassium from the cell to the extracellular compartment to which the plasma belongs.
Two causes are at the origin of this dysfunction: the destruction, usually by necrosis, of a large number of cells and the acidosis which facilitates the exit of potassium from the cell compartment.
Finally, it is appropriate to cite an exceptional cause of genetic origin, periodic paralysis with hyperkalemia or Gamstorp’s disease which causes acute attacks of hyperkalemia with muscular paralysis.
Treatment of hyperkalemia depends on its severity and origin.
When it reaches or exceeds 7 mmol / l, which is seen almost exclusively in renal failure, hemodialysis is urgently needed to quickly rid the extracellular compartment of excess potassium to avoid sudden death by a heart attack.
While awaiting or in the impossibility of hemodialysis, substitution treatments should be started: injection of calcium gluconate to decrease hyperexcitability, injection of insulin, and infusion of sodium bicarbonate to transfer potassium to the blood cell compartment, resin enemas fixing potassium in the intestine.
The occurrence of hyperkalemia associated with acidosis, if not accidental, in the final phase of chronic renal failure requires the initiation of a dialysis program in the patient.
The prevention of hyperkalemia in patients with chronic renal failure can be obtained by the diet “without potassium”, the prescription of diuretics promoting the elimination of potassium (diuretics of the loop of Henle which is a segment of the nephron shaped hairpin and thiazide diuretics) and drugs that trap dietary potassium in the intestine and thus prevent its absorption.
The treatment of adrenal cortical insufficiency is provided by deficient hormones, minerals- and glucocorticoids.
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