Hypokalemia: diagnosis and treatment of intensive care
The severity of manifestations of hypokalemia, which tends to be proportional to the extent and duration of hypokalemia
Potassium enters the body through oral or intravenous infusion, is largely stored in the cells, and is then excreted in the urine. Therefore, decreased intake, increased intracellular migration, or, most often, increased loss through urine, gastrointestinal tract, or sweat can lead to decreased serum potassium concentrations.
Potassium intake is usually 40 to 120 mEq per day, most of which is then excreted in the urine. The kidneys can lower potassium excretion to a minimum of 5 to 25 mEq per day with potassium depletion. Therefore, reducing intake alone rarely causes significant hypokalemia. This was demonstrated in a study in normal subjects, where a reduction in potassium intake to 20 mEq per day was associated with a decrease in serum potassium from 4.1 mEq/L at baseline to 3. 5 mEq/L.
However, a low potassium intake can contribute to the severity of potassium depletion when another cause of hypokalemia contributes, such as diuretic therapy.
More than 98 percent of total body potassium is intracellular, mainly in muscle. The normal distribution of potassium between cells and extracellular fluid is mainly maintained by the Na-K-ATPase pump in the cell membrane. Increased Na-K-ATPase pump activity and/or alterations in other potassium transport pathways may lead to transient hypokalemia due to increased intracellular potassium.
Most of the potassium filtered at the glomerulus is reabsorbed in the proximal tubules and loops of Henle, while most of the potassium is excreted from the main cell ducts in the junction and ducts. Aldosterone plays a central role in this process. An increase in plasma potassium stimulates aldosterone secretion, which then appropriately increases potassium excretion to return plasma potassium to normal.
Decreased Potassium Secretion by Major Cells - The effects of hypokalemia and decreased potassium excretion by primary cells are at least in part by the renin-angiotensin-aldosterone system. Hypokalemia inhibits aldosterone secretion, resulting in decreased sodium reabsorption by primary cells. Reduced sodium reabsorption by these cells reduces electrical stimulation, which is negative for potassium excretion through the apical potassium channels. In addition, potassium depletion increases renin release and systemic angiotensin II formation, which in turn downregulates apical secretory potassium channels, thereby directly inhibiting potassium excretion. Hypokalemia also activates the Na-Cl cotransporter (NCC) in the distal tubular complex cells, increasing sodium reabsorption by the distal tubule and decreasing sodium delivery to principle cells, thereby reducing decrease potassium excretion.
Increased active potassium reabsorption by type A interstitial cells – Decreased potassium activates the HK-ATPase pump in the apical membrane of type A interstitial cells, which are adjacent to the primary cells in the collecting duct. These pumps reabsorb potassium and secrete hydrogen.
Although hypokalemia can be transiently caused by the entry of potassium into the cells, most cases are caused by gastrointestinal or urinary losses that are not treated, for example, by vomiting. vomiting, diarrhea or diuretic therapy.
Potassium replacement is mainly indicated when hypokalemia is caused by potassium loss, and there is a significant deficiency of potassium in the body. It is also warranted for acute treatment in disorders such as periodic paralysis, hypokalemia or thyrotoxicosis in which hypokalemia is caused by redistribution of potassium into cells, often associated with significant symptoms. important. Potassium is cautioned in redistributive hypokalemia due to transient hypokalemia, and the use of potassium can lead to hyperkalemia as the basal process is corrected and potassium moves out of the cells.
The optimal treatment in patients with hypokalemia due to potassium loss depends on the severity of the potassium deficit. In addition, several different considerations are required to minimize ongoing urinary loss from diuretic therapy, or less frequently for primary hyperaldosteronism.
The severity of the manifestations of hypokalemia tends to be proportional to the extent and duration of the decrease in serum potassium. Symptoms usually do not manifest until serum potassium is below 3.0 mEq/L unless serum potassium falls rapidly or the patient has predisposing factors, such as a predisposition to arrhythmias associated with digitalis use. Symptoms usually resolve with the correction of hypokalemia.
Hypokalemia is a common electrolyte disturbance in the intensive care unit. Can be fatal if not treated promptly.
Normal blood potassium: 3.5-5mmo/l.
Hypokalemia < 3.5 mmol/l.
Clinical signs of hypokalemia
Muscle weakness (extremities, respiratory muscles...), muscle pain, muscle cramps.
Abdominal distention decreased intestinal motility, constipation, vomiting, nausea.
Signs of hypokalemia on electrocardiogram
There are tumor waves, flattened T waves, ST depression, QT prolongation, and severe electrocardiographic signs: ventricular arrhythmias (ventricular tachycardia, torsades de pointes).
Blood potassium < 3.5 mmo/l.
Mild level: 2.5mmol/l < kall < 3.5mmol/l. No symptoms.
Moderate: potassium <2.5mmol/l (<3mmol/l if taking digoxin). There was no muscle weakness and no signs of severity on the electrocardiogram.
Severe: potassium < 2.5mmol/l (< 3mmol/l if taking digoxin). muscle weakness or severe ECG findings.
Lost through the kidneys
Frequent urination for any reason.
Hypomagnesaemia, hypochloremia, hypercalcemia.
Renal tubular acidosis type 1 or type 2.
Fanconi syndrome, Bartter syndrome.
Vomiting or loss due to nasogastric drainage.
Bile drainage, ileostomy, after small bowel surgery.
Enemas or laxatives.
Due to drugs
Potassium excreting diuretic.
Insulin, glucose, natri bicarbonate.
Antibiotics: aminoglycosides, penicillin, ampicillin, rifampicin, ticarcillin.
Treatment of vitamin B12 and folic acid deficiency.
Insufficient potassium intake
Lack of food, alcoholism, diet.
Excess corticosteroids to metabolize salt and water
Primary hyperaldosteronism (Conn's syndrome), secondary hyperaldosteronism.
Cushing's syndrome, kidney cancer, para-glomerular cell tumor, drinking a lot of licorice...
Westphalian paralysis with primary hypokalemia
It is common in children up to the age of 30 years.
The course lasts from a few hours to a week, usually in the morning, and recurs many times.
Mild to severe muscle weakness.
Blood potassium compensation
Blood potassium compensation regimen
In case of hypokalemia with changes in the electrocardiogram, monitor the ECG continuously on the monitor until the ECG returns to normal.
Monitor blood potassium tests. Severe hypokalemia every 3 hours, moderate level every 6 hours, mild level every 24 hours until blood potassium returns to normal.
Avoiding glucose infusion in hypokalemic patients will cause increased insulin secretion, which leads to hypokalemia.
The concentration of potassium chloride phase should not exceed 40mmol/l (3g) if using a peripheral route (must be compensated through a central venous catheter).
The rate of potassium chloride compensation should not exceed 40 mmol/hour (3g).
An increase in pH of 0.1 is equivalent to a decrease in potassium by 0.4 mmol/l.
1g kali clorid has 13,6g mmol.
Find and treat the cause
Adequate oral potassium replacement for those at risk of hypokalemia. Foods and fruits that are high in potassium include potatoes, bananas, oranges, and peaches.