Potassium in the human body is the main cation that maintains cell physiological activities, is necessary to maintain the body's normal osmotic pressure and acid-base balance, participate in sugar and protein metabolism, and ensure the normal function of neuromuscles.

Basic knowledge about serum potassium

Potassium in the human body is the main cation that maintains cell physiological activities, is necessary to maintain the normal osmotic pressure of the body and acid-base balance, participate in the metabolism of sugar and protein , and ensure the normal function of neuromuscles.

potassium ion is mostly found in the cells, a small amount is found in the extracellular fluid, and the concentration is relatively constant. potassium salt in the human body mainly comes from food. Serum potassium salt determination is actually a potassium ion assay for extracellular fluids, but potassium ions in the body are often constantly exchanged between cells and body fluids to maintain dynamic equilibrium. Therefore, the serum potassium concentration can also indirectly reflect the level of potassium ions in the cell to a certain extent.

The source of potassium in the body mainly includes dietary intake and reabsorption of digestive tract secretion; excretion is mainly through the kidneys, and very little is excreted through the intestines.

Normal reference value

Normal serum potassium is 3.5~5.5mmol/L;

less than 3.5mmol/L is hypokalemia ;

higher than 5.5mmol/L is hyperkalemia .

Little knowledge points

You may have heard that the main method of death penalty in my country is to inject a large dose of potassium chloride in a short time, which induces ventricular fibrillation in the prisoner and leads to death. This is also the reason why potassium chloride is listed as a high-risk drug in hospitals.

Potassium ion physiological effects

. Potassium is the material basis for maintaining the static potential of in the cell membrane. The static potential of is mainly determined by the permeability of the cell membrane to potassium and the difference in the internal and external potassium concentrations. This potential is an important factor affecting the excitability of neuromuscular tissue.

. Potassium participates in various metabolic processes, and is closely related to glycogen and protein synthesis. Some enzymes in the cell that are related to sugar metabolism , such as phosphorylases and thiodosases, must be present in high concentrations of potassium to be active.

. Regulates the osmotic pressure and acid-base balance of the internal and external fluids in the cell. Because a large number of potassium ions exist in the cell (about 20 times that of the outside of the cell), it not only maintains the osmotic pressure and acid-base balance of the intracellular fluids, but also affects the osmotic pressure and acid-base balance of the extracellular fluids.

Metabolism process of potassium ions

. Absorption: For surgery, absorption is nothing more than two ways: vein and gastrointestinal tract.

. Distribution: Because Na-K-ATP actively transports , most of the potassium in the body is in the cells. Intracellular accounts for 98% of the total potassium and extracellular accounts for 2%. When the blood potassium inside and outside the cell is redistributed, changes in blood potassium homeostasis can be caused. When potassium moves into the cell in large quantities, it can cause hypokalemia; when potassium moves out large quantities, it can cause hyperkalemia .

. The main excretion is: kidney, digestive tract, and skin.

The kidneys account for the majority. It is discharged mainly through distal nephron and collection tube. It is mainly regulated by the renin-angiotensin-aldosterone system. Another major cause of hyperkalemia is the poor excretion function of the kidneys, such as the reduction of glomerular filtration rate (CKD), tubular dysfunction (AKI), and RAAS system disorders (Addison’s disease aldosterone secretion).

The body regulates the K concentration at three levels: absorption, distribution and excretion, so that the potassium remains at a steady state level. The ultimate goal is to enable potassium to perform its ultimate physiological function.

Causes and mechanisms of hypokalemia

The occurrence of hypokalemia is nothing more than the following three reasons: Inadequate intake, excessive excretion, and abnormal distribution .

. Potassium intake is insufficient

is seen in long-term hunger, low-energy diet, absorption disorders, etc.

Because the potassium content in a normal diet is much higher than the body needs to maintain potassium balance, insufficient intake of short-term diet generally does not cause hypokalemia.

2. Excessive potassium excretion

The channels that can excrete potassium include the kidneys, gastrointestinal tract, and skin. It is often divided into renal potassium loss and non-renal potassium loss. It is better to clarify the non-renal potassium loss.

. Nonrenal loss transgastrointestinal loss is found in the loss of intestinal fluid caused by severe diarrhea, vomiting, gastric juice drainage, and fistomy. In addition to direct loss of K+, the above factors can cause secondary increased aldosterone secretion, resulting in increased urinary potassium excretion. Because the small intestinal fluid is alkaline, it is often accompanied by metabolic acidosis. In addition, excessive sweating, large-scale burns in the skin, long-term high-temperature operation without supplementation with sweat, and maintenance peritoneal dialysis patients may also cause hypokalemia.

. Renal loss

⑴. Diuretics: diuretics (thiazides, furosemide), permeable diuretics (diabetes, mannitol ).

diabetic ketoacidosis hyperglycemia causes permeable diuretic effects and a large number of negatively charged ketone bodies are excreted from the urine and promote the excretion of potassium in urine. In the early stage of acidosis, hypokalemia may not be obvious due to the redistribution of potassium in and outside the cells. If potassium supplementation is not given when treated with insulin or alkaline drugs, it can cause severe or even fatal hypokalemia.

⑵. mineralocorticosteroid (or mineralocorticosteroids) enhances the effects of: such as primary aldosterone , secondary aldosterone dysfunction, Cushing syndrome , congenital adrenal hyperplasia, 11β steroid dehydrogenase defect, etc.

⑶. Tubular Disease : Liddle syndrome, Bartter syndrome, and Gitelman syndrome are all congenital tubular diseases; renal tubular acidosis and Fancoin syndrome can be primary or secondary.

. Distribution abnormally, means that K+ enters the cell too much.

. During metabolic alkalosis, H+ intracellular is transferred to the outside of the cell, promoting K+ into the cell.

. Hypokalemia periodic paralysis (including thyrotoxicity) often occurs when eating a large amount of carbohydrate exercise and stress, which can promote potassium ions to transfer into cells.

. Injection of insulin and a large amount of glucose can also promote potassium ions to transfer into cells. For example, 10 units of insulin plus 50 grams of glucose can reduce blood potassium by 0.6-1.2 mmol/L.

    . Unexpected or induced hypothermia can cause K+ to enter the cells.

  • . The significant increase in potassium intake of newborn cells when blood cells are generated too quickly can cause hypokalemia, which is commonly found in the treatment of granulocyte colony stimulation factor for granulocytopenia or the use of folate and vitamin B12 for megacillary erythrocyte anemia .

    Clinical manifestations of hypokalemia

    . Skeletal muscle weakness

    We said above that potassium ions are an important component in maintaining muscle function. If hypokalemia occurs, muscle function will be dysfunction, manifested as muscle weakness, fatigue, weakness, limb paralysis, etc. Severe patients will have diaphragm, respiratory muscle weakness, dyspnea, dysphagia, etc. There will also be sensory disorders such as numbness and pain in the limbs.

    . Digestive system

    Hypokalemia will cause gastrointestinal dysfunction, manifested as nausea, vomiting, anorexia, abdominal distension, constipation, weakening or disappearing intestinal peristalsis, intestinal paralysis, etc. These symptoms are not specific, and many diseases will have these symptoms.

    .Central nervous system expression

    Hydkalemia can cause brain dysfunction, because the maintenance of brain function also requires potassium ions to participate.Therefore, hypokalemia can lead to listlessness, slow response, dysdirectional force, lethargy and even coma, etc. There was once a coma patient with unknown reasons. Later, after checking for blood potassium, it was only 1.9 mmol/L (normal 3.5-4.5), which was considered to be a coma caused by hypokalemia.

      , blood pressure drop manifestations

      various arrhythmia , mild patients have sinus tachycardia , atrial or ventricular pre-syndroop , atrioventricular block; severe patients have paroxysmal atrial or ventricular tachycardia , and even ventricular fibrillation, which can lead to death.

    • . The circulatory system shows

      This is a very serious manifestation. We say that the function of the heart, especially the myocardial function, highly requires the cooperation of potassium ions. If potassium ions are lacking, myocardial function will be significantly dysfunction, manifested as tachycardia, premature beats, etc., and even ventricular fibrillation, cardiac arrest and death. Therefore, when we clinicians encounter hypokalemia, the most feared thing is that it will cause arrhythmia.

    • , radial muscle lysis

      When there is severe potassium deficiency, radial muscle lysis may occur, which can sometimes induce acute renal failure.

    . Urinary system symptoms: shows polyuria, nocturnal urine, thirst, etc.

    . The clinical manifestation of potassium deficiency depends on the amount of potassium deficiency in

    • : Most of the loss of potassium in comes from intracellular fluid, and the intracellular potassium content is very high. When the loss is below 350 mmol, symptoms generally do not appear.
    • potassium deficiency rate: Whether symptoms appear after clinically deficient potassium depends not only on the amount of potassium deficiency, but also on the rate of potassium deficiency. Potassium deficiency occurs in a short period of time, although the quantity is small, the clinical symptoms can also be very obvious. On the contrary, if potassium is slowly lost, the symptoms will be mild.
    • is accompanied by sodium deficiency: When hypokalemia is accompanied by hyponatremia , the clinical manifestations are mild.

    ECG manifestations of hypokalemia

    When the blood potassium concentration is less than 2.7 mmol/L, some patients may experience corresponding electrocardiogram changes due to delay in ventricular repolarization.

    . Characteristics of mild hypokalemia:

    • changes less and not significant;
    • U wave is obvious, P wave amplitude and time limit increase;
    • PR interval and QRS time limit extend;
    • T wave is low or inverted, and ST segment mild progressive depression (no significant correlation with blood potassium concentration).

    , Surawicz, etc. proposed the following three characteristics of electrocardiograms:

    ① ST segment depression is ≥0.5 mm;

    ② U wave amplitude > 1 mm;

    ③ The amplitude of the same lead U wave exceeds the T wave amplitude.

    When there are three characteristics on the electrocardiogram in two leads on the electrocardiogram, the ECG expression of common hypokalemia is typical of hypokalemia, and the two characteristics mentioned above or one of them related to U waves is shown, it is the electrocardiogram expression of common hypokalemia.

    . Mechanism of U wave generation: U wave is generally related to the 3-phase repolarization of Purkinje fiber , and is generally masked by the repolarization wave of the ventricular muscle and is not obvious. During hypokalemia, the inward rectified potassium channel on the Purkinje cell membrane decreases K+ permeability and K+ outflow decreases, so the resting potential of Purkinje cells decreases, the excitability increases, the conductivity decreases, and the conductivity decreases. The automatic depolarization accelerates in the fourth phase, and the self-discipline increases.

    Hypokalemia has greater impact on Purkinje fiber than on the ventricular muscle, which prolongs the repolarization process of Purkinje fiber than the repolarization process of the ventricular muscle. The repolarization process of Purkinje fiber is manifested, and U wave enlargement occurs.

    As the blood potassium decreases, U wave gradually becomes obvious

    In addition, T wave and U wave can produce the performance of QT interval prolongation (T wave becomes smaller, U wave becomes larger, U wave is higher than T wave). However, since T wave and U wave are difficult to distinguish, it is manifested as a prolongation of the QU interval, while the actual QT interval is normal.

    Hydkalemia, it is manifested as

    ST segment depressed, U wave is enlarged, and QU interval prolonged

    . It should be noted that U wave is not a specific manifestation of hypokalemia, and can also occur in bradycardia or left ventricular hypertrophy.

    If hypokalemia further develops, it may lead to fatal ventricular arrhythmias in severe cases, such as ventricular speed, ventricular fibrillation and torsional ventricular speed.

    Classification of the severity of hypokalemia

    . Common blood test indicators: Serum potassium concentration decreases, less than 3.5 mmol/L, blood pH is at the normal upper limit or greater than 7.45, and Na+ concentration is at the normal lower limit or less than 135 mmol/L.

    , commonly used urine test indicators

    urine potassium concentration is reduced (except for renal tubular function impairment or "occult tubular function impairment"), urine pH is acidic, and urine sodium is discharged more.

    potassium ions are crucial to regulating normal electrical activity of the heart. Reduced extracellular potassium ions lead to increased myocardial excitability and may develop reentrant arrhythmias.

    serum potassium is less than 3.5 mmol/L. It is called hypokalemia.

    Among them, those with blood potassium between 3.0 and 3.4 mmol/L are mild hypokalemia;

    .5 to 2.9 mmol/L are moderate hypokalemia;

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    Common clinical potassium supplementation pathways

    Know the cause of hypokalemia, and we will start treating hypokalemia next. The first thing is to actively treat the primary disease, try to eliminate the onset factors, and prevent the loss of potassium. Do you know these common ways to supplement potassium?

    , oral potassium supplementation

    For those with mild symptoms or chronic diseases, oral potassium deficiency is generally preferred, oral potassium supplementation is the most direct and convenient, and the maintenance time is also long.

    However, oral potassium supplementation will have a stimulating effect on the patient's gastrointestinal mucosa. Patients may experience gastrointestinal adverse reactions such as nausea, vomiting, and diarrhea. In severe cases, gastrointestinal ulcers and bleeding will occur.

    Therefore, in order to reduce adverse gastrointestinal reactions, it is recommended that oral potassium supplementation should be placed after a meal, or the 10% potassium chloride solution is diluted into milk or juice for taking.

    , intravenous potassium supplementation

    Intravenous infusion of potassium chloride is the most commonly used method of potassium supplementation in clinical practice. Note that the concentration does not exceed 0.3%, and the drop speed cannot exceed 40~60 drops/min. It is suitable for patients with severe hypokalemia. In order to correct hypokalemia in a timely and quickly, and reduce the occurrence of complications.

    , dietary potassium supplementation

    guides patients to eat foods rich in potassium: such as grapes, watermelon, bananas, spinach, mushrooms, etc. to prevent the production of hypokalemia. Potassium salt can also be taken orally.

      , atomized inhalation potassium supplementation

      This method is not only convenient to administer and has no adverse reactions, but also avoids the stimulation of oral and intravenous potassium supplementation to the gastrointestinal tract and venous blood vessels. It is especially suitable for patients who must strictly control the intake volume.

      Principles for potassium supplementation

      . It is not advisable to supplement potassium too early, see urine.

      . It should not be too concentrated, and the concentration should not exceed 0.3% [referring to the concentration of KCl (potassium chloride)].

      . It should not be too fast. Generally, the rate of potassium supplementation intravenously is 20-40 mmol/h (reduce it if children are careful).

        . It is not advisable to have too much, and the adults should not exceed 200 mmol per day (equivalent to 15 g of potassium chloride).

        Potassium supplementation amount

        In addition to seeing the principle of urine potassium supplementation, there are also secrets of 3, 6 and 9.

        Mild potassium deficiency: serum potassium (3.0-3.5 mmol/L) supplement 3 g of potassium chloride one day;

        Moderate potassium deficiency: serum potassium (2.5-3.0 mmol/L) supplement 6 g of potassium chloride one day;

        Severe potassium deficiency: serum potassium (<2.5>

        Note, what is said here is extra, that is, if the patient cannot eat, remember to add the daily physiological potassium supplement to 6 g of potassium chloride; pay special attention to potassium supplementation and potassium chloride supplementation are not the same thing, pay attention to conversion!

        Types of potassium supplementation

        Drug potassium chloride, potassium citrate and potassium magnesium aspartate (especially applicable to those who lack both potassium and magnesium).

        ① Potassium chloride: contains 13-14 mmol/g, most commonly used;

        ② Potassium citrate: contains about 9 mmol/g, heart failure or severe myocardial damage, peptic ulcer ;

        ③ Potassium acetate: contains about 10 mmol/g, potassium citrate and potassium acetate are suitable for the treatment of hyperchloremia (such as renal tubular acidosis);

        ④ Potassium glutamate: contains about 4.5 potassium glutamate: contains about 4.5 potassium glutamate: contains about 4.5 potassium glutamate: contains about 4.5 potassium glutamate: contains about 4.5 potassium glutamate: contains about 4.5 potassium glutamate: contains about 4.5 potassium glutamate;

          Potassium glutamate: contains about 4.5 potassium glutamate: contains about 4.5 potassium glutamate: contains about 4.5 potassium glutamate;

            Potassium glutamate: contains about 4.5 potassium glutamate: contains about 4.5 potassium glutamate: contains about 4.5 potassium glutamate;

              Potassium glutamate: contains about 4.5 potassium glutamate: contains about 4.5 potassium glutamate;

              html mmol/g, suitable for those with liver failure and hypokalemia. Excessive dose of this product can cause alkalemia. Use it with caution or contraindication for those with alkalineemia;

              ⑤L-Potassium magnesium aspartate: contains 3.0 mmol/10 mL of potassium, 3.5 mmol/10 mL of magnesium, aspartic acid and magnesium help potassium to be carried out in cells. Hyperkalemia, acute and chronic renal failure , Addison's disease, III atrioventricular block, cardiogenic shock (blood pressure below 90 mmHg) is contraindicated.

              Warm reminder: Remember to convert the amount of potassium chloride or potassium between different drugs!

              Precautions for potassium supplementation

              (1) Potassium supplementation requires checking renal function and urine volume, 500 mL/d or 30 mL/h, which is safer, otherwise you should be vigilant about hyperkalemia.

              (2) During hypokalemia, potassium chloride is added to normal saline and drip intravenously. If the blood potassium is normal, add potassium chloride to glucose and drip intravenously, which can prevent hyperkalemia and correct potassium deficiency. If the blood potassium is still normal after 24 hours of stopping intravenous potassium supplementation, it can be changed to oral supplementation (3.5 mmol/L of blood potassium, and still lacking potassium is about 10%).

              (3) Potassium enters the cell slowly, and the potassium equilibrium time inside and outside the cell takes about 15 hours or more. Therefore, special attention should be paid to the strict observation after infusion and infusion to prevent transient hyperkalemia.

              (4) Refractory hypokalemia should be paid attention to correcting alkaline poisoning and hypomagnesemia ;

              (5) Potassium supplementation can aggravate the original hypocalcemia . Hand and foot convulsions should be given in time. calcium agent ;

              (6) It is not advisable to use potassium enteric-coated tablets for a long time to avoid the small intestine being in a high potassium state causing complications such as small intestine stenosis, bleeding, obstruction, etc. The amount of

              !

              How to prevent pain intravenous potassium supplementation

              . Select solvent to prevent and treat pain: Glucose saline and normal saline as solvents can reduce the occurrence of pain.

              Reason: Because potassium ions are pain-causing factors, they act on nerve ending receptors after entering the tissue, depolarizing them, thereby causing pain; and after sodium ion enters the tissue, the nerve cells are superimposed, its excitability is reduced, and the pain area is increased, thereby alleviating pain.

              . Apply external medicine to relieve pain: When pain occurs during infusion, immediately dip sterile dry cotton swab in nitroglycerin ml and apply it locally to relieve pain.

              Reason: Nitroglycerin is an antiangina pectoris that relaxes smooth muscles and relieves vasospasm. Local external coating can be absorbed through the skin to dilate blood vessels, which can directly work and relieve pain.

              . Change the operation method to relieve pain: flip the needle handle 180° plus the hot compress method can significantly relieve local pain in the infusion.

              Reason: Because the needle faces obliquely to the lower wall of the blood vessel, the flow direction of the drug has fundamentally changed, which is relatively far away from or avoids stimulation of the sensitive nerve endings to the body surface.

              In addition, the use of a precision infusion device can effectively reduce the stimulation of blood vessels by particles in the liquid and reduce pain.

              Drugs that can easily lead to hypokalemia