The classification of hypokalemia can be broadly divided into four categories: acute hypokalemia (acute hypokalemia), chronic hypokalemia (chronic hypokalemia), metastatic hypokalemia, and dilutional hypokalemia.
(a) Acute hypokalemia, referred to as acute hypokalemia. It is a condition in which the serum potassium ion concentration drops below the normal level within a short period of time due to increased potassium loss or combined with insufficient intake, while the potassium content of the body decreases and various types of cardiac arrhythmias or muscle weakness are likely to occur.
1.Cause
Insufficient intake
(1) Fasting or anorexia Since both the general diet and the enteral nutrition diet contain more potassium (as mentioned above, most intracellular K+ concentrations are more than 30 times higher than extracellular ones) and the kidneys have a strong capacity for potassium retention, hypokalemia does not easily occur with a general reduction in diet; however, it occurs when there is a serious lack of intake and a lack of potassium in intravenous rehydration, mainly seen in coma, after surgery, digestive tract diseases, etc. Patients who cannot eat or are severely underfed. Patients with chronic wasting diseases, with little muscle tissue and low overall potassium stores, are also prone to hypokalemia when they do not eat enough. Patients with cardiac insufficiency, liver cirrhosis, hematological diseases, and tumor diseases are prone to severe under-eating.
(2) Individual patients with severe eccentricities may also develop hypokalemia.
Increased loss is mainly seen in acute loss of various secretory fluids; or in patients with massive diuresis and inadequate potassium supplementation, when it often coexists with hyponatremia and hypochlorhydria.
(1) Loss through the digestive tract because the concentration of potassium in all kinds of digestive fluids is almost always higher than that of plasma, and the secretion volume is larger, and the secretion volume is even higher when stimulated by inflammation and other pathological factors; once such diseases occur, the amount of food eaten is significantly reduced, or even completely fasted, so that diseases of the digestive tract are very prone to hypokalemia, and easily combined with other electrolyte ion disorders. The composition of the digestive fluid varies from one part of the body to another, so the type of combined electrolyte disorders also varies. For example, the gastric juice has a high content of Cl- and H+, so vomiting and gastric drainage can easily be combined with hypokalemia, hypochlorhydria and metabolic alkalosis. The concentration of HCO-3 in intestinal fluid is high, so bile duct and pancreatic drainage and diarrhea are prone to combined hyperchloremic acidosis. Hypokalemia can also occur in patients who use laxatives improperly.
(2) Loss via the kidney Various primary or secondary renal tubular dysfunctions are prone to excessive potassium loss, and diseases or factors other than the kidney can also increase potassium excretion from the kidney, mainly the following problems.
(1) Renal tubular impairment of various causes of proximal or distal tubular acidosis can lead to severe hypokalemia due to decreased reabsorption or increased secretion of potassium. Others such as aminoglycoside antimicrobials, immunosuppressants (especially routinely applied in organ transplant patients), antiviral drugs or chronic potassium or magnesium deficiency tend to impair renal tubular function and hypokalemia occurs. The renal function (creatinine) of these patients is mostly normal or even negative for urine protein, but may be combined with other electrolyte ion deficiencies, uremia, metabolic acidosis, etc. Therefore, it can be called “occult renal tubular impairment”, which is essentially an abnormality of renal tubular reabsorption or secretion function.
(2) Hypokalemia occurs during the polyuric phase of renal insufficiency, which is accompanied by a large amount of electrolyte loss, such as sodium and potassium.
(3) Elevated levels of adrenal glucocorticoids or salt corticoids or enhanced effects of adrenal glucocorticoids or aldosterone have the function of sodium retention and potassium excretion, especially the latter, so that hypokalemia is likely to occur when its concentration in the blood is increased. The breakdown is as follows.
Increased secretion: Cortisol and aldosterone have certain similar stimulating factors and production sites (adrenal cortex), and in pathological states, they can be manifested as a separate increase in the level of one hormone or as a simultaneous increase in the level of the two hormones. Increased secretion (increased renin secretion is described separately) is mainly seen in: adrenocortical hyperplasia and increased secretion due to hypothalamic and pituitary diseases, adrenocortical adenoma or cancer; stressful increase due to various acute and severe diseases, such as trauma, severe infection, surgery, etc.
Exogenous increase: various diseases requiring extensive oral or intravenous application of glucocorticoid therapy. Hypokalemia may also occur in individual patients with inappropriate use of inhaled hormones.
Decreased inactivation: seen in cirrhosis and right heart insufficiency.
Increased function of the renin-angiotensin-aldosterone system is a relatively common endocrine disorder.
Glycocorticoids and their derivatives: Because the receptor structures of salt corticosteroids and glucocorticoids in the distal renal tubule initiation and the cortical collecting duct are very similar, both hormones can bind to each other with both receptors, and the plasma concentration of glucocorticoids is much higher than that of salt corticosteroids and should have a stronger effect, but in fact this is not the case because there is a substance called 11β hydroxysteroid dehydrogenase in these sites that prevents glucocorticoids from Corticosteroid binding to the salt corticosteroid receptor, so glucocorticoids have a limited effect on electrolyte metabolism, and glycoconjugates can block this binding, leading to a salt corticosteroid-like effect and producing hypokalemia.
Diuretics: These include tab diuretics such as tachyphylaxis and thiazide diuretics such as dihydrocortisone, and osmotic diuretics such as mannitol and hypertonic glucose, all of which can lead to large excretion of urinary potassium.
(5) Excessive anion in the renal tubule: it increases the negative charge in the tubular lumen and facilitates the secretion of K+, such as the application of high-dose penicillin, especially when combined with blood volume deficiency.
⑥Other: such as hypomagnesemia, Bartter syndrome, cotton phenol poisoning, etc.
2.Pathophysiology and clinical manifestations
(1) neuromuscular system
(1) Skeletal muscle weakness and paralysis: hypokalemia, the concentration difference between intra- and extracellular K+ increases, the negative value of the resting potential increases, the value of the trigger domain of the action potential increases, the excitability and conductivity of the nerve-muscle decreases, and muscle weakness occurs. Muscle weakness usually starts in the lower extremities, especially in the quadriceps, and manifests as difficulty walking and unsteadiness in standing; as hypokalemia increases, muscle weakness worsens and involves the trunk and upper extremity muscles until it affects the respiratory muscles and respiratory failure occurs. In general, muscle weakness can occur when the serum potassium concentration is below 3 mmol/L, and paralysis can occur when it is below 2.5 mmol/L. It is also easy to complicate respiratory failure.
In patients with pulmonary insufficiency, hypokalemia leading to respiratory failure or exacerbation of respiratory failure is more common, but is easily overlooked clinically.
(2) Smooth muscle weakness and paralysis: manifested as abdominal distension, constipation, and in severe cases, paralytic intestinal obstruction, and also urinary retention.
(2) Circulatory hypokalemia can lead to dysfunction of cardiac muscle cells and their conduction tissues, as well as multiple, small focal necrosis of the myocardium, mononuclear and lymphocyte infiltration, and finally scar formation.
① Arrhythmia: It is related to the abnormalities of excitability of autonomic cardiac cells and conduction tissue conduction, mainly manifested as decreased excitability of sinus node, slowed conduction of atrioventricular junctional zone, and increased excitability of ectopic rhythm cells, so a variety of arrhythmias can occur, including sinus bradycardia, premature atrial or ventricular beats, supraventricular tachycardia and atrial fibrillation, atrioventricular block, and even ventricular tachycardia and ventricular fibrillation. Susceptibility to digitalis toxicity.
Electrocardiographic manifestations are valuable in the diagnosis of hypokalemia. As hypokalemia worsens, P-wave widening, QRS wave widening and the above-mentioned arrhythmias may appear.
(ii) Cardiac insufficiency: Changes in myocardial function and structure caused by severe hypokalemia may directly induce or aggravate cardiac insufficiency, especially in patients with poor underlying cardiac function.
(③) Hypotension: It may be related to vasodilatation due to phytonadic dysfunction.
(3) In transverse myelolysis, under normal conditions, K+ is released from the transverse muscle during muscle contraction and the blood vessels dilate to accommodate the increased energy metabolism. In patients with severe hypokalemia, the above effects are diminished, muscle tissue is relatively ischemic and hypoxic, and rhabdomyolysis can occur, with a large amount of myosin entering the renal tubules, which can induce acute renal failure. When the serum potassium concentration is lower than 2.5 mmol/L, there is a possibility of rhabdomyolysis.
(4) The main pathological changes of renal impairment are renal tubular hypofunction, epithelial cell degeneration, renal interstitial lymphocyte infiltration, and in severe cases, fibrous changes. Clinical manifestations are: (1) reduced sodium pump activity of renal tubular epithelial cells, reduced intracellular K+, increased hydrogen-sodium exchange, acidic urine, and metabolic alkalosis; increased intracellular Na+, reduced tubular fluid Na+ reabsorption, and hyponatremia. (ii) Decreased concentration function: polyuria, increased nocturia, low specific gravity urine, hypotonic urine, poor response to antidiuretic hormone. ③Increased ammonia production capacity, increased acid excretion, increased HCO-3 reabsorption, and metabolic alkalosis. (iv) Chronic hyperalgesia. It is more common in patients with chronic, long-term hypokalemia or hypomagnesemia.
(5) Digestive system mainly leads to hypotonia of smooth muscle of gastrointestinal tract, prone to loss of appetite, nausea, vomiting, abdominal distension, constipation, and even intestinal paralysis.
(6) In acid-base and other electrolyte disorders hypokalemia, sodium pump activity is weakened, active transport of ions inside and outside the cell is reduced (passive diffusion is relatively increased), hydrogen-sodium exchange ratio exceeds potassium-sodium exchange, and decreased serum Na+ concentration or hyponatremia, extracellular alkalosis, increased intracellular Na+ concentration and acidosis occur. As mentioned above, the sodium pump activity of renal tubular epithelial cells is weakened, aggravating alkalosis and hyponatremia; ammonia production capacity is increased, further metabolic alkalosis with a corresponding decrease in chlorine retention capacity, and lower blood chloride occurs.
It should be emphasized that the effect of K+ on the body is also related to the lack of sodium. When sodium and potassium are lacking at the same time, the symptoms of potassium deficiency are mild; however, when potassium deficiency and sodium intake is normal, the symptoms of potassium deficiency are more obvious. If potassium is deficient while the sodium content of the body is normal, K+ transfers to the extracellular area and Na+ to the intracellular area, leading to intracellular ion disorder, which directly affects the metabolism of the body; Na+ transfers to the intracellular area, which can lead to intracellular edema; K+ and Na+ transfers in large amounts lead to a serious imbalance in the ratio of intra- and extracellular K+ and intra- and extracellular Na+, which directly affects the resting potential and action potential, resulting in obvious clinical symptoms. However, when Na+ and K+ are lacking at the same time, the intra- and extracellular ion transfer is not obvious, and the effect on cell metabolism and electrophysiology is rather small. Therefore, the sodium intake should be strictly controlled in severe hypokalemia.
3.Laboratory examination
(1) Commonly used blood test indicators are decreased serum potassium concentration, less than 3.5 mmol/L, blood pH at normal high limit or greater than 7.45, Na+ concentration at normal low limit or less than 135 mmol/L.
(2) Commonly used urine laboratory indicators, urine potassium concentration is reduced (except for renal tubular impairment or “occult renal tubular impairment”), urine pH is acidic, and urine sodium excretion is high.
4.Treatment
(1) The principle of acute hypokalemia is that most of the acute hypokalemia has a clear underlying disease or triggering factors, especially the medical factors, so prevention should be the main focus. First of all, we should try to remove the causative factors and resume normal diet as soon as possible. Since food contains a large amount of potassium salts, once the patient resumes a normal diet and tries to correct the large amount of potassium loss. In the case of temporary failure to correct a large amount of potassium loss, potassium should be appropriately supplemented and hypokalemia will be easily prevented and treated.
(2) The amount of supplementation Once acute hypokalemia occurs, rehydration in proportion to the body fluid electrolytes is sufficient. The amount of potassium supplementation (mmol) = (4.2 – measured value) x body weight (kg) x 0.6 + continued loss + physiological requirements. Since it takes about 15h for the exchange of potassium inside and outside the cells to reach equilibrium, the general rule is to supplement 2/3 on the first day and 1/3 on the next day, and the speed of rehydration should be controlled, faster at the beginning and slower thereafter, so that the liquid is inputted more evenly within 24h, and reviewed once in 2 to 6h if necessary. Generally choose potassium chloride solution. After the blood K+ concentration is normalized, it is still necessary to supplement potassium chloride solution for several days.
(3) Precautions As mentioned before, after giving glucose rehydration solution, because it can stimulate the secretion of insulin, accompanied by the allogenic effect of glycogen (bound potassium), it can lower the serum potassium concentration; when giving saline or sodium bicarbonate rehydration solution, the sodium concentration of both extracellular and intracellular fluid increases, activating Na+-K+-ATPase, which causes potassium to be transported into the cells and lowering the blood potassium. Therefore, in the treatment of hypokalemia, if potassium salts are given intravenously in 5% or 10% glucose solution (sugar concentration is significantly higher than blood glucose concentration) or saline (sodium concentration is higher than blood sodium concentration), the potassium concentration may be temporarily lowered if the infusion is too fast. 5% sugar saline as a common rehydration solution may worsen the hypokalemia through the dual transport of K+ by glucose and Na+. Special attention is needed.
In patients with oliguria or anuria, potassium supplementation is generally not indicated, except in severe hypokalemia, because the serum potassium concentration can increase by 0.3 mmol/L after 1 day of anuria.
(4) Oral potassium-preserving diuretics such as ambrisentine or aminoglutethimide help recovery from hypokalemia.
(5) Oral ACE inhibitors such as Kepone preserve potassium by inhibiting the production of aldosterone. In general, the application of ACE inhibitors has a major difference in the regulatory effect on the kidneys and the systemic hypotensive effect, with the former requiring significantly smaller doses than the latter. The combination of potassium-preserving diuretics, ACE inhibitors and potassium is the strongest theoretical combination to raise blood potassium and has a certain regulatory effect on renal function, which has a high promotion value, but attention should be paid to regular rechecking of blood potassium to avoid hyperkalemia.
(6) Potassium supplementation In patients with mild hypokalemia, oral potassium chloride solution should be the mainstay, about 3g per day, and the same dose can be given for intravenous application if it cannot be taken orally. In patients with moderate hypokalemia, both oral and intravenous applications should be given, about 6 g/day. in severe patients, both potassium chloride and potassium glutamate should be given, about 9 g/day.
If the serum K+ concentration is at the low limit of normal (3.5 to 4.0 mmol/L) and the dynamic follow-up shows a decreasing trend, it often means that the body is potassium deficient, especially in the elderly or in patients treated with digitalis, and must be supplemented with potassium.
(7) Treatment of severe hypokalemia Our treatment experience is to use 15ml of 10% potassium chloride added to 500ml of 5% glucose solution intravenously, 1000-1500ml daily; 20-40ml of 31.5% potassium glutamate added to 500ml of 5% glucose solution, 500-1000ml daily; 30-40ml of oral potassium chloride daily, divided into 3-4 times Orally, the blood potassium should be rechecked once in about 2h, with each increase of 0.1~0.3mmol/L until normal. Patients who need to strictly control the amount of fluid intake can choose deep vein placement to increase the concentration, reduce the amount of water intake and use micro-pump. If the blood K+ concentration continues not to rise or even decreases, an indwelling intravenous catheter is also an option to increase the potassium concentration and to monitor the electrocardiogram.
Patients in this category also need to apply potassium-protective diuretics and ACE inhibitors at the same time, avoid Na+ input or intake, and avoid the simultaneous application of large amounts of glucose, amino acids and insulin.
(2) Chronic potassium-deficit hypokalemia (chronicpotassium-deficithypokalemia) refers to the gradual decrease of serum potassium ion concentration below the normal level due to increased potassium loss or combined with insufficient intake, and the decrease of potassium content in the body. Because of the slow onset and mild degree of compensation and adaptation, the clinical symptoms are mild, with weakness, loss of appetite, polyuria and insidious damage to the renal tubules as the main manifestations (see acute potassium loss hypokalemia for details). The principles of treatment are similar to those of acute hypokalemia and will not be repeated. However, since this group of patients has certain adaptations and compensations, it is emphasized that the rate of potassium supplementation does not need to be too fast, and it is usually sufficient to increase the blood K+ concentration by 0.2 to 0.4 mmol/day. In moderate and severe hypokalemia Na+ intake or input should be avoided, otherwise it will lead to persistent transfer of K+ into the cells and persistent excretion via the renal tubules, and recalcitrant hypokalemia will occur. Because of the long onset of the disease, the body’s potassium level is significantly reduced, while the kidney’s ability to reabsorb potassium is reduced. Therefore, potassium chloride supplementation should be continued for about a week or even longer after the blood K+ concentration is normalized, so that the body’s potassium level is eventually normalized. In addition, chronic hypokalemia is often accompanied by magnesium and phosphorus deficiency, while phosphorus and Mg2+ deficiency often lead to a decrease in sodium pump activity and cellular metabolic disorders, resulting in a decrease in intracellular potassium concentration and a decrease in the kidney’s ability to reabsorb K+. ). Insufficient water-soluble vitamins in the body due to poor diet or inadequate supplementation can also lead to reduced sodium pump activity and chronic hypokalemia. It is also important to emphasize that K+ may continue to be lost during the course of treatment, so the actual amount of supplementation should be increased, especially in patients with “occult renal tubular impairment” (chronic hypokalemia itself can lead to tubular dysfunction and organic damage). Patients whose blood potassium does not rise significantly after potassium supplementation should be routinely checked and followed up with urine electrolytes and other electrolyte ion and water-soluble vitamin supplements.
Chronic hypokalemia often leads to reduced sodium pump activity in somatic cells and metastatic hyponatremia; reduced sodium pump activity in renal tubular epithelial cells and increased renal sodium excretion aggravate hyponatremia, so patients with chronic hypokalemia combined with hyponatremia should focus on correcting hypokalemia.
(iii) Shifted hypokalemia (shiftedhypokalemia) is hypokalemia caused by potassium ions entering the cells, mainly seen in patients with periodic paralysis, various causes of alkalosis or insulin application. It is mainly divided into two conditions as follows.
1. Primary significant enhancement of the sodium pump function results in rapid entry of K+ into the cells, leading to hypokalemia, mainly seen in periodic paralysis and unexplained hypokalemia. It is characterized by a rapid progression of the disease with obvious clinical symptoms and no change in the body’s K+ content. the transfer of K+ into the cell is inevitably accompanied by the transfer of Na+ into the cell, while the transfer of H+ into the cell is reduced, with mild hypernatremia and mild metabolic acidosis, and the acidosis leads to a compensatory increase in Cl- concentration. This is the exact opposite of potassium deficiency hypokalemia leading to extracellular metabolic alkalosis and hyponatremia, which is worth noting. The principles of treatment are.
(i) Avoid K+ transfer or increased excretion due to glucose. If hypertonic sugar is not used, choose 5% glucose solution, and for faster rehydration, establish a deep venous line to increase the potassium concentration and infuse with a micropump.
②As the increase of Na+ concentration can promote the transfer and excretion of K+ and aggravate hypokalemia, it is necessary to avoid the simultaneous application of various forms of sodium chloride solution, as saline and 5% sugar saline are often used inadvertently, special attention should be paid.
(iii) Excessive Cl- intake should also be avoided due to compensatory increase in Cl- concentration. Therefore, potassium chloride should not be supplemented too much and can be supplemented with potassium glutamate at the same time. Since this type of hypokalemia occurs very fast and the transfer of potassium is mostly still going on during the treatment, there are more chances of respiratory muscle weakness, respiratory failure and cardiac arrhythmia, and the treatment should be especially aggressive.
2. Transferred hypokalemia due to other causes is more common clinically, mainly in patients with increased ventilation from various causes, alkalosis, or the application of insulin, hypertonic sugar, or amino acids.
Increased ventilation from various causes, such as fever, pulmonary edema, pneumonia and other site infections, trauma, and acute respiratory distress syndrome can lead to respiratory alkalosis and acute hyperkalemia. Since patients have high catabolism and K+ release from cells, hypokalemia is not serious and should be treated mainly by treating the original disease and reducing ventilation. In a small number of patients, the blood K+ concentration decreases significantly, so potassium should be supplemented appropriately.
Mechanical ventilation for chronic respiratory failure is one of the most important causes of chronic metastatic hypokalemia. The main therapeutic measure at this time should be to rapidly and substantially reduce the ventilation volume, which is generally 1/3 to 1/2 or even greater, with the main focus on slowing down the respiratory rate. In patients with chronic acidosis and normal blood K+ concentration, there is a true lack of potassium in the organism, so the improvement of acidosis is often accompanied by hypokalemia. pH increases by 0.1 and blood K+ concentration decreases by about 0.1 mmol/L. Therefore, the principle of treatment is to control the speed of improvement of acidosis, while appropriately supplementing potassium chloride and potassium glutamate to avoid alkalosis. Once alkalosis occurs, measures should be taken to bring down the pH appropriately. However, avoid applying arginine hydrochloride, because it can quickly enter the cell through the cell membrane, aggravate the intracellular acidosis and further affect the cell metabolism. The stability of the intracellular environment is the basis of normal cell metabolism, and its role is much more important than that of the extracellular environment (i.e., the “internal environment” of the body), so clinicians should pay more attention to the electrolyte disorders of the “intracellular environment” than just the “internal environment” of the body. Therefore, clinicians should pay more attention to the electrolyte disorders in the “intracellular environment” than just the disorders in the “internal environment” of the body.
During the improvement of diabetic ketoacidosis, stress hyperglycemia or other conditions of hyperglycemia, severe hypokalemia can occur due to the dual effect of pH increase and insulin.
Other factors, such as the application of catecholamine preparations, can also activate sodium pump activity and lead to hypokalemia, but to a lesser extent and with less clinical value.
In the acute phase of various wasting diseases or critical illnesses, due to the vigorous cellular catabolism and intracellular K+ release, the renal elimination also increases in order to keep the blood K+ concentration normal, leading to potassium deficiency in the organism. In the process of disease improvement, hypokalemia can occur due to enhanced anabolic metabolism, so the daily requirement of potassium increases accordingly. Of course other electrolyte ions, water-soluble vitamins, energy and protein supplements should also be increased.
(iv) Dilutional hypokalemia (dilutional hypokalemia) is hypokalemia caused by an increase in blood volume or extracellular fluid volume, accompanied by dilutional hyponatremia. There is usually a limited decrease in blood potassium. Treatment should be based on strict control of water intake and appropriate diuresis on the basis of potassium chloride and sodium chloride supplementation.
Edit this section Commonly used potassium-containing substances 1. 10% potassium chloride solution packed in 10ml with 1g of potassium chloride (13.4mmol) can be used for intravenous drip, micro-pump injection, oral or nasal feeding.
2.Potassium chloride extended-release tablets are packed as 0.5g/tablet and 1g/tablet, the latter has the same potassium chloride content as the solution and is used for oral administration.
3, 31.5% potassium glutamate package for 20ml, the content of potassium glutamate is 6.3g (34mmol), so 31.5% potassium glutamate 20ml is equivalent to 2.5g of potassium chloride.
4, potassium magnesium menthylate package has a solution and tablets. Solution for 10ml / branch, intravenous application, each containing 33.7mg of magnesium, potassium 103.3mg; tablets for oral use, each containing 11.8mg of magnesium, potassium 36.2mg. because of the low potassium content, mainly for the prevention and treatment of hypomagnesemia.
5, normal diet as mentioned above, the normal diet contains high potassium, restore the normal diet should be used as the basic means of potassium supplementation.
Edit this paragraph hypokalemia in patients with different diseases 1, chronic hypercapnia with hypokalemia
(1) Causes ① Decreased potassium intake; ② Weak sodium pump function, poor potassium retention function of the kidney, a certain degree of urinary K+ excretion despite low blood K+ concentration; increased excretion after application of diuretics or mechanical ventilation; ③ Renal function compensation, increased Cl- exclusion, supplementation of potassium chloride must be accompanied by increased K+ exclusion, i.e. further weakening of the potassium retention function of the kidney; ④ Potassium transfer: early stage of respiratory failure, the acidosis leads to weakened intra- and extracellular K+-Na+ exchange, and the level of K+ in the cell is low. Once the respiratory acidosis is corrected, K+-Na+ exchange is enhanced, which will lead to a rapid increase in K+ entry into the cells; the elimination via renal tubules and collecting ducts is also increased. Therefore, patients with chronic hypercapnia are prone to hypokalemia.
(2) Prevention and control principles For patients with chronic respiratory failure, if the blood K+ concentration is lower than normal or even at the low limit of normal, potassium chloride should be supplemented first; and the amount of mechanical ventilation must be gradually increased to make hypercapnia gradually improve, otherwise it may lead to severe hypokalemia. In the case of moderate normal blood K+ concentrations, potassium chloride is supplemented along with mechanical ventilation. In the case of very low blood K+ concentration, potassium glutamate and potassium chloride should be supplemented at the same time to improve the efficiency of potassium supplementation. While ensuring a gradual increase in blood K+ concentration, ventilation should be increased so that PaCO2 decreases slowly. Once there is a trend that blood K+ concentration does not increase or decreases, ventilation should be rapidly reduced, and ventilation should be increased after blood K+ concentration increases to avoid ” Hyperventilation” and alkalosis should be avoided.
Emphasis should also be placed on avoiding high Cl- and Na+ intake and avoiding rapid hypertonic glucose drip. This is because alkalosis and hypertonic glucose accelerate K+ transfer, and alkalosis and Cl- and Na+ promote K+ transfer and excretion.
Severe hypokalemia due to pH rebound (which can be normal or above normal) must be rapidly reduced by ventilation to bring pH back to near pre-treatment levels.
2. Hypokalemia combined with hyponatremia
Hypokalemia combined with hyponatremia is relatively common in clinical practice. In acute cases, it is mostly due to acute loss of digestive juices, which can be treated by replenishing both Na+ and K+, for example, by applying Ringer’s solution or potassium chloride in saline intravenously. However, chronic cases are more difficult to manage. Because both hypokalemia and hyponatremia lead to a weakening of sodium pump activity, resulting in intracellular transfer of Na+ and extracellular transfer of K+, improper supplementation may lead to further ion transfer and ion disorders. Because the concentration of K+ in rehydration fluid often needs to be strictly controlled, generally the concentration of potassium chloride does not exceed 0.3%; while the concentration of Na+ in rehydration fluid can be allowed to be higher, generally up to 3%, the latter is 10 times of the former, and at the same time, saline is a routinely used fluid, its concentration is 0.9%, which is also three times of the highest concentration of potassium chloride allowed in general, so clinically there are often cases where sodium supplementation exceeds potassium supplementation. Therefore, in clinical practice, sodium supplementation often exceeds potassium supplementation, and the increase in blood sodium increases the concentration of Na+ entering the cells, which activates the sodium pump and promotes the transfer of K+ into the cells and further excretion through the kidneys, resulting in persistent “hypokalemia”. Hypokalemia, in turn, inhibits the activity of the sodium pump, further promoting the intracellular transfer of Na+ and its excretion through the kidneys, resulting in a failure to effectively increase Na+ concentration, which may in turn combine with “intractable hyponatremia”. As mentioned above, if Na+ is replenished to normal levels, the symptoms of hypokalemia may be aggravated. Therefore, in hypokalemia combined with hyponatremia, especially in chronic patients, K+ supplementation should be the main focus, and with the recovery of K+, the sodium pump activity will be enhanced, intracellular Na+ will be transferred to the extracellular level, and Na+ concentration will naturally increase or return to normal, accompanied by the reduction of intracellular edema and the recovery of cellular function. In patients with severe hyponatremia, effective K+ supplementation is required along with Na+ supplementation.
Finally, it is important to emphasize that this group of patients is often combined with Mg2+ deficiency and may also be combined with “occult renal tubular impairment”, so attention should be paid to the examination of urinary electrolytes and the corresponding ion supplementation.
Hypokalemia combined with hypernatremia is mainly seen in patients with severe infections, trauma and other critical illnesses resulting in stress, or combined with the application of glucocorticoids; it is also common in endocrine disorders caused by cerebral hemorrhage, trauma or hypothalamic-pituitary disorders. As mentioned above, the role of most hormones is to conserve sodium and drain potassium; while the commonly used rehydration solution has a high content of sodium chloride and a low content of potassium chloride, so hypokalemia and hypernatremia are likely to occur, and also easily combined with reactive hyperglycemia at the same time.
The principles of prevention and treatment emphasize prevention, while treating the primary disease and correcting the triggering factors, controlling Na+ intake and input, increasing K+ supplementation, avoiding alkalosis and blood glucose falling too fast, and rechecking electrolytes, blood glucose and liver and kidney functions once in 1~2d. Once hypokalemia and hypernatremia occur, all Na+ intake and input, including gastrointestinal intake and sodium bicarbonate input, should be stopped if possible; continue to increase K+ supplementation. The presence of this condition is often a sign of critical illness, and monitoring and treatment efforts should be intensified.