Potassium chloride Relative molecular mass KCl 39+35.5=74.5g/mol
1 mol of potassium chloride is 74.5 g. 1 mmol of potassium chloride is 0.0745 g.
1 g divided by 0.0745 g equals 13.4228 mol, which is approximately 13.4 mol.
Total amount of potassium supplementation: (Note! It is the total amount, not the daily amount! This includes intravenous and oral!)
Mild potassium deficiency: serum potassium 3.0~3.5 mmol/L, 100 mmol of potassium supplementation (equivalent to 8.0 grams of potassium chloride)
Moderate potassium deficiency: serum potassium 2.5~3.0mmol/L, can be supplemented with 300mmol of potassium (equivalent to 24g of potassium chloride)
Severe potassium deficiency: serum potassium 2.0~2.5 mmol/L, potassium supplementation 500 mmol (equivalent to 40 grams of potassium chloride)
Intravenous potassium supplementation has limits of concentration and speed. The amount of potassium contained in each liter of infusion should not exceed 40mmol (equivalent to 3g of potassium chloride), and the amount of potassium input should be controlled at 20mmol/h (equivalent to 1.5g/h of potassium chloride) or less. The total daily intravenous amount should not exceed 6g in general.
Potassium supplementation (mmol) = (4.2 – actual value) x body weight (kg) x 0.6 + continued loss + physiological requirements. Recheck once in 2-6 h 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.
When glucose rehydration solution is given, it can lower the serum potassium concentration because it can stimulate the secretion of insulin, accompanied by the allogenic effect of glycogen (bound potassium); when saline or sodium bicarbonate rehydration solution is given, the sodium concentration of both extracellular and intracellular fluid increases, activating the Na+-K+-ATPase, which transports potassium into the cells and lowers the blood potassium. Therefore, 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) in the treatment of hypokalemia, 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+, so special attention is also needed. Therefore, special attention is needed.
2. Pathophysiology and clinical manifestations
(1) Neuro-muscular system
(1) Skeletal muscle weakness and paralysis: In hypokalemia, the difference between the concentration of K+ inside and outside the cell 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 unstable standing; with the aggravation of hypokalemia, muscle weakness increases 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 system Hypokalemia can lead to dysfunction of cardiac muscle cells and their conduction tissues, as well as to 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 vegetative dysfunction. [2]
(3) 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) Renal function damage
The main pathological changes 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) Acid-base and other electrolyte disturbances
In 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 increases, 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, and the main reason may be related to sodium transfer, and also related to the change of sodium and potassium ratio affecting resting potential and action unit. 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.
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) Compensated renal function, increased Cl- exclusion, supplementation of potassium chloride must be accompanied by increased K+ exclusion, i.e., further weakened potassium retention function of the kidney; (4) Potassium transfer: early respiratory failure, acidosis resulting in K+-Na+ exchange inside and outside the cell is weakened, 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 the renal tubules and collecting ducts is also increased. Therefore, patients with chronic hypercapnia are prone to hypokalemia.
(2) Prevention and control principles
In patients with chronic respiratory failure, if the blood K+ concentration is below normal or even at the low limit of normal level, potassium chloride should be supplemented first; and the amount of mechanical ventilation must be gradually increased so that the hypercapnia gradually improves, otherwise it may lead to severe hypokalemia. At 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 resulting from 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 fluid, which can be treated by replenishing both Na+ and K+, such as applying Ringer’s solution or adding potassium chloride to saline intravenously. However, chronic cases are more difficult to manage. Because both hypokalemia and hyponatremia lead to a weakening of the 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 the rehydration solution often needs to be strictly controlled, the general concentration of potassium chloride does not exceed 0.3%; while the Na+ in the rehydration solution can allow a higher concentration, generally up to 3%, the latter is 10 times of the former, while saline is a routinely used liquid, the concentration of which is 0.9%, which is also three times the highest concentration of potassium chloride allowed under normal circumstances, 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”. In turn, hypokalemia inhibits the activity of the sodium pump, which further promotes the intracellular transfer of Na+ and its excretion through the kidneys, resulting in a failure to effectively increase Na+ concentration, which may in turn lead to a combination of “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+, sodium pump activity is enhanced, intracellular Na+ is transferred to the extracellular level, and Na+ concentration naturally increases or returns 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”, which requires attention to urinary electrolyte examination and corresponding ion supplementation.
3. Hypokalemia combined with hypernatremia
Hyponatremia 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.