Respiratory failure and electrolyte imbalance are caused by this.

Respiratory failure and electrolyte imbalance are common conditions in life, but most people don’t really understand what is going on. In fact, electrolyte imbalance in respiratory failure is caused by external respiratory disorder. External respiratory disorder can not only cause electrolyte imbalance, but also may cause renal dysfunction.

In case of respiratory failure, acid-base imbalance may occur not only due to external respiratory disorders, but also due to complications such as renal dysfunction, infection, shock, and certain improper treatment measures. Therefore, the patient's presentation may be diverse. Severe external respiratory dysfunction may cause respiratory acidosis, respiratory alkalosis, metabolic acidosis, or respiratory acidosis combined with metabolic acidosis.

(I) Respiratory acidosis In type II respiratory failure, a large amount of carbon dioxide is retained, which can cause primary plasma carbonic acid excess. Those with sudden onset often have incomplete compensation and develop decompensated respiratory acidosis. If the onset is slower, compensated respiratory acidosis may occur. At this time, the main changes in blood electrolytes are as follows. ① Increased serum potassium concentration: In acute respiratory acidosis, the increase in serum potassium concentration is mainly due to changes in the distribution of ions inside and outside the cells, which causes the outward movement of intracellular potassium. In chronic respiratory acidosis, the increase in serum potassium concentration is due to increased hydrogen secretion and reabsorption of sodium bicarbonate by renal tubular epithelial cells and decreased potassium excretion. ② The serum chloride concentration decreases and the bicarbonate increases; when carbon dioxide is retained in the blood, the bicarbonate generated in red blood cells increases under the action of carbonic anhydrase and the buffer system, and thus the bicarbonate entering the plasma also increases. At the same time, chloride transfer occurs, and the chloride ions in the plasma increase entering the red blood cells. Therefore, the serum chloride ions decrease and the bicarbonate increases. On the other hand, due to increased tubular hydrogen secretion, sodium bicarbonate reabsorption and regeneration increase, and more chloride ions are excreted in the urine in the form of sodium chloride and ammonium chloride, which can also cause a decrease in serum chloride ions and an increase in bicarbonate.

(ii) Metabolic acidosis or respiratory acidosis combined with metabolic acidosis Due to severe hypoxia, anaerobic metabolism is enhanced and acidic metabolites increase, which can cause metabolic acidosis or respiratory acidosis combined with metabolic acidosis. If the patient has concurrent renal insufficiency, infection, shock, etc., metabolic acidosis will be aggravated due to impaired renal acid excretion and alkaline conservation function or increased fixed acid production in the body. At this time, the increase in serum potassium concentration may be more obvious.

(III) Respiratory alkali poisoning Patients with a significantly decreased Paco2 may develop respiratory alkali poisoning due to primary hypocapnia. Due to the rapid onset, most cases are decompensated respiratory alkali poisoning. At this time, the serum potassium concentration may decrease due to the entry of extracellular potassium ions into the cells. Due to excessive carbon dioxide excretion, more bicarbonate in the plasma moves into the red blood cells, and chloride ions move out of the red blood cells. In addition, the renal excretion of chloride also decreases, so the serum chloride concentration increases. Plasma bicarbonate concentration decreases due to transfer into red blood cells and decreased tubular reabsorption and regeneration of bicarbonate.

In addition, some patients with respiratory failure may develop metabolic alkali poisoning, which is mostly iatrogenic and occurs during or after treatment. If an artificial ventilator is used, a large amount of carbon dioxide will be discharged too quickly, and the compensatory increase in bicarbonate cannot be discharged quickly, thus causing metabolic alkali poisoning. Insufficient potassium intake, the use of potassium-excreting diuretics and cortical hormones can lead to hypokalemic alkali poisoning.