Normal human body fluids maintain a certain H + concentration, i.e., a certain pH (arterial plasma has a pH of 7.40 +-0.05). to maintain normal physiological and metabolic functions. The body produces both acids and bases during metabolism, so the H+ concentration in body fluids changes frequently. However, the human body is able to maintain the pH value of blood between 7.35-7.45 through the buffer system of body fluids, the role of lung respiration and kidney regulation, so that the concentration of H+ in the blood changes only within a small range. The most important pair of buffering substances in the blood are HCO-3 and H2CO3. The normal value of HCO-3 averages 24 mmol/L and H2CO3 averages 1.2 mmol/L, with a ratio of HCO-3/H2CO3 = 24/1.2 = 20/1. The concentration of carbonic acid in the plasma is determined by the amount of CO2 that is dissolved in a physical state and the amount of carbonic acid that is produced with water. Since CO2 in body fluids exists mainly in a physically dissolved state, the amount of H2CO3 is very small and can be ignored. Therefore, H2CO3 can be calculated by partial pressure of carbon dioxide (PCO2) and its solubility coefficient (0.03).The normal value of PCO2 is 40mmHg, i.e., H2CO3=0.03*40=1.2.Thus, HCO-3/H2CO3= HCO-3/0.03*PCO2=24/1.2=20/1.As long as the ratio of HCO-3/H2CO3 is maintained at 20/1, the plasma pH will remain at 7.40.As far as the regulation of acid-base balance is concerned, the respiration of the lungs is responsible for the expulsion of CO2 and for the regulation of the respiratory component of the blood, i.e., PCO2, which is the regulation of the blood’s H2CO3.A malfunctioning of the respiratory function of the body, therefore, can cause both a direct disturbance of acid-base balance and an effect of the compensatory response to the disturbance of acid-base balance. The regulatory role of the kidneys is the primary acid-base homeostatic system, excreting fixed acids and excess alkalinity in order to maintain a stable plasma HCO-3 concentration. Renal dysfunction can both affect the normal regulation of acid-base balance and cause acid-base balance disorders. The mechanisms by which the kidney regulates acid-base balance are: 1, H+-Na+ exchange; 2, reabsorption of HCO-3; 3, secretion of NH3 that combines with H+ to form NH+4 for excretion; and 4, acidification of the urine and excretion of H+. Differential diagnosis of fluid balance disorders: 1, isotonic dehydration, also known as acute or mixed dehydration. Surgical patients are most susceptible to this type of dehydration. Water and sodium are lost proportionally, but serum sodium remains in the normal range and the osmolality of the extracellular fluid remains normal. It results in a rapid decrease in extracellular fluid volume, including circulating blood volume. Stimulation of pressure receptors in the walls of the small renal entry arterioles by a decrease in intratubular pressure and a decrease in Na+ in the distal tubular fluid due to a decrease in glomerular filtration rate causes excitation of the renin-aldosterone system and an increase in aldosterone secretion. Aldosterone promotes sodium reabsorption in the distal tubule, and there is an increase in the amount of water that is reabsorbed along with the sodium, causing extracellular fluid volume to rebound. Since the lost fluid is isotonic and essentially does not change the osmolality of the extracellular fluid, initially the intracellular fluid does not transfer to the extracellular space to compensate for the lack of extracellular fluid. Therefore, the amount of intracellular fluid does not change. But this fluid loss lasts for a long time, the intracellular fluid will also gradually move out, along with the loss of extracellular fluid, so as to cause the cells, water shortage. 2, hypotonic dehydration, also known as chronic dehydration or secondary dehydration. Water and sodium loss at the same time, but less water than sodium loss, so the serum sodium is lower than the normal range, the extracellular fluid is hypotonic. The body reduces the secretion of antidiuretic hormone, so that the reabsorption of water in the renal tubules is reduced, and the urinary output is increased to increase the osmolality of the extracellular fluid. However, the volume of extracellular fluid decreases even more, and the interstitial fluid enters the circulation, which partially compensates for the blood volume but makes the decrease in interstitial fluid more than the decrease in plasma. Faced with a marked reduction in circulating blood volume, the body will no longer be concerned with osmolality and will try to maintain blood volume. Excitation of the renin-aldosterone system causes the kidneys to decrease sodium excretion and increase reabsorption of CI- and water. Therefore, the urinary sodium chloride content is significantly reduced. Decreased blood volume in turn stimulates the posterior pituitary gland, causing increased secretion of antidiuretic hormone and increased water reabsorption, resulting in oliguria. If blood volume continues to decrease, shock will occur when the above compensatory function is no longer able to maintain blood volume. This kind of shock caused by massive sodium loss is also called hyponatremic shock. 3.Hypertonic dehydration is also known as primary dehydration. Although water and sodium are lacking at the same time, but the lack of water is more than the lack of sodium, so the serum sodium is higher than the normal range, and the extracellular fluid is hypertonic. The thirst center located in the lower part of the optic thalamus is stimulated by hypertonicity, and the patient feels thirsty and drinks water, so that the body water increases in order to reduce the osmotic pressure. On the other hand, hypertonicity of extracellular fluid can cause increased secretion of antidiuretic hormone so that water reabsorption by renal tubules increases and urine output decreases to lower the osmolality of the extracellular fluid and restore its volume. If water deprivation continues, increased aldosterone secretion caused by a significant decrease in circulating blood volume enhances reabsorption of sodium and water to maintain blood volume. In severe cases of water deprivation, the intracellular fluid moves to the extracellular space because of the increased osmotic pressure of the extracellular fluid, with the result that there is a reduction in both intracellular and extracellular fluid volumes. Eventually, the degree of intracellular fluid dehydration exceeds the degree of extracellular fluid dehydration. Brain cell dehydration will cause brain dysfunction. 4, too much water, also known as water intoxication or dilute hyponatremia. It means that the total amount of water entering the body exceeds the amount of water discharged, so that the water is retained in the body, causing a decrease in blood osmotic pressure and an increase in circulating blood volume. Water overload occurs less frequently. It is only in the case of excessive secretion of antidiuretic hormone or renal insufficiency, when the body takes in too much water or receives too much intravenous fluids, that water accumulates in the body, leading to water intoxication. At this time, the volume of extracellular fluid increases, serum sodium concentration decreases, and osmolality decreases. Because the osmotic pressure of the intracellular fluid is relatively high, water moves into the cells, resulting in a decrease in osmotic pressure and an increase in the volume of both intracellular and extracellular fluid. In addition, the increased volume of extracellular fluid inhibits aldosterone secretion, causing the distal tubules to reduce Na+ reabsorption and Na+ excretion from the urine to increase, resulting in an even lower serum sodium concentration. Dysregulation of fluid metabolism and acid-base balance is often a concomitant finding or consequence of a primary disease. Prompt measures should be taken to prevent the occurrence of such disorders. Generally, about 1500 ml of 5%-10% glucose solution, 500 ml of 5% grapefruit saline, and 130-40 ml of 10% KC can be administered intravenously daily to supplement the daily water and glucose requirements to conserve proteolytic metabolism and to avoid the ketoacidosis that may occur when excessive fat burning occurs. In febrile patients, supplementation can generally be increased according to the criterion of about 3-5 ml/kg of hypotonic body fluid lost from the skin for every 1C0 rise in body temperature. In patients with moderate sweating, the loss of body fluids is about 500-1000 ml (containing 11.25-2.50 g of NaC); in cases of profuse sweating, the loss of body fluids is about 1,000-1,500 ml. In patients with tracheotomy, the daily evaporation of water from respiration is 2-3 times more than that of the normal ones, which counts to be about 1,000 ml. All of them need to be increased during rehydration.