What Is an Acid-Base Imbalance?

The pH of normal human blood, that is, the pH value, is always maintained at a certain level, and the range of its variation is small. The relatively constant blood pH ^[1] is one of the basic conditions for the body to perform normal physiological activities. Daily metabolism

Disorders of acid-base balance

Disorders of acid-base balance

Under normal conditions, the body has a set of mechanisms that regulate the acid-base balance. In the course of disease, despite the increase and decrease of acid-base substances, acid-base balance disorders are generally not easy to occur. Only in severe cases, the body produces or loses too much acid-base and exceeds the body's ability to regulate, or the body regulates acid-base. When the mechanism is impaired, the acid-base balance is imbalanced. Although the body has a large buffering capacity and effective regulating function for acid-base load, many factors can cause excessive acid-base load or obstacles to the regulation mechanism to cause the stability of body fluid pH to be disrupted. This stability disruption is called acid-base balance disorder.

Disturbance of acid-base balance

The pH of normal human blood, that is, the pH value, is always maintained at a certain level, and the range of its variation is small. The relatively constant blood pH ^[1] is one of the basic conditions for the body to perform normal physiological activities. Daily metabolism

Disorders of acid-base balance

Both of them will produce a certain amount of acidic or alkaline substances and continuously enter the blood, which may affect the pH of the blood. However, the pH of the blood is still between pH 7.35 and 7.45. The healthy body is so. During the course of the disease, the human body is still trying to keep the blood pH constant within this narrow range. The reason why the blood pH is so stable is because the human body has a set of mechanisms to adjust the acid-base balance. It first depends on some acidic or alkaline substances in the blood and is completed by a certain proportion of the buffer system, and this ratio is constant. However, it depends on the regulating effects of the lungs and kidneys and other organs to eliminate excess acid or alkali and maintain a relatively balanced state of pH in the body. The process of adjusting the acid-base content and the ratio of the body to maintain the blood pH within the normal range is called acid-base balance.

Too much acidic or alkaline substances in the body, beyond the body's ability to regulate, or lung and kidney dysfunction that impairs the regulation of acid-base balance, can cause changes in plasma HCO3- and H2CO3 concentrations and their ratios to exceed normal ranges and cause Disorders of acid-base balance such as acidosis or alkalosis. Disturbance of acid-base balance is a common clinical symptom, and various diseases may occur.

Typing of acid-base disorders

According to the level of blood pH, <7.35 is acidosis and> 7.45 is alkalosis. HCO3-concentration that is mainly affected by metabolic factors is called metabolic acidosis or alkalosis; H2CO3 concentration that is mainly increased or decreased by the influence of respiratory factors is called respiratory acidosis or alkalosis. In the case of simple acidosis or alkalosis, although the body's HCO3- / H2CO3 value has changed, the pH is still within the normal range due to the body's regulation, becoming compensatory acidosis or alkalosis. If the pH is abnormal, it is called decompensated acidosis or alkali

Disorders of acid-base balance

Poisoning.

Disorders of acid-base balance are mainly divided into the following five types:

Metabolic acidosis ^[2] can be divided into AG-increasing type and AG-normal type according to the AG value

Respiratory acidosis can be divided into acute respiratory acidosis and chronic respiratory acidosis according to the course of disease

Metabolic alkalosis is divided into saline responsiveness and saline resistant acidosis according to whether it can be relieved after administration of physiological saline.

Respiratory alkalosis can be divided into acute and chronic respiratory alkalosis according to the course of the disease

Mixed acid-base disorders can be subdivided into acid-base consistency and acid-base mixing

Regulation mechanism of acid-base balance disorder

Disturbance of acid- base balance

1. Carbonic acid, a volatile acid that can be excreted through the lungs; is the most acidic substance produced in the body. H2CO3 HCO3- + H +

2. Fixed acids excreted by the kidney-mainly include sulfuric acid, phosphoric acid, uric acid ^[3] , pyruvate, lactic acid, tricarboxylic acid, -hydroxybutyric acid, and acetoacetic acid.

3. Alkaline substances are mainly derived from the metabolism of amino acids and organic acid salts in food.

Acid-base balance treatment device

Disturbance of acid-base balance

1. Blood buffering system: HCO3- / H2CO3 is the most important buffering system with the strongest buffering capacity (most content; open buffering system). The ratio of the two determines the pH. The normal value is 20/1, and the pO value is 7.4. Secondly, there are Hb- / HHb in red blood cells, as well as HPO42- / H2PO4- and Pr- / HPr.

2, lung breathing: through the central or peripheral aspects. Central: PaCO2 makes the cerebrospinal fluid PH , stimulates the hydrogen ion-sensitive central chemoreceptor located in the superficial part of the ventrolateral medulla, and excites the respiratory center. If the carbon dioxide concentration is higher than 80 mmHg, the respiratory center is suppressed. Peripheral: It is mainly carotid body chemoreceptor, which is stimulated by hypoxia, pH and carbon dioxide, and reflexively excites the respiratory center, deepens breathing and expels carbon dioxide.

3. Kidney ^[4] excretion and reabsorption:

H + secretion and reabsorption: Proximal tubules and distal tubules collect hydrogen to reabsorb sodium bicarbonate;

Acidification of buffered saline in the renal tubule: Hydrogen pump actively bleeds hydrogen into the lumen and HPO42 into H2PO4-

NH4 + secretion: glutamine in the tubules (under the action of glutaminase) NH3 + HCO3- NH3 + H + NH4 +, secreted into the lumen through Na + / NH4 + exchange. The manifold is combined with NH3 in the lumen to form NH4 + through the hydrogen pump.

4. Ion exchange inside and outside the cell: H + -K +, H + -Na +, Na + -K +, Cl--HCO3- inside and outside the cell, mostly located in red blood cells, muscle cells, and bone tissue. Acidosis is often accompanied by hyperkalemia, and alkalosis is often accompanied by hypokalemia.

Note: Blood buffering is rapid, but not long lasting. Pulmonary regulating effect is great, reaching peak in 30 minutes, only effective for H2CO3; intracellular fluid buffering is stronger than extracellular fluid, but it can cause changes in blood potassium concentration; renal regulation is slower. It only takes effect within 12-24 hours, but it is efficient and lasting. Reflects acid-base balance.

Common indicators of acid-base disorders

Common indicators reflecting acid-base balance are: pH and H + concentration, arterial blood CO2 partial pressure, standard bicarbonate and actual bicarbonate, buffered alkali ^[5] , alkali residue, and anion gap.

Classification of acid-base disorders

Metabolic acidosis

It refers to the disorder of acid-base balance characterized by the decrease of plasma HCO3- caused by the increase of extracellular fluid H + and / or loss of HCO3-. [AG increased acid replacement: refers to metabolic acidosis when the plasma concentration of any fixed acid other than chlorine is increased. Features: increased AG, normal blood chlorine.

AG normal acid replacement: refers to a reduction in HCO3- concentration, accompanied by a compensatory increase in Cl- concentration, which is normal to AG

Disorders of acid-base balance

Type or hyperchloric metabolic acidosis. Features: Normal AG, elevated blood chlorine. AG anion gap

Difference between undetermined anion and undetermined cation in plasma ^[6]

Compensatory acid replacement: HCO3- / H2CO3 tends to 20: 1 by compensatory regulation of blood cells, lungs, and kidneys in the body, and the pH tends to be normal.

Decompensated acid: HCO3- / H2CO3 tends to 20: 1 through the compensatory regulation of the lungs and kidneys of the blood cells of the body, and the pH is less than normal.

Respiratory acidosis

It refers to the type of acid-base balance disorder characterized by increased plasma H2CO3 concentration caused by CO2 excretion disorder or excessive inhalation.

Acute exhaled acid: common in acute airway obstruction, acute cardiogenic pulmonary edema, central or respiratory muscle paralysis, and apnea caused. Due to the slow compensatory effect of the kidney, it is mainly regulated by intracellular and extracellular ion exchange and intracellular buffering, which is often manifested as compensatory

Disorders of acid-base balance

Inadequate or decompensated status.

Chronic exhaled acid: seen in COPD (chronic obstructive pulmonary disease) and extensive fibrosis or atelectasis caused by chronic inflammation of the airways and lungs, generally refers to those with high concentration of PaCO2 for more than 24 hours. When it happens, it is mainly compensated by the kidney, which can be compensated.

Metabolic alkalosis

It refers to the disturbance of acid-base balance characterized by increased plasma HCO3- caused by extracellular fluid alkali or H + loss.

Respiratory alkalosis

It refers to a disorder of acid-base balance characterized by a primary decrease in plasma H2CO3 concentration caused by pulmonary ventilation.

Disorders of acid -base balance metabolic acidosis

Classification of acid-base disorders

Metabolic acid ^[7] poisoning can be divided into two types: increased AG (normal blood chlorine) and normal AG (high blood chlorine).

Causes and mechanisms of acid-base balance disorders

Excessive H + production or renal H + disorders are two basic causes of metabolic acidosis.

1. AG increased metabolic acidosis (acid storage) The plasma concentration of any fixed acid increases, and AG increases. At this time, the HCO3- concentration decreases and the Cl- concentration does not change significantly. Poisoning. It can be seen that in the case of AG-increasing metabolic acidosis, AG = [HCO3-].

(1) Lactic acidosis: seen in hypoxia (shock, pulmonary edema, severe anemia, etc.), liver disease (lactic acid utilization disorder), diabetes, etc. When lactic acidosis, the HCO3-concentration is reduced and the AG is increased by buffering, but the blood chlorine is normal.

Disorders of acid-base balance

(2) Ketoacidosis: seen in diabetes, hunger, alcoholism, etc. -hydroxybutyric acid and acetoacetic acid in the ketone body release H + in the plasma, and the plasma HCO3- combines with H + to buffer, thereby reducing the HCO3- concentration.

(3) Uremic acidosis: The glomerular filtration rate is reduced, and the non-volatile acidic metabolites in the body cannot be normally excreted by the urine, especially sulfuric acid, phosphoric acid, etc. are accumulated in the body, which increases unmeasured anions in plasma , HCO3- concentration decreased.

(4) Salicylic acid ^[8] poisoning: For medical reasons, ingestion or administration of salicylic acid preparations in large quantities.

2. Normal metabolic acidosis of AG When the HCO3-concentration in plasma is reduced primary, it can cause metabolic acidosis (alkaline acid replacement), meanwhile, the blood Cl- concentration is compensatory, and there is no change in AG. It is a normal type of hyperchloric acidosis in AG. In this type of acidosis, [HCO3-] = [Cl-].

(1) HCO3- loss in the digestive tract: HCO3- concentrations in intestinal fluid, pancreatic juice and bile are higher than blood. Therefore, severe diarrhea, small intestine and biliary fistula, and intestinal drainage can cause a large loss of HCO3-, which will cause the blood chlorine to compensate, and AG will be normal.

(2) HCO3-excessive urine: common in

Mild to moderate chronic renal failure: due to renal tubular epithelial dysfunction, H + and NH4 + secretion decrease

Disorders of acid-base balance

Less, the reabsorption of NaHCO3 is reduced and the excretion is excessive.

Proximal tubular acidosis: The ability of epithelial cells in proximal tubules to weaken H + is reduced, so H + -Na + exchange and HCO3- reabsorption in proximal tubules are reduced, and the reabsorption of NaCl in renal tubules is correspondingly increased. A large amount of HCO3- Urine is excreted and urine is alkaline.

Distal renal tubular acidosis: Distorted tubule epithelial cells secrete H +, and urine cannot be acidified (urine pH> 6.0). As a result, H + is retained in the body, and HCO3- is continuously excreted in the urine. Mild to moderate AG normal hyperchloric acidosis occurred.

Application of carbonic anhydrase inhibitors: It can reduce the production of H2CO3 in the cells due to the inhibition of carbonic anhydrase activity in renal tubular epithelial cells. As a result, the secretion of H + and the reabsorption of HCO3- can be reduced.

Excessive intake of chlorine-containing acidic drugs: The increase in Cl- can promote the reabsorption of Na + in the form of NaCl in the proximal tubules, and decrease the Na + content in the distal tubules, thus reducing H + -Na + exchange and HCO3-resorption. HCO3- can be consumed after buffering, leading to normal hyperchloric acidosis of AG. In the same way, a large amount of saline infusion can also cause normal hyperchloric acidosis in AG.

Acid-base balance disorder body compensation regulation

1. Blood buffering Excessive metabolic H + in plasma can be immediately combined with HCO3- and non-HCO3-buffering bases such as Na2HPO4 and buffered, so that HCO3- and BB are continuously consumed, that is: HCO3- + H + H2CO3 CO2 + H2O, CO2 are excreted by the lungs, with the result that HCO3- in the plasma is continuously consumed.

2. When intracellular and extracellular fluid ion exchange and intracellular fluid buffer metabolic acidosis, as the extracellular fluid H + concentration increases, too much H + can penetrate the cell membrane to enter the cell, and the buffering of intracellular fluid such as Pr- / HPr, HPO42- / H2PO4, Hb- / HHb and other buffer reactions occurred.

H ++ Pr HPr H ++ HPO42- H2PO4- H ++ Hb- HHb

When a large amount of H + in the extracellular fluid enters the intracellular fluid, in order to maintain the charge balance, the K + in the intracellular fluid is transferred to the extracellular fluid. As a result, the extracellular fluid is often accompanied by an increase in blood K + concentration.

3. The compensation of the lung regulates the excitement of the medullary respiratory center, which causes the breathing to deepen and accelerate. As the lung ventilation increases, CO2 emission increases, and the blood [H2CO3] can decrease accordingly. To a certain extent, it can help maintain [HCO3 -] / [H2CO3] ratio.

4. When renal compensation compensates for acidosis, the activity of carbonic anhydrase and glutaminase ^{[10] in} renal tubular epithelial cells is enhanced, and the renal compensation compensatory effects are mainly manifested in: increased renal tubular excretion of H + and reabsorption of NaHCO3 ; Renal tubular production of NH3 increased, excretion of NH4 + increased; acid phosphate increased.

Changes in acid-base indicators of acid-base disorders

Indicators reflecting metabolic factors (such as SB, AB, and BB) all decrease, and negative BE values increase; PaCO2, an indicator reflecting respiratory factors, can decrease due to the body's compensatory activities; pH <7.35 (body decompensation ) Or in the normal range (acidosis is fully compensated by the body).

Effects of acid-base disturbances on the body

Metabolic acidosis mainly causes dysfunction of the cardiovascular system and central nervous system. Severe acidosis also has a certain effect on the skeletal system.

1. Severe metabolic acidosis of the cardiovascular system can cause arrhythmia, weakened myocardial contractility and cardiovascular

Disorders of acid-base balance

The system is less responsive to catecholamines.

(1) Arrhythmia: Arrhythmia caused by metabolic acidosis is closely related to elevated blood K +. Severe hyperkalemia can cause cardiac block, ventricular fibrillation, and even cardiac arrest. Mechanism of elevated blood K +: In metabolic acidosis, due to acidosis, H + -K + ion exchange can cause intracellular K + spillover; renal tubular epithelial cells increase H + and K + decrease.

(2) Decreased myocardial contractility: Ca2 + is a myocardial excitation-contraction coupling factor. In severe acidosis, myocardial contractility is weakened because H + competes with Ca2 +.

(3) Decreased sensitivity of the cardiovascular system to catecholamines: Increasing H + concentration can reduce the responsiveness of resistance vessels (arterioles, arterioles, and precapillary sphincter) to catecholamines, causing vasodilation; it can reduce blood pressure and even cause shock.

2. In the case of metabolic acidosis in the central nervous system, the central nervous system dysfunction mainly manifests as inhibitory effects such as fatigue, muscle weakness, and dull feeling. In severe cases, it can cause conscious disturbance, lethargy, and coma. Central vascular motility paralyzed and died. The mechanism may be related to the increased glutamate decarboxylase activity during acidosis and the increased production of the inhibitory neurotransmitter -aminobutyric acid; and the acidosis affects oxidative phosphorylation leading to a decrease in ATP and insufficient energy supply to the brain.

Prevention and care of acid-base balance disorders

1. Prevention and treatment of primary disease, which is the basic principle for prevention and treatment of metabolic acidosis.

2. Correct water and electrolyte metabolism disorders, restore effective circulating blood volume, and improve renal function.

3, supplement alkaline drugs.

(1) NaHCO3: It can directly supplement HCO3-. Therefore, NaHCO3 is the medicine of choice for metabolic acidosis and alkali replenishment.

(2) Sodium lactate: Sodium lactate can be combined with H + in the body to become lactic acid, and lactic acid can be completely oxidized into H2O and CO2 in the liver to provide energy for the body. Therefore, sodium lactate is an alkaline drug that can neutralize H +, its product lactic acid, and can be used by the body. It is also commonly used in clinical practice; however, it should not be used in patients with lactic acidosis and liver damage.

Acid-base balance disorder respiratory acidosis

Acid-base balance disorder concept

Respiratory acidosis is a disorder of acid-base balance characterized by CO2 retention in the body and an increase in the concentration of H2CO3 in the plasma.

Causes and mechanisms of acid-base balance disorders

The reason is nothing more than CO2 exhaustion or excessive CO2 inhalation. In clinical practice, CO 2 exhaustion caused by pulmonary ventilation dysfunction is the main cause.

1. Inhibition of the respiratory center, craniocerebral injury, encephalitis, cerebrovascular accident, anesthetic or sedative overdose, etc. can cause pulmonary ventilation insufficiency due to respiratory central inhibition, which causes CO2 retention in the body, often acute respiratory acidosis .

2. Respiratory muscle paralysis, severe acute polio, myasthenia gravis, organophosphate poisoning, severe hypokalemia, etc., due to loss of power in respiratory movement, can cause CO2 retention in the body and cause respiratory acidosis.

3. Laryngeal edema, convulsion, severe airway obstruction, foreign body, large amount of secretions, edema fluid or vomit, etc. block the airway, which can cause alveolar ventilation dysfunction and cause acute respiratory acidosis.

4. Severe pneumothorax, pleural effusion, severe chest trauma, and certain chest deformities in the thoracic and thoracic conditions can affect the ventilation function of the lungs and cause CO2 retention in the body.

5. Pulmonary diseases Chronic obstructive pulmonary diseases such as emphysema and chronic bronchitis are the most common clinical causes of respiratory acidosis.

6. Improper use of ventilator causes too low carbon dioxide accumulation in the body

7. Excessive CO2 inhalation

Acid-base balance disorder body compensation regulation

1. Intracellular and extracellular ion exchange and intracellular fluid buffering Intracellular and extracellular ion exchange and intracellular fluid buffering are the main compensation methods in the early stage of acute respiratory acidosis. The sharply increased CO2 in the plasma can enter the red blood cells through dispersion, and quickly generate H2CO3 under the catalysis of carbonic anhydrase, and further dissociate into H ++ HCO3-, H + can combine with Hb to HHb, and HCO3- escapes from the red blood cells. Exchange with plasma Cl-. The result is a decrease in plasma Cl- concentration and a slight increase in HCO3- concentration. In addition, H + can be exchanged into the cell through H + -K + exchange and bind to hemoglobin.

2. The compensatory regulation of the kidney The main compensation method for chronic respiratory acidosis is the compensation of the kidney.

In acute respiratory acidosis, the kidneys are often too late to compensate. Chronic respiratory acidosis, more than 24 hours, with the increase of PaCO2 and the increase of H + concentration, can increase the activity of carbonic anhydrase and glutaminase in renal tubular epithelial cells, so that renal tubules can produce NH3 and excrete H + , NH4 + increased, renal tubular reabsorption NaHCO3 increased.

Acid-base balance disorder acid-base indicator change form

The index reflecting respiratory factors increased, Pa CO2> 6.25kPa (47mmHg), AB , AB> SB; the indexes reflecting metabolic factors changed differently depending on whether the kidneys participated in compensation. In acute respiratory acidosis, the pH value is often less than 7.35. Because the kidneys are too late to compensate, indicators that reflect metabolic factors (such as SB, BE, BB) can rise in the normal range or slightly; in chronic respiratory acidosis As the kidneys participate in compensation, SB and BB increase, and the positive value of BE increases, pH <7.35 (decompensation of the body) or in the normal range (acidosis is fully compensated by the body).

Effects of acid-base disturbances on the body

The effects of respiratory acidosis on the body are mainly dysfunctions of the central nervous system and cardiovascular system.

1. Severe respiratory acidosis in the central nervous system. The typical central nervous system dysfunction is "pulmonary encephalopathy". Patients may experience persistent headaches and anxiety in the early stages, and further development may include insanity, delirium, tremor, lethargy, coma Wait. Its mechanism is:

(1) High concentrations of CO2 can directly cause cerebral vasodilation and increase in cerebral blood flow, resulting in increased intracranial pressure and cerebral edema.

(2) CO2 is fat-soluble and can quickly cross the blood-brain barrier, while HCO3- is water-soluble and passes through the blood-brain barrier very slowly. Therefore, the high concentration of CO2 can significantly reduce the pH value of the cerebrospinal fluid and last for a long time.

(3) Respiratory acidosis can also cause inadequate supply of ATP in brain tissue and increase the inhibitory transmitter -aminobutyric acid.

(4) High concentration of CO2 has a significant inhibitory effect on the central nervous system, which is called "CO2 anesthesia".

2. The cardiovascular system is similar to metabolic acidosis. Respiratory acidosis can also cause arrhythmias, weakened myocardial contractility, and reduced responsiveness of the cardiovascular system to catecholamines.

3. The accumulation of carbon dioxide in the body causes hypoxia.

Prevention and care of acid-base balance disorders

1. Prevention and treatment of primary disease. Chronic obstructive pulmonary disease is the most common cause of respiratory acidosis. Clinically, anti-infection, antispasmodic and expectorant should be actively combated. Acute respiratory acidosis should be promptly removed to cause the ventilation disorder.

2. Increase alveolar ventilation. Improve the ventilation function as soon as possible and keep the airway unobstructed to facilitate the discharge of CO2. If necessary, tracheal intubation or tracheotomy and respirator can be used to improve ventilation.

3. Proper oxygen supply should not simply give high concentration of oxygen, because it does not help to improve respiratory acidosis, but it can inhibit the respiratory center, further decrease the ventilation and increase CO2 retention and cause CO2 hemp.

4, cautious use of alkaline drugs for patients with severe respiratory acidosis, sodium bicarbonate must be applied under sufficient ventilation, because NaHCO3 and H + can produce H2CO3 after buffering, which further increases PaCO2, but worsens respiratory Harm of acidosis.

Acid-base balance disorder metabolic alkalosis

Disturbance of acid-base balance

Metabolic alkalosis is a disorder of acid-base balance characterized by a primary increase in plasma HCO3-concentration.

Causes and mechanisms of acid-base balance disorders

According to the therapeutic effect on physiological saline, metabolic alkalosis is divided into two categories: metabolic alkalosis that is effective in treatment with physiological saline and metabolic alkalosis that is ineffective in treatment with physiological saline.

1. Effective metabolic alkalosis treated with normal saline

(1) Excessive loss of H + in the gastrointestinal tract: It is common in severe vomiting caused by pyloric obstruction, high intestinal obstruction and gastrointestinal drainage due to the loss of gastric juice containing a large amount of HCl. At this time, HCO3- in the intestinal fluid cannot be neutralized with HCl as normal, and a large amount of human blood is absorbed by the small intestinal mucosa, which causes the plasma to increase in HCO3- concentration and cause metabolic alkalosis. The loss of gastric juice is often accompanied by the loss of Cl- and K +, so it can cause hypochloremia and hypokalemia. The latter two can aggravate or promote the occurrence of metabolic alkalosis.

(2) Hypochlorine alkalosis: A large amount of chlorine loss and insufficient chlorine intake can lead to hypochlorine alkalosis, which is common in patients with long-term diuretics. Diuretics such as furosemide (fast urine) and itanilic acid (diuretic acid) can inhibit the reabsorption of Na + and Cl- by the proximal tubules, increase the excretion of Na + and Cl- and play a diuretic effect. As Na + reabsorption decreases in the proximal tubule, Na + concentration in the distal tubule increases, leading to enhanced H + -Na + exchange, increased K + -Na + exchange, increased hydrogen secretion and potassium secretion in the distal tubule, and increased reabsorption of HCO3-. At the same time, due to the increased exchange of HCO3--Cl-, Cl- is excreted from the urine in the form of NH4Cl and hypochlorine alkalosis occurs. In addition, the above-mentioned loss of a large amount of gastric fluid can also cause hypochlorine alkalosis. Hypochlorine alkalosis can be corrected after normal saline is added, so it is also called "chlorine-reactive alkalosis".

2. Ineffective metabolic alkalosis treated with saline

(1) Excessive secretion of mineralocorticoids: When primary mineralocorticoids are excessive, it can increase the reabsorption of Na + and H2O by renal tubules and collecting ducts, and promote the excretion of K + and H +. Therefore, too much aldosterone can lead to the loss of H + through the kidney and increase in NaHCO3 reabsorption, causing metabolic alkalosis, and can also cause hypokalemia. At this time, supplementation with normal saline could not be corrected, so it was called "non-reactive alkalosis with chlorine".

(2) potassium deficiency: potassium deficiency can cause metabolic alkalosis. This is because in hypokalemia, the concentration of extracellular fluid K + decreases, intracellular K + is transferred to the extracellular, and H + in the extracellular fluid moves into the cell; at the same time, lack of K + in renal tubular epithelial cells can lead to increased H + secretion Therefore, H + -Na + exchange increases, HCO3- reabsorption increases, and metabolic alkalosis occurs. At this time, the patient's urine is still acidic, which is called abnormal acidic urine. Potassium salts need to be added during treatment, and sodium chloride solution alone cannot correct this type of metabolic alkalosis.

(3) Excessive input of alkaline substances: It has been seen that patients with ulcer disease take too much NaHCO3 for a long time, and these drugs have rarely been used to treat peptic ulcers. Therefore, alkalosis caused by this reason is rare. Entering a large amount of sodium bicarbonate and stock blood can cause iatrogenic metabolic alkalosis, and the citrate anticoagulant input into the blood can produce excessive HCO3- by metabolism.

Acid-base balance disorder body compensation regulation

1. Buffering effect of blood The buffering effect of blood on alkalosis is small, because most of the buffer system components have more alkaline components than acidic components (such as the ratio of HCO3- / H2CO3 is 20/1). Therefore, the blood's buffering capacity for increased alkaline substances is limited. When the extracellular H + concentration decreases, OH- increases, and OH- can be neutralized by weak acids in the buffer system.

OH- + H2CO3 HCO3- + H2O

OH- + HPr Pr + H2O

2. When the lung is compensated to regulate metabolic alkalosis, the HCO3-concentration and pH value of the extracellular fluid increase, and the H + concentration decreases, all of which have an inhibitory effect on the respiratory center, making the breathing movement shallower and slower, and alveolar ventilation reduced. And CO2 emission is reduced, so that the plasma H2CO3 concentration increases, and the HCO3- / H2CO3 ratio approaches 20/1 again. However, the compensation regulation of the lungs is limited, and breathing is also affected by other factors. Although shallow and slow breathing can increase PaCO2, it also causes a decrease in PaO2. When the latter reaches a certain level (PaO27.45, alkalosis is fully compensated by the body, the pH value can be within the normal range.

3. The compensatory regulation of the kidney reduces the release of potassium and ammonium, increases the reabsorption of bicarbonate, and increases the urine pH.

Effects of acid-base disturbances on the body

The clinical manifestations of metabolic alkalosis are often obscured by the primary disease and lack typical symptoms or signs. However, in severe metabolic alkalosis, the following functional and metabolic disorders may occur.

1. Severe metabolic alkalosis caused by central nervous system dysfunction, patients may show signs of increased excitability in the central nervous system such as irritability, delirium, and insanity. Its mechanism may be:

(1) Decreased content of inhibitory transmitter -aminobutyric acid: When metabolic alkalosis occurs, glutamic acid decarboxylase activity decreases, -aminobutyric acid transaminase activity increases, and aminobutyric acid decomposition is enhanced to reduce production. As the content of -aminobutyric acid is reduced, its inhibitory effect on the central nervous system is weakened, so the symptoms of central nervous system excitement appear.

(2) Hypoxia: Metabolic alkalosis, increased pH value, shifts the oxygen separation curve to the left, increases the affinity of hemoglobin and oxygen, and makes it difficult for HbO2 to release O2 in the tissue, causing tissue hypoxia. Brain tissue is particularly sensitive to hypoxia and is prone to central nervous system dysfunction.

2. Neuromuscular stress increased serum calcium exists in two forms of free calcium and bound calcium, and the pH value can affect the mutual conversion between the two. Free calcium can stabilize cell membrane potentials and inhibit neuromuscular stress. In metabolic alkalosis, although total calcium remains unchanged, free calcium decreases and neuromuscular stress increases. In addition, the decrease in -aminobutyric acid content may also play a role. The most common symptoms of patients are hand and foot twitching, facial and limb muscle twitching, hyperreflexia, and convulsions.

3 When hypokalemia is caused by alkalosis, the H + concentration of extracellular fluid decreases, the H + of the intracellular fluid overflows, and the K + of the extracellular fluid shifts inwardly; at the same time, the renal compensatory effect causes the renal tubular epithelial cells to reduce H +, so H + -Na + exchange is reduced, while K + -Na + exchange is enhanced, and K + is increased in the renal row, leading to hypokalemia.

Prevention and care of acid-base balance disorders

1. Treat the primary disease and actively remove the causes that can cause metabolic alkalosis.

2. Mild cases can be corrected by simply entering normal saline or glucose saline. For severe alkalosis, a certain amount of weakly acidic or acidic drugs can be given, such as dilute solution of hydrochloric acid or arginine hydrochloride solution to quickly exclude excessive HCO3-.

3. Patients with excessive mineralocorticoids should use myelin or thiazide diuretics as little as possible, and can be treated with carbonic anhydrase inhibitor acetazolamide; those who are caused by chlorine loss or potassium loss need to be supplemented with potassium chloride at the same time Promote the correction of alkalosis.

4. Use of chlorinated acid drugs

Acid-base balance disorder respiratory alkalosis

Acid-base balance disorder concept

Respiratory alkalosis is a disorder of acid-base balance characterized by a primary reduction in plasma H2CO3 concentration caused by pulmonary hyperventilation.

Causes and mechanisms of acid-base balance disorders

Hyperventilation is the basic mechanism of respiratory alkalosis. The reasons are as follows:

1. Hypotonic hypoxic external respiratory dysfunction such as pneumonia, pulmonary edema, etc., as well as inhaled partial oxygen pressure can cause reflex excitation of the respiratory center due to PaO2 reduction, deep breathing, and increased CO2 emission.

2. Hyperventilation may occur during the onset of hyperventilation such as rickets or crying in children.

3, central nervous system diseases cerebrovascular accidents, encephalitis, brain trauma and brain tumors, etc., when they stimulate the respiratory center can cause hyperventilation.

4. Certain drugs such as salicylic acid and ammonia can directly stimulate the respiratory center and enhance ventilation.

5. Excessive metabolism of the body, such as hyperthyroidism, high fever, etc. Due to increased body metabolism and increased body temperature, it can stimulate the respiratory center, causing patients to deepen and accelerate breathing.

6. Improper use of respirators often causes acute respiratory alkalosis due to excessive ventilation.

Acid-base balance disorder body compensation regulation

1.Internal and external ion exchange and intracellular fluid buffering

(1) In acute respiratory alkalosis, the extracellular fluid H2CO3 decreases and the HCO3-concentration increases relatively, so the H + spillage of the intracellular fluid, combined with HCO3- to form H2CO3, can increase the H2CO3 concentration in the plasma. When the H + of the intracellular fluid overflows, the K + of the extracellular fluid moves internally, and as a result, the K + concentration of the extracellular fluid decreases.

(2) In acute respiratory alkalosis, the concentration of HCO3- in plasma is relatively high, and plasma HCO3- can be exchanged with Cl- in red blood cells. After HCO3- enters red blood cells, it can combine with H + in red blood cells to form H2CO3 and release CO2. CO2 can enter the plasma from red blood cells to form H2CO3, which can increase the plasma H2CO3 concentration. Due to HCO3--C1-exchange, plasma Cl- concentration can be increased.

2. The role of compensatory regulation of the kidney The compensatory regulation of the kidney is the main compensation method for chronic respiratory alkalosis. With acute respiratory alkalosis, the kidneys are too late to compensate. In chronic respiratory alkalosis, PaCO2 decreases, plasma H + concentration decreases, and carbonic anhydrase and glutaminase activities in renal tubular epithelial cells decrease. Therefore, renal tubules produce NH3, excrete H +, NH4 +, and renal tubular reabsorption. NaHCO3 decreases.

Variations of acid-base indicators

The index reflecting respiratory factors decreased, PaCO27.45; chronic respiratory alkalosis, because the kidneys participated in compensation, the SB and BB decreased, and the negative value of BE increased. When the body is decompensated, the pH is greater than 7.45. If alkalosis is fully compensated, the pH can be within the normal range.

Effects of acid-base disturbances on the body

1. Central nervous system dysfunction In acute respiratory alkalosis, the central nervous system dysfunction is not only related to the decrease of -aminobutyric acid content and hypoxia, but also to cerebral vasoconstriction and cerebral blood caused by hypocapnia. Related to reduced traffic. Patients are prone to headaches, dizziness, irritability, and convulsions. In severe cases, they are even unconscious.

2. Increased neuromuscular stress is associated with a decrease in free calcium concentration.

3. Hypokalemia Hypokalemia is related to extracellular K + influx and increased renal K +.

Prevention and care of acid-base balance disorders

1. Prevent the primary disease and remove the cause of hyperventilation.

2. Inhalation of CO2-containing gas. Acute respiratory alkalosis can inhale a mixed gas of 5% CO2 or cover the patient's mouth and nose with paper to inhale the exhaled gas and increase PaCO2 and H2CO3.

3, symptomatic treatment of patients with repeated seizures, intravenous injection of calcium; those with obvious K + deficiency should be supplemented with potassium salts; those with obvious hypoxia symptoms, can take oxygen.

Acid -base balance disorder

Disorders of dual acid-base balance include acid-base consistency and acid-base mixing. There are also two forms of triple acid-base disorders.

Acid-base consistency: acid exhalation and acid replacement; alkali replacement and exhalation.

Acid-base mixing: exhaled acid, substituted alkali; exhaled acid, substituted acid;

Disorders of triple acid-base balance: acid exhalation, acid replacement, and alkali replacement;

Basic principles for judging acid-base disorders

1. Judging acidosis or alkalosis by pH;

2. Judging by respiratory factors or metabolic imbalances based on primary factors;

3. Judge whether it is simple or mixed acid-base imbalance according to the compensation situation.

Clinical analysis

In a disease state, the increase or decrease of acid-base substances in the body exceeds the body's ability to compensate for adjustments, or obstacles to the mechanism of acid-base regulation, disrupt the relative stability of body fluid pH, which is called acid-base balance disorder.

Acidic substances in the body can be divided into: volatile acids that can be excreted through the lungs-carbonic acid; fixed acids that can be excreted through the kidney-mainly including sulfuric acid, phosphoric acid, uric acid, pyruvate, lactic acid, tricarboxylic acid, -hydroxybutyric acid Acetoacetate, etc.

Basic substances in the body are mainly derived from the metabolism of amino acids and organic acid salts in food.

The mechanisms that regulate the body's acid-base balance include the blood buffering system, lung respiration, renal excretion and reabsorption, and ion exchange inside and outside the cell.

Common indicators reflecting acid-base balance are: pH and H + concentration, arterial blood CO2 partial pressure, standard bicarbonate and actual bicarbonate, buffered alkali, alkali residue, and anion gap.

Simple acid-base balance disorders can be divided into metabolic acidosis, respiratory acidosis, metabolic alkalosis and respiratory alkalosis.

Metabolic acidosis can be divided into two types of increased AG and normal AG. Mainly seen in severe diarrhea and other causes of HCO3- direct loss, or loss of HCO3- buffer when acidosis such as lactic acid, ketosis, salicylic acid and so on. AB, SB, BB, PaCO2 decreased in patients with acid replacement, AB <SB.

Cardiovascular system abnormalities in patients with acid replacement often manifest as arrhythmia, weakened myocardial contractility, and decreased vascular response to catecholamines; central nervous system abnormalities are mainly due to increased production of the inhibitory neurotransmitter r-aminobutyric acid and brain tissue oxidase Class activity is inhibited.

Respiratory acidosis is mainly seen in the weakened alveolar ventilation caused by respiratory central depression, respiratory muscle paralysis, airway obstruction, thoracic and lung lesions. Can be divided into two types of acute and chronic. Tissue cell buffering is the main compensation method for the body during acute exhalation, and renal compensation is the main compensation method for the body during chronic exhalation. Generally, PaCO2 increases, pH decreases, AB, SB, and BB increase, AB> SB, and the positive value of BE increases.

Metabolic alkalosis is mainly seen in severe vomiting, excessive mineralocorticoids, and excessive H + loss due to insufficient effective circulating blood volume; HCO3- overload, potassium deficiency, etc. are also common causes. Alkaline generation can be divided into two types of saline reactivity and saline resistance. The patient's pH, PaCO2, AB, SB, and BB all increased, and the positive value of BE increased, AB <SB.

R-aminobutyric acid production increased, oxygen dissociation curve shifted leftward, hypoxia, and central disorder; free calcium decreased, neuromuscular excitability increased; patients often had hypokalemia.

Respiratory alkalosis is mainly seen in pulmonary hyperventilation caused by various reasons. During exhalation, the pH increased, PaCO2, AB, SB, and BB all decreased, AB <SB, and the negative value of BE increased.

Acid-base balance disorders Honey regulates acid-base disorders

Honey ^[11] contains a large amount of basic element salts, so it is an alkaline "food". Regular servings of honey can neutralize acidic metabolites in the body and alkalize body fluids, thereby adjusting the body's acid-base balance and regulating metabolism To avoid causing an acidic constitution and prevent the occurrence of diseases, it is conducive to preventing disease and prolonging life and delaying anti-aging. It is recommended to drink 1-3 times a day, 2-3 spoons each time. If you like honey, you can add more, you can adjust the acid-base balance disorder in the body, warm milk with honey at night can help sleep.