What Is Hypocapnia?

Carbon dioxide retention, like hypoxia, is a specialized pathological term. Various causes cause respiratory dysfunction, leading to hypoxia, which causes carbon dioxide to increase, accumulate, and retain, which affects the normal metabolism of cells and gas exchange, which leads to a series of carbon dioxide retention. Clinical manifestations.

Carbon dioxide retention

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Carbon dioxide retention, like hypoxia, is a specialized pathological term. Various causes cause respiratory dysfunction, leading to hypoxia, which causes carbon dioxide to increase, accumulate, and retain, which affects the normal metabolism of cells and gas exchange, which leads to a series of carbon dioxide retention. Clinical manifestations.

Chinese name

Carbon dioxide retention

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Special pathology nouns

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Causes respiratory dysfunction, resulting in hypoxia

The main form of carbon dioxide in the blood is bicarbonate, which accounts for about 88% of the total carbon dioxide in the blood. Carbon dioxide enters the blood from tissues and reacts with water to form carbonic acid. This reaction occurs mainly in red blood cells. Carbonic acid ionization is hydrogen ions and bicarbonate ions. The concentration of bicarbonate ions in red blood cells gradually increases, and at the same time diffuses into the plasma, and combines with sodium ions in the plasma to form bicarbonate, which is dissolved in plasma and transported. At the same time, the chloride ion in the plasma is transferred to the red blood cells. On the other hand, the hydrogen ions ionized by carbonic acid can quickly combine with oxyhemoglobin, generate reduced hemoglobin, and release oxygen at the same time. The combination of hydrogen ions and hemoglobin not only promotes the conversion of more carbon dioxide into bicarbonate ions, which facilitates the transport of more oxygen-released carbon dioxide, but also promotes the release, which is beneficial to the supply of tissue oxygen.

Impact of carbon dioxide retention

(A) acid-base balance disorders and electrolyte disorders

Normal humans have a certain amount of fixed acid excreted daily by the kidneys, while H ₂ CO ₃ (volatile acids) excreted by the lungs are quite large. Therefore, the regulation of acid-base balance and body fluid and electrolyte content are seriously affected during respiratory failure.

1, acid-base balance disorder due to respiratory failure caused by respiratory failure, due to a large amount of CO ₂ retention, PaCO ₂ increased, causing respiratory acidosis; at the same time due to severe hypoxia, oxidation process disorders, acid metabolites increased, often can Complicated by metabolic acidosis. If the patient is complicated by renal insufficiency or infection, shock, etc., metabolic acidosis will be exacerbated by renal dysfunction of acid excretion and alkali retention or increased production of fixed acid in the body. Respiratory failure caused by impaired ventilation can cause modern compensatory ventilation due to hypoxia, which causes excessive CO ₂ emission. Therefore, respiratory alkalosis can be concurrent with metabolic acidosis. The metabolic alkalosis that occurs in some patients with respiratory failure is mostly iatrogenic, and often occurs after treatment. For example, if the artificial respirator is used improperly in the treatment of chronic respiratory acidosis, CO _{2 is} discharged too quickly and the blood H ₂ CO _{3 is} significantly reduced, and at this time the HCO ₃ increased through compensatory regulation cannot be quickly excreted with urine, so metabolic alkalosis can occur; excessive alkali supplementation can also cause metabolic alkalosis when correcting acidosis For example, insufficient potassium intake and the application of a large amount of potassium-releasing diuretics and adrenocortical hormones can lead to hypokalemia alkalosis.

2. Electrolyte disorders When respiratory acidosis occurs, blood Cl ^- decreases and HCO3 ^- increases, which is due to: increased renal tubular hydrogen secretion, increased NaHCO3 reabsorption, and more Cl ^- in the form of NH4Cl Urinary excretion; Long-term use of diuretics or elevated intracranial pressure may cause excessive Cl ^- loss during vomiting ^. When CO2 accumulates in the blood, HCO3 in red blood cells exchanges with plasma Cl ^- causing blood Cl ^-to decrease. Changes in blood potassium, blood sodium, and blood calcium are affected by acid-base balance disorders, treatment measures, and renal function. Their concentrations can be normal, and they can be increased or decreased.

(Two) changes in the central nervous system-pulmonary encephalopathy

1. CO ₂ retention increases the concentration of hydrogen ions in the cerebrospinal fluid, affects brain cell metabolism, reduces brain cell excitability, and inhibits cortical activity; with the increase of CO ₂ , the stimulation of the subcortex is enhanced, causing cortical excitement; if CO ₂ continues to increase, The subcortex is suppressed, leaving the central nervous system under anesthesia. Patients before anesthesia often have aura symptoms of insomnia, mental excitement, and restlessness.

2. Pulmonary encephalopathy refers to a syndrome mainly due to central nervous system dysfunction caused by respiratory failure. Clinically, due to the enhancement of the excitatory process in the early stage, patients manifested with memory loss, headache, dizziness, restlessness, hallucinations, and mental disorders. When PaCO2 reached 10.6kPa (80mmHg) or more, the cerebral cortex was inhibited, and the patient gradually became indifferent. Drowsiness, unconsciousness, coma, etc. Pulmonary encephalopathy is mostly a functional disorder in the early stages, with cerebral vasodilation and congestion. There may be severe lesions such as cerebral edema and cerebral hemorrhage in the late stage. Pulmonary encephalopathy is the result of a combination of hypoxia, hypercapnia, acidosis, and microthrombosis in the brain.

3. The increase of PaCO ₂ in hypercapnia and acidosis not only inhibits the function of the central nervous system, but also directly affects the cerebral blood vessels. When PaCO2 exceeds the normal level of 1.33 kPa (10 mmHg), cerebral blood vessels dilate and cerebral blood flow can increase by 50 %. PaCO _{2 is} too high, which can significantly dilate and congest cerebral blood vessels, and increase the permeability of capillary walls, causing vascular-derived cerebral edema, increased intracranial pressure, and optic nerve papillary edema. In severe cases can also lead to the formation of a brain hernia. The effect of CO2 accumulation on the center can also play a role by changing the pH of cerebrospinal fluid and brain tissue. The buffering capacity of cerebrospinal fluid is lower than that of blood. The pH of normal cerebrospinal fluid is low (7.33 to 7.40), but PCO2 is about 1.0kPa (7.5mmHg) higher than arterial blood. Therefore, when PaCO2 is increased, the CO2 in cerebrospinal fluid also increases. The pH value is lower and the blood is worse, so it can aggravate brain cell damage, such as enhancing the activity of phospholipase, causing damage to the cell membrane structure and increasing permeability; the stability of the lysosomal membrane is reduced, and various hydrolytic enzymes can be released to break down tissue components Promote edema, degeneration and necrosis of brain cells.

(Three) changes in the respiratory system

1. A certain concentration of PCO2 is an important physiological stimulus to maintain respiratory movement. The stimulating effect of CO2 on breathing is achieved in two ways. Stimulation of peripheral chemoreceptors: When PCO2 rises, the peripheral chemoreceptors of the carotid body and the aortic body are stimulated, which increases the afferent impulses of the sinus and aortic nerves, acts on the medullary respiratory center to excite, and accelerates the deepening of breathing. Stimulation of central chemoreceptor: The central chemoreceptor is located on the superficial part of the ventrolateral medulla and is sensitive to H +. The surrounding cells are also cerebrospinal fluid. The blood-cerebrospinal fluid barrier and the blood-brain barrier are relatively impermeable to H + and HCO ₃ , but CO2 is easy to pass through. When PCO2 in the blood rises, CO2 enters the cerebrospinal fluid through the above barrier, combines with H2O in it to form HCO3-, and then dissociates out H + to stimulate the central chemoreceptor. Through certain neural connections, the medullary respiratory central neurons are excited, and breathing is enhanced. Among the two pathways of PCO2 on respiratory regulation, the central chemoreceptor pathway is the main one. Within a certain range, increased arterial blood PCO2 can enhance breathing, but exceeding a certain limit can cause respiratory depression.

2. Hypoxemia and hypercapnia caused by respiratory failure can further affect respiratory function. PaO2 reduces the stimulation of the carotid body's primary aortic body chemoreceptor, and PaCO2, the increase of the effect on the medullary central chemoreceptor can deepen the breathing and increase the alveolar ventilation, which has compensatory significance. However, when PaO2 is lower than 4kPa (30n1mHg) or PCO2 is higher than 10.6KPa (80mmHg), it will inhibit the respiratory center and weaken the breathing. Changes in respiratory function in patients with respiratory failure are also related to many primary diseases. For example, obstructive ventilation disorder, due to different obstruction sites, restrictive insufficient ventilation due to decreased lung compliance manifested as inspiratory dyspnea (upper airway obstruction) or expiratory dyspnea (lower airway obstruction), often occurs Shallow and fast breathing; central respiratory failure often shows shallow and slow breathing, and in severe cases, respiratory rhythm disturbances can occur, such as tidal breathing, medullary breathing, sigh-like breathing, and sobbing-like breathing. Tidal breathing is more common. Its characteristic is that the breathing gradually changes from shallow to deep, and then gradually slows down. After a short breath stop, the above breathing process is repeated. Such respiration is seen when intracranial pressure is elevated, uremia, severe hypoxia, and damage or suppression of the respiratory center. The mechanism is generally considered to be due to reduced excitability of the respiratory center. At this time, stimulation of normal concentration of CO2 in the blood can not cause excitement of the respiratory center, so apnea occurs. Subsequently, the CO2 in the blood gradually increases to a concentration sufficient to excite the respiratory center. When breathing occurs, CO2 is gradually discharged, and the concentration of CO2 in the blood decreases with apnea. Repeatedly alternating like this, the performance is tide, so it is called tide breathing. Medullary respiration is an advanced manifestation of central respiratory failure, with irregular rhythms and amplitudes and apnea. The respiratory rate is less than 12 breaths / min. Sigh-like breathing and sobbing-like breathing are end-of-life breathing performances, which are characterized by breathing : Deep and irregular, open mouth breathing and respiratory assistance muscle activity increase, and finally the breathing weakens and stops. These two types of breathing indicate that the respiratory center is in a deeply suppressed state.

4. Changes in the circulatory system

PaO2 reduction and PaCO2 increase to a certain degree can stimulate peripheral chemoreceptors (carotid body and aorta body), make the heart beat faster, strengthen myocardial contractility, and increase blood pressure; it can also cause sympathetic nerve excitement and adrenal marrow reflectively Mass secretion increases, which causes faster heartbeat, stronger myocardial contractility, increased blood pressure, skin and abdominal visceral blood vessels contraction, and heart and cerebral blood vessels dilate. These changes are compensatory. A certain degree of CO2 retention also has a direct effect on peripheral small blood vessels, causing them to expand (except lung and renal arteries). Skin vasodilation can make limbs warm and ruddy with profuse sweating; conjunctival and cerebral vasodilation and congestion. Severe hypoxia and CO2 retention can directly inhibit the cardiovascular center and heart activity, aggravate vasodilation, lead to lower blood pressure, and reduce myocardial contractility. Both O2 and CO2 retention can cause pulmonary artery vasoconstriction and increase pulmonary circulation resistance, leading to pulmonary hypertension and increasing right heart burden.

Respiratory failure is often accompanied by heart failure, especially right heart failure, the main cause of which is pulmonary hypertension and myocardial damage. The mechanism is closely related to severe hypoxia. Hypercapnia can also aggravate heart damage due to acidosis.

(E) Changes in renal function

Mild CO2 retention will dilate the renal blood vessels, increase renal blood flow, and increase urine output. When PaCO2 exceeds 8.64 kPa and blood pH drops significantly, renal vasospasm, blood flow decreases, HCO3- and Na + reabsorption increase, and urine output decreases. Respiratory failure due to hypoxia and CO2 accumulation can cause persistent renal arteriolar spasm, reduce renal blood flow, renal glomerular: reduced ball filtration rate, light urine protein, red blood cells, white blood cells and casts, etc. In severe cases, acute renal failure may occur, with changes such as oliguria, azotemia, and metabolic acidosis.

(6) Gastrointestinal changes

CO2 retention can increase gastric acid secretion, so gastric mucosal erosion, necrosis and ulceration can occur during respiratory failure. Causes gastrointestinal bleeding.

Clinical manifestations of CO2 retention

The partial pressure of carbon dioxide can accurately reflect the state of respiratory function. Carbon dioxide partial pressure> 6kPa is hypercapnia, which indicates insufficient ventilation, showing CO2 retention, which is respiratory acidosis; <5.99kPa, hypocapnia, which indicates excessive ventilation, which indicates excessive CO2 excretion, which is respiratory alkalinity Poisoning; respiratory failure may occur when pCO2> 4.66kPa, and> 7.32kPa is one of the signs of diagnosing respiratory failure; when the partial pressure of carbon dioxide rises above 10.64kPa, the symptoms of central nervous system depression appear, which are first manifested as unresponsive nerve, headache, Disorientation, and further insanity, lethargy, semi-coma to coma, and even convulsions. When the carbon dioxide partial pressure rises to 15.96kPa, a coma is almost unavoidable, with the disappearance of the plantar reflex, the pupils generally shrink, the intracranial pressure rises, and it is life-threatening. The degree of impact of the elevated carbon dioxide partial pressure on the condition is related to the individual The obvious difference is directly related to the speed of CO2 retention. When CO2 is abruptly retained (acute respiratory failure), coma may occur even if the carbon dioxide partial pressure does not exceed 10.64kPa.

main performance:

First, dyspnea is manifested in changes in frequency, rhythm, and amplitude, such as central respiratory failure with tidal, intermittent or sobbing breathing; COPD is changing from slow and deep breathing to shallow and fast breathing to assist respiratory muscle activity Strengthening, nodding or lifting shoulders, central nervous system drug poisoning manifested as slow breathing and lethargy; when severe pulmonary heart disease was accompanied by carbon dioxide anesthesia with respiratory failure, shallow and slow breathing occurred,

Second, the mental symptoms of acute respiratory failure are more obvious than chronic ones.Acute O2 deficiency can cause symptoms such as insanity, mania, coma, and convulsions. Chronic O2 deficiency often has mental or directional dysfunction, and CO2 retention appears before central depression. Exciting symptoms, such as insomnia, irritability, restlessness, but at this time do not use sedatives or sleeping pills to avoid aggravating CO2 retention, pulmonary encephalopathy, manifested as indifferent, muscle tremors, intermittent convulsions, lethargy, even coma, etc., pH compensation, Can still carry out daily personal life activities, acute CO2 retention, pH 7.3, psychological symptoms will occur, severe CO2 retention may appear weakened or disappeared tendon reflex, positive cone tract sign, etc.

Symptoms of the circulatory system Severe deficiency of O2 and CO2 retention causes pulmonary hypertension, right heart failure can occur, with signs of systemic circulation congestion, CO2 retention fills peripheral body surface veins, skin ruddy, sweaty, humid, blood pressure rises, heart Increased pulse volume caused a large pulse; due to cerebral vasodilation, pulsatile headaches were generated; late in the course of severe O2 deficiency, acidosis caused myocardial damage, peripheral circulation failure, decreased blood pressure, arrhythmia, and cardiac arrest,

Fourth, severe digestive and urinary symptoms, respiratory failure has an impact on liver and kidney function, such as elevated alanine aminotransferase and non-protein nitrogen, proteinuria, red blood cells and casts in the urine, often due to gastrointestinal hyperemia and edema, Erosion and bleeding, or upper gastrointestinal bleeding caused by stress ulcers, these symptoms can disappear with the correction of O2 and CO2 retention,

Determination of CO2 retention

Arterial blood gas analysis can objectively reflect the degree of CO2 retention, and is of great value in guiding the adjustment of various parameters of oxygen therapy, mechanical ventilation, and correcting acid-base balance and electrolytes.

First, the partial pressure of carbon dioxide in arterial blood (PaCO2) refers to the pressure generated by physically dissolved CO2 molecules in the blood.The normal PaCO2 is 4.6kPa-6kPa (35-45mmHg), and greater than 6kPa is hypoventilation. Acute hypoventilation, when PaCO26.6kPa (50mmHg), calculated according to the Henderson-Hassellbalch formula, the pH has been lower than 7.20, which will affect circulation and cell metabolism. Chronic respiratory failure due to the body's compensation mechanism, PaCO26.65kPa (50mmHg) as respiratory failure Diagnostic indicators.

Second, the pH value is the negative logarithm of the hydrogen ion concentration in the blood.The normal range is 7.35 to 7.45, with an average of 7.40. Below 7.35 is decompensated acidosis. Above 7.45 is decompensated alkalosis, but it cannot be explained. What kind of acid-base poisoning is, clinical symptoms are closely related to pH shift.

Third, excess alkali (BE) at 38 ° C, CO2 partial pressure 5.32kPa (40mmHg), 100% oxygen saturation measurement, the amount of acid and alkali required to titrate the blood to pH 7.4, it is the human metabolic acid and alkali Quantitative indicator of imbalance. The positive acid amount is BE, which is a metabolic alkalosis; the negative amount EB is a negative value, which is a metabolic acidosis. The normal range is 02.3mmol \ / L. When correcting the metabolic acid-base imbalance It can be used as a reference for estimating the dosage of antacids or alkali resistance drugs.

Fourth, buffer base (BB) is the total content of various buffer bases in the blood, including bicarbonate, phosphate, plasma protein salt, hemoglobin salt, etc., which reflects the body's buffering ability to resist acid-base interference, and the body's The specific situation of acid-base imbalance compensation, the normal value is 45mmol \ / L.

Fifth, the actual bicarbonate (AB) AB is the content of bicarbonate contained in human plasma under the actual partial carbon dioxide pressure and blood oxygen saturation, the normal value is 22-27mmol \ / L, the average value is 24mmol \ / L, HCO3- content is related to PaCO2. With the increase of PCO2, the plasma HCO3- content also increases. On the other hand, one of the HCO3-plasma buffer bases. When there is too much fixed acid in the body, the pH can be stabilized by HCO3- buffering. The HCO3- content decreases, so AB is affected by both breathing and metabolism. Nine, standard bicarbonate (SB) refers to a whole blood specimen that is isolated from the air. At 38 ° C, PaCO2 is 5.3kPa, and the hemoglobin is 100% oxygenated, the measured bicarbonate (HCO3-) content in the plasma. The normal value is 22-27mmol \ / L, with an average of 24mmol \ / L. SB is not affected by respiratory factors.The increase or decrease of its value reflects the amount of HCO3-reserve in the body, so it explains the trend and degree of metabolic factors, metabolic acid. SB decreased during poisoning; SB increased during metabolic alkalosis, and CO2 retention was indicated at ABSB.

Sixth, the normal value of carbon dioxide binding power (CO2CP) is 22-29mmol \ / L, which reflects the main alkali reserve in the body. When metabolic acidosis or respiratory alkalosis, CO2CP decreases; when metabolic alkalosis or respiratory acidosis, CO2CP increases, but when respiratory acidosis is accompanied by metabolic acidosis, CO2CP may not necessarily increase. Due to respiratory acidosis, the kidneys excrete H + in the form of NH4 + or H +, and absorb HCO3- for compensation, and the alkali reserve increases. Therefore, the increase of CO2CP reflects the severity of respiratory acidosis to a certain extent, but it cannot reflect the rapid changes of CO2 in the blood, and it is also affected by metabolic alkali or acidosis. Therefore, CO2CP has its one-sidedness, and it must be combined with clinical and electrolytes. For full consideration,

CO2 retention treatment

First, establish an unobstructed airway

Before oxygen therapy and improving ventilation, various measures must be taken to keep the airway open. For example, use a porous catheter to suck secretions or reflux in the stomach through the mouth and throat. The sputum is sticky and difficult to cough. It can also retain the ring when inhaled with bromine spray. Hypothyroidism plastic tube is injected with normal saline to dilute secretions or bronchial antispasmodics 2 stimulants are used to dilate the bronchial tubes. If necessary, adrenal corticosteroids can be given to inhale bronchospasm; in addition, the secretions can be sucked out with a bronchoscope. Nasal tracheal intubation or tracheotomy to create an artificial airway

Second, oxygen therapy

The principle of oxygen therapy should be given a low concentration (<35%) of continuous oxygen. Patients with CO2 retention cannot inhale high concentrations of O2. Because of patients with hypercapnia, their respiratory central chemoreceptors are poorly responsive to CO2, and the maintenance of breathing is mainly based on hypoxia. Driving effect of chemoreceptors on carotid sinus and aortic body. If inhaled high concentration of oxygen, PaO2 rises rapidly, causing peripheral chemoreceptors to lose the stimulation of hypoxemia, the patient's breathing becomes slower and shallower, PaCO2 rises accordingly, and in severe cases can fall into a state of CO2 anesthesia. This mental change is often associated with PaCO2 Speed of rise

Methods of oxygen therapy: The commonly used oxygen therapy is nasal catheter or nasal inhalation. The concentration of inhaled oxygen (F1O2) and the flow of inhaled oxygen have the following relationship: F1O2 = 21 + 4 × inhaled oxygen flow (L / min). However, it should be noted that the same flow rate, the inhaled oxygen concentration of the nasal plug changes with the inhalation minute ventilation. For low ventilation, the actual oxygen concentration is higher than the calculated value; for high ventilation, the oxygen concentration is lower than the calculated value.

Application of ventilator: Use a two-level ventilator. To put it plainly, it is possible to set two pressures, high and low, and use the pressure difference to expand and contract the lungs and expel carbon dioxide.

Third, increase ventilation and reduce CO2 retention

CO2 retention is caused by inadequate alveolar ventilation. Only increasing alveolar ventilation can effectively expel CO2. Mechanical ventilation has affirmed the efficacy of treatment; however, the application of respiratory stimulants is still controversial due to its different effects. The brief introduction is as follows:

(1) Reasonable application of respiratory stimulants Respiratory stimulants stimulate the respiratory center or surrounding chemoreceptors. By increasing respiratory center excitability, increase breathing frequency and tidal volume to improve ventilation. At the same time, the patient's oxygen consumption and CO2 production also increase correspondingly and Ventilation volume is positively related. Because it is simple and economical to use and has a certain effect, it is still widely used in clinical practice. However, patients with low ventilation rate should have mastery of clinical indications. It is better if the main respiratory stimulant is central depression. Chronic obstructive pulmonary disease respiratory failure Low ventilation due to bronchial-pulmonary lesions with low central responsiveness or respiratory muscle fatigue at this time The pros and cons of applying respiratory stimulants at this time should be determined according to the major and minor factors of the above three factors in the nervous conduction system and respiratory muscle disease and pneumonia and pulmonary edema Breathing dysfunction in patients with extensive interstitial fibrosis of the lung is not good for respiratory stimulants. It should not be used. When applying respiratory stimulants, attention should be paid to reducing the mechanical load on the chest, lungs and airways, such as the drainage of bronchial spasmolytic agents. Application to eliminate pulmonary interstitial edema and other factors affecting chest and lung compliance, otherwise ventilation drive will increase shortness of breath and increase exhalation. At the same time, you need to increase the concentration of inhaled oxygen in addition to taking advantage of the conscious return of some breathing stimulants. Encourage patients to cough and sputum to keep the airway open. If necessary, cooperate with nasal or oronasal mask mechanical ventilation support.

Nicoxamib is a commonly used respiratory central stimulant to increase ventilation and also has a certain effect on thallium. Patients who are drowsy can slowly inject 0.375g-0.75g intravenously and then add 3-3.75g to 500ml of liquid and press 25-30 drops. / min intravenous drip Closely observe the patient's eyelash response conscious changes and respiratory frequency amplitude and rhythm follow up arterial blood gas in order to adjust the dose. If there are side effects such as skin itching and irritability, the drip rate must be slowed down. If no effect is seen after 4h-12h or a severe reaction to muscle twitching occurs You should disable mechanical ventilation support if necessary

Fourth, correct acid-base balance disorders and electrolyte disorders

The following types of acid-base balance disorders are common in the diagnosis and treatment of respiratory failure.

(1) Respiratory acidosis due to insufficient alveolar ventilation, CO2 retention in the body produces hypercapnia, changes the normal ratio of BHCO3 / H2CO3 1/20 of patients with chronic respiratory failure who produce acute respiratory acidosis through the blood buffering system and the kidneys Adjustment (H + secretion combined with Na + combined with HCO3- to form NaHCO3) to bring the pH close to normal respiratory failure and deacidification. Alkali (5% NaHCO3) can be used to temporarily correct the pH value but it will reduce ventilation and further increase CO2 retention so it is not removed. The root cause of acidosis can only correct respiratory acidosis by increasing alveolar ventilation

(2) Respiratory acidosis combined with metabolic acidosis due to hypo-O2emia, insufficient blood volume, decreased cardiac output, and peripheral circulation disorders. Fixed acids such as lactic acid in the body increase renal function damage and affect the discharge of acidic metabolites. On the basis, it can be accompanied by metabolic acidosis. The fixed acid in the anion increases. HCO3- correspondingly decreases the pH value. Acidosis causes potassium ions to transfer blood from the cell to the outside of the cell. K + increases HCO3-. Reduces blood CI. Except for severely affecting blood pressure due to acidosis during mobile therapy or adding alkaline agents at pH <7.25, NaHCO3 will increase the risk of CO2 retention (NaHCO3 + HAC NaAC + H2O + CO2) At this time, ventilation should be increased to correct CO2 retention and Treating the Causes of Metabolic Acidosis

(3) Respiratory acidosis combined with metabolic alkalosis During the treatment of chronic respiratory acidosis, CO2 is often expelled too quickly due to the application of mechanical ventilation; supplementary alkaline drugs are overdose; glucocorticoid diuretics are used to increase potassium excretion; or Because the correction of acid intoxication potassium ions into the cell produces hypokalemia, vomiting or diuretics to reduce blood chlorine can also produce metabolic alkalosis. The pH is high. BE is a positive value. The above medicinal factors of alkalosis should be prevented during treatment. And avoid CO2 exhaustion too fast and give an appropriate amount of thallium chloride to relieve alkalosis should be treated in time

(4) Respiratory alkalosis This is a case of respiratory alkalosis caused by heartbeat breathing in patients without respiratory disease. The use of mechanical ventilation due to excessive venting of excessive CO2.

(5) Respiratory alkalosis combined with metabolic alkalosis is a chronic respiratory failure patient with mechanical ventilation that excretes excessive CO2 in a short period of time and is lower than the normal value; it is also caused by the absolute increase of renal bicarbonate in the body

In addition, due to improperly treated patients with respiratory failure, the tribasic acid-base imbalance caused by low potassium and low chlorine on the basis of respiratory and metabolic acidosis

V. Other treatments: anti-infective treatment, prevention and treatment of gastrointestinal bleeding, correction of shock, rational use of diuretics, and nutritional support.