Chronic respiratory failure

Introduction to Chronic Respiratory Failure Chronic respiratory failure occurs on the basis of existing lung diseases such as chronic obstructive pulmonary disease, severe tuberculosis, pulmonary interstitial fibrosis, pneumoconiosis, thoracic lesions and chest surgery, trauma, extensive pleural thickening, and thoracic deformity. Common diseases because of COPD, early manifestations of type I respiratory failure, as the condition gradually worsens, lung function is getting worse and worse, can be expressed as type II respiratory failure. In the stable phase of chronic respiratory failure, although PaO2 is lowered and PaCO2 is elevated, patients can be stabilized within a certain range by compensation and treatment, and patients can still engage in general work or daily life activities. Once the respiratory infection is aggravated or other causes, PaO2 can be significantly decreased, PaCO2 is significantly increased, which can be called acute exacerbation of chronic respiratory failure, which is the most common type of chronic respiratory failure in China. Chronic respiratory failure has a certain number of basic diseases, but acute seizures have decompensated respiratory failure, which can directly endanger life, and must be promptly and effectively rescued. basic knowledge The proportion of the disease: 0.05%-0.08% in the respiratory system Susceptible people: no specific population Mode of infection: non-infectious Complications: pulmonary encephalopathy, gastrointestinal bleeding, shock, metabolic acidosis

Causes of chronic respiratory failure

Causes

Chronic respiratory failure is often caused by bronchial-pulmonary disorders such as COPD, severe tuberculosis, bronchiectasis, diffuse pulmonary interstitial fibrosis, pneumoconiosis, etc. Among them, COPD is the most common, thoracic lesions such as thoracic surgery, trauma, extensive pleural thickening Thoracic deformity can also cause chronic respiratory failure.

Bronchiectasis (26%):

Due to chronic suppurative inflammation and fibrosis of the bronchus and its surrounding lung tissue, the muscles and elastic tissues of the bronchial wall are destroyed, resulting in bronchial deformation and persistent expansion. Typical symptoms are chronic cough, massive cyanosis, and repeated hemoptysis.

Diffuse pulmonary interstitial fibrosis (20%):

It is an inflammatory disease of the interstitial lung caused by various causes. The lesion mainly affects the interstitial lung, and may also involve alveolar epithelial cells and pulmonary blood vessels. The cause is clear and some are unknown. The clear causes are inhalation of inorganic dust such as asbestos, coal, organic dust such as mold dust, cotton dust, gases such as smoke, sulfur dioxide, viruses, bacteria, fungi, parasitic infections, drug effects and radiation damage.

Pneumoconiosis (10%):

It is a systemic disease mainly caused by diffuse fibrosis (scarring) of lung tissue caused by long-term inhalation of productive dust (dust) in occupational activities and retention in the lungs. Pneumoconiosis can be divided into inorganic pneumoconiosis and organic pneumoconiosis according to the type of dust inhaled. The pneumoconiosis caused by the inhalation of inorganic dust in production labor is called inorganic pneumoconiosis. Most of the pneumoconiosis is inorganic pneumoconiosis.

Pathogenesis

The main physiological function of the lung is gas exchange. This exchange mainly involves the body's carbon dioxide production from the body through the lung tissue and the carbon dioxide produced by the body's metabolism. The transportation of gas in the body depends on blood circulation. The cells take oxygen from the blood or tissue fluid environment and emit carbon dioxide. The whole process of breathing includes three interconnected links:

1. External respiration refers to the exchange of gas between the external environment and blood in the lungs. It includes two processes: lung ventilation (gas exchange between the lungs and the outside world) and lung ventilation (gas exchange between the alveoli and blood).

2. Transportation of gas in the blood.

3. Internal respiration refers to the exchange of gas between blood or tissue fluid and tissue. The mechanism involved in respiratory failure is mainly external respiration, which includes pulmonary ventilation and pulmonary ventilation, which are described below.

1. Lung ventilation dysfunction: Gas exchange in the lung refers to the exchange of gas in the alveoli with the blood in the alveolar capillaries, mainly the exchange of oxygen and carbon dioxide. The exchange of lung gas is mainly determined by the ventilation/blood perfusion ratio (V/ Q) With diffuse function, the main pathogenesis of type I respiratory failure is ventilation dysfunction, mainly including ventilation/blood flow imbalance and diffuse dysfunction.

(1) Ventilation/blood flow imbalance: effective gas exchange in the lung requires not only adequate ventilation and blood flow, but also a proper ratio of the two. At rest, the alveolar ventilation of healthy people is about 4L/min. The pulmonary blood flow is about 5L/min, and the average lung V/Q is about 0.8. When the ventilation is greater than the pulmonary blood flow, V/Q>0.8, the gas entering the alveoli cannot fully fully contact the blood in the alveolar capillaries. Therefore, sufficient gas exchange is not obtained, that is, there is not enough blood exchange in the alveolar excessive gas exchange, resulting in ineffective cavity ventilation, such as clinically common emphysema, bullous bullae and pulmonary embolism, when pulmonary blood flow When the lung ventilation increased, V/Q<0.8, when the venous blood flow through the poorly ventilated alveolar capillaries did not fully oxygenate back to the left heart, forming an arterial blood venous blood doping, called functional movement - venous blood shunting, such as functional shunt in patients with severe COPD, decreased lung gas or no gas in the atelectasis, and blood flow continues, V / Q = 0, at this time the blood flowing through the lungs is completely without gas exchange Incorporating arterial blood, similar to anatomical shunt , also known as true shunt, or pathological arteriovenous blood shunt, V / Q ratio imbalance mainly causes hypoxemia, is also the most common mechanism of hypoxemia, has little effect on PaCO2, the reason is :

1 movement, intravenous carbon dioxide partial pressure difference is only 6mmHg, and the difference between dynamic and venous oxygen partial pressure is about 60mmHg, when V / Q <0.8 mixed venous blood added to arterial blood, the effect on PaO2 is significantly greater than PaCO2.

When 2V/Q>0.8 or V/Q<0.8, both of them can show a compensatory increase in normal alveolar ventilation with V/Q, while the diffusion rate of carbon dioxide is about 21 times that of oxygen, and the dissociation curve of carbon dioxide is linear. As long as the normal alveolar ventilation increases, more carbon dioxide can be discharged, and the result is as follows: PaO2 decreases without PaCO2 elevation.

(2) Dispersion dysfunction: Gas dispersion refers to the process of moving gas molecules from high concentration zone to low concentration zone. Dispersion is a passive movement process, so there is no need to consume energy. The mechanism of dispersion is the random movement of gas molecules, dispersion. As a result, the molecules at different concentrations eventually reach equilibrium. The gas in the alveoli and the exchange of gas in the blood of the alveolar wall (mainly oxygen and carbon dioxide) are diffused. The ability of the lung to diffuse is not only affected by the alveolar capillary membrane, but also by the The effect of pulmonary capillary blood flow, healthy adult lung diffusion (DL) is about 35ml O2 / (mmHg · min), can affect the alveolar capillary membrane area, alveolar capillary bed volume, diffuse membrane thickness and gas and hemoglobin binding The factors can affect the diffusion function. In clinical practice, the diffuse dysfunction is the only pathological factor. The diffuse dysfunction in the disease process is always accompanied by the ventilatory/blood flow imbalance, because the alveolar membrane thickens or the area. Decreased often leads to a ventilatory/blood flow imbalance, due to the rate of diffusion of carbon dioxide through the alveolar capillary membrane 21 times, so the diffuse dysfunction is mainly affecting the exchange of oxygen. The hypoxemia caused by diffuse dysfunction can be corrected by inhaling high concentration of oxygen, because the increase of alveolar oxygen partial pressure can overcome the increased diffusion resistance, which is often used in clinical practice. Oxygen correction hypoxemia, can also use oxygen to correct hypoxemia to identify hypoxemia caused by diffuse dysfunction caused by hypoxemia or arteriovenous shunt.

2. Lung ventilation dysfunction: Lung ventilation refers to the process of exchanging alveolar gas with outside air through respiratory movement. Any factors that can affect lung ventilation and resistance can affect lung ventilation function, normal ventilation and ventilation volume. It is not only the size of the motility that drives the lung ventilation, but also the resistance of the lung ventilation. Under the control of the respiratory center, the lungs are expanded and contracted by the contraction and relaxation of the respiratory muscles. In the resting air, the total alveolar ventilation is about 4L/min to maintain normal oxygen and carbon dioxide partial pressure. When the lung ventilation is dysfunctional, the alveolar ventilation is insufficient, the alveolar oxygen partial pressure decreases, and the carbon dioxide partial pressure rises. Type II respiratory failure can occur, that is, PaO2 decline and PaCO2 increase simultaneously. Lung ventilation dysfunction can be divided into two types: restricted ventilation and obstructive ventilation. Restricted ventilation is caused by restriction of alveolar contraction. Because of the increased airway resistance, the obstructive ventilation is insufficient, which is explained below.

(1) Insufficient ventilation: Insufficient alveolar ventilation caused by restriction of alveolar contraction during inhalation is called restrictive hypoventilation. Usually, inspiratory movement is the active process of inspiratory muscle contraction, exhalation. It is the passive process of elastic retraction of the alveoli and the reduction of the ribs and sternum by gravity. The active process is prone to obstacles and the alveolar expansion is limited. It mainly involves the compliance of the respiratory muscles, thorax, respiratory center and lungs. Disorders can be collectively referred to as respiratory pump failure.

1 respiratory pump failure is mainly due to lack of respiratory drive, such as sleeping pills poisoning, central nervous system disorders can affect the lack of respiratory drive, respiratory movement is limited, such as respiratory muscle function caused by a variety of diseases such as Guillain-Barre syndrome, Hypokalemia and other thoracic disorders such as thoracic deformity, posterior scoliosis, massive pleural effusion and pneumothorax, etc., have recently been recognized as one of the important causes of respiratory pump failure in patients with COPD.

2 Reduced lung compliance is also one of the causes of limited ventilation in patients with COPD.

(2) obstructive ventilation deficiency: due to airway stenosis or obstruction caused by increased airway resistance caused by ventilatory disorders called obstructive hypoventilation (obstructive hypoventilation), bronchial wall congestion, swelling, hyperplasia, smooth wall tendon, lumen Increased secretion of endocrine, obstruction of foreign bodies, lung tissue damage caused by alveolar wall destruction and loss of alveolar space, so that the traction of the airway wall is weakened, etc., the airway inner diameter can be narrowed or irregular and the airway can be increased. Resistance, which causes obstructive ventilation, and increased oxygen consumption is one of the causes of aggravation of hypoxemia. Fever, chills, dyspnea, and convulsions can increase oxygen consumption, as increased oxygen consumption can lead to mixed venous oxygen. The partial pressure drops, which aggravates the hypoxemia caused by the arteriovenous shunt, the oxygen consumption increases, and the alveolar oxygen partial pressure decreases. The normal person can increase the ventilation to prevent hypoxia, and the oxygen consumption increases the ventilatory dysfunction patients. The alveolar oxygen partial pressure is continuously increased, and the lack of oxygen is also difficult to alleviate.

Pathophysiology

Hypoxia and carbon dioxide retention during respiratory failure can affect the metabolism and function of various systemic organs of the body. The degree of damage to the body depends on the rate, extent and duration of hypoxia and carbon dioxide retention, if both hypoxia and carbon dioxide remain In the presence of the body damage is more obvious, in which hypoxia is more important to the body damage, in all organs caused by hypoxia, heart, brain, pulmonary blood vessels, liver, kidney are most sensitive to hypoxia, below Deficiency of hypoxia and carbon dioxide retention are described separately.

(1) Pathophysiology of hypoxia:

1 Impact on the respiratory system: Patients with chronic respiratory failure have respiratory symptoms due to the original lung disease, but hypoxia and carbon dioxide retention can further affect respiratory function, sometimes difficult to distinguish between the two, in the absence of oxygen, located in the carotid artery The peripheral chemoreceptors of the body and aortic arch can produce excitement and stimulate the respiratory center, and reflexively enhance respiratory movement. It has compensatory significance. This reaction is obvious when PaO2 is less than 60mmHg, which can be clinically manifested as increased respiratory rate and lung ventilation. Increase, but this protective reflex effect is limited. When PaO2 is lower than 30mmHg, hypoxia has a direct inhibitory effect on the respiratory center. This effect can be greater than the reflective excitatory effect, and the respiratory depression is expressed as the respiratory rate. And the lung ventilation is significantly reduced or reduced, so that the respiratory rhythm slows down, the amplitude becomes shallow, and finally the breathing stops completely. In addition, the long-term enhanced breathing exercise can increase the oxygen consumption of the respiratory muscles, and the blood oxygen supply is insufficient. Can cause respiratory muscle fatigue, weaken respiratory muscle contraction, slower and faster breathing, reduced alveolar ventilation, can be added Respiratory failure.

2 Effects on the circulatory system: The effects of hypoxia on the circulatory system include the heart and blood vessels, early hypoxia, a certain degree of PaO2 reduction can excite the cardiovascular motor center, accelerate heart rate, increase myocardial contractility, peripheral vasoconstriction, peripheral blood vessels Contraction can increase the effective circulating blood volume and increase cardiac output, but at this time, the heart and cerebral blood vessels are dilated, which ensures the blood supply to the heart and brain, and the late stage of severe hypoxia or hypoxia. A. For the cardiovascular center Direct inhibition, direct inhibition of cardiac activity and dilation of blood vessels, B. Tissue and cells do not receive adequate oxygen supply or when severe metabolic acidosis occurs, the ability of tissues and cells to take up oxygen and utilize oxygen also decreases. The irreversible damage of the myocardium caused by hypoxia, the above three factors can cause slow heart rate, decreased myocardial contractility, decreased cardiac output, arrhythmia, and even severe consequences such as cardiac arrest. Hypoxia can cause a wide range of Contraction of pulmonary arterioles, increased resistance to pulmonary circulation, pulmonary hypertension, especially in patients with respiratory failure caused by COPD, due to the presence of pulmonary arteriolar wall Hypertrophy and hyperplasia of synovial cells and fibroblasts, increased synthesis of collagen and elastin, resulting in thickening and sclerosis of the pulmonary vascular wall, narrowing of the lumen, which is the anatomical basis for the formation of persistent and stable chronic pulmonary hypertension. At the time, the contraction of pulmonary arterioles caused by hypoxia is an important factor for aggravating pulmonary hypertension. Long-term pulmonary hypertension will lead to right ventricular hypertrophy, dilatation, and increased right ventricular load, eventually causing chronic pulmonary heart disease.

3 effects on the central nervous system: the brain is very sensitive to hypoxia, the cerebral cortex is particularly sensitive, hypoxia is most likely to cause brain dysfunction, hypoxia can cause cerebral vasodilation and damage to the vascular endothelium to increase its permeability, leading to the brain Quality edema, hypoxia can also cause cell oxidation process disorders, intracellular ATP production is reduced, Na+-K+ pump requires less energy, plus increased lactate production, decreased intracellular pH, can cause intracellular Na+ and water increase , causing brain cell edema, cerebral congestion, edema, increased intracranial pressure, oppression of cerebral blood vessels, more severe cerebral hypoxia, thereby forming a vicious circle, oxygen supply can be stopped for 4 to 5 minutes, irreversible damage to brain tissue, early light, medium Degree of hypoxia can be manifested as increased excitability, decreased judgment, anxiety and confusion, severe hypoxia or hypoxia can be converted from inhibition to inhibition, expression apathy, lethargy, even coma, convulsions, and finally due to breathing, circulation center Suppress and die.

4 Influence on the blood system: Chronic hypoxia stimulates the enhancement of bone marrow hematopoietic function, which can cause the increase of red blood cells and hemoglobin. The increased red blood cells can increase the oxygen carrying capacity of the blood and increase the oxygen supply of the tissue, which is beneficial to the body, but Long-term red blood cells will increase blood viscosity, which will increase the burden on the heart. This is a negative side. In addition, long-term hypoxia can cause damage to vascular endothelial cells, leading to platelet adhesion, aggregation, dissolution, and release of platelet factor, promoting blood coagulation. The formation of living enzymes causes the blood to enter a hypercoagulable state, which is easy to form blood clotting and thrombosis, and induces disseminated intravascular coagulation (DIC).

5 effects on the kidney, liver, digestive system: hypoxia can reflect the renal vasoconstriction through the sympathetic nerve, renal blood flow is seriously reduced, can cause renal insufficiency, such as heart failure, diffuse intravascular coagulation and shock At the time, the blood circulation and renal dysfunction of the kidney are more serious. Usually, protein, red blood cells, white blood cells, etc. appear in the urine of the light, and oliguria and azotemia may occur in severe cases, but the renal structure does not change significantly at this time. For functional renal insufficiency, as long as hypoxia is corrected, renal function can return to normal quickly, and hypoxia can also cause hepatic vasoconstriction, which can cause degeneration and necrosis of liver cells in the central region of the lobules, and liver function is impaired, but it is more common. Functional changes, with the improvement of hypoxia can return to normal, only hepatocellular necrosis can occur when severe hypoxia, such as COPD complicated by pulmonary heart disease, chronic right ventricular dysfunction can cause liver congestion, swelling, long-term can lead to cirrhosis, However, it is less common that severe hypoxia can cause vasoconstriction of the gastric wall, thereby reducing the barrier function of the gastric mucosa, and carbon dioxide retention can enhance the carbonic anhydrase activity of the gastric parietal cells. Increased gastric acid secretion, it can occur gastric mucosal erosion, necrosis, bleeding and ulcer formation.

(2) Pathophysiology of carbon dioxide retention: The effect of carbon dioxide retention on the body is often closely related to hypoxia, because the type II respiratory failure seen in the clinic is often accompanied by hypoxia, carbon dioxide retention and no hypoxia. Type II respiratory failure under oxygen inhalation conditions, so carbon dioxide retention and hypoxia are often difficult to distinguish the damage to the body, and the damage to the body is more obvious.

1 Influence on the respiratory system: The increase of PaCO2 is mainly caused by the stimulation of the respiratory central chemoreceptor, which excites the respiratory center, causing the respiratory deepening to accelerate and increase the ventilation. When the PaCO2 exceeds 80 mmHg, the respiratory center is inhibited. The stimulation of the peripheral chemoreceptors of the carotid body and the aortic arch is mainly maintained by hypoxemia. Especially for patients with chronic type II respiratory failure, the respiratory center adapts to the internal environment of high PaCO2 due to the high PaCO2 for a long time. Therefore, no longer excited, if the high concentration of oxygen will relieve the hypoxemia of breathing stimulation, so that the ventilation is reduced, so in the clinical oxygen therapy for patients with type II respiratory failure, the inhaled oxygen concentration is considered to be <33%.

2 The impact on the circulatory system: The most prominent effect of carbon dioxide retention on the circulatory system is vasodilation, such as peripheral skin vessels, cerebrovascular, coronary vessels, etc., so patients with type II respiratory failure caused by COPD often have conjunctival edema. Facial flushing, warm skin of the limbs, patients often complain of headache, dizziness, and blood pressure drop may occur in severe cases, which may be the result of vasodilation, a certain degree of PaCO2 elevation, can also stimulate the cardiovascular motor center and sympathetic nerves, so that Increased heart rate, increased cardiac contractility, increased cardiac output, visceral vasoconstriction, and elevated blood pressure. According to reports in the literature, carbon dioxide retention is proportional to the increase in cardiac output, ie, the higher the PaCO2, the greater the cardiac output, but the higher the PaCO2 At a certain level, the cardiac output will decrease, and arrhythmia may occur. The reason: A. Severe carbon dioxide retention can directly inhibit the cardiovascular movement center. B. Severe carbon dioxide retention can cause severe respiratory acidosis, when pH<7.20 When it can cause myocardial contraction weakness, cardiac output decreases, peripheral blood vessels to vascular actives Decreased sensitivity, causing decreased blood pressure, decreased cardiac fibrillation threshold can lead to ventricular fibrillation.

3 effects on the central nervous system: carbon dioxide retention inhibits the central nervous system, clinically seen chronic chest disease caused by type 2 respiratory failure patients, once neuropsychiatric symptoms, can be diagnosed as pulmonary encephalopathy (pulmonary encephalopathy) The reason is related to carbon dioxide retention and hypoxia. Carbon dioxide retention can cause cerebral vasodilation, increased cerebral blood flow, increased intracranial pressure, early headache, dizziness, lethargy, and coma in the late stage. Symptoms and signs of insanity, tremors, convulsions, and other intracranial hypertension. However, a large number of clinical data indicate that changes in the central nervous system caused by carbon dioxide retention are not only related to the degree of carbon dioxide retention, but also related to the rate of carbon dioxide retention. Can not be ignored, the central nervous system changes caused by carbon dioxide retention is also associated with the degree of hypoxia, acidosis, especially acidosis in brain cells, severe hypoxia and acidosis can aggravate cerebral edema, increased intracranial pressure and nerve cells Damage.

4 on the acid-base balance and electrolytes: carbon dioxide retention can cause respiratory acidosis, at this time the body through the blood buffer, intracellular and extracellular ion exchange, kidney compensation and other compensation mechanisms, can make blood HCO3- compensatory increase, The blood Cl- correspondingly decreased, the result is to maintain the relative range of HCO3-/PCO2, pH=PK log(HCO3-/PCO2) varies within a small range, but the body compensates a certain range, that is, chronic respiratory acidosis The estimated compensation formula is HCO3-=0.35×PCO2±5.58. Respiratory acidosis can cause intracellular and extracellular ion exchange due to the decrease of PH, ie, extracellular Na+, 1H+ and intracellular 3K+, and renal tubule Na+-H+ The exchange is strengthened, and the Na+-K+ exchange is reduced. Both of the above factors can lead to an increase in the extracellular fluid K+ concentration, that is, acidosis and high potassium.

Chronic respiratory failure prevention

Cold protection measures

1. Persevere in exercising, enhance physical fitness and enhance cold resistance.

2. Appropriately increase the temperature in the living room.

3. When the weather is cold, especially when the temperature drops suddenly, increase the warm clothes properly.

Heatstroke prevention measures : In the severe summer heat, taking measures to reduce the temperature of work, living environment and humidity, it is beneficial to prevent respiratory failure caused by chronic obstructive pulmonary disease. The mechanism is:

1, avoid excessive sweat, prevent a lot of water loss, blood viscosity increased, blood flow slowly stagnant, lung tissue blood circulation disorders.

2, to avoid excessive sputum sputum, difficult to cough up, hinder alveolar ventilation.

When using respiratory central stimulants in patients with chronic respiratory failure, care should be taken to keep the airway open, and if necessary, increase the oxygen concentration, because the use of respiratory central stimulants increases the body's oxygen consumption.

Chronic respiratory failure complications Complications, pulmonary encephalopathy, gastrointestinal hemorrhagic shock, metabolic acidosis

There may be fatal airway infections, secretions blocking the airway, high blood pressure and other complications, and may also be complicated by pulmonary encephalopathy, gastrointestinal bleeding, shock and metabolic acidosis.

1. Pulmonary encephalopathy, also known as pulmonary heart and brain syndrome, is a brain tissue damage and cerebral circulation disorder caused by chronic bronchitis complicated with emphysema, pulmonary heart disease and pulmonary failure.

2, gastrointestinal bleeding is a common clinical serious symptom, the digestive tract refers to the pipeline from the esophagus to the anus, including the stomach, duodenum, jejunum, ileum, cecum, colon and rectum. The upper gastrointestinal bleeding site refers to the esophagus, stomach, duodenum, upper jejunum, and pancreatic duct and bile duct bleeding above the ligamentous ligament. Intestinal hemorrhage below the ligamentous ligament is called lower gastrointestinal bleeding.

3, shock (shock) is a clinical syndrome caused by insufficient acute tissue perfusion, which is a common complication in clinical serious diseases. The common feature of shock is that the effective circulation is insufficient. The blood perfusion of tissues and cells is severely limited by compensation, resulting in poor blood perfusion of whole body tissues and organs, resulting in hypoxia, microcirculation, and organ visceral organs. A series of pathophysiological changes such as dysfunction and abnormal metabolism of cells.

4. Metabolic acidosis is the most common acid-base balance disorder, which is caused by an increase in extracellular fluid H+ or loss of HCO3- with a decrease in primary HCO3- (<21mmol/L) and a decrease in pH (<7.35). ) as a feature. In the clinical judgment of metabolic acidosis, anion gap (AG) has important clinical value. According to different AG values, it can be divided into high AG normal chlorine type and normal AG high chlorine type metabolic acidosis.

Symptoms of Chronic Respiratory Failure Common Symptoms Respiratory Failure Breathing Arrhythmia Attention Deficit Respiratory Inhibition Respiratory Reflex Regulatory Impaired Right Heart Failure Hair Loss Low Blood Pressure Consciousness Loss

The clinical manifestations of chronic respiratory failure include the original clinical manifestations of primary diseases and various organ damage caused by hypoxia and carbon dioxide retention. The harm to the body caused by hypoxia and carbon dioxide retention is not only due to the degree of hypoxia and carbon dioxide retention, but also Depending on the speed and duration of hypoxia and carbon dioxide retention, when acute respiratory failure is acutely exacerbated, hypoxia and carbon dioxide retention occur sharply, so clinical manifestations are often severe, and hypoxia and carbon dioxide retention are not the same. However, there is a lot of overlap. For a patient with respiratory failure, the clinical manifestations are often the result of a combination of hypoxia and carbon dioxide retention. Therefore, the clinical manifestations of hypoxia and carbon dioxide retention are combined. set forth.

1, respiratory dysfunction: hypoxia and carbon dioxide retention can affect respiratory function, dyspnea and respiratory rate increase is often the earliest clinically important symptoms, manifested as breathing effort, accompanied by increased respiratory rate, shallow breathing, nose Fanning, assisted muscles participate in respiratory activities, especially in COPD patients with airway obstruction, respiratory pump failure factors, breathing difficulties are more obvious, and sometimes respiratory rhythm disorders, manifested as tidal breathing, sigh-like breathing, etc., mainly seen in When the respiratory center is inhibited, respiratory failure does not necessarily have difficulty breathing, and respiratory depression occurs in severe cases.

2, cyanosis: cyanosis is a reliable sign of hypoxemia, but not sensitive enough. In the past, the view that blood-reduced hemoglobin exceeds 50g/L has been turned off. In fact, when PaO2 is 50mmHg, blood oxygen saturation ( When SaO2) is 80%, cyanosis can occur, the tongue color is more cleft than the lips, and the nail bed appears earlier, more obviously, the cyanosis mainly depends on the degree of hypoxia, and also on the amount of hemoglobin, skin pigmentation and cardiac function. influences.

3, neuropsychiatric symptoms: mild hypoxia can have inattention, disorientation. People with severe hypoxia, especially with carbon dioxide retention, may experience headache, excitement, depression, lethargy, convulsions, loss of consciousness or even coma. Acute respiratory failure caused by chronic chest disease is acute, hypoxemia and carbon dioxide retention occur rapidly. Therefore, obvious neuropsychiatric symptoms can occur, and at this time, it can be called pulmonary encephalopathy.

4, cardiovascular dysfunction: severe carbon dioxide retention and hypoxia can cause palpitations, conjunctival congestion and edema, arrhythmia, pulmonary hypertension, right heart failure, hypotension and so on.

5, digestive system symptoms: 1 ulcer disease symptoms. 2 upper gastrointestinal bleeding. 3 abnormal liver function, the above changes are related to carbon dioxide retention and severe hypoxia.

6, renal complications: renal insufficiency may occur, but more common is functional renal insufficiency, severe carbon dioxide retention, renal failure may occur in the late stage of hypoxia.

7, acid-base imbalance and electrolyte imbalance: respiratory failure often due to hypoxia and / or carbon dioxide retention, as well as clinical application of glucocorticoids, diuretics and loss of appetite and other factors can be complicated by acid-base imbalance and electrolyte imbalance, common abnormalities Arterial blood gas and acid-base imbalance types are:

(1) severe hypoxia accompanied by respiratory acidosis (hook acid).

(2) severe hypoxia accompanied by acid reflux and metabolic alkalosis (alkali).

(3) severe hypoxia accompanied by acid reflux and metabolic acidosis (acid).

(4) Hypoxia is accompanied by respiratory alkalosis (alkali).

(5) Hypoxia accompanied by alkali and alkali.

(6) Hypoxia is associated with triple acid-base disorders with respiratory akalosis (TABD).

Chronic respiratory failure check

Laboratory tests can objectively reflect the nature and extent of respiratory failure, and have important value in guiding oxygen therapy, adjustment of various parameters of mechanical ventilation, and correcting acid-base balance and electrolytes.

First, arterial oxygen partial pressure (PaO2)

Refers to the pressure generated by the physical dissolved oxygen molecules in the blood. The PaO2 of healthy people gradually decreases with age, and the physiological influence of the receptor position. According to the relationship between oxygen partial pressure and oxygen saturation, the dissociation curve of oxyhemoglobin is S. Morphology, when PaO2>8kPa (60mmHg) or more, flat curve at the curve, blood oxygen saturation is above 90%, PaO2 changes 5.3kPa (40mmHg), and blood oxygen saturation changes little, indicating that the oxygen partial pressure is much higher than oxygen saturation. Sensitivity, but when PaO2<8kPa or less, the curve is steep and straight, the oxygen partial pressure drops slightly, and the blood oxygen saturation drops sharply. Therefore, PaO2 is less than 8kPa (60mmHg) as a diagnostic indicator of respiratory failure.

Second, arterial oxygen saturation (SaO2)

Is the oxygen percentage of the unit hemoglobin, the normal value is 97%, when PaO2 is lower than 8kPa (60mmHg), the hemoglobin oxygen dissociation curve is in the steep section, the oxygen saturation reflects the hypoxic state, so in severe respiratory failure During the rescue, the pulse oximeter is used to help evaluate the degree of O2 deficiency, and the concentration of O2 is adjusted to make the patient's SaO2 reach more than 90%, so as to reduce the blood gas analysis of the traumatic arterial blood. positive effects.

Third, arterial blood oxygen content (CaO2)

Is the number of milliliters of oxygen in 100 ml of blood, including the sum of hemoglobin binding oxygen and physical dissolved oxygen in plasma, CaO2 = 1.34 × SaO2 × Hb + 0.003 × PaO2, healthy CaO2 reference value is 20ml%, mixed venous blood oxygen saturation Degree (SVO2) is 75%, and its oxygen content CVO2 is 15ml%. After every 100ml of arterial blood, about 5ml of oxygen is used for tissue utilization, hemoglobin is reduced, SaO2 is lower than normal, and blood oxygen content is still in the normal range.

Fourth, arterial blood carbon dioxide partial pressure (PaCO2)

Refers to the pressure generated by the physically dissolved CO2 molecules in the blood. The normal PaCO2 is 4.6kPa-6kPa (35-45mmHg). If the pressure is greater than 6kPa, the ventilation is insufficient. If the pressure is less than 4.6kPa, the ventilation may be excessive. The acute ventilation is insufficient. PaCO2>6.6kPa (50mmHg) When calculated according to the Henderson-Hassellbalch formula, the pH is below 7.20, which will affect circulation and cell metabolism. Chronic respiratory failure due to the body compensatory mechanism, PaCO2>6.65kPa (50mmHg) as a diagnostic indicator of respiratory failure.

V. pH

For the negative logarithm of the concentration of hydrogen ions in the blood, the normal range is 7.35-7.45, the average is 7.40, which is less than 7.35 for decompensated acidosis, and higher than 7.45 for decompensated alkalosis, but it is not indicative of the nature. Acid-base poisoning, clinical symptoms and pH shift are closely related.

6. Alkali excess (BE)

At 38 ° C, CO2 partial pressure 5.32 kPa (40 mmHg), blood oxygen saturation measurement 100% conditions, the blood titration to pH 7.4 required amount of acid and alkali, it is a quantitative indicator of metabolic acid-base imbalance in humans, acid The positive value of BE is metabolic alkalosis, and the amount of alkali added EB is negative. It is metabolic acidosis, and the normal range is 0±2.3mmol/L. It can be used as an estimate when correcting metabolic acid-base imbalance. Reference for the dose of acid or alkali resistant drugs.

7. Buffer base (BB)

It is the total content of various buffer alkalis in the blood, including bicarbonate, phosphate, plasma protein salt, hemoglobin salt, etc. It reflects the buffering ability of the human body against acid-base interference, and the body's specific compensation for acid-base imbalance In the case, the normal value was 45 mmol/L.

Eight, the actual bicarbonate (AB)

AB is the content of bicarbonate contained in human plasma under actual carbon dioxide partial pressure and oxygen saturation. The normal value is 22-27mmol/L, the average value is 24mmol/L, and the HCO3- content is related to PaCO2. PCO2 is increased and plasma HCO3- content is also increased. On the other hand, one of HCO3-plasma buffer bases, when the acid is too much fixed in the body, the pH can be stabilized by HCO3-buffering, while the HCO3- content is decreased, so AB is breathed and The dual effects of metabolism.

Nine, standard bicarbonate (SB)

Refers to whole blood specimens that are isolated from air. At 38 ° C, PaCO 2 is 5.3 kPa, and hemoglobin is 100% oxygenated, the measured plasma bicarbonate (HCO3-) content, the normal value is 22-27 mmol / L, The average 24mmol/L, SB is not affected by respiratory factors, the increase or decrease of its value reflects the amount of HCO3-reservoir in the body, thus indicating the trend and degree of metabolic factors, SB decreased in metabolic acidosis, SB in metabolic alkalosis Increase, AB> SB, indicating CO2 retention.

X. Carbon dioxide binding capacity (CO2CP)

The normal value is 22-29mmol/L, reflecting the main alkali reserve in the body. When the metabolic acidosis or respiratory alkalosis is reduced, the CO2CP is decreased. When the metabolic alkalosis or respiratory acidosis occurs, the CO2CP is elevated, but the respiratory acid is When poisoning is accompanied by metabolic acidosis, CO2CP does not necessarily increase. Due to respiratory acidosis, the kidney discharges H+ in the form of NH4+ or H+, and absorbs HCO3- to compensate, and the alkali reserve increases. Therefore, the increase of CO2CP reflects to some extent. The severity of respiratory acidosis, but can not reflect the rapid changes of CO2 in the blood, is also affected by metabolic alkali or acidosis, so CO2CP has its one-sidedness, must be considered in combination with clinical and electrolyte.

Among these indicators, PaO2, PaCO2 and pH are the most important, reflecting the lack of O2 and CO2 retention during respiratory failure. In case of acid-base imbalance, if BE is added, it can reflect the body's compensation situation, whether or not it contains metabolic acid or Alkali poisoning, as well as electrolyte imbalance.

Diagnosis and diagnosis of chronic respiratory failure

diagnosis

Chronic respiratory failure decompensation, according to the patient's respiratory system chronic disease or other history of respiratory dysfunction, there is a lack of O2 and / or CO2 retention clinical manifestations, combined with relevant signs, diagnosis is not difficult, arterial blood gas analysis can be objective Reflecting the nature and extent of respiratory failure, it has important value for guiding oxygen therapy, regulating various parameters of mechanical ventilation, and correcting acid-base balance and electrolytes.

According to the cause, history, inducement, clinical manifestations and signs can be used to diagnose chronic respiratory failure. Arterial blood gas analysis is of great significance for definite diagnosis, classification, guiding treatment and prognosis. The diagnostic criteria are: Type I respiratory failure is sea level. PaCO2 is normal or decreased under calm breathing air conditions, PaO2 <60mmHg. 2 Type II respiratory failure is PaCO2>50mmHg and PaO2<60mmHg under the condition of calm sea level breathing air. 3 Under the condition of O2 absorption, calculate the oxygenation index=PaO2/FiO2<300mmHg, suggesting respiratory failure.

Differential diagnosis

The disease must be differentiated from atelectasis, spontaneous pneumothorax, persistent asthma state, upper respiratory airway obstruction, acute pulmonary embolism, cerebrovascular accident and cardiogenic pulmonary edema. By asking about medical history, physical examination and chest x-ray examination, apricot can be identified. Patients with cardiogenic pulmonary edema have difficulty breathing in bed, cough pink foamy sputum, wet sputum at the bottom of both lungs, treatment for heart, diuresis, etc. The effect is better, if it is difficult, it can be identified by measuring PAwP and echocardiography.

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