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hypercarbonic respiratory failure


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hypercarbonic respiratory failure

Introduction
Respiratory failure (Figure 1) respiratory failure (respiratory failure) is caused by various reasons, lung ventilation and (or) ventilation with severe dysfunction, which can not be effective gas exchange, leading to hypoxia with (or without) of carbon dioxide retention, which led to a series of physiological functions and metabolic disorders in the clinical syndrome. Atmospheric pressure at sea level, in resting conditions, breathing room air, and the exclusion of intracardiac shunt and primary anatomic cardiac output and decreased in the situation, the arterial oxygen tension (PaO2) less than 8kPa (60mmHg), or accompanied by carbon dioxide partial pressure (PaCO2) above 6.65kPa (50mmHg), is the respiratory failure (referred to as respiratory failure). It is a state of dysfunction, not a disease, lung disease can be caused by various diseases may be complications. Cause
Respiratory function of the respiratory system damage can lead to respiratory failure of various factors. Causes of common clinical aspects are as follows. First, respiratory diseases bronchitis spasm, upper respiratory tract tumors, foreign body airway obstruction, etc., causing inadequate ventilation, the gas led to uneven distribution of ventilation / perfusion imbalance, the occurrence of oxygen and carbon dioxide retention. Second, the lung disease pneumonia, severe tuberculosis, emphysema, diffuse pulmonary fibrosis, pulmonary edema, adult respiratory distress syndrome (ARDS), silicosis, can cause lung capacity, ventilation, reducing the effective diffusion area, ventilation / kind of imbalance lead to pulmonary blood flow shunt, causing hypoxia and (or) carbon dioxide retention. Third, pulmonary vascular disease, pulmonary embolism, pulmonary infarction, pulmonary capillary hemangioma, so that part of the blood flow into the pulmonary veins, the occurrence of hypoxia. Fourth, thoracic lesions such as thoracic trauma, deformity, surgical trauma, pneumothorax, and pleural effusion, lung expansion affect the activity and thorax, leading to uneven ventilation reduce the impact of inhalation of gas ventilation function. Fifth, the nerve center of its transmission system, respiratory muscle disorders and cerebrovascular disease, encephalitis, brain trauma, shock, poisoning, etc., directly or indirectly inhibit the respiratory center; poliomyelitis and polyneuritis induced neuromuscular block connector affect conduction; myasthenia gravis and other damage caused by hypoventilation respiratory drive. Signs
Respiratory failure (Figure 2) Clinically, there are several classification respiratory failure: arterial blood gas analysis at 1, â…  respiratory failure: oxygen-free CO2 retention, or with reduced CO2 (â…  type
) is found in dysfunction of ventilation (ventilation / blood flow ratio and the damage and pulmonary diffusing capacity - venous shunt-like) cases. Oxygen therapy is the indication. 2, â…¡-type respiratory failure: lack of O2 with CO2 retention (â…¡), Department of alveolar hypoventilation due to lack of O2 and CO2 retention, pure hypoventilation, lack of O2 and CO2 in the retention level is parallel, if with ventilation function damage, lack of O2 is more serious. Only by increasing alveolar ventilation, oxygen therapy when necessary to resolve the increase. By the lesion can be divided into central and peripheral respiratory failure. According to the course can be divided into acute and chronic. Acute respiratory failure is the original normal respiratory function, the cause of the precipitating cause of the aforementioned five, causing ventilation, or ventilatory function serious damage, sudden clinical manifestations of respiratory failure, such as cerebrovascular accidents, poisoning inhibiting the respiratory center, respiratory muscle paralysis, pulmonary embolism, ARDS, etc., because the body can not quickly compensate, if not rescued, would endanger the lives of patients. Chronic respiratory failure more common in chronic respiratory diseases such as chronic obstructive pulmonary disease, severe tuberculosis, and its more severe respiratory dysfunction, although the lack of O2, or with CO2 retention, but the compensation through the body to adapt, able to engage in personal activities called compensated chronic respiratory failure. Once the concurrent respiratory tract infection, or for other reasons, the physiological burden caused by increased respiratory decompensation, severe lack of O2, CO2 retention and acidosis in the clinical presentation, known as decompensated chronic respiratory failure, this chapter will be highlights. According to etiology
Respiratory failure (Figure 3) in recent years, some academics have suggested classification under respiratory failure can be divided into: 1, pump failure: the lack of the respiratory drive (respiratory motor center), or respiratory movement is limited (peripheral nerve paralysis, respiratory muscle fatigue, chest deformity ), said pump failure caused by respiratory failure; 2, lung failure: As the airway obstruction, lung disease and pulmonary vascular disease called respiratory failure due to pulmonary failure. Treatment should be handled for the cause. In accordance with the degree of respiratory insufficiency can be focused into the oxygenation failure, respiratory failure and ventilatory failure, such as interstitial lung disease, pneumonia. ARDS mainly oxygenation failure, and chronic obstructive pulmonary disease, both of the two. Diagnostic medical history and symptoms
Respiratory failure (Figure 4) (1) Multi-bronchial, lung, pleura, pulmonary vascular, cardiac, neuromuscular or serious organic disease history. (2) In addition to the onset of symptoms, mainly oxygen and carbon dioxide retention performance, such as difficulty breathing, shortness, neuropsychiatric symptoms, pulmonary encephalopathy, may also have gastrointestinal bleeding. Examination that may have cyanosis, unconsciousness, conjunctival congestion, edema, flapping wing-like tremor, optic disc edema. Secondary inspection (1) blood gas analysis; suck air resting arterial oxygen pressure (PaO2) <8.0Kpa (60mmHg), arterial carbon dioxide partial pressure (PaCO2)> 6.7Kpa (50mmHg) type â…¡ respiratory failure, simply arterial partial pressure of oxygen was reduced type 1 respiratory failure. (2) The incidence of other tests based on the original corresponding to different findings. Identification 1. Tracheal airway obstructive disease - inflammation of bronchial spasm tumor fibrosis, foreign body, such as short-scar severe chronic obstructive pulmonary disease such as asthma and pulmonary airway obstruction caused by inadequate ventilation and blood flow associated with ventilation imbalance. Oxygen and carbon dioxide lead to respiratory failure caused by left coast 2. Lung alveolar and pulmonary interstitial lesions of various diseases. Such as pneumonia, tuberculosis, emphysema, pulmonary fibrosis, severe pulmonary edema and other pneumoconiosis may also lead to diffuse alveolar reduce the effective ventilation area of reduction of the government of reducing the imbalance Air flow oxygen and carbon dioxide lead to respiratory failure caused by left over 3. Pulmonary vascular disease pulmonary embolism pulmonary capillary blood perfusion go far to reduce the ventilation / Air flow imbalance or part of the venous oxygenation dK not been directly into the pulmonary vein resulting in respiratory failure 4. thorax and pleural disease caused by chest trauma, flail chest severe spinal deformity various reasons pleural thickening due to severe adhesion of spontaneous or traumatic pneumothorax cases of pleural effusion such a large number of activities can affect the thoracic chest fat profits to the lungs than the negative force the gas shortage caused by limited expansion and inhalation of gas distribution and small-for-all contribute to lung ventilation respiratory dysfunction caused by benign gas exhaust 5. neuromuscular disease and cerebrovascular disease, encephalitis, brain trauma and sedative hypnotic intoxication can inhibit the respiratory center; spinal cord paralysis between the entropy change to help myasthenia gravis, and potassium may be involved metabolic disorders such as respiratory muscle weakness caused by paralysis of respiratory muscle function decline in respiratory drive lung ventilation inadequate. Treatment
Respiratory failure (Figure 5) one. In the outpatient treatment of mild to serious cases should be hospitalized, the first active treatment of primary disease, an infection antibiotics should be used to remove the predisposing factors. II. Maintain airway patency and effective ventilation can be given in the lifting of bronchospasm, expectorant drugs such as albuterol (salbutamol), terbutaline sulfate (Bricanyl), half-light acetyl acid (sputum and easy net), hydrochloric acid, bromine has a new (must cough ping) and other drugs. There must be available when nikethamide, adrenal cortex hormones intravenous drip. III. Correct hypoxemia, available oxygen nasal cannula or mask, accompanied by severe hypoxia and hypercapnia PaO2 <7.32Kpa (55mmHg), PaCO2 significantly increased or serious disturbance of consciousness, encephalopathy, pulmonary ventilation should be used to improve hypoxemia. IV. Treatment of acid-base imbalance, arrhythmia, heart failure complications. Prevention 1. Lifting of bronchospasm to reduce energy consumption, elimination of bronchial mucosal edema, reduced bronchial secretions, remove stubborn phlegm, lower airway resistance, reduce energy consumption. 2. Enhanced to improve the nutritional status of the body to improve nutrition of sugar, protein and intake of vitamins, if necessary, intravenous infusion of compound amino drums, plasma, albumin. 3. Breath every day for gymnastics, and enhance the activities of respiratory muscle function. 4. Use of in vitro diaphragm pacemaker respiratory muscle fatigue, you can use the external diaphragm pacing to improve alveolar ventilation, exercise the diaphragm, and enhance the activities of diaphragmatic function. Health
Respiratory failure (Figure 6) 1, primary disease prevention and control methods are commonly used: (1) Clear the contents or airway secretions; (2) the lifting of bronchospasm; (3) anti-inflammatory treatment to reduce swelling of the airways and secretion; (4) necessary for endotracheal intubation or tracheostomy; (5) give respiratory stimulants; (6), indications, proper use of mechanical ventilation. Respiratory failure with severe hypoxia must therefore correct the hypoxia, levels increased Pao2 is necessary for each patient. 2, to prevent and remove the role of incentives: for the disease may cause respiratory failure, but must also prevent the incentive effect. For example, trauma, shock patients, to avoid high oxygen concentration, loss of blood or blood bank Jiucun fluid overload, etc., so as not to induce adult respiratory distress syndrome. Patients with respiratory diseases, surgery must be made, should first check the patient's pulmonary function reserve force. On lung function has been damaged or chronic respiratory failure patients should actively prevent and remove the role of various incentives, so as not to induce acute respiratory failure. Chronic respiratory failure, lack of O2 and CO2 retention mechanism of
Respiratory failure (Figure 7) (a) lack of ventilation breathing air at rest, the total alveolar ventilation is about 4L/min, in order to maintain normal alveolar partial pressure of oxygen and carbon dioxide. Decreased alveolar ventilation, alveolar oxygen partial pressure decreased, carbon dioxide partial pressure increased. Breathing air condition (20.93% inspired oxygen concentration, carbon dioxide close to zero), alveolar oxygen and carbon dioxide partial pressure and the relationship between alveolar ventilation, shown in Figure 2-6-1. Figure 2-6-1 alveolar oxygen and carbon dioxide partial pressure and the relationship between alveolar ventilation (b) of the ventilation / perfusion imbalance of ventilation and perfusion of alveolar capillary blood flow around the ratio must be coordinated to ensure effective gas exchange. Normal alveolar ventilation per minute (VA) 4L, pulmonary capillary blood flow (Q) 5L, the ratio between the 0.8. If alveolar ventilation is greater than the rate on blood flow (> 0.8). Increase in physiological dead space is formed, that is, dead space effect; alveolar ventilation in the ratio of less than the blood flow (<0.8), mixed venous blood to the pulmonary artery into the pulmonary vein without adequate oxygenation, the formation of arteriovenous-like shunt (Figure 2-6-2). Ventilation / perfusion imbalance, resulting in lack of O2, but no CO2 retention. This is due to mixed venous and arterial blood oxygen difference is much greater than the CO2 partial pressure, the former 7.98kPa, while the latter only 0.79kPa, a difference of 10 times. It may, by a healthy alveolar hyperventilation, and expel more CO2, the compensatory alveolar hypoventilation retention of CO2, or even release more CO2, respiratory alkalosis. The hemoglobin oxygen dissociation curve characteristics, the normal alveolar capillary oxygen saturation has been in the flat segment, the increase in ventilation, breathing air, the alveolar oxygen partial pressure despite the increase, but little increase in oxygen saturation, so by improve alveolar ventilation can not be compensated over the alveolar hypoventilation due to lack of oxygen uptake, which occurred missing O2. Ventilation> normal blood flow> ventilation (dead space effect) (effective ventilation) (Static artery shunt effect) Figure 2-6-2 ventilation / perfusion ratio on gas exchange (c) of the pulmonary artery - vein-like shunt As lung disease such as alveolar collapse, atelectasis, pulmonary edema and pneumonia-like consolidation may lead to pulmonary shunt increased, so that no contact with alveolar gas blood gas exchange opportunities. Therefore, raising the oxygen concentration does not improve arterial oxygen tension. Fractional flow greater increase arterial blood oxygen partial pressure of oxygen after the worse effects, such as sub-flows more than 30%, and oxygen on the partial pressure of oxygen is limited. (D) diffusion barriers to oxygen diffusing capacity of carbon dioxide is only 1 / 20, so in the diffusion barrier, the resulting hypoxia. (E) the increase in oxygen consumption increased oxygen consumption O2 missing one of the reasons, fever, chills, breathing difficulties and seizures are to increase oxygen consumption. Chills oxygen consumption up to 500ml/min, severe asthma, with increased work of breathing, oxygen consumption can be ten times as normal. Increased oxygen consumption, alveolar oxygen partial pressure decreased to normal with increased ventilation to prevent hypoxia. Figure 2-6-3 that breath the air, the change of oxygen consumption and alveolar ventilation, alveolar oxygen partial pressure relations. The figure the dashed curve and the point of intersection for different oxygen consumption, the maintenance of normal alveolar oxygen partial pressure required for alveolar ventilation, with the increase in oxygen consumption, was a corresponding increase in oxygen consumption per minute, respectively, 200ml, 400ml, 800ml, the alveolar ventilation respectively 3L, 6L, 12l. From the figure, each curve steep front, features a flat rear section also shows that the increase in oxygen consumption in patients with ventilatory dysfunction, alveolar oxygen partial pressure does not improve, hypoxia hardly eased. Figure 2-6-3 when different oxygen consumption and alveolar ventilation, the relationship between alveolar oxygen partial pressure (oxygen consumption curve next to the numbers indicate ml / min) lack of O2, CO2 retention effects on the body (a) the impact on the central nervous whole body oxygen consumption of brain tissue about consumption of 1/5-1/4. Central cortical neuron cells are most sensitive to hypoxia, lack of O2 occurred Jihuan the extent and production second highest bid on the central nervous students differently. Such as a sudden break for O2, 20 seconds to change the nitrogen absorption can occur deep coma and convulsions. Decreasing the concentration of O2 absorption, the slow onset of symptoms, mild lack of O2 can cause lack of concentration, mental deterioration, disorientation; with the lack of increased O2, arterial oxygen pressure (PaO2) less than 6.66kPa can cause irritability, trance, delirium; below 3.99kPa, makes the loss of consciousness and even coma; below 2.66kPa is irreversible brain cell damage. CO2 retention to increase the hydrogen ion concentration in cerebrospinal fluid and affect brain cell metabolism, reducing brain cell excitability, inhibition of cortical activity; as CO2 increases, the lower stimulation of the cortex to strengthen, causing cortical excitability; if CO2 continues to rise, subcortical suppression so nervous in the anesthetized state. Appeared before anesthesia in patients often have insomnia, excitement, restlessness, a harbinger of excitement symptoms. Lack of O2 and CO2 retention are cause cerebral vasodilation, vascular resistance decreases, blood flow to compensate it. O2 serious shortage of brain cells occurs within the edema, increased vascular permeability, interstitial edema caused by the brain, leading to increased intracranial pressure, brain tissue extrusion, pressure vessels, thus increasing shortage of brain tissue O2, a vicious circle. (B) of the heart, circulation of lack of O2 can stimulate the heart, the heart rate and stroke volume increased, increased blood pressure. O2 in the absence of coronary artery blood flow is significantly increased blood flow to the heart far more than the brain and other organs. Very sensitive to the lack of myocardial O2, early mild lack of O2 that is displayed on the ECG appearance of acute severe shortage of O2 can cause ventricular fibrillation or cardiac arrest. Lack of O2 and CO2 retention can lead to increased pulmonary vasoconstriction of small pulmonary vascular resistance, resulting in increased pulmonary hypertension and right heart burden. CO2 concentration in the inhaled air, can heart rate, stroke volume increased, the brain, coronary vasodilation, superficial skin capillaries and veins expand, leaving the spleen and muscle vasoconstriction, coupled with increased stroke volume, so blood pressure remains elevated. (C) lack of respiratory effects of O2 on the respiratory effects than CO2 retention is small. O2, mainly through lack of carotid sinus and aortic body chemoreceptor reflexes stimulated ventilation, such as the lack of O2 levels increased slowly, this reflex slow. CO2 is a strong respiratory stimulants, inhalation of CO2 concentration, ventilation doubled, acute CO2 retention occurs deep rapid breathing; when inhaled    12% CO2 concentration, did not increase ventilation, the respiratory center in the be restrained. And chronic hypercapnia, there is no corresponding increase in ventilation, but declined, this slow reaction with the respiratory center, through the kidney bicarbonate reabsorption and H + excretion, so that no significant decrease of blood pH values, but also with patients Air resistance increases, a serious lung damage, chest movement dysfunction related to ventilation. (D) of the liver, kidney and hematopoietic system of lack of O2 can be made directly or indirectly damage the liver alanine aminotransferase increased, but with the lack of O2 correction, liver function gradually returned to normal. Arterial oxygen is reduced, renal blood flow, glomerular filtration volume, urinary excretion of sodium excretion and an increase in volume; when PaO2 <5.3kPa, the renal blood flow decreased and renal function was inhibited. Low oxygen tension increases the organization to promote red blood cell proliferation of erythropoietin. Kidney and liver produces an enzyme activity of the blood-Africa erythropoietin activation of the precursor material into the EPO, to stimulate the bone marrow caused by secondary polycythemia. Help to increase blood oxygen carrying capacity, but also increased blood viscosity, increased pulmonary circulation and right heart burden. CO2 retention would expand mild renal vessels and increase renal blood flow, urine volume increased; when PaCO2 than 8.64kPa, blood pH decreased, the renal vascular spasm, decreased blood flow, HCO3-and Na + resorption increased, decreased urine output. (V) the impact of acid-base balance and electrolytes serious shortage of energy on behalf of O2 inhibited cell in the middle of the process of shooting, such as the citric acid cycle, oxidative phosphorylation and related enzymatic activities. This not only reduces the efficiency of energy production, but also because of lactic acid and inorganic phosphorus induced metabolic acidosis. Because energy is insufficient, the body of the sodium pump was damaged ion transport, intracellular potassium ion to the bloodstream, while Na + and H + into the cell, causing intracellular acidosis and hyperkalemia. Metabolic acidosis resulting in a fixed acid and bicarbonate buffer system works, producing carbonic acid, carbon dioxide partial pressure increased an organization. PH value depends on the ratio of bicarbonate and carbonate, the former regulation by the kidney (1-3 days), and regulation by lung carbonic acid (several hours). Discharged from the lung health of people every day as much carbonate of 15000mmol, so retention of acute respiratory failure on the pH of CO2 very quickly, often with metabolic acidosis exist, due to severe acidosis caused by decreased blood pressure, arrhythmia and even cardiac arrest . And chronic respiratory failure due to the slow development of CO2 retention, reduced renal bicarbonate excretion, does not result in significantly lower pH. Because the main anion in blood HCO3-and CI-of and is a constant, when HCO3-increases, the CI-be reduced, resulting in low chlorine hyperlipidemia. Acute respiratory failure in acute respiratory failure (ARF) is common in children during the emergency, one refers to the variety of diseases involving the respiratory center / or respiratory organs caused by respiratory function (ventilation and gas exchange) barrier, manifested as hypoxemia or with high hypercapnia, and the resulting series of physiological functions and metabolic disorders in the clinical syndrome. Common causes of ARF in children with severe pneumonia, bronchiolitis, laryngeal edema, nosocomial infections. Once the clinical diagnosis and should be actively rescue, otherwise it will cause irreversible damage to the vital organs, children with life-threatening. â‘  rescue matters of effective antibiotics used to actively improve the infection control ventilation time for turning back shot sputum sputum discharge time add enough water Collaborative Application expectorants reduce the viscosity of sputum to facilitate the discharge using bronchodilators (aminophylline receptor stimulants etc.) can relieve airway spasm improve ventilation and help expectoration glucocorticoid anti-inflammatory effects have mainly non-specific respiratory mucosal edema reduce congestion optional dexamethasone or hydrocortisone intravenously through the treatment center is still valid or began to participate in those who belong to severe respiratory failure can accumulate tracheal intubation or tracheostomy for mechanical ventilation. â‘¡ - hypoxia in patients with chronic respiratory failure have been respiratory center to carbon dioxide stimulation is not sensitive to the excited by hypoxia is mainly done to maintain the pure oxygen, especially if high concentrations of oxygen and oxygen is the core of the problem while temporary relief departments, but because decrease the excitability of the respiratory center of the carbon dioxide retention and even lead to more serious claims of low concentration of carbon dioxide anesthesia so continuous low flow oxygen nasal cannula nasal oxygen means method can be used masks and France found that inhalation of oxygen at the same time attention should be actively heated humidification prevent respiratory failure â‘¢ rescue and treatment of various complications, such as acid-base imbalance in water and electrolyte disturbance dic gastrointestinal bleeding heart arrhythmia shock liver and kidney failure and so on. Confusing disease and respiratory failure and the diseases easily confused with 1. Airway obstructive airway disease - bronchial inflammation, spasm, foreign body, tumor, fibrosis short marks, such as chronic obstructive pulmonary disease, severe asthma, airway obstruction and pulmonary hypoventilation, ventilation and blood flow associated with imbalance. Lead to oxygen and carbon dioxide left coast, causing respiratory failure. 2. Lung alveolar and pulmonary interstitial lesions of various diseases. Such as pneumonia, emphysema, severe pulmonary fibrosis, pulmonary tuberculosis, pulmonary edema, pneumoconiosis, etc., can lead to lung reduction of the effective diffusion area of reducing the government reduced ventilation Air flow imbalance, leading to oxygen and carbon dioxide left over , causing respiratory failure. 3. Pulmonary embolism pulmonary vascular disease, pulmonary vascular go far to reduce pulmonary capillary perfusion and ventilation / Air flow imbalance, or part of the vein dK not been directly into the pulmonary vein oxygenation, leading to respiratory failure. 4. Thorax and pleural disease caused by chest trauma, flail chest, severe spinal deformity, pleural thickening caused by various reasons, adhesions, severe cases of spontaneous or traumatic pneumothorax, large pleural effusion, thoracic activities can affect the benefits of negative chest fat ratio, the lung expansion is limited, resulting in forced inhalation of gas shortages and gas distribution are small, leading to dysfunction of pulmonary ventilation and gas exchange, causing respiratory good exhaust. 5. Neuromuscular disease and cerebrovascular disease, brain trauma, encephalitis, and sedative hypnotic intoxication, can inhibit the respiratory center; spinal entropy change, to help inter-neuritis, myasthenia gravis, and metabolic disorders such as potassium, may involve respiratory muscle function, cause respiratory muscle weakness, paralysis, respiratory drive down the lack of lung ventilation. Book 1 Book Information
Name: respiratory failure on: Yin Kai Publisher: Science Press Publication date: 2010-6-1ISBN: 9787030279354 Book Size: 16 Open Price: 148.00 yuan Introduction This book describes the respiratory system in the system's basic structure and function, respiratory movement and regulation, gas exchange and transport and other infrastructure on the basis of reason perish, and comprehensively expounded the cause of respiratory failure, pathophysiology, diagnosis and treatment of various special cases of respiratory failure occurred in the clinical features and treatment are detailed instructions, combined with clinical case describes the diagnosis and treatment of respiratory failure experts, experience and understanding. Illustrated book, not only for the low years of tertiary hospital physicians, training physicians and one, two or more hospitals and their attending physicians to read, but also in intensive care nursing, teaching and research staff of the reference books. Library catalog first chapter the basic theory of basic structure and function of the respiratory system Chapter II Chapter III of the physical properties of gases respiration and regulation of pulmonary circulation and lung Chapter Chapter ventilation and non-defense function of lung respiratory function VI Chapter VII of pulmonary surfactant and blood oxygen transport and tissue oxygen ventilation Chapter VIII of the second blood gas analysis in clinical practice the clinical application of Chapter IX of the etiology of respiratory failure and pathophysiology Chapter diagnosis and treatment of respiratory failure in the first Chapter XI the treatment of respiratory failure XII wet oxygen inhalation therapy and mechanical ventilation connection Chapter XIII Chapter XIV Chapter XV ventilator ventilator based on the clinical application of Chapter XVI respiratory intensive care Room and its management of severe pneumonia in Chapter XVII Chapter XVIII of the diagnosis and treatment of respiratory failure bronchoscopy in Chapter XIX of nutritional support in patients with respiratory failure, respiratory arrest Chapter Chapter XXI of first aid caused by chronic obstructive pulmonary disease diagnosis and treatment of respiratory failure in the twenty-second chapter of severe bronchial asthma diagnosis and treatment of acute lung injury twenty-three chapters and the acute respiratory distress syndrome in twenty-four chapters of the nervous system causes respiratory failure first twenty-five chapters of Chapter sleep apnea syndrome caused by pulmonary edema with respiratory failure Respiratory Failure Chapter XXVII surgical treatment of severe acute respiratory syndrome in the twenty-eight chapters of Article IX of cases of respiratory failure Introduction and diagnosis and treatment
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