Pediatric acute respiratory failure

　　1. Etiology

　　The causes of respiratory failure can be divided into three major categories, namely respiratory tract obstruction, pulmonary parenchymal lesions, and respiratory pump abnormalities.

　　1. Respiratory tract obstruction

　　Upper respiratory tract obstruction is common in infants and young children. The larynx is the narrow part of the upper respiratory tract and the main site of obstruction, which can be caused by infection, neurohumoral factors (laryngospasm), foreign bodies, or congenital factors (laryngeal cartilage softening). Lower respiratory tract obstruction includes obstructions caused by asthma, bronchiolitis, etc. Secretions during severe pulmonary infection and necrotic material in viral pneumonia can also block bronchioles, causing lower respiratory tract obstruction.

　　2. Pulmonary parenchymal diseases

　　(1) General pulmonary parenchymal diseases: Including various pulmonary infections such as pneumonia, bronchiolitis, interstitial lung diseases, pulmonary edema, etc.

　　(2) Neonatal respiratory distress syndrome (RDS): Mainly due to the underdevelopment of the lungs in premature infants, leading to widespread atelectasis due to the lack of pulmonary surfactant.

　　(3) Acute respiratory distress syndrome (ARDS): Often occurs during severe infection, trauma, major surgery, or other serious diseases, characterized by severe lung injury. The pathological feature is the infiltration and edema of interstitial tissue and alveoli in both lungs.

　　3. Abnormalities in the respiratory pump

　　Abnormalities in the respiratory pump include lesions in various parts from the respiratory center, spinal cord to the respiratory muscles and chest wall, which have the common feature of causing insufficient ventilation. Brain edema and intracranial hypertension caused by various reasons can affect the respiratory center. Lesions in the nervous system can be flaccid paralysis, such as acute infectious polyneuritis, or rigidity and spasm, such as tetanus. Abnormalities in the respiratory pump can also lead to weak expectoration, causing respiratory tract obstruction, atelectasis, and infection, thereby aggravating the original respiratory failure. Respiratory failure caused by chest surgery also often belongs to this type.

　　II. Pathogenesis

　　1. Pathophysiology of respiratory failure

　　Due to abnormal respiratory function, the lungs cannot complete the gas exchange required for the body's metabolism, leading to decreased arterial oxygen and CO2 retention, which is known as respiratory failure. The occurrence of respiratory failure has two causes: insufficient ventilation and gas exchange disorders. The three types of etiology mentioned above can all cause insufficient ventilation, the main result being increased PCO2 with varying degrees of hypoxemia. Gas exchange disorders are caused by various pulmonary diseases, mainly causing a decrease in PO2, with PCO2 varying depending on the severity of the condition. It should be pointed out that in clinical practice, there are often various factors coexisting or influencing each other, such as in children with central respiratory failure, difficulty in swallowing and weak sputum, which can be complicated with pneumonia; severe pneumonia can also lead to central respiratory failure.

　　Respiratory failure has adverse effects on the function of brain substance, kidney, and circulatory system. The combined action of hypoxia, CO2 retention, and respiratory acidosis can cause cerebral edema, damage to the respiratory center, reduce ventilation, and further exacerbate respiratory acidosis and hypoxia, forming a vicious cycle. In addition, hypoxia can cause vasoconstriction of the pulmonary arterioles, leading to pulmonary hypertension, increased workload on the right heart, and severe respiratory acidosis affects myocardial contractility, resulting in circulatory failure and a significant drop in blood pressure. Due to circulatory dysfunction, tissue hypoxia and renal insufficiency can occur, leading to metabolic acidosis, which further makes respiratory acidosis difficult to compensate, aggravating the degree of acidosis. As a result, the ability of hemoglobin to bind oxygen decreases, and the oxygen saturation further decreases, forming another vicious cycle.

　　2. Types of respiratory failure

　　(1) Hypoxemia-type respiratory failure: Also known as Type I respiratory failure or gas exchange disorder-type respiratory failure. It is mainly caused by pulmonary parenchymal lesions. The main change in blood gas is the decrease in arterial oxygen partial pressure. These children often have hyperventilation in the early stage of the disease, so the arterial PCO2 is often reduced or normal. If there are factors such as airway obstruction or in the later stage of the disease, PCO2 can also increase. Due to pulmonary lesions, lung compliance decreases, and the dysfunction of gas exchange is the main pathophysiological change. The imbalance of ventilation/perfusion ratio is the main cause of the decrease in blood oxygen, and there is also an increase in pulmonary shunting to varying degrees.

　　(2) Respiratory Function Failure: Also known as Type II respiratory failure. The characteristics of arterial blood gas changes are increased PCO2, with a simultaneous decrease in PO2, which can be caused by pulmonary reasons (airway obstruction, increased physiological dead space) or extrapulmonary reasons (respiratory center, respiratory muscle, or chest wall abnormalities). The basic pathophysiological change is insufficient alveolar ventilation. For children of this type without pulmonary lesions, the main problem is CO2 retention and respiratory acidosis. Hypoxemia caused by insufficient ventilation alone is not very severe, and treatment is relatively easy. Before the oxygen partial pressure in the artery decreases to a dangerous level due to insufficient ventilation, the increase in PCO2 is sufficient to be fatal.

　　The complications of respiratory failure include the impact on the normal function of various systems of the body during respiratory failure, as well as the hazards brought by various treatment measures (mainly respiratory machine treatment), such as: respiratory tract infection, atelectasis, respiratory machine and lung injury, complications of tracheal intubation and tracheotomy, pulmonary edema and water retention, complications of the circulatory system, kidney and acid-base balance, etc.

　　The manifestations of respiration

　　Due to respiratory failure caused by pulmonary diseases, there is often varying degrees of dyspnea, three凹陷, nasal flaring, etc., the respiratory rate is often increased, and it may slow down in the late stage. Central respiratory failure is mainly characterized by changes in respiratory rhythm, and severe cases may have apnea. It should be pointed out that the respiratory manifestations of children with respiratory failure may not be obvious, and the manifestations of dyspnea may also be caused by non-respiratory factors, such as severe metabolic acidosis. It is difficult to make an accurate diagnosis of respiratory failure based solely on clinical manifestations.

　　The effects of hypoxia and carbon dioxide retention

　　The early symptoms of hypoxia include an increased heart rate, and the blood pressure may rise at the beginning of hypoxia, followed by a decrease. In addition, there may be cyanosis or pallor of the skin, restlessness at the onset of acute severe hypoxia, and further development may lead to loss of consciousness, convulsions. When PaO2 is below 5.3 kPa (40 mmHg), the brain, heart, kidneys, and other important organs are insufficiently supplied with oxygen, posing a serious threat to life. Common symptoms of carbon dioxide retention include sweating, restlessness, and disturbance of consciousness. Due to the dilation of superficial capillaries, there may be redness of the skin, dark red lips, congestion of the conjunctiva. In the early stage or mild cases, the heart rate may be fast, and the blood pressure may rise. In severe cases, the blood pressure may drop. Elderly children may have muscle tremors, but they are not common in infants. The exact diagnosis of carbon dioxide retention depends on blood gas examination. The above clinical manifestations are for reference only and are not often seen. It is generally believed that when PaCO2 rises to about 10.6 kPa, clinical symptoms such as drowsiness or delirium may occur, and in severe cases, coma may occur. The degree of influence on consciousness is related to the speed of PaCO2 increase. If PaCO2 increases gradually over several days, the body has a certain degree of compensation and adaptation, and the blood pH value may only be slightly low or within the normal range, with less impact on the child. If the ventilation volume decreases sharply, and PaCO2 suddenly increases, the blood pH value may significantly decrease. When it drops below 7.20, it will seriously affect the circulatory function and cell metabolism, posing a great danger. The severe consequences of carbon dioxide retention are closely related to the decrease in arterial pH. Hypoxia and carbon dioxide retention often coexist, and the clinical manifestations are often the combined effects of both.

　　3. Changes in other systems during respiratory failure

　　1. Nervous system

　　Restlessness is an early sign of hypoxia, and older children may have headaches. A decrease in arterial pH value, CO2 retention, and severe hypoxemia can all affect consciousness, even leading to coma and convulsions. The severity of symptoms is related to the speed of onset of respiratory failure. Respiratory failure caused by pulmonary diseases can lead to cerebral edema and central respiratory failure.

　　2. Circulatory system

　　Early hypoxia can cause an increase in heart rate and blood pressure, and severe cases may have a decrease in blood pressure and arrhythmia. Reports from Peking University Health Science Center indicate that pulmonary artery pressure in infants and young children with severe pneumonia is increased, which may be related to increased plasma endothelin caused by hypoxia. Marked cyanosis of the lips and nail beds is a sign of hypoxemia, but it may not be obvious in cases of anemia.

　　3. Digestive system

　　Severe respiratory failure can lead to intestinal paralysis, and some cases may have gastrointestinal ulcers, bleeding, or even increased alanine aminotransferase levels due to impaired liver function.

　　4. Water and electrolyte balance

　　During respiratory failure, blood potassium levels are often elevated, blood sodium levels change little, and some cases may have hyponatremia. Some cases have a tendency to retain water, and sometimes edema occurs. In cases with respiratory failure lasting for several days, plasma chloride levels are often reduced to compensate for respiratory acidosis. Prolonged severe hypoxia can affect kidney function, leading to oliguria or anuria in severe cases, even acute renal failure.

　　4. Respiratory failure in infants and young children

　　Pneumonia is an important common disease in infancy and early childhood, and also the most important cause of death in hospitalized children; most deaths are due to respiratory failure and its complications caused by uncontrollable infection. In-depth understanding of the pathophysiology of respiratory failure in infantile pneumonia and rational treatment based on this are important tasks in pediatric emergency care. This section focuses on the changes in respiratory function and characteristics of respiratory treatment in severe pneumonia.

　　1. Ventilation dysfunction

　　The characteristics of respiratory changes in children with pneumonia are primarily small tidal volume, rapid breathing, and superficial breathing (related to decreased lung compliance). When the condition is severe, the tidal volume further decreases due to increased effort in breathing, although the minute ventilation is higher than normal, the actual alveolar ventilation does not increase due to the increased physiological dead space, remaining at normal levels or slightly lower; arterial oxygen saturation decreases, and the partial pressure of carbon dioxide slightly increases. In critical conditions, the child is extremely exhausted, unable to breathe, and the respiratory rate decreases, with the tidal volume not even reaching half of normal. The physiological dead space is further increased, and the ventilation effect is even lower, resulting in a significant decrease in alveolar ventilation (only 1/4 of normal), leading to severe hypoxia, serious obstruction of carbon dioxide excretion, and a marked increase in arterial carbon dioxide partial pressure, presenting non-compensatory respiratory acidosis. The pH value drops to a life-threatening level, averaging below 7.20. Hypoxia and respiratory acidosis are the main causes of death in severe pneumonia. In the resuscitation of critically ill pneumonia, the key is to improve ventilation function, correct hypoxia, and respiratory acidosis.

　　2. Arterial blood gas examination

　　The degree of arterial blood oxygen decrease in the acute phase of infantile pneumonia varies with the type of pneumonia, with bronchiolitis being the mildest and the most extensive consolidation pneumonia being the most severe. In infants under 4 months of age with pneumonia, due to weak compensatory capacity, narrow airways, and other factors, PaO2 decreases significantly. Gas exchange dysfunction is the most important cause of PaO2 decrease. Hypoxia caused by intrapulmonary shunting is the most severe. In children with congenital heart disease, PaO2 decreases even lower. The changes in PaCO2 in arterial blood of pneumonia children are not always consistent with PaO2. An increase in PaCO2 can have both pulmonary and central causes.

　　3. Compliance and pulmonary surfactant

　　During pneumonia, the lung compliance usually decreases to varying degrees. The more severe the condition, the more obvious the decrease. The reasons are multifaceted, including inflammation exudation, edema, and tissue destruction, which can all increase elastic resistance. On the other hand, inflammation destroys lung type II cells, leading to a decrease in pulmonary surfactant and its inactivation in inflammatory exudates, which can increase the surface tension at the air-liquid interface of alveoli, reduce lung compliance. We have observed that the severity of lung lesions is consistent with compliance and changes in tracheal aspirates of phospholipids. The heavier the lung lesions, the lower the saturated lecithin (the main component of pulmonary surfactant), and the poorer the compliance. The decrease in compliance is a basic cause of atelectasis, causing gas exchange disorders and a decrease in blood oxygen, as well as difficulties in lung expansion and insufficient ventilation volume. Pneumonia children with a significant decrease in lung compliance indicate severe lung lesions and poor prognosis. These changes provide a basis for the use of pulmonary surfactant in the treatment of these children.

　　4. Two different types of respiratory failure

　　(1) Respiratory obstruction as the main problem: The lung lesions in these children are not necessarily severe. Due to the obstruction caused by secretions and inflammation, there is a widespread obstruction of the bronchioles, leading to fatigue of the respiratory muscles due to difficult breathing. The ventilation volume cannot meet the body's needs, and hypoxia is accompanied by severe respiratory acidosis, which causes cerebral edema and leads to central respiratory failure early on, mainly manifested as changes or pauses in respiratory rhythm. This type is more common in infants.

　　(2) Prolonged lung lesions as the main problem: Although such children may also have severe respiratory obstruction, hypoxia is more prominent than carbon dioxide retention. This is because the lung lesions in these children are widespread and severe, and once mechanical ventilation is applied, it often requires a longer time to maintain.

　　The above is a relatively typical situation. What is common in clinical practice is a mixed type, which is difficult to distinguish exactly. However, regardless of the type, if timely treatment is not received and sufficient ventilation cannot be maintained, it will be the common basic cause leading to death.

　　1. Ensure prenatal care (In order to ensure the health of mothers and infants, improve the quality of the population, and give full play to the law of the People's Republic of China on Maternal and Child Health Care, prenatal care services are emphasized, including: health, nutrition, psychology, counseling, regular prenatal examinations, prenatal diagnosis of suspected congenital or hereditary fetal abnormalities, and special attention to high-risk pregnant women and fetuses, etc.), prevent premature birth, difficult labor, birth injuries, and so on.

　　2. Actively prevent and treat pediatric pneumonia and various infectious diseases.

　　3. Actively prevent various accidents from occurring.

　　4. Prevent drug poisoning or other intoxications.

　　5. Ensure various preventive vaccinations are done.

　　1. Acid-base index

　　pH is an acid-base index, normally ranging from 7.35 to 7.45, with an average value of 7.40. The pH of venous blood is about 0.03 lower than that of arterial blood. A pH greater than 7.45 indicates alkalosis, and it is difficult to survive when the pH reaches 7.8. Humans have a strong tolerance for acid, and they can still survive even if [H] increases to three times the normal level. However, the tolerance for alkali is较差, and life-threatening conditions can occur when [H] decreases to half the normal level. If both metabolic acidosis and respiratory alkalosis exist simultaneously, the pH may also be normal. Therefore, a single pH value can only indicate the presence of acid or alkalosis, and it is necessary to combine other acid-base indicators (such as PaCO2, HCO3-, BE, etc.), biochemical indicators (such as blood potassium, chloride, calcium), and medical history to correctly judge whether acid (alkali) poisoning occurs or complex acid-base poisoning.

　　2. Standard Bicarbonate (SB) and Actual Bicarbonate (AB)

　　SB refers to whole blood specimens isolated from air, and the concentration of bicarbonate ion [HCO3-] measured under standard conditions (temperature 38℃, PaCO2 5.33kPa, hemoglobin fully oxygenated, i.e., blood oxygen saturation reaches 100%). Since the PaCO2 and SaO2 affecting [HCO3-] have been reduced to normal conditions, the influence of respiratory acid-base imbalance on [HCO3-] has been eliminated. Therefore, the increase or decrease of SB reflects the reserve of [HCO3-] in the body and is a quantitative indicator of metabolic acid-base balance, with normal values ranging from 22 to 27 mmol/L. AB is the concentration of [HCO3-] measured directly from plasma, which is the whole blood specimen isolated from air, and the value of bicarbonate ion measured without any treatment. It is affected by both metabolic and respiratory factors. Normally, AB = SB, and the difference between AB and SB reflects the extent of the impact of respiratory factors on acid-base balance. When AB > SB, it indicates CO2 retention in the body, which is more common in respiratory acidosis or metabolic alkalosis caused by insufficient ventilation function.

　　3. Alkali excess (BE) or alkali deficiency (-BE)

　　Alkali excess or alkali deficiency refers to the amount of acid or alkali required to titrate 1L of blood to pH 7.4 under standard conditions (38℃, PaCO2 25.33kPa, hemoglobin 150g/L, blood oxygen saturation 100％). If pH is greater than 7.40, acid titration is required and called alkali excess (BE); if pH

　　4. Carbon dioxide binding power (CO2CP)

　　CO2CP refers to the plasma CO2 content obtained after the venous plasma sample is balanced with normal alveolar gas (PaCO2 of 5.33kPa), which is the amount of carbon dioxide contained in HCO3- in plasma, mainly referring to the amount of CO2 in the combined state, which is an approximate value of HCO3-. The normal value for adults is 23～31mmol/L (55～70Vo1％), and for children it is lower, 20～29mmol/L (45～65Vo1％). CO2CP is affected by both metabolic and respiratory factors. A decrease in CO2CP suggests metabolic acidosis (decrease in HCO3-) or respiratory alkalosis (excessive excretion of CO2), and vice versa. However, it has no decisive significance in mixed acid-base disorders, for example, in respiratory acidosis, pH decreases while CO2CP increases; conversely, in respiratory alkalosis, CO2CP decreases. Therefore, CO2CP cannot reflect the true acid-base balance state in the body during respiratory acid-base balance.

　　5. Total carbon dioxide (T-CO2)

　　It refers to the total sum of carbon dioxide existing in various forms in plasma, including the ionized part of HCO3-, existing in HCO3-, CO3-, and RNH2COO, as well as the non-ionized HCO3- and physically dissolved CO2, etc. The normal value for adults is 24～32mmol/L, and for children is 23～27mmol/L.

　　6. Partial pressure of oxygen in arterial blood (PaO2)

　　It refers to the pressure produced by oxygen molecules physically dissolved in plasma. The partial pressure of oxygen in arterial blood can well reflect the lung function, and is mainly used to reflect the oxygen deficiency in respiratory insufficiency, including PaO2, SaO2 (oxygen saturation), and O2CT (oxygen content or CO2, referring to the total amount of oxygen in 100ml of blood, including oxygen carried by hemoglobin and dissolved oxygen). However, the sensitivity is not uniform. SaO2 and O2CT are affected by hemoglobin, for example, children with anemia may still be hypoxic even if SaO2 is normal, while PaO2 is not affected by it, so PaO2 is a good indicator for judging whether there is oxygen deficiency. However, when analyzing the results, it is necessary to understand whether oxygen is inhaled, because the meaning of inhaling oxygen and not inhaling oxygen is completely different. Therefore, it is best to measure it without inhaling oxygen.

　　7. Carbon Dioxide Partial Pressure (PaCO2)

　　It refers to the pressure produced by dissolved carbon dioxide in arterial blood. Due to the high diffusion capacity of CO2, which is about 25 times that of oxygen, it can be considered that PaCO2 basically represents the alveolar carbon dioxide partial pressure, and PaCO2 can reflect the size of alveolar ventilation volume, which is a good indicator reflecting alveolar ventilation function. Therefore, when there is interstitial edema, congestion, and exudation in the alveoli, the oxygen exchange has decreased significantly, but the carbon dioxide exchange can still be normal. If the patient's arterial blood oxygen partial pressure decreases and the carbon dioxide partial pressure is normal, it indicates dysfunction in gas exchange. However, if the arterial blood oxygen partial pressure decreases and is accompanied by an increase in carbon dioxide partial pressure, it indicates insufficient ventilation.

　　Placenta Porridge

　　One bovine or porcine placenta, 100 grams of glutinous rice. Wash the bovine or porcine placenta clean, cut into pieces, cook until soft with an appropriate amount of water, then add glutinous rice to cook into porridge, add seasonings and eat. It can be eaten for breakfast and dinner, and is effective for preventing the recurrence of asthma or for those with chronic respiratory failure who have had asthma for many years without relief.

　　1. First, actively treat the primary disease. When complications such as bacterial infections occur, sensitive antibiotics should be used to remove the triggering factors.
　　2. Maintain clear airways and effective ventilation volume, and may be given bronchodilator and expectorant drugs, such as salbutamol (Ventolin), terbutaline sulfate (Bricanyl) for bronchodilation, acetylcysteine, and ambroxol hydrochloride (Mucosolvan) for expectoration. In necessary cases, adrenal cortical hormones can be administered intravenously.
　　3. Correct hypoxemia, which can be treated with nasal cannula or oxygen mask. In severe hypoxemia and with carbon dioxide retention, accompanied by severe consciousness disorders, and the appearance of pulmonary encephalopathy, mechanical ventilation should be used to improve hypoxemia.
　　4. Correct acid-base imbalance, arrhythmia, heart failure, and other complications.