Pediatric respiratory failure

Introduction to Pediatric Respiratory Failure Respiratory failure (respiratory failure) is a serious clinical syndrome. It is one of the common emergencies in pediatrics. It is also a common cause of death. It is referred to as respiratory failure. Respiratory failure refers to the central and/or peripheral causes due to various reasons. Sexual respiratory physiology dysfunction, the arterial partial pressure of oxygen (PaO2) <8kPa (60mmHg) or associated with arterial carbon dioxide partial pressure (PaCO2)>6.67kPa (50mmHg), and clinical symptoms of dyspnea symptoms. Children often see acute respiratory failure. basic knowledge The proportion of illness: 0.001% more common in severe pneumonia Susceptible people: young children Mode of infection: non-infectious Complications: gastrointestinal bleeding, arrhythmia, pneumothorax, pulmonary embolism

Causes of respiratory failure in children

Classified by age (20%):

(1) Neonatal stage: generally refers to respiratory failure caused by respiratory or other systemic diseases within 28 days after birth, mostly due to asphyxia, hypoxia, immature lung development, inhalation of amniotic fluid meconium, lung or systemic infection, In addition, congenital malformations and developmental disorders lead to obstruction of the upper and lower respiratory tract, and the lungs are compressed, which can also lead to respiratory failure.

(2) Infant and child stage: mostly caused by bronchial pneumonia, central infection, etc., but also due to imperfect development of the airway and lung immune system, easy to infect bacteria and viruses, leading to pneumonia and respiratory failure.

(3) Child stage: more may be due to pneumonia, congenital heart disease, persistent state of asthma, infectious diseases, lung and organ failure, etc. In addition, trauma, surgical trauma, airway foreign body, drowning, poisoning, etc. It can also seriously affect respiratory function, leading to acute respiratory failure.

Classification according to central and peripheral causes (20%):

(1) Centrality: primary disease damage to the brain, cerebral edema or intracranial hypertension affects the normal function of the respiratory center, resulting in abnormal release of central respiratory motor neurons, and respiratory frequency and rhythm abnormalities, mainly in clinical Abnormal ventilatory function, such as intracranial infection, bleeding, head trauma, asphyxia and hypoxia, drug poisoning, acidosis, liver and kidney dysfunction can also lead to central respiratory failure.

(2) Peripheral: Primary disease in the respiratory organs, such as airways, lungs, thoracic and respiratory muscles, or various diseases secondary to diseases of the organs other than the lungs and chest.

Classification based on infectious and non-infectious causes (20%):

(1) Infectious diseases: such as bacteria, viruses, fungi, protozoal pneumonia complicated with respiratory failure, or systemic infections such as sepsis leading to acute lung inflammation, injury, edema, hemorrhage and other diseases, central infection is also an important cause of respiratory failure .

(2) Non-infectious: Central and peripheral respiratory failure caused by surgery, trauma, inhalation, drowning, poisoning, etc.

4. Meningitis with respiratory failure, or multiple organ failure with respiratory failure.

Classification according to pathophysiological characteristics (20%):

(1) Acute respiratory failure: mostly acute attacks and persistent hypoxemia, relying on emergency resuscitation.

(2) Chronic respiratory failure: more manifested as progressive damage to the basic diseases of the lungs, leading to decompensation, hypercapnia and acidosis.

(3) Blood oxygen and carbon dioxide levels: There are also clinically diagnosed respiratory failure according to blood gas analysis type I (hypoxemia type) and type II (hypoxemia with hypercapnia).

The causes of respiratory failure can be divided into three major categories: respiratory obstruction, pulmonary parenchymal lesions and abnormal breathing pump, and the three are interrelated.

Pathogenesis

The cause is caused by obstruction of upper and lower respiratory tract, lung disease and central nervous system disease or myopathy, which causes serious damage to respiratory function, and cannot effectively exchange gas to cause O2 deficiency, CO2 normal or decrease (type I), or Multiple (type II), a series of physiological dysfunctions and metabolic disorders such as decreased lung capacity, decreased compliance and increased respiratory function, normal ventilation and ventilation, relying on the regulation of the respiratory center, sound thoracic, respiratory muscles and Nerve innervation, unobstructed airway, perfect alveolar and normal pulmonary circulation, any cause that can seriously damage one or more of the links, can cause ventilatory ventilation process disorders, resulting in respiratory failure, due to its etiology and pathological basis Differently, the use of only one standard as a guide for all respiratory failure is not comprehensive enough. According to clinical manifestations, combined with blood gas analysis, it can be divided into two types of ventilation and ventilation failure.

1. Type I respiratory failure

Ventilation failure is mainly caused by lung parenchymal lesions, which is caused by gas diffusion disorder between alveoli and blood and abnormal ratio of ventilation to blood flow, so that the lungs cannot have sufficient O2 to pulmonary capillaries, and arterial blood is low. O2, while CO2 excretion is normal or even increased, PaCO2 is normal or decreased, and individual atrophic respiration can lead to respiratory alkalosis, which often occurs in a wide range of lung diseases, including bacteria, viruses, fungal infections, etc. Aspiration pneumonia, interstitial pneumonia, irritating gas inhalation, respiratory distress syndrome, shock lung, pulmonary edema and extensive atelectasis are also of this type. When inhaling indoor air at rest state under sea level atmospheric pressure, blood gas The characteristic of the change is PaO2<8kPa (60mmHg), PaCO2 can be normal or reduced, and its pathogenesis is:

(1) Dispersion of gas: due to pulmonary congestion, pulmonary edema, alveolitis and other severe changes in alveolar capillaries and reduction of effective capillary bed, emphysema, pulmonary embolism, etc., resulting in gas diffusion dysfunction, due to CO2 dispersion ability It is 20 to 25 times larger than O2, so not only does CO2 retention occur in the blood flow filling area, but under the stimulation of low O2, the alveolar is hyperventilated, and more CO2 is discharged. As a result, the pH value increases, but it cannot be ingested more. O2, the body is lacking O2. If the heart rate is increased at the same time, there is no sufficient time for dispersion, resulting in respiratory failure. (2) Inhomogeneous ventilation and blood flow ratio (V/Q) are abnormal: alveolar gas exchange rate is high or low. It depends on the ratio of the alveolar per minute ventilation to the per minute blood flow of the capillaries around the alveoli. If there is respiratory disease, the area of the alveolar ventilation is insufficient, the ventilation/blood flow is less than 0.8, the lung tissue still maintains blood flow, and the venous blood is not. After sufficient oxygenation, it enters the artery and forms a pulmonary shunt to produce hypoxemia. This is more common in atelectasis. If the ventilation/blood flow is greater than 0.8, the ventilation of the lesion remains good, and the blood flow is reduced. Entering this area can not carry out normal gas exchange, form ineffective ventilation, increase the amount of ineffective cavity, reduce the amount of alveolar gas, resulting in the lack of O2, increase the number of breaths to increase the amount of ventilation to compensate, so that PCO2 maintains normal or even lower, common in Diffuse pulmonary vascular disease.

2. Type II respiratory failure

Ventricular failure is mainly caused by pulmonary causes (respiratory obstruction, increased physiological ineffective cavity) or extrapulmonary causes (respiratory center, thoracic, respiratory muscle abnormalities), low O2 with hypercapnia, All the lesions that weaken the lung power or increase the resistance can cause the alveolar ventilation to decrease due to the decrease of the total ventilation. Even if the total ventilation is not reduced, the alveolar ventilation will decrease due to the increase of the residual volume. O2 and CO2 retention, clinical manifestations of respiratory distress, wheezing, severe cyanosis, respiratory secretions or a large number of secretions blocked, may be accompanied by obstructive emphysema or regional atelectasis, children with irritability or Consciousness disorder, blood gas analysis PaCO2 is greater than 6.67kPa (50mmHg), PaO2 is reduced to less than 8kPa (60mmHg), this type can be divided into two main groups:

(1) Restricted respiratory failure: seen in thoracic deformity, pleural thickening, pleural effusion or accumulation of gas, lung hardening, etc. caused by elastic decline of the chest wall or lung tissue, in addition to neuromuscular diseases such as polyneuritis, Polio, respiratory muscle paralysis caused by respiratory center inhibition or loss of function, such as morphine, barbiturates, anesthetics and other poisoning, severe brain deficiency O2, encephalitis, meningitis, increased intracranial pressure, etc., make breathing The action is limited, the O2 of the outside entering the alveoli is reduced, and the elimination of CO2 is also reduced, resulting in the lack of O2 and CO2 retention.

(2) Obstructive respiratory failure: mainly refers to poor breathing or difficulty caused by obstruction of the lower respiratory tract, most commonly in bronchiolitis, emphysema, bronchial asthma and mediastinal tumors such as compression or obstruction, so that exhalation resistance is increased Large, alveolar ventilation is insufficient, some areas are even in an airless state, the total lung capacity and vital capacity are normal, and even increased, but the residual gas volume is significantly increased compared with the total lung capacity, the maximum ventilation is reduced, and the time lung capacity is obvious. Prolonged, sometimes mixed with both groups, have low O2emia, due to its rapid onset, so that the increased partial pressure of CO2 can not be compensated from the bicarbonate retained by the kidney in time, resulting in respiratory acidosis, hypercapnia Symptoms increase pulmonary resistance, cerebral vasodilation, increased intracranial pressure and cerebral edema. Both types of respiratory failure are deficient in O2, while CO2 retention is only seen in type II, but late stage I can also occur, central nervous system and Neuromuscular diseases can only produce type II respiratory failure, and diseases involving lung and bronchus can not only produce type I, but also type II. If only type I is present, the lungs must be involved.

Pediatric respiratory failure prevention

To actively treat diseases that cause respiratory failure, when treating shock and serious infections, it is necessary to control the infusion rate and the balance of inflow and outflow, and avoid inhaling high concentrations of oxygen for a long time. It is an effective measure to prevent acute respiratory failure, and the clinical application of blood gas microanalysis. It can be used to observe changes in the state of work, help to detect abnormalities early, analyze the cause, and deal with them in time to save lives.

Pediatric respiratory failure complications Complications, gastrointestinal bleeding, arrhythmia, pneumothorax, pulmonary embolism

There are mainly gastrointestinal bleeding, arrhythmia, pneumothorax, DIC, superficial venous thrombosis and pulmonary embolism, complications of tracheal intubation or incision, secondary infection.

1. Development of severe lung injury and acute respiratory distress syndrome: central respiratory failure can develop into ventilator-associated pneumonia and lung injury, poor respiratory management during continuous mechanical ventilation, can lead to airway alveolar dysplasia, respiratory bacterial infection In the development of pneumonia, exacerbation of respiratory failure, chemotherapy and immunosuppression, intestinal ischemia and hypoxia-reperfusion injury can lead to severe pulmonary infection and develop into ARDS.

2. Development of pulmonary dysfunction: persistent hypoxemia during respiratory failure can lead to pulmonary and pulmonary dysfunction, mainly due to the accumulation of inflammatory cells in the lungs, release of pro-inflammatory mediators into the circulation, attacking the lungs Organs, which cause damage to the function and structure of the extrapulmonary organs, can develop into multiple organ dysfunction and failure.

Pediatric respiratory failure symptoms common symptoms irritability, difficulty breathing, cyanosis, arrhythmia, respiratory failure, fatigue, three concave signs, heart sound, low blunt blood pressure, drop, convulsion

In children with acute respiratory failure, in addition to the performance of the primary disease, hypoxemia, or hypercapnia, a variety of clinical abnormalities.

Respiratory system

Because the lung capacity of children is small, in order to meet the metabolic needs, lung compensatory ventilation mainly relies on the increase of respiratory rate. When the respiratory rate is >40 times/min, the effective alveolar ventilation shows a downward trend, so the dyspnea is often shallow, infants and young children. It can even reach 80-100 times/min, and there are three concave signs. When the respiratory muscles are fatigued, the breathing rate becomes slow, accompanied by severe hypoxia and high carbon dioxide retention, and various clinical abnormalities appear; when the blood oxygen saturation is <80 At the time of % (PaO2<6.67kPa), there is a cyanosis; however, if the child is anemia, the cyanosis may not be obvious. When hypercapnia is present, skin flushing may occur, and the lips are reddish cherry, which does not reflect the improvement of circulation, and must be distinguished if PaCO2> At 12.0 kPa (90 mmHg), anesthesia can be exerted on the respiratory center. Respiratory movement can only be maintained by the stimulation of chemoreceptors by hypoxia. At this time, if high concentration of oxygen is given, the breathing can be inhibited.

2. The nervous system

Hypoxemia occurs when irritability, confusion, lethargy, coma, convulsions, central respiratory failure, respiratory rhythm, tidal breathing; when respiratory nerves are oppressed in the late stage of respiratory failure, there may be large changes in pupils.

3. Cardiovascular system

Early hypoxemia, heart rate increased, cardiac output increased, blood pressure increased; later heart rate slowed down, heart sounds were low, blood pressure decreased, arrhythmia.

4. Other organ systems

Hypoxia can lead to visceral vascular stress contraction, gastrointestinal bleeding and necrosis, abnormal metabolic enzymes in liver function damage, proteinuria, oliguria and anuria.

5. Acid-base balance disorders and water-salt electrolyte imbalance

Hypoxemia and acidosis can cause abnormal metabolism of tissue cells, plus insufficient energy intake, restriction of fluid replacement, diuretic application, etc., can cause blood potassium biochemical examination, high blood potassium, hypokalemia, hyponatremia, high blood Chlorine and hypocalcemia, pediatric kidney has limited regulation of acid-base, water-salt electrolyte balance, especially in hypoxemia, renal blood flow decline, further limiting the regulation of the kidney, can increase systemic acid-base balance Disorders and water, salt electrolytes are disordered.

Pediatric respiratory failure examination

Suspected children with respiratory failure should be blood, urine routine, blood urea nitrogen or serum creatinine determination, blood chlorine, sodium determination, blood gas determination, laboratory examination can objectively reflect the nature and extent of respiratory failure, to guide oxygen therapy The adjustment of various parameters of mechanical ventilation, as well as the correction of acid-base balance and electrolytes are of great value.

1. Urine routine and serum creatinine

Normal, can rule out renal acidosis.

2. Blood gas analysis

It can accurately reflect the specific conditions of hypoxia and acidosis in respiratory failure. The method is simple. It can be repeated several times since the application of micro-assay to observe its dynamic changes, and also to understand the compensation degree of acid poisoning. And the circulation function, and the clinical phenomenon, simple ventilation measurement, electrolyte examination, etc. for comprehensive judgment, is of great significance for guiding treatment.

(1) Analysis of hypoxemia:

1 The significance of arterial oxygen partial pressure change: A. Change of blood oxygen partial pressure when breathing air: If PaO2 is in the normal range, it means that the ventilation function of the lung of the child is normal, generally PaO2 is above 8.0 kPa (60mmHg), it will not cause In the state of hypoxia, the value of blood oxygen partial pressure drop is not linear with the severity, which is determined by the oxygen dissociation curve: PaO2 is at 10.6 kPa (80 mmHg), which is equivalent to 94% of SO2, which is normal adult PaO2. The lower limit, PaO2 is 8.0 kPa (60 mmHg), which is equivalent to 90% of SO2. This is the starting point of the oxygen dissociation curve. Below, with the decrease of PaO2, the decrease of SO2 is obvious, and PaO2 is at 5.3 kPa (40 mmHg). It is equivalent to 75% of SO2. When the arterial blood reaches this value, there is obvious clinical cyanosis. Below this, there will be severe hypoxia. 5.3 kPa (40 mmHg) is also the normal average value of mixed venous oxygen partial pressure, which represents the circulation function. Normally, the level of oxygen in the blood after consumption by the whole body tissue, PaO2 is 2.7 kPa (20 mmHg), SO2 32%, the arterial blood reaches the limit that the value is near to survival, PaO2 is lower than normal, indicating that the lung has ventilation function. Insufficient obstacles or ventilation, the difference between the two: if PaCO2 is normal or low, while PaO2 is low, it is definitely a ventilatory dysfunction, not a lack of ventilation. If PaCO2 is increased, PaO2 decline indicates insufficient ventilation, but it may also incorporate ventilation dysfunction, further determined to be combined with clinical Whether there is lung disease, and the alveolar-arterial oxygen pressure difference is calculated. The alveolar-arterial oxygen pressure difference is in the normal range, indicating that the ventilation function is normal, and there is no important lesion in the lung. If the alveolar-arterial oxygen pressure difference is increased, it indicates that there is lung. Ventilation dysfunction, for PaO2 decline, the following simple method can be used to infer the cause: calculate the sum of PCO2 and PaO2, this value is 14.6 ~ 18.6kPa (110 ~ 140mmHg) suggesting insufficient ventilation, this value is less than 14.6kPa (110mmHg) (including oxygen inhalation patients), suggesting ventilation function dysfunction, this value is greater than 18.6kPa (140mmHg), suggesting that there may be technical errors, B. The significance of oxygen partial pressure change during oxygen inhalation: changes in PaO2 after inhalation of different concentrations of oxygen It can make a preliminary judgment on the cause of the decline of PaO2. When the concentration of oxygen is low (the concentration of inhaled oxygen is about 30%), it can be divided into three types according to the increase of PaO2: PaO2 is obviously improved after oxygen absorption, which is due to dispersion. Functional barrier Obstruction of oxygen partial pressure decline; PaO2 has a certain degree of change after oxygen inhalation, which is caused by ventilatory/blood flow imbalance caused by ventilation dysfunction; due to pathological intrapulmonary shunt, oxygen partial pressure rise after oxygen inhalation The height is not obvious. In the same child, there may be three reasons for ventilatory dysfunction, and the lesions of the child are not the same as the degree of PaO2 decline. Therefore, the above judgment method can only be roughly calculated, and the concentration of oxygen is high. When the concentration of inhaled oxygen can be 30% to 60%, the PaO2 of most children can rise to the normal level of 10.6 to 13.3 kPa (80 to 100 mmHg) or close to the normal level of 8.0 to 10.6 kPa (60 to 80 mmHg). PaO2 is still below 8.0 kPa (60 mmHg), indicating that there is a serious lesion in the lung or a problem with the oxygen supply method. If the fixed oxygen concentration is constant, the PaO2 gradually increases, indicating that the lung lesions gradually improve.

2 degree and type of hypoxia: clinical hypoxia and hypoxemia are not completely equivalent definitions, some sick children may have hypoxia, but not necessarily hypoxemia, according to PaO2, SaO2 can be low Oxygenemia is divided into: mild hypoxemia: SaO2>80%, PaO2 5060mmHg (no cyanosis), moderate hypoxemia: SaO2 60%80%, PaO2 4050mmHg (has hairpin), Severe hypoxemia: SaO2<60%, PaO2<40mmHg (severe cyanosis), according to the cause, hypoxia can be divided into four categories: respiratory, circulatory, anemia and tissue, different types of hypoxia, blood oxygen The changes in arteries and veins are different. See Table 1. Respiratory hypoxia is caused by lung ventilation and ventilatory disorders, resulting in insufficient intravascular oxygenation (PaO2, SO2 and blood oxygen levels are reduced), while venous oxygen The content is also reduced, right-to-left shunt congenital heart disease, venous blood flows into the artery to reduce blood oxygen, blood oxygen changes and respiratory causes are the same, it is also classified as respiratory hypoxia, cyclic In the absence of oxygen, the circulation is too slow, so that the tissue is insufficiently oxygenated, and the oxygen taken from the blood is in units of blood per milliliter. Increased, it shows that the difference between arterial and venous oxygen is increased, anemia and hypoxia are mainly due to the decrease or qualitative change of hemoglobin, although there is no significant decrease in arterial oxygen partial pressure and oxygen saturation (hemoglobin abnormality, blood may be present The oxygen saturation is reduced, but the oxygen carrying is limited, the oxygen content is reduced, and the tissue hypoxia is caused by the tissue enzyme system disorder, and the oxygen supplied by the artery cannot be utilized, so the venous oxygen content is increased.

(2) Type of respiratory failure:

Type 1 type respiratory failure: PaO2 < 6.67 kPa (50 mmHg).

2 type II respiratory failure: PaO2 <6.67kPa (50mmHg), PaCO2>6.67kPa (50mmHg), A. Mild: PaCO2 6.67 ~ 9.33kPa (50 ~ 70mmHg), B. Moderate: PaCO2> 9.33 ~ 12.0kPa (70 90 mmHg), C. Severity: PaCO2>12.0 kPa (90 mmHg).

3. Heart, liver, kidney function and electrolytes

Serum myocardial zymogram, urea chloride, creatinine, transaminase, electrolyte determination, etc., contribute to the diagnosis of heart, kidney, liver function impairment and electrolyte imbalance.

4. Vital capacity

The lung capacity is measured at the bedside. The first second time lung capacity or peak expiratory flow rate (PEER) can help to understand the extent of ventilatory damage. For example, if the vital capacity accounts for 1/2 of the predicted value, mechanical respiration should be considered, which is less than 1/3 of the predicted value. Should be mechanical breathing, should be an electrocardiogram, chest X-ray and B-ultrasound, CT and other examinations.

Diagnosis and diagnosis of respiratory failure in children

diagnosis

According to the above respiratory system performance, together with the manifestations of changes in the nervous system, cardiovascular and visceral functions, combined with blood gas analysis, the clinical diagnosis of respiratory failure can be initially made. It is generally considered that at sea level atmospheric pressure level, when inhaling air at rest, PaO2<8.0kPa, PaCO26.0kPa, SO2<91% for respiratory insufficiency; PO26.65kPa, PCO26.65kPa, SO2<85% suggest respiratory failure, according to PaCO2 PaO2 value can be inferred the cause of respiratory failure, this value 14.6 ~18.6kPa (110 ~ 140mmg), suggesting insufficient ventilation; if <14.6kPa (<110mmg), suggesting ventilation disorder; if >18.6kPa (>140mmg) (no oxygen) suggesting technical errors, blood gas analysis can provide Indicators of different types of acid-base disorders.

Differential diagnosis

1. Insufficient respiratory function

It is not accurate to use blood gas value alone as the diagnosis basis of respiratory failure. For example, 30 to 60 minutes after inhalation of 30% to 40% oxygen, PaCO2>8 kPa in children may be respiratory insufficiency. Therefore, when symptoms of dyspnea occur. Continuous non-invasive positive pressure ventilation, or airway cannula mechanical ventilation and airway cleaning to relieve the airway obstruction caused by thick secretions, the rapid relief of dyspnea symptoms, therefore, need to be simple with the primary lung Differences in severe dyspnea that develop or develop extra-pulmonary diseases, dynamic examination of blood gas, heart rate and respiratory monitoring.

2. Acute respiratory distress syndrome (ARDS)

Children with ARDS are mostly acute onset, with a history of infection of the lungs and other organs, mainly manifested as respiratory distress symptoms, radiological examination for bilateral diffuse inflammation and exudation changes, blood gas analysis suggests severe hypoxemia, Severe intrapulmonary shunt and pulmonary hypertension can be combined. Conventional mechanical ventilation often has poor results, and the clinical mortality rate can be as high as 60% or more.

3. Septic shock and systemic inflammatory response syndrome

Infantile septic shock leads to severe lung damage and respiratory dysfunction. The primary cause should be treated in time, and anti-infective and anti-shock measures should be taken to relieve the main cause of respiratory dysfunction.

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