Acute respiratory failure (ARF, respiratory failure) refers to a clinical syndrome in which the body, due to various reasons affecting the respiratory system, prevents the lungs from effectively exchanging gases, leading to hypoxia, carbon dioxide retention, and respiratory acidosis, thereby causing a series of physiological and metabolic disturbances. Respiratory failure is one of the common pediatric emergencies and a frequent cause of death in children.

The classification of respiratory failure includes the following types:

1. Classification by primary site of disease:
   1. Central (respiratory center failure).
   2. Peripheral (respiratory organ or respiratory muscle failure).
2. Classification by functional abnormality:
   1. Ventilatory failure.
   2. Gas exchange dysfunction.
3. Classification by blood gas type:
   1. Type I respiratory failure: hypoxemic respiratory failure.
   2. Type II respiratory failure: hypercapnic respiratory failure.
4. Classification by clinical course:
   1. Potential respiratory insufficiency.
   2. Respiratory insufficiency.
   3. Respiratory failure.

bubble_chart Etiology

1. Hypoxic respiratory failure (ventilatory failure, Type I respiratory failure) occurs due to impaired gas diffusion between the alveoli and blood, resulting in insufficient oxygen entering the pulmonary capillaries. This leads to reduced oxygen content in the arterial blood (decreased PaO₂), while carbon dioxide elimination remains normal or even increases (normal or decreased PaCO₂). This type of respiratory failure is primarily characterized by hypoxia and is commonly seen in severe respiratory conditions such as infectious pneumonia (bacterial, viral, etc.), aspiration pneumonia, interstitial pneumonia, extensive atelectasis, pulmonary edema, shock lung, inhalation of irritant gases, and neonatal respiratory distress syndrome.
2. Hypercapnic respiratory failure (ventilatory failure, Type II respiratory failure) arises from airway obstruction or weakened respiratory effort, leading to reduced ventilation. This decreases the amount of oxygen entering the alveoli from the external environment (decreased PaO₂) and correspondingly reduces carbon dioxide elimination (increased PaCO₂). This type of respiratory failure involves both hypoxia and carbon dioxide retention and is commonly seen in: (1) Obstructive respiratory disorders (severe lung disease, alveolar hypoventilation, increased dead space), such as severe bronchopneumonia, bronchiolitis, bronchial asthma, pulmonary emphysema, or mediastinal tumors compressing the trachea or bronchi. (2) Restrictive respiratory disorders (respiratory center dysfunction or respiratory muscle paralysis, with normal lungs), such as encephalitis, meningoencephalitis, polyradiculitis, drug poisoning diseases that suppress the respiratory center, or chest trauma.

bubble_chart Clinical Manifestations

Respiratory failure can occur suddenly or result from the gradual decline of respiratory function. In addition to the symptoms of the primary disease, it mainly manifests as respiratory symptoms and those caused by hypoxia (hypoxemia) and carbon dioxide retention (hypercapnia).

1. The respiratory symptoms primarily present as dyspnea. Central respiratory failure and peripheral respiratory failure each have distinct characteristics of dyspnea.
   1. Central respiratory failure is often caused by cerebral edema or brain herniation due to intracranial infections, craniocerebral injury, toxic encephalopathy, etc., while the respiratory organs themselves may remain unaffected. The dyspnea mainly manifests as changes in respiratory rhythm and rate. The respiratory rhythm becomes irregular, with uneven depth and speed, and may exhibit various abnormal breathing patterns, such as Cheyne-Stokes respiration, Biot's respiration, sighing respiration, double inhalation, mandibular breathing, slowed breathing, or even respiratory arrest.
   2. Peripheral respiratory failure occurs when there are lesions in the respiratory organs or respiratory muscles. The dyspnea mainly manifests as changes in respiratory depth and rate, while the respiratory rhythm remains consistent throughout. In mild cases or the early stages of the disease, shallow breathing and increased respiratory rate may be observed. In severe cases, obvious dyspnea accompanied by accessory respiratory muscle movements—such as the "three depressions" sign—may appear. In advanced or critical stages, breathing becomes slow and shallow, weak and feeble, and severe signs such as nodding or bubo-like breathing may emerge.
2. **Symptoms of Hypoxemia and Hypercapnia**
   1. **Symptoms of Hypoxemia**
      1. Cyanosis is a typical symptom of hypoxia. It first appears as bluish discoloration in the fingertips, nail beds, earlobes, nose tip, lips, and around the mouth. Generally, when PaO₂ > 7.32 kPa (55 mmHg), cyanosis is often absent. When PaO₂ < 5.32 kPa (40 mmHg), cyanosis is definitely present. However, the degree of cyanosis does not always correlate precisely with the severity of hypoxia. For example, in severe shock, bluish discoloration may appear in the lips and nail beds due to slowed blood flow, even though PaO₂ is normal. Conversely, in anemia, even if PaO₂ is reduced, cyanosis may not be obvious. Therefore, hypoxia cannot be judged solely based on cyanosis. In cases of carbon dioxide retention, cyanosis is often more pronounced than in hypoxemia.
      2. Neurological symptoms may initially include dysphoria, restlessness, and irritability. Later, symptoms of central nervous system depression, such as apathy, confusion, drowsiness, or even convulsions and unconsciousness, may appear. Severe cases may exhibit signs of increased intracranial pressure or brain herniation. In early respiratory failure, the pupils often constrict, dilating only in critical conditions. Due to hypoxia, pathological reflexes such as a positive Babinski sign may also occur, though these are nonspecific.
      3. **Cardiovascular Symptoms** Heart rate increases, heart sounds become muffled, and blood pressure initially rises before falling. Severe hypoxia often leads to arrhythmias and conduction blocks, potentially resulting in heart failure or cardiogenic shock. Increased capillary permeability due to hypoxia and acidosis may cause pulmonary edema, skin and mucosal bleeding, etc.
      4. **Digestive Symptoms** Hypoxia and congestion lead to widespread mucosal hyperemia and erosion in the gastrointestinal tract, causing bleeding. Severe respiratory failure in children may result in intestinal paralysis, with severe abdominal distension and fullness restricting diaphragmatic movement, further impairing respiration and creating a vicious cycle.
      5. **Renal Dysfunction** Protein, red and white blood cells, and casts may appear in the urine, along with oliguria or anuria. Severe hypoxia can lead to renal failure.
   2. Symptoms of hypercapnia When PaCO₂ increases by 0.67–1.33 kPa (5–10 mmHg) above normal, the child exhibits profuse sweating and restlessness; due to dilation of superficial capillaries, the limbs may feel warm and the skin may appear flushed. Other manifestations include constricted pupils, rapid pulse, and elevated blood pressure. If PaCO₂ increases by ≥1.99 kPa (15 mmHg) above normal, symptoms progress to lethargy, limb tremors, increased heart rate, and conjunctival congestion. Should PaCO₂ continue to rise, convulsions, unconsciousness, and optic disc edema may occur. When PaCO₂ exceeds 10.64 kPa (80 mmHg), severe hypoxia can lead to death.

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bubble_chart Diagnosis

The early diagnosis primarily relies on clinical manifestations, underlying diseases, and blood gas analysis. The key diagnostic points are:

1. the presence of disease causes leading to respiratory failure.
2. Clinical manifestations: respiratory distress with distinct features of either central or peripheral respiratory failure, along with various symptoms caused by hypoxemia or hypercapnia.
3. Blood gas analysis: the diagnosis is more accurate and reliable based on the results of arterial blood (or arterialized capillary blood) gas analysis (see Table 7-3).

1. Type I respiratory failure, i.e., hypoxemic respiratory failure. PaO₂ is decreased; PaCO₂ is normal. It occurs in the early stages and mild cases of respiratory failure.
2. Type II respiratory failure, i.e., hypercapnic respiratory failure. PaO₂ is decreased; PaCO₂ is increased. It is seen in the advanced stages of respiratory failure, and while all children with respiratory failure have hypoxemia, not all have hypercapnia.

bubble_chart Treatment Measures

The fundamental key lies in eliminating the disease cause, treating the primary condition and its triggers, improving respiratory function, increasing PaO₂ and SaO₂, altering ventilation, and reducing PaCO₂.

1. **Preventing and Treating Infections** Infections of the lungs and central nervous system are common causes of respiratory failure and should be diagnosed and managed early. If the disease cause is unclear, broad-spectrum antibiotics may be administered first.
2. **Maintaining Airway Patency** Airway obstruction is primarily caused by mucosal swelling, mucus accumulation, and bronchospasm. Obstruction due to mucus buildup is often a major factor in causing or worsening respiratory failure. Therefore, before employing other treatments, accumulated mucus or foreign objects should be promptly suctioned or removed. Mucus in the mouth, nose, and pharynx can be suctioned with a catheter. For blockages caused by thick secretions in the lower respiratory tract, endotracheal intubation should be performed for suctioning. Simultaneously, ultrasonic nebulization can be administered via the tube 2–3 times daily. The nebulized solution may include expectorants (such as bromhexine, acetylcysteine, α-chymotrypsin), bronchodilators (such as isoproterenol, salbutamol, clenbuterol, dexamethasone), and antibiotics.
3. **Oxygen Therapy** The goal of oxygen therapy is to increase PaO₂ and SaO₂ to alleviate hypoxia. For grade I and grade II hypoxia, 100% pure oxygen can be delivered via nasal cannula at a flow rate of 0.5–1 L/min, with an actual inspired oxygen concentration of about 30%. The inhaled oxygen should ideally be humidified and warmed by passing it through a glass bottle containing water at around 40°C before entering the nasal cannula. For grade III hypoxia, a mask with pressurized oxygen delivery may be used, with the flow rate increased to 3–5 L/min, achieving an actual inspired oxygen concentration of about 60%. Continuous use of pure oxygen should not exceed 12 hours, after which it should be switched to approximately 50% oxygen to avoid oxygen toxicity and respiratory suppression.
   Previously, intermittent oxygen delivery was thought to prevent oxygen toxicity, but current evidence favors continuous oxygen therapy. This is because when oxygen is administered, hypoxia improves, and alveolar ventilation decreases accordingly, increasing alveolar PaO₂. When oxygen delivery is interrupted, a large amount of carbon dioxide dilutes the oxygen concentration in the alveoli, causing PaO₂ to drop, while carbon dioxide in the lungs has not yet been expelled, leading to more severe hypoxia and carbon dioxide retention. Therefore, once the condition improves with oxygen therapy, the flow rate can be gradually reduced while maintaining continuous oxygen delivery.
4. **Use of Respiratory Stimulants** The primary role of respiratory stimulants is to excite the respiratory center, increase ventilation, and expel carbon dioxide. They are suitable for children with unobstructed airways but shallow, weak breathing, inadequate gas exchange, irregular respiratory rhythms, or early-stage respiratory failure. Commonly used drugs include nikethamide, lobeline, dimefline, and pentylenetetrazol, which can be alternated. For children with severe airway obstruction or mucus accumulation, respiratory stimulants merely increase respiratory effort without improving ventilation. They are also ineffective for respiratory failure caused by neuromuscular disorders and should not be used when respiratory muscles are already under high workload. Respiratory stimulants can be administered subcutaneously, intramuscularly, intravenously, or via drip, as needed. Medication can continue until respiratory symptoms improve, after which the interval can be extended or the dosage reduced until discontinuation.
   Respiratory stimulants are only one part of comprehensive treatment and should not be overly relied upon, as their effects are not long-lasting. Excessive doses may lead to convulsions.
5. In the correction of acidotic respiratory failure, it is often uncompensated respiratory acidosis. The main principles of management are to improve ventilation, provide adequate calories, water, and electrolytes to prevent dehydration and ketosis. When respiratory failure is accompanied by metabolic acidosis (blood pH < 7.20), alkaline drugs should be appropriately used, commonly 5% sodium bicarbonate, 2–3 ml/kg each time, with subsequent doses adjusted as needed. Special attention must be paid to the fact that sodium bicarbonate can only correct acidosis effectively when there is sufficient ventilation. Otherwise, the administered sodium bicarbonate may decompose in the body to produce carbon dioxide and water. If the carbon dioxide cannot be expelled through the lungs, PaCO₂ will rise, and the pH will drop further, exacerbating the condition.
6. Diuretics and Dehydrating Agents During respiratory failure, hypoxia increases capillary permeability, which can easily lead to pulmonary edema and cerebral edema. Therefore, diuretics are often required. For example, furosemide has a strong diuretic effect and can improve pulmonary edema. Recent studies have found that furosemide can also dehydrate brain tissue, reduce cerebrospinal fluid production by 40–70%, lower intracranial pressure, inhibit the entry of sodium and chloride into cells, thereby alleviating glial cell swelling and blocking the catalytic effect of cAMP on active transport mechanisms. For cerebral edema, the combined use of furosemide and mannitol has a synergistic effect and can reduce the dosage of mannitol.
7. Cardiotonics and Vasoactive Drugs In cases of respiratory failure complicated by heart failure, fast-acting digitalis preparations such as cedilanid or digoxin can be used to enhance myocardial contractility and slow the heart rate, thereby reducing oxygen consumption by the heart and brain. During respiratory failure, myocardial hypoxia increases the risk of digitalis toxicity, so the dosage should be relatively small.
   Respiratory failure is often accompanied by cardiovascular dysfunction due to hypoxia and carbon dioxide retention. Vasoactive drugs can relieve small vessel spasms, improve microcirculation, and increase tissue perfusion. They can also reduce preload and afterload, improve heart failure and pulmonary edema, enhance cerebral hypoxia and circulation to allow dehydrating agents to take effect, and increase glomerular filtration rate and renal blood flow to protect the kidneys. Clinically, phentolamine is commonly used at a dose of 0.3–0.5 mg/kg per administration, generally not exceeding 10 mg per dose, administered intravenously with 10% glucose solution. Scopolamine or 654-2 may also be used.
8. Artificial Assisted Respiration If the above aggressive treatments are ineffective for children with respiratory failure, the following artificial respiration methods can be employed based on the child's condition and available medical resources.
   1. Mouth-to-Mouth Respiration: In critical situations where rescue equipment is unavailable and the child’s breathing is about to stop, mouth-to-mouth respiration should be performed immediately. Lay the child on their back with the head tilted back as much as possible. The rescuer should hold the child’s jaw with one hand and pinch the nostrils with the other, then blow air into the mouth. Release the nostrils when stopping the blow to allow passive exhalation as the chest collapses naturally. The ratio of blowing to exhalation time should be 1:2. The blowing frequency should be 30–40 times per minute for infants and 20–24 times per minute for children.
      
   2. Endotracheal Intubation: This is suitable for unconscious children or when sudden respiratory arrest does not respond to mouth-to-mouth respiration. Intubation ensures airway patency, improves ventilation, and facilitates sputum suction, pressurized oxygen delivery, or intratracheal medication. After intubation, connect to a resuscitation bag or ventilator, with a breathing frequency of 30–40 times per minute for infants and 18–24 times per minute for children. The gas volume should cause moderate chest rise, equal breath sounds in both lungs, good basal breath sounds, and pink lips and mucous membranes. Intubation time generally should not exceed 48 hours to avoid laryngeal edema and severe dyspnea after extubation.
   3. Tracheostomy: This should be performed without delay when laryngeal conditions preclude intubation, when intubation for 48 hours shows improvement but extubation is not possible, or when there is significant sputum obstruction in the lower airways or extensive atelectasis. For conditions like polyradiculitis or encephalitis B, tracheostomy is crucial for maintaining airway patency and ensuring the child’s safety, so it should not be delayed to avoid missing the optimal treatment window. After tracheostomy, a ventilator should be used for assisted respiration to ensure safety.
   4. Application of Artificial Respirators: After endotracheal intubation or tracheotomy, an artificial respirator is connected to replace manual artificial respiration. Clinically used automatic artificial respirators are classified into three types: pressure-controlled, volume-controlled, and time-controlled. Quantitative types are mostly used for neurological diseases, while pressure-controlled or time-controlled types can be used for respiratory diseases. In pediatric clinics, intermittent positive pressure electric respirators are commonly used. After applying an artificial respirator, close monitoring is essential, requiring dedicated nursing staff to observe and record all changes in detail.