bubble_chart Overview

Chronic respiratory failure occurs when respiratory dysfunction gradually worsens on the basis of chronic pulmonary or thoracic diseases, leading to respiratory failure. Clinically, it is mainly classified as type II, with occasional cases of type I respiratory failure. Those who can still perform light work and daily activities under natural breathing conditions are referred to as having compensated chronic respiratory failure. However, when respiratory function deteriorates sharply due to respiratory infections or other causes, resulting in more severe dyspnea, hypoxemia, and hypercapnia, it is termed decompensated respiratory failure.

bubble_chart Etiology

Chronic respiratory failure can be caused by various factors, with its underlying disease causes primarily being chronic pulmonary and thoracic diseases, particularly chronic obstructive pulmonary disease (COPD), including chronic bronchitis, obstructive emphysema, and bronchial asthma. Other significant causes include severe pulmonary tuberculosis, pneumoconiosis, diffuse pulmonary fibrosis, and thoracic deformities. The most common direct trigger for acute exacerbation leading to decompensated respiratory failure is respiratory tract infection.

bubble_chart Clinical Manifestations

Since chronic respiratory failure is secondary to chronic pulmonary and thoracic diseases, it presents with corresponding clinical manifestations of various primary diseases, and is often accompanied by chronic pulmonary heart disease.

All clinical manifestations of chronic respiratory failure itself are the results of hypoxia and/or carbon dioxide retention, as both can lead to multi-organ system damage and physiological and metabolic dysfunction.

1. Dyspnea and cyanosis Dyspnea is the earliest clinical symptom, often manifested as rapid breathing, increased respiratory rate, and the involvement of accessory respiratory muscles in breathing, which may present as orthopnea, open-mouth breathing, nodding, or shrugging-like respiration. This is due to the reflex compensatory mechanism triggered by the stimulation of the carotid and aortic chemoreceptors when the body is hypoxic, as well as the increased PaCO₂, which strongly excites the respiratory center, leading to enhanced ventilation. However, severe hypercapnia, especially when PaCO₂ rises rapidly to exceed 10.7 kPa (80 mmHg), can instead inhibit the respiratory center, reducing ventilation and resulting in shallow, slow breathing, or even respiratory arrest. Severe respiratory failure may complicate cerebral edema, affecting the respiratory center and causing abnormal respiratory rhythms, such as Cheyne-Stokes respiration or Biot's respiration. Cyanosis is a manifestation of severe hypoxia, where hemoglobin cannot be fully oxygenated. When reduced hemoglobin increases significantly or when oxygen saturation falls below 85%, cyanosis appears as bluish discoloration of the lips, nail beds, and oral mucosa. However, in patients with significant polycythemia, cyanosis may occur even with grade I reduction in oxygen saturation. Additionally, patients with severe anemia or darker skin pigmentation may not exhibit obvious cyanosis.
2. Neuropsychiatric symptoms Although the brain accounts for only 2% of body weight, its oxygen consumption reaches 20–25% of the total. Therefore, the central nervous system is extremely sensitive to hypoxia. Hypercapnia can exacerbate hypoxia and inhibit the cerebral cortex while enhancing subcortical excitability. Thus, in the early stages of respiratory failure, symptoms such as headache, impaired orientation and timing, and difficulty concentrating may appear. As the condition worsens, symptoms like confusion, drowsiness, dysphoria, restlessness, spasms, delirium, and even unconsciousness may occur, along with neurological signs and positive flapping tremors. Patients with cerebral edema may exhibit symptoms of increased intracranial pressure, such as headache, vomiting, and papilledema. Carbon dioxide retention can cause cerebral vasodilation, leading to pulsatile headaches. The severity of neuropsychiatric symptoms is not only related to the degree of hypoxia and hypercapnia but also closely associated with the speed of onset and compensatory mechanisms.
3. Cardiovascular manifestations Hypoxia and hypercapnia can increase sympathetic excitability, leading to compensatory tachycardia, increased cardiac output, elevated blood pressure, pulmonary arteriolar spasm, pulmonary hypertension, and accentuated pulmonary second heart sound. Myocardial hypoxia increases irritability, predisposing to premature beats, atrial fibrillation, and other arrhythmias, and in severe cases, even ventricular fibrillation and cardiac arrest. Reduced myocardial contractility and decreased cardiac output can lead to hypotension and shock. Long-term pulmonary hypertension can cause chronic pulmonary heart disease.
   Grade I carbon dioxide retention can also relax vascular smooth muscles and dilate peripheral blood vessels, presenting as warm, flushed skin, profuse sweating, elevated blood pressure, and bounding pulses. Severe carbon dioxide retention can cause hypotension or even shock.
4. Gastrointestinal bleeding Hypoxia and hypercapnia can increase gastric acid secretion, cause widespread congestion, edema, and erosion of the gastric mucosa, and, combined with factors such as hydrogen ion back-diffusion and long-term high-dose corticosteroid use, can lead to upper gastrointestinal bleeding. Massive bleeding often indicates a poor prognosis. Early signs of gastrointestinal bleeding include loss of appetite, nausea, and epigastric fullness, which should be detected early.
5. Chronic hypoxia due to abnormalities in the blood system can lead to compensatory increases in red blood cells, resulting in secondary polycythemia and causing hyperviscosity, which easily induces pulmonary embolism and increases cardiac load, leading to heart failure. Severe hypoxia, acidosis, infection, shock, etc., can cause circulatory stasis, triggering disseminated intravascular coagulation (DIC), and subsequently leading to multiple organ damage.
6. Damage to organs such as the liver and kidneys can manifest as increased transaminase levels, decreased serum albumin, elevated blood urea nitrogen and creatinine, and adrenal cortical dysfunction.
7. Acid-base imbalance and electrolyte disturbances During chronic respiratory failure, factors such as hypoxia and hypercapnia can lead to various complex acid-base imbalances and electrolyte disturbances (see Table 2-13-2).

(1) Respiratory acidosis ranks first in incidence among chronic respiratory failure cases. It results from impaired carbon dioxide elimination leading to hypercapnia, increased hydrogen ion concentration, and decreased pH, known as uncompensated respiratory acidosis. Over time, compensatory increases in HCO₃^- (bicarbonate) can normalize or restore pH, transitioning to compensated respiratory acidosis.

(2) Respiratory acidosis with metabolic alkalosis ranks second. It often occurs due to low potassium and chloride caused by insufficient intake, vomiting, or diuretic use on the basis of respiratory acidosis, or excessive supplementation of alkaline drugs. Blood gas analysis may show decreased, increased, or normal pH, elevated PaCO₂, and significantly increased HCO₃^-.

(3) Respiratory acidosis with metabolic acidosis ranks third. Factors such as hypoxia, insufficient intake, infection, and shock increase acidic metabolites, while poor kidney function reduces acid excretion, leading to metabolic acidosis superimposed on respiratory acidosis. Due to the dual acidosis, pH often drops significantly, PaCO₂ increases, and HCO₃^- remains normal or decreases.

(4) Metabolic alkalosis is less common. It may occur when excessive respiratory stimulants or diuretics are used during compensated respiratory acidosis, or when mechanical ventilation removes carbon dioxide too rapidly, leading to hypocapnia, or when inappropriate alkali supplementation is given in type I respiratory failure. Blood gas analysis shows increased pH and HCO₃^-, with normal or elevated PaCO₂.

(5) Respiratory alkalosis is rare and often related to excessive carbon dioxide removal during mechanical ventilation. It may also occur in type I respiratory failure patients inappropriately given respiratory stimulants. Blood gas analysis reveals increased pH and decreased PaCO₂

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During respiratory failure, serum potassium levels often follow certain patterns based on acid-base status: hyperkalemia in acidemia and hypokalemia in alkalemia. Serum sodium changes are less predictable, but hyponatremia is more common. Serum magnesium often decreases, and hypoosmolality may occasionally occur.

bubble_chart Diagnosis

1. Pre-existing chronic pulmonary and thoracic diseases, especially chronic bronchitis with obstructive emphysema and cor pulmonale, serve as the foundation for chronic respiratory failure, with most cases having a recent history of respiratory tract infection.
2. The clinical features of respiratory failure primarily include dyspnea, cyanosis, profuse sweating, increased heart rate or arrhythmia, and impaired consciousness.
3. Arterial blood gas analysis showing PaO₂ < 8 kPa (Type I) or accompanied by PaCO₂ > 6.67 kPa (Type II) can confirm the diagnosis. It can also be classified as mild, moderate, or grade III respiratory failure based on multiple indicators.
4. When mental and neurological symptoms and pathological signs appear during respiratory failure, and other causes such as cerebrovascular disease, toxic encephalopathy due to infection, or severe electrolyte imbalances are excluded, pulmonary encephalopathy can be diagnosed, which is a manifestation of severe respiratory failure.

bubble_chart Treatment Measures

The treatment principles involve comprehensive therapies to correct hypoxia, improve ventilation, treat acid-base imbalance and electrolyte disturbances, and eliminate precipitating factors.

1. Controlled oxygen therapy: Hypoxia is the root cause of multi-system damage and must be corrected as soon as possible to ensure aerobic metabolism in tissue cells. For type II respiratory failure, low-flow (1–2 L/min) and low-concentration (25–30%) continuous oxygen supply, known as controlled oxygen therapy, is recommended. The oxygen concentration can be calculated using the formula: 21 + 4 × flow rate. For example, at a flow rate of 2 L/min, the concentration would be 21 + 4 × 2 = 29%. Nasal cannulas or stuffy nose oxygen delivery are commonly used. The rationale for controlled oxygen therapy in type II respiratory failure is that the relationship between PaO₂ and SaO₂ lies on the steep part of the oxygen dissociation curve. A slight increase in PaO₂ leads to a significant rise in SaO₂, greatly improving tissue oxygenation. More importantly, it prevents the rapid relief of hypoxia, which could otherwise eliminate the hypoxic stimulus to respiration, leading to respiratory depression, reduced ventilation, and further elevation of PaCO₂, potentially causing unconsciousness. For type I respiratory failure, higher oxygen concentrations can be inhaled. However, nasal cannulas or stuffy nose delivery are often poorly tolerated at flow rates exceeding 5 L/min due to local airflow irritation. In such cases, mask oxygen therapy may be used.
2. Ensuring airway patency is crucial for effective oxygenation, improved ventilation, and alleviation of carbon dioxide retention. This includes the use of bronchodilators such as β2-agonists (e.g., salbutamol 4 mg three times daily, terbutaline 2.5 mg three times daily), oral or intravenous aminophylline, as well as mucolytic and dispelling phlegm therapies (e.g., bromhexine 16 mg three times daily, ammonium chloride 1.0 g three times daily, fresh Bomboo Juice 20 ml three times daily). Ultrasonic nebulization can also be employed. Patients should be encouraged to cough actively to expel sputum. For those unable to cough effectively or with impaired consciousness, measures such as turning, back patting, or catheter suction may be necessary. In severe cases, seasonal epidemic intubation or tracheostomy may be required to ensure airway patency and effective ventilation. However, strict respiratory care is essential, including maintaining airway dampness transformation with saline or 1% sodium bicarbonate drops, sterile suctioning, and infection prevention.
3. Promoting carbon dioxide elimination: In cases of significantly elevated PaCO₂, especially with impaired consciousness, respiratory stimulants such as nikethamide (0.75 g [2 ampoules] intravenously, followed by 3.75 g [10 ampoules] in 500 ml of 5% glucose or saline for continuous infusion) can increase respiratory depth and frequency, improving ventilation and facilitating CO2 elimination. This also aids in restoring consciousness, enhancing cough reflexes, and improving sputum expulsion. However, it should be noted that respiratory stimulants generally increase metabolic rate and oxygen consumption, so concurrent oxygen therapy is necessary. Diaphragmatic pacing can enhance diaphragmatic contraction and increase ventilation, aiding CO2 elimination. Aminophylline and digoxin also improve diaphragmatic contraction, thereby increasing ventilation. These measures are most effective when the airway is unobstructed.
4. Mechanical ventilation should be administered to patients whose hypoxemia, hypercapnia, and consciousness do not improve after the aforementioned treatments, or who exhibit shallow, slow, or ceased breathing. Commonly used methods include the manual resuscitation bag and mechanical ventilator, connected via endotracheal intubation or tracheostomy tube, to assist, control spontaneous breathing, or replace respiration. This aims to increase ventilation volume, reduce venous admixture, improve the ventilation/perfusion ratio, and decrease the work of breathing, thereby elevating PaO2 and lowering PaCO₂. The manual resuscitation bag is suitable for emergencies due to its simplicity and rapid deployment. Mechanical ventilators are more appropriate for prolonged artificial ventilation and are categorized into volume-controlled and pressure-controlled types. Volume-controlled ventilators automatically switch upon reaching a preset tidal volume, ensuring adequate ventilation, and are suitable for patients with increased airway resistance, reduced lung compliance, weak or absent spontaneous breathing. Pressure-controlled ventilators use preset pressure as the switching signal and are suitable for patients with relatively milder conditions and some spontaneous breathing. Both types now come with synchronization devices. Regardless of the mechanical ventilation method used, familiarity with its functions and proficient operation are essential. The delivered air volume and pressure must be appropriately managed—excessive levels may lead to hyperventilation, respiratory alkalosis, or complications like barotrauma and pneumothorax, while insufficient ventilation fails to alleviate hypoxia and carbon dioxide retention. Additionally, intensive care is crucial, with close monitoring of the patient's condition and vital indicators. Regular clearance of airway secretions and strict aseptic techniques must be maintained to prevent cross-infection.
5. Management of Water-Electrolyte and Acid-Base Imbalances For respiratory acidosis, the primary approach is to improve ventilation and actively eliminate retained carbon dioxide. Alkaline drugs are generally not recommended, except in cases of severe acidemia (pH < 7.20), where a small amount of sodium bicarbonate may be considered. In cases of respiratory acidosis accompanied by metabolic alkalosis or pure metabolic alkalosis, in addition to enhancing ventilation, potassium chloride and normal saline should be supplemented. For patients with significantly elevated pH, intravenous infusion of 20g arginine can be administered to appropriately lower the pH. For respiratory acidosis accompanied by metabolic acidosis with a significant drop in pH, alkaline drugs should be used for correction. However, the correction of acidemia, especially under hypoxic conditions, should not be too rapid to avoid a sharp rise in pH, which could shift the oxygen dissociation curve to the left, reduce oxygen release, and exacerbate tissue hypoxia. Electrolyte supplementation should follow the principle of "replenishing what is deficient" based on clinical manifestations and laboratory data. Dehydration often occurs due to insufficient intake, vomiting, sweating, or diuretic use, and should be supplemented as needed. Additionally, nutritional support and supportive therapy are crucial for the recovery of patients with chronic respiratory failure.
6. **Disease Cause** The acute exacerbation of chronic respiratory failure often has precipitating factors, with respiratory infections being the most common. Therefore, active infection control is a key measure in alleviating respiratory failure. The optimal antimicrobial therapy is based on sputum culture results to select highly sensitive drugs. However, since cultures take time, empirical therapy can be initiated based on the patient's condition, sputum characteristics, and hospital-acquired infections. Options include penicillin with gentamicin, erythromycin with chloramphenicol, ampicillin, cefazolin, etc. Fluoroquinolones such as ciprofloxacin are also effective, often requiring intravenous administration. Adjustments should be made once culture results are available. If heart failure or arrhythmias occur, appropriate treatment should be administered. For concurrent gastrointestinal bleeding, intravenous cimetidine is effective. The underlying disease causing respiratory failure should also be treated simultaneously.

bubble_chart Prognosis

In cases where the underlying pulmonary or thoracic disease causing respiratory failure is relatively mild, with clear and easily removable triggers, most respiratory failures can be alleviated with the aforementioned aggressive treatment. However, patients with severe underlying diseases, recurrent respiratory failure, or multiple serious complications have a poor prognosis.

bubble_chart Prevention

1. Efforts should be strengthened to prevent and treat the primary disease to prevent its progression to respiratory failure.
2. Enhance physical exercise to improve the body's disease resistance and prevent common colds and respiratory infections.
3. The direct trigger for chronic respiratory failure transitioning from compensation to decompensation is often respiratory infection. Once it occurs, immediate treatment is necessary to control it as soon as possible and prevent the worsening of respiratory failure.