Etiology
Respiratory system diseases such as severe respiratory infections, acute obstructive airway diseases, severe or critical asthma, acute pulmonary edema caused by various causes, pulmonary vascular diseases, thoracic trauma or surgical injury, spontaneous pneumothorax, and rapidly increasing pleural effusion can lead to pulmonary ventilation and/or gas exchange disorders. Acute intracranial infections, traumatic brain injury, and cerebrovascular lesions (cerebral hemorrhage or infarction) can directly or indirectly suppress the respiratory center. Conditions like poliomyelitis, myasthenia gravis, organophosphate poisoning, and cervical spine injuries can damage the neuromuscular conduction system, causing inadequate pulmonary ventilation. These factors can all result in acute respiratory failure.
Clinical manifestations
The clinical manifestations of acute respiratory failure are primarily due to dyspnea and multiorgan dysfunction caused by hypoxemia.
Dyspnea is the earliest symptom of respiratory failure. Most patients experience significant dyspnea, which may be manifested by changes in frequency, rhythm, and amplitude of breathing. Initially, there is tachypnea, and as the condition progresses, dyspnea occurs with increased accessory muscle activity, such as the presence of three concave sign. Respiratory failure due to central nervous system diseases or central nervous system depressants may present with altered respiratory rhythms, such as Cheyne-Stokes respiration and Biot respiration.
Cyanosis is a typical sign of hypoxia, and can occur on the lips and nails when arterial oxygen saturation drops below 90%. It is important to note that the severity of cyanosis is related to the level of reduced hemoglobin, so it is more pronounced in polycythemia and less prominent or absent in anemia. Patients with peripheral circulation disorders caused by severe shock may exhibit cyanosis even if arterial oxygen tension is normal, which is termed peripheral cyanosis. Cyanosis due to reduced arterial oxygen saturation is termed central cyanosis. Cyanosis is also influenced by skin pigmentation and cardiac function.
Acute hypoxia can cause obfuscation, agitation, coma, and seizures. If acute CO2 retention occurs, symptoms like drowsiness, apathy, asterixis, and even respiratory arrest may be present.
Most patients experience tachycardia. Severe hypoxemia and acidosis can cause myocardial damage, peripheral circulatory failure, hypotension, arrhythmias, and cardiac arrest.
Severe respiratory failure affects liver and kidney function. Some cases may show elevated alanine aminotransferase and plasma urea nitrogen levels, and urine may contain protein, erythrocytes, and casts. Impaired gastrointestinal mucosal barrier function can lead to congestion, edema, erosion, hemorrhage, or stress ulcers in the gastrointestinal tract, resulting in gastrointestinal hemorrhage.
Diagnosis
In addition to the clinical manifestations caused by the primary disease, hypoxemia, and CO2 retention, the diagnosis of respiratory failure mainly relies on arterial blood gas analysis. This analysis helps determine the type and severity of respiratory failure. Further investigations, such as chest imaging, pulmonary function tests, and fiberoptic bronchoscopy, are used to identify the etiology.
Blood gas analysis is used to determine whether it is hypoxemic respiratory failure (Type I respiratory failure) or hypercapnic respiratory failure (Type II respiratory failure). If it is hypoxemic respiratory failure, the primary cause is usually V/Q mismatch. If chest imaging (chest x-ray) is roughly normal, the focus is on right heart-pulmonary vascular disease. If imaging shows significant abnormalities, further assessments based on medical history, symptoms, signs, risk factors, ECG, echocardiography, and cardiac enzymes are needed to determine whether it is due to pulmonary disease or left heart-related pulmonary edema. Hypercapnic respiratory failure is mainly caused by increased CO2 production and reduced CO2 elimination. Due to the compensatory mechanisms, Type II respiratory failure caused solely by increased CO2 production is less common; the main cause is reduced CO2 elimination, seen in ventilation dysfunction and/or increased dead space.
Arterial blood gas analysis
This is crucial for assessing the severity of respiratory failure and acid-base imbalance, as well as guiding treatment. The pH reflects the compensatory status and helps distinguish between acute and chronic respiratory failure. When PaCO2 is elevated and pH is normal, it is termed compensatory respiratory acidosis; if PaCO2 is elevated and pH < 7.35, it is termed decompensated respiratory acidosis. It is important to note that blood gas results are influenced by factors such as age, altitude, and oxygen therapy, so clinical context must be considered.
Pulmonary function tests
Although limited in some critically ill patients, these tests can determine the nature of ventilation dysfunction (obstructive, restrictive, or mixed) and assess if there is a concurrent gas exchange dysfunction. They also help evaluate the severity of ventilation and gas exchange disorders. Respiratory muscle function tests can indicate the cause and severity of respiratory muscle weakness.
Chest imaging
This includes conventional chest x-ray, chest CT, ventilation/perfusion scintigraphy, pulmonary angiography, and ultrasound.
Fiberoptic bronchoscopy
This is significant for identifying airway diseases and obtaining pathological evidence.
Treatment
Acute respiratory failure has many causes, and treatment plans vary depending on the primary disease. The general treatment principles include respiratory support, etiological treatment, and management of complications.
Respiratory support
Hypoxemia and hypercapnia can affect the metabolism and function of various organ systems and even alter tissue structure. In the initial stage of respiratory failure, compensatory reactions occur in organ systems to improve oxygen supply, regulate acid-base balance, and adapt to changes in the internal environment. In severe stages, compensation fails, leading to severe dysfunction and metabolic disorders in organ systems, potentially resulting in failure. Therefore, respiratory support should be provided promptly to improve hypoxemia and hypercapnia, correct internal environment disorders, maintain circulatory stability, and prevent decompensation.
Etiological treatment
As mentioned earlier, there are various primary diseases that can cause acute respiratory failure. It is crucial to identify and appropriately treat the specific primary disease, while managing the harm caused by respiratory failure itself, as this is fundamental to the treatment of respiratory failure.
Management of complications
Respiratory failure often affects other vital organs, so it is important to monitor and support organ function, and to prevent and treat complications such as pulmonary hypertension, cor pulmonale, pulmonary encephalopathy, renal insufficiency, gastrointestinal dysfunction, and disseminated intravascular coagulation (DIC).