Tuberculosis is the second leading cause of respiratory failure after chronic obstructive pulmonary disease. Although combination chemotherapy has been widely used in the treatment of tuberculosis and has achieved remarkable results, cases of tuberculosis combined with respiratory failure are still frequently seen in clinical practice. Respiratory failure is both a major cause of disability and one of the serious complications of death from tuberculosis. The most common types of tuberculosis with respiratory failure are post-tuberculosis and severe tuberculosis. Post-tuberculosis sequelae are disfiguring lesions such as emphysematous changes, pulmonary fibrosis, bronchiectasis, pulmonary alveoli and cavities, lobectomy and atelectasis, pleural thickening, thoracic reshaping, and spinal deformity caused by tuberculosis.
I. Pathogenesis of pulmonary tuberculosis combined with respiratory failure
1. Insufficient alveolar ventilation due to pulmonary tuberculosis is associated with the following mechanisms.
(1) increased respiratory muscle burden: pulmonary fibrosis, lobectomy and atelectasis, pleural thickening, thoracic reshaping and massive pleural effusion due to pulmonary tuberculosis reduce pulmonary compliance and increase elastic resistance; bronchiectasis and infection, emphysema, and the coexistence of pulmonary tuberculosis and COPD increase airway resistance significantly, and increase elastic resistance and airway resistance increase respiratory muscle burden.
(2) Respiratory muscle fatigue: Respiratory muscle fatigue refers to the inability of the force and endurance generated by respiratory muscle contraction to counteract the respiratory muscle load, so that the driving pressure required to maintain adequate alveolar ventilation cannot be generated. Respiratory muscle fatigue is the main cause of ventilatory failure during acute exacerbation of chronic respiratory insufficiency. Respiratory muscle fatigue is due to an increased respiratory muscle load, and also to inadequate supply of nutrients to the respiratory muscles due to chronic malnutrition in patients with tuberculosis.
2. Ventilation/blood flow ratio imbalance.
V/Q ratio dysregulation mainly causes hypoxemia and has less effect on PaCO2. This is because.
(1) Although both hypoxia and CO2 retention can stimulate ventilation and increase alveolar ventilation, because the oxygen dissociation curve and CO2 dissociation curve are different, alveoli with normal or higher than normal V/Q can compensate for the increased ventilation by expelling more CO2, and the partial pressure of oxygen in blood flow in these regions is already in the flat part of the dissociation curve, and the oxygen saturation will not improve more even if PaO2 is further increased .
(2) The partial pressure difference between arterial and venous blood oxygen is 50 mmHg, while the partial pressure difference between CO2 is only 6 mmHg. When a static arterial shunt occurs, the effect on PaO2 is significantly greater than that on PaCO2.
3, intrapulmonary shunt.
The total cardiopulmonary shunt flow is only 5% of the cardiac output in normal time. Severe tuberculosis, pulmonary atelectasis, and severe tuberculosis complicated by ARDS can lead to an increase in intrapulmonary shunt flow, and unoxygenated venous blood is mixed with arterial blood to cause hypoxemia. In hypoxemia caused by right-to-left shunt, increasing oxygen concentration does not significantly improve arterial partial pressure of oxygen, and the larger the shunt flow, the less effective oxygen inhalation is in improving arterial partial pressure of oxygen. When the fractional flow rate exceeds 30%, the effect of oxygen inhalation on the arterial partial pressure of oxygen is minimal. As long as the VA is maintained, right-to-left shunt rarely results in CO2 retention, and only when the fractional flow rate is >50% does it lead to hypercapnia.
4. Diffusion disorders.
Diffusion dysfunction due to pulmonary tuberculosis is seen in the following conditions.
(1) Reduced diffusion area due to lesions such as severe emphysema and/or pulmonary atelectasis, and increased blood flow velocity due to destruction of the capillary bed, resulting in reduced diffusion volume.
(2) Chronic fibro-cavitary lesions cause significant thickening and mechanization of alveolar capillaries, resulting in a significantly greater time for oxygen to diffuse through the respiratory membrane than for red blood cells to pass through pulmonary capillaries, thereby affecting diffusion function. Since the diffusing power of CO2 is approximately 20 times that of oxygen, diffusion disorders alone do not cause hypercapnia. Unless the diffusion disorder is extreme, it usually does not lead to hypoxemia in the resting state.
II. Pathophysiology
Hypoxemia and hypercapnia due to pulmonary tuberculosis complicated by respiratory failure can have a series of adverse effects on the physiological functions of the body.
1.Central nervous system.
2.Respiratory system.
3.Cardiovascular system.
4.Digestive system.
5. Acid-base imbalance and electrolytes.
Clinical manifestations of pulmonary tuberculosis complicating respiratory failure
The clinical manifestations of pulmonary tuberculosis complicating respiratory failure include the clinical manifestations of tuberculosis itself and respiratory failure. The manifestations of pulmonary tuberculosis have been described in detail in the relevant chapters of this book. Respiratory failure is mainly a clinical condition caused by multiple organ dysfunction due to hypoxia and CO2 retention.
1, dyspnea: increased respiratory rate, dyspnea, increased nasal agitation and auxiliary respiratory muscle activity. Those with obvious airway obstruction often show prolonged expiration and labored expiration. In severe cases, abnormal respiratory rhythm and slowing and stopping of respiration may also occur.
2. Cyanosis: It is a typical manifestation of hypoxia. When the arterial oxygen saturation is lower than 85% or the intravascular reduced hemoglobin is more than 50g/L, cyanosis can appear in the lips, mucous membrane and nail bed where the blood flow is high. Cyanosis is more pronounced in those with increased hemoglobin, but is less pronounced or absent in those with anemia, while peripheral cyanosis can occur in those with severe shock and terminal circulation stasis, even if the partial pressure of arterial blood oxygen is normal. In addition, cyanosis is also affected by skin pigmentation and cardiac insufficiency.
3. Psychoneurological symptoms: Mild hypoxia and CO2 retention may manifest as mental inattention, headache, excitement or drowsiness, irritability and disorientation, while in severe cases, agitation, convulsions and coma may occur. It is worth mentioning that excitement, insomnia and irritability caused by CO2 retention are generally contraindicated with sedatives and hypnotics to avoid aggravating the retention.
4. Circulatory system symptoms; accelerated heart rate and elevated blood pressure appear in the early stage of hypoxia, while heart rate slows down, arrhythmia and blood pressure drops in the severe period. In addition, long-term hypoxia and CO2 retention can lead to constriction of small pulmonary arteries, pulmonary hypertension and right heart failure. The clinical manifestations are jugular vein filling, hepatosplenomegaly and lower limb edema, etc. CO2 retention may cause skin vasodilation, warm and sweaty skin, conjunctival congestion and edema, and large pulse rate.
5. Other systemic symptoms of severe respiratory failure may lead to gastrointestinal mucosal congestion, erosion and bleeding, elevated hepatic glutamate transaminase, jaundice, and oliguria and anuria, etc.
IV. Diagnosis of pulmonary tuberculosis with respiratory failure
The following three questions should be clarified in the diagnosis.
1. Whether it is complicated by respiratory failure: It is mainly determined by the clinical manifestations and the results of arterial blood gas analysis. However, for patients clinically suspected of complicating acute respiratory failure, there is no need to sit and wait for the results of arterial blood gas analysis, and emergency treatment should be carried out immediately to avoid delaying the time of resuscitation.
2. Type and severity of respiratory failure: Arterial blood gas analysis can determine the type and severity of respiratory failure and acid-base imbalance, providing a basis for clinical treatment of respiratory failure. In addition, electrocardiogram, central venous pressure measurement, liver and kidney function, blood enzymology, urine volume and other measurements can help to understand the degree of damage to other system organs, and also provide a basis for the prevention and treatment of respiratory failure.
3. Type of tuberculosis and precipitating factors of respiratory failure: In the emergency diagnosis and treatment of pulmonary tuberculosis complicated by respiratory failure, the type and severity of tuberculosis should be clarified as soon as possible, whether there are other precipitating factors of respiratory failure, and the correct and effective anti-tuberculosis treatment and removal of precipitating factors should be started as early as possible. Oxygen therapy or mechanical ventilation can maintain relatively normal PaO2 and PaCO2 levels, but if the underlying etiology and triggers are not removed, the patient is still not free from the risk of reoccurring respiratory failure. A detailed history and physical examination can make a preliminary determination of the cause of respiratory failure. Chest radiographs are important to identify the cause of respiratory failure. Diffuse pulmonary infiltrates in both lungs are most often seen in hematogenous disseminated pulmonary tuberculosis, ARDS, interstitial fibrosis, interstitial pneumonia, and alveolar cell carcinoma. Restricted pulmonary infiltrates are mostly seen in severe pneumonia, caseous pneumonia, pulmonary atelectasis, and lung cancer.
Treatment of pulmonary tuberculosis with respiratory failure
1.Maintain airway patency and establish artificial airway.
2.Rational oxygen therapy.
3.Maintain acid-base and electrolyte balance.
4.Mechanical ventilation.