Respiratory muscle fatigue

Introduction to respiratory muscle fatigue Respiratory muscle fatigue or respiratory muscle dysfunction is common in patients with chronic lung disease and ICU hospitalization. For a long time, respiratory muscle fatigue or exhaustion has not received much attention. The breathing rate is increased, and the breathing is not synchronized (such as periodic abdominal pressure and chest pressure breathing alternately, disordered and non-parallel abdominal pressure breathing, abdominal bimodal breathing exercise) and chest and abdomen contradictory breathing. Timely detection and treatment of respiratory muscle fatigue can correct respiratory mechanics abnormalities, reduce respiratory work, improve oxygenation, and shorten the time of mechanical ventilation. Therefore, in recent years, the evaluation of respiratory muscle function in critically ill patients has become an important part of intensive care. basic knowledge The proportion of illness: 0.003% Susceptible people: no specific population Mode of infection: non-infectious Complications: diaphragmatic paralysis

Causes of respiratory muscle fatigue

(1) Causes of the disease

Respiratory muscle fatigue in most patients is caused by the disease itself. Sepsis, multiple organ failure, mechanical ventilation, hypercapnia (acidosis) and various drugs have been found to cause neuromuscular processes. Functional abnormalities and become an important part of the pathophysiological process of the above diseases. In short, respiratory muscle fatigue and weakness are very common in chronic diseases such as critical illness and COPD. In addition to the role of the disease itself, a variety of drugs such as glucocorticoids, muscle relaxants, aminoglycoside antibiotics can induce or aggravate respiratory muscle fatigue. Inappropriate application of ventilator can also cause diaphragmatic dysfunction. The method of detecting respiratory muscle fatigue is poor in specificity and accuracy, and it is difficult to routinely apply clinically. It is important to pay attention to the presence of respiratory muscle fatigue in clinical examination.

(two) pathogenesis

Respiratory muscles include diaphragm, intercostal muscle, abdominal muscle, sternocleidomastoid and scalene muscle. According to function classification, respiratory muscle can be divided into inspiratory muscle (diaphragm, intercostal muscle, sternocleidomastoid, etc.) and Breathing muscles (intercostal muscles, abdominal muscles) can be divided into red muscle fibers (also known as slow-shrinkage anti-fatigue fibers or class I fibers) and white muscle fibers (also known as fast-shrink fibers or class II) according to the properties of muscle fibers. Fiber), class II fiber can be divided into fast shrinkage fatigue fiber (IIA fiber) and fast shrinkage fast fatigue fiber (IIB).

The main function of the respiratory muscles is to complete the respiratory movement, and then participate in the cough, sputum, vomiting and other processes, in which the diaphragm function is the most important, about 3% to 90% of the total respiratory function, and 2/3 of the tidal volume is produced by the contraction of the diaphragm. When the ventilation per minute increases or there is diaphragmatic fatigue, the assisted respiratory muscles participate in contraction. During calm breathing, the expiratory muscles do not participate in contraction, but when the respiratory function increases, the expiratory muscles such as the intercostal muscles and abdominal muscles contract. The diaphragm is squeezed into the thoracic cavity, so that the diaphragm muscle fibers are in the best initial tension position.

1. COPD patients

It is currently believed that skeletal muscle (including respiratory muscle) dysfunction is directly related to the decline of exercise tolerance in patients with COPD. The structural changes of skeletal muscle in patients with COPD are characterized by a decrease in muscle weight and a change in muscle fiber structure (a decrease in the proportion of type I fibers, the proportion of type II fibers). Increase, type I and IIA fiber atrophy, class I and class II fiber diameter reduction, etc.), the number of capillary trees per unit area of skeletal muscle decreased and metabolic changes (oxidative enzyme activity decreased), functional changes expressed as muscle strength decreased, The main reasons for the decline in endurance, local oxygen uptake and oxygen transport during maximum exercise, and the resulting structural and functional changes are:

1 long-term hypoxemia, hypercapnia, infection and chronic malnutrition;

2 accompanied by electrolyte imbalance (low potassium, low phosphorus, low magnesium), heart failure, muscle atrophy; 3 glucocorticoid-induced acute and chronic myopathy, in patients with severe airway obstruction, due to lung Excessive inflation causes significant changes in the mechanical characteristics of the respiratory system. The diaphragm is in an unfavorable initial position of contraction, and the contraction efficiency is significantly reduced. In addition, the effects of various factors mentioned above can easily lead to diaphragmatic fatigue and functional failure.

2. Sepsis (Sepsis)

Patients with sepsis are characterized by normal or increased systemic blood flow, decreased tissue oxygen uptake, decreased local perfusion, and hypoxemia. For respiratory muscles, total perfusion during sepsis and shock is Increased, but local microvascular perfusion disorders and increased work of breathing can still cause respiratory muscle hypoxia and respiratory muscle dysfunction.

3. The effect of mechanical ventilation on respiratory muscles

The effect of mechanical ventilation on respiratory muscle function has two sides. On the one hand, replacing or assisting the respiratory muscles to make the fatigue of the respiratory muscles rest, on the other hand, the respiratory muscles are atrophic, and the strength and endurance of the respiratory muscles are reduced, resulting in breathing. Machine dependence, major changes in skeletal muscle atrophy include:

(1) The muscle weight is significantly reduced.

(2) Decreased protein synthesis.

(3) Muscle fiber mesh, reduced in diameter.

(4) The number of slow-shrinkage anti-fatigue fibers is reduced.

(5) Decreased mitochondrial glucose oxidation and decomposition ability, although the respiratory muscle has different characteristics from ordinary skeletal muscle, but in the long-term controlled mechanical ventilation, the activity of the diaphragm electromyography can be found to decrease, the cross-pressure drop and breathing Reduced muscle endurance, Brochard et al. 11 days of controlled ventilation of healthy sputum, found that Pdi decreased by 25%, endurance decreased by 36%, the other major determinant of respiratory muscle atrophy during mechanical ventilation is the length of the fiber If the length of the muscle fiber is fixed below its normal length for a long time, it is easy to produce fatigue; when it exceeds its base length, muscle atrophy can be avoided.

4. Respiratory muscle function during weaning

For patients who have undergone mechanical ventilation for a period of time, respiratory muscle function is one of the key factors in determining whether to withdraw the machine. Most patients with clinical difficulty in weaning have respiratory muscle fatigue. Cohen et al. The patient's study found that 7 patients had changes in EMG spectrum and suggested diaphragmatic fatigue, 6 patients had abnormal abdominal breathing, and 6 patients had increased respiratory rate. Some patients experienced increased respiratory rate and PaCO2 after changes in EMG spectrum. Increased, suggesting that the increase in respiratory rate and PaCO2 in these patients is related to diaphragmatic fatigue, respiratory muscle fatigue is a common cause of failure to wean.

5. Critically ill patients with multiple neuropathy

In patients with sepsis and multiple organ failure (MOF), polyneuropathy with sensory-motor nerve damage may occur. Currently referred to as critically ill polyneuropathy, approximately 70% of patients in the ICU have different degrees of occurrence. Multi-neuropathy, Bolton electrophysiological examination of 43 patients with sepsis and MOF found that 30 patients had axonal degeneration with sensory and motor potential abnormalities, 15 patients showed clinical weakness, withdrawal failure, and reduced reflex Or disappear, the main clinical manifestations of critically ill multi-neuronal lesions are weakened limb muscle strength with atrophy, abnormal sensory function, deep reflex or disappear, cranial nerve function is normal, critically ill multi-neuropathy has self-limiting, after a period of time After the full recovery, but the EMG can be abnormal, it is now considered that this secondary polymuscular disease is one of the important factors that cause difficulty in weaning and prolong the length of ICU hospitalization, 62% of patients with difficulty in weaning related.

The mechanism of critically ill multi-neuronopathy is still not fully understood. Nutritional disorders, poisoning, metabolic abnormalities and vascular factors may be involved in the occurrence of neuropathy. It is also suggested that hypoxic edema and blood-neural barrier damage caused by neuro-ischemia It is the main cause of nerve injury. The diagnosis of critically ill multi-neuropathy mainly depends on electrophysiological examination. Peripheral axon injury is the main electrophysiological change. The typical manifestation is fibrillation potential at 7 days after onset of resting myoelectric examination. The latency changes and positive-point waves. The neuropotential map usually shows that the proximal and distal nerve segment impulse conduction velocity is normal and the mixed muscle potential amplitude is decreased, but the typical changes of primary demyelination such as the nerve conduction velocity are significantly reduced. The extension of the latent latency, the scattering of the complex muscle activity potential, the conduction block and the increase of the F wave potential are rarely found in patients with critically ill multipathopathy.

6. Effects of drugs on respiratory muscle function

(1) corticosteroids: high-dose or long-term application of glucocorticoids can cause a variety of side effects, including myopathy, animal experiments confirmed that corticosteroids can significantly reduce the contractility of the diaphragm, the pathological basis of hormone-induced myopathy may be fast contraction Fiber (type I) protein synthesis is reduced, and catabolism is enhanced by this type of muscle fiber atrophy. At present, although the exact mechanism of corticosteroid-induced myopathy is not fully understood, the shrinkage of fast-shrinking fiber will inevitably lead to a decrease in muscle maximum contractility. When the work of breathing increases, the diaphragm is prone to fatigue. If the muscle relaxant is applied at the same time or the patient is accompanied by poor tissue perfusion, the respiratory muscle function may be further deteriorated. It has been reported that corticosteroid-induced acute muscle in the onset of severe asthma The incidence of the disease is as high as 10%.

(2) Neuromuscular blockers: The purpose of applying neuromuscular blockers (NBA) during mechanical ventilation is to help the smooth implementation of mechanical ventilation, improve man-machine coordination, reduce oxygen consumption, and avoid cranial in patients with intracranial hypertension. Fluctuations in internal pressure, etc., a survey in the United Kingdom in the late 1970s showed that 90% of ICU patients routinely applied muscle relaxants. In the past 20 years, due to the emergence of potent sedatives, ventilator performance improvement and pharmacological properties of NBA In-depth understanding, especially found that NBA can cause muscle relaxation delay and myopathy, the application of muscle relaxant has a decreasing trend, the direct toxicity of NBA on muscle is not very clear, but it can enhance existing muscles Abnormal function, increase the role of muscle toxic drugs or drug metabolites, so that the effect of muscle relaxation can be prolonged and can cause acute myopathy, and the application of certain drugs can prolong and enhance the role of NBA.

Respiratory muscle fatigue prevention

Precautionary principle

If respiratory muscle fatigue or functional failure plays an important role in the occurrence of respiratory failure, the cause of respiratory muscle dysfunction should be corrected and removed first. The general principles are:

1 Ensure adequate energy supply to the respiratory muscles, including supplemental nutrition, correct electrolyte abnormalities, especially phosphorus and magnesium abnormalities, correct hypoxemia and hypercapnia, and improve cardiac output.

2 specific treatment for respiratory muscle fatigue, including nutritional supplementation, respiratory muscle function exercise, respiratory muscle rest and so on.

1. Supplementary nutrition studies have shown that most patients with COPD have nutritional metabolic disorders, mainly in patients with high metabolic status, energy demand is greater than energy supply, and various factors can affect the patient's energy supply, such as loss of appetite and poor gastrointestinal nutrition. Role, hypoxemia during eating, increased CO2 production when eating high carbohydrates exceeds ventilation capacity, animal experiments and human studies have confirmed that malnutrition can cause type II muscle fiber atrophy, resulting in muscle weakness, when the patient's actual weight Below 71% of the average standard weight, the maximum oral inspiratory pressure, vital capacity and maximum voluntary ventilation are significantly lower than normal people. Supplemental nutrition can increase inspiratory pressure and body weight, and appropriate supplementation during the weaning process. Calories can enhance respiratory muscle function and improve the success rate of weaning. Of course, there is still some controversy about the effect of supplemental nutrition on muscle fatigue, resulting in different reasons and the degree of malnutrition, the way of nutritional supplement, time and other factors. In addition, in addition, whether supplemental nutrition can affect the prognosis of patients with COPD needs further confirmation. real.

2. Functional exercise Targeted exercise of respiratory muscle function can not only improve respiratory muscle function, but also increase overall exercise capacity. It is generally considered that respiratory exercise is only suitable for patients with moderate ventilatory function impairment and shortness of breath, for severe ventilation function. It is not advisable to apply respiratory exercise to the injured. Respiratory exercise should follow three basic principles: load, pertinence and reversibility. Exercise should be gradual, not eager to achieve, and should be exercised for a specific function for a long time under a certain intensity load. The goal is to increase the strength and endurance of the respiratory muscles and enhance the ability to resist fatigue. Excessive exercise may increase respiratory muscle fatigue and cause muscle damage.

There are three main methods of breathing muscle exercise:

(1) Resistance method: The patient breathes through a respirator with a small hole, and increases the respiratory muscle load when inhaling, and exhalation is not affected.

(2) Excessive breathing method: The patient performs autonomous rapid ventilation through a repetitive breathing device that can indicate the target ventilation level, and maintains the alveolar oxygen concentration and carbon dioxide concentration within physiological limits. The ventilation level should reach 70%-90 of the maximum voluntary ventilation. %, in patients with COPD should reach the upper limit of the above range.

(3) Domain value load method: preset the inspiratory pressure. When the inspiratory pressure of the patient reaches this value, the inhalation valve is opened to complete the inhalation. If the inspiratory pressure does not reach the preset pressure value, the inspiratory pressure cannot be breathed. Other methods include whole body exercise, abdominal breathing, deep and slow breathing, lip breathing, and external diaphragmatic pacing.

The exact effect of muscle function training needs to be further evaluated. Most studies suggest that reasonable exercise can increase respiratory muscle strength and endurance, improve patient's exercise capacity, reduce breathing difficulties, and improve quality of life. However, some studies suggest that muscles undergo muscle muscle exercise. The function has improved, but the total athletic ability has not increased.

3. Respiratory muscle rest and fatigue of the respiratory muscles can restore function after rest. At present, positive pressure ventilation is used instead of or partially to replace the respiratory muscles to complete ventilation, so that the fatigued respiratory muscles can be rested. The ventilation method can be used with non-invasive positive pressure of oral and nasal masks. Ventilation, unconsciousness, lack of cooperation, respiratory secretions, hemodynamic instability patients should take tracheal intubation to establish artificial airway ventilation, the current respiratory muscle dysfunction in patients with chronic respiratory failure advocate non-invasive Compressive ventilation has also achieved good results in patients with chronic respiratory diseases such as chronic neuromuscular disorders and thoracic deformities, but the effects in patients with COPD are quite different. The main question is whether non-invasive ventilation actually reduces the activity of the diaphragm. The diaphragmatic muscle has been fully rested, the length of ventilation time, the size of the auxiliary ventilation pressure, the severity of the patient's underlying disease and the medication can affect the judgment of the efficacy of non-invasive ventilation. Most of the viewpoints tend to apply the non-invasive ventilation correctly. By reducing respiratory muscle work and improving respiratory muscle function, many patients can avoid tracheal intubation. Non-invasive ventilation to improve the disease and other mechanisms such as: re-set the sensitivity of the respiratory center to carbon dioxide, improve blood gas to reduce the impact of hypoxia and CO2 retention on respiratory muscle function, excessive rest can lead to respiratory muscle atrophy, Caused by ventilator dependence, it is difficult to determine the ideal limit of complete rest and load of respiratory muscles. The general principle is that after 24 to 48 hours of controlled ventilation or high level of pressure support ventilation, the fatigued respiratory muscles should be fully rested. Reduce the intensity of ventilation support, gradually increase the patient's respiratory load, and actively prepare for the withdrawal.

Respiratory muscle fatigue complications Complications, diaphragmatic paralysis

Complicated with muscle fatigue.

Symptoms of respiratory muscle fatigue Common symptoms Fatigue, shortness of breath, shortness of breath, shortness of breath, ring finger, nail depression, emotional fatigue, sports fatigue

The breathing rate is increased, and the breathing is not synchronized (such as periodic abdominal pressure and chest pressure breathing alternately, disordered and non-parallel abdominal pressure breathing, abdominal bimodal breathing exercise) and chest and abdomen contradictory breathing.

Examination of respiratory muscle fatigue

1. Maximum inspiratory pressure (MIP) refers to the maximum inspiratory pressure generated by the maximum effort inhalation in the residual gas position (RV) or functional residual gas position (FRC), airway blockage, measured by MIP The main clinical significance is:

1 In the neuromuscular disease, the function of the inspiratory muscle is evaluated, which provides a reference for the diagnosis and severity of the disease. When the MIP is 30% of the normal predicted value, respiratory failure is prone to occur;

2 to evaluate the respiratory muscle function of patients with pulmonary disease (COPD), thoracic deformity and drug poisoning;

3 is used to predict the weaning. It is generally considered that the probability of successful weaning when MIP<-30cmH20 is large, but the false negative rate is high when MIP is used to predict the weaning. The main reason is that the patient can't cooperate well when measuring.

Maximum expiratory pressure (MEP) refers to the maximum oral expiratory pressure that can be generated by maximal effort after expiration of the airway (TLC). These are indicators that reflect the strength of all respiratory muscles. It fully represents the function of the diaphragm. For patients undergoing mechanical ventilation, the MIP and MEP can be measured by the pressure sensor at the proximal end of the endotracheal tube. The measurement is repeated several times, and the reproducible value is taken as the measured value when there is obvious airflow. When obstructed, the measurement of these indicators is affected, and the variation of each measurement is increased. In addition, the results are also affected by the subjective efforts of patients. There is no uniform standard for the normal value of MIP, and the reports of different laboratories vary greatly. Orientals and the West There must be a difference between races.

2. Trans-compression (Pdi) Pdi refers to the diaphragmatic muscle in the contraction of the diaphragm, the pressure difference on the ventral side, which represents the contraction ability of the diaphragm, and the maximum trans-compression (Pdimax) refers to the functional residual position (or residual position). In the airway obstruction state, Pdimax reflects the pressure generated by maximal contraction when the diaphragm is maximally inhaled. It is a reliable index for evaluating the muscle strength of the respiratory muscles. Pdi and Pdimax are reduced when the diaphragm is fatigued. When Pdi can not maintain the Pdimax level of 40%, it indicates that there is diaphragmatic fatigue. The method of measuring the trans-compression is complicated. It is necessary to measure the esophageal pressure and intragastric pressure through the esophageal balloon and the intragastric balloon respectively. The difference between the two is Pdi.

3. Diaphragm tension-time index (TTdi) This index is a good indicator of respiratory muscle endurance. For respiratory muscles, evaluating endurance is more important than strength. Muscle endurance depends on energy supply, muscle fiber composition and work size. The size of work depends on the strength and duration of muscle contraction. The strength of the diaphragm muscle varies greatly. To reduce individual differences, the ratio of the average value of Pdi produced by diaphragm contraction and Pdimax is used to reflect the contraction intensity. The ratio of time (Ti) to the total time of the respiratory cycle (Ttot) reflects the duration of diaphragmatic contraction. The product of the two is TTdi, which is expressed as: TTdi=Pdi/Pdimax×Ti/Ttot, in the case of inspiratory resistance load In the case of existence, when the TTdi value is <0.15, diaphragmatic fatigue is not easy to occur, and when the TTdi value is >0.15, the time of diaphragmatic fatigue will be significantly shortened. It should be noted that the measurement of TTdi is done under artificially set resistance. There may be a large gap with spontaneous breathing, so how to determine the domain value of respiratory muscle fatigue under various disease states needs to be further explored.

4. Muscle electromyography EMG can be used to detect the electrophysiological activities of the diaphragm, intercostal muscles and abdominal muscles, but it is difficult to carry out electromyography during the mechanical ventilation of critically ill patients, and the interference factors are many and can be repeated. Sexuality and accuracy of results are poor. The percutaneous puncture electrode that passes the fine needle through the skin to the diaphragm is more accurate and reliable than the transcutaneous electrode. The EMG is composed of different frequencies, and its spectrum is mainly between 20 and 250 Hz. The change of distribution is the early manifestation of the fatigue process. It is lower than the decrease of muscle strength. When the diaphragm muscle is fatigued, the low-frequency component (L) of the EMG spectrum increases, and the high-frequency component (H) decreases. When the H/L decreases by 20% from the baseline value, it means There is a significant change in the spectrum. The high-frequency components are caused by the accumulation of metabolic toxic substances in the muscles. The recovery period is short (several minutes), while the low-frequency components are caused by changes in muscle structure. It takes more than 24 hours to recover. Dynamic observation of EMG can detect respiratory muscles early. The existence of fatigue, clinically, during the evacuation of mechanical ventilation, such as the increase of low frequency components, suggesting that it takes at least 24 to 48 hours to restore the contractile function of the fatigued respiratory muscles.

5. nerve electrical stimulation nerve stimulation of the diaphragm contraction is mainly dominated by the phrenic nerve, using the body surface or acupuncture electrodes to stimulate the phrenic nerve to observe Pdi or EMG. Can reflect the diaphragm function, the advantage of this method is to objectively evaluate The contraction performance of the diaphragm and the mechanical characteristics of the chest wall are not affected by the degree of self-motivation or breathing. The disadvantage is that it stimulates local pain and the electrode is accurately positioned. Especially when the patient is irritated, the position change will affect the accuracy of the measurement, COPD and In obese patients, if there is hypertrophy of sternocleidomastoid muscle, it is difficult to accurately stimulate the phrenic nerve. Therefore, diaphragm stimulation is limited in the application of critically ill patients, mainly for the study of patients with stable disease. Recently, some people have used electromagnetic stimulation. The neurological method studies the function of the diaphragm and finds that the magnetic stimulation can effectively stimulate the diaphragm contraction compared with the method of directly stimulating the phrenic nerve. It can overcome the shortcomings of the direct stimulation method and use it for the study of diaphragmatic function in critically ill patients. Good results.

Diagnosis and diagnosis of respiratory muscle fatigue

diagnosis

1. According to the medical history, there is a history of basic respiratory diseases.

2. The clinical manifestations are that the respiratory rate is faster and the breathing is not synchronized.

3. The increase of creatine phosphokinase in the blood can be diagnosed according to 3 items.

Differential diagnosis

Prolongation of muscle relaxation is more common in patients with long-term or large-scale application of muscle relaxants or drugs that have an effect on neuromuscular function. The incidence in ICU is about 5%, which can prolong ICU hospitalization and NBA-induced acute myopathy. The rate of prolongation of muscle relaxation is lower than that of high-dose hormones and NBA in acute exacerbation of asthma. In a prospective clinical study, Leatherman performed 25 patients with asthma who received both Vecuronium and corticosteroids. Observations revealed that 19 patients had elevated creatine phosphokinase (CPK) and 19 had clinical signs of myopathy. The severity was related to the duration of mechanical ventilation. The main clinical manifestation of NBA-associated myopathy was after discontinuation of muscle relaxants. Long-term sustained muscle weakness, difficult to identify with multi-neuronopathy and hormone-induced myopathy caused by critical illness, some patients with acute myopathy may have elevated serum CPK, but some patients have no increase in CPK, and the severity of myopathy, blood collection The timing of the examination and other factors are related. Regular dynamic review of CPK is helpful in determining the occurrence of myopathy. Table 4 lists the various causes of muscle weakness. Features for clinician reference.

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