Respiratory muscle fatigue-What is the respiratory muscle fatigue?
Respiratory muscle fatigue or respiratory muscle dysfunction is very common in chronic lung disease and ICU hospitalized patients. For a long time, respiratory muscle fatigue or failure is not taken seriously. Timely detection and treatment of respiratory muscle fatigue can correct abnormal respiratory mechanics, and reduce the work of breathing, improve oxygenation, to shorten the duration of mechanical ventilation. Therefore, evaluation of respiratory muscle function in critically ill patients in recent years has become an important part of the intensive care.
Edit Summary- Overview of respiratory muscle fatigueBreathing exercise breathing exercise is a prerequisite to change thoracic volume depend on the activities of the respiratory muscles, causing lung contraction provide the driving force for the realization of pulmonary ventilation.Respiratory muscles of the human body is the belch muscle and intercostal muscles (including aid room, outside the muscle), there are the muscles of the abdomen and the neck accessory muscles of breathing only difficulty breathing when involved in assisted breathing.
Respiratory muscles and other muscles of the body, all belong to the skeletal muscle. Respiratory muscle are different from most skeletal muscle, it is the only life depends on skeletal muscle contraction regularly throughout the life course, and never-ending. Therefore, the respiratory muscles is an important part of the respiratory pump, is the completion of the power of the external respiratory function. In order to guarantee enough power breathing, respiratory muscle strength and endurance must maintain a certain strength. Due to illness and other reasons, the respiratory muscles to long-term overload, can not produce and maintain muscle strength, namely atony called respiratory muscle fatigue. Effective alveolar ventilation due to respiratory muscle weakness, reduce, and eventually can lead to respiratory failure.
Generally believed that chronic obstructive pulmonary disease patients (including chronic bronchitis, emphysema, asthma), the air over the resistance continues to increase, and the long period of hypoxemia, carbon dioxide retention and systemic malnutrition state, prone to respiratory muscle fatigue. Followed by neuromuscular diseases, such as bilateral diaphragm paralysis, myasthenia gravis, Guillain-Barre syndrome, some poisoning, and cardiogenic shock, septic shock, toxic shock can cause respiratory muscle weakness, fatigue, Finally, leading to respiratory failure.
Respiratory muscle fatigue - academic explainRespiratory muscle fatigue treatment instrument 1 definition of respiratory muscle fatigue according to the definition set by the 1988 U.S. Heart, Lung, and Blood Institute (NHLBI), respiratory muscle fatigue refers to the force of contraction of the respiratory muscles bear the load and (or) contraction speed reduced, and this reduction can rest and recover.2, the so-called respiratory muscle fatigue muscle activity under load and cause it to produce a reduced ability of the strength and speed of the decline in this ability can rest and recovery. Discuss endometriosis endometrial growth function The parts of the tissue outside the uterine cavity covering mucosa.
3, respiratory muscle fatigue is caused by a variety of respiratory muscle contraction and relaxation activities can not produce the need to maintain a certain amount of alveolar ventilation pleural pressure, the muscle itself can be manifested as muscle strength, and (or) systolic and diastolic velocity decreased, and The decline in this ability after a rest can be restored.
, Respiratory muscle fatigue respiratory muscle contraction can not produce the gas required to maintain adequate alveolar pressure, thereby affecting gas exchange, respiratory muscle fatigue is the development of a variety of clinical conditions hypercapnia respiratory failure final common pathway.
, Respiratory muscle fatigue is not against the burden of respiratory muscle strength and endurance respiratory muscle contraction that can not produce the driving pressure required to maintain adequate alveolar ventilation which is the main reason ventilator dependent. The factors leading to respiratory muscle fatigue: the endogenous end expiratory positive pressure (PEEP).
Respiratory muscle fatigue, respiratory muscle fatigue is the respiratory muscle activity under load and cause it to generate force and (or) the speed of a reduced ability to decline in this ability can rest and recovery. Respiratory muscle fatigue (pump failure) is breathing failure an important part of the disease process.
7, the so-called respiratory muscle fatigue is the case of the continued contraction of the respiratory muscles, can no longer maintain the required or intended muscle occlusion side: right nine cases, 17 cases left. The occlusive reasons: cerebral thrombosis nine cases of cerebral infarction 17 atrial fibrillation patients (9 cases).
Respiratory muscle fatigue - etiologyThe majority of patients with respiratory muscle fatigue in patients with respiratory muscle fatigue is caused by the disease itself, has been found to sepsis (sepsis), multiple organ failure, mechanical ventilation hypercapnia (acidosis), and a variety of drugs can cause abnormal neuromuscular function and become the important disease pathophysiology process.In short, the respiratory muscle fatigue and weakness, health search is very common in the critically ill COPD and other chronic diseases in addition to the effects of the disease itself, a variety of drugs, such as glucocorticoids muscle relaxants aminoglycoside antibiotics can induce or aggravate respiratory muscle fatigue, breathing specificity, and accuracy of the machine improper application can also be caused by diaphragmatic dysfunction various checks respiratory muscle fatigue are poor and difficult routine clinical applications attention to clinical examination to detect the presence of respiratory muscle fatigue.
Respiratory muscle fatigue - pathogenesisTreatment of respiratory muscle fatigue instrument respiratory muscles, including the diaphragm intercostal muscles, the abdominal muscles can be divided into inspiratory muscles (diaphragm, intercostal muscle, sternocleidomastoid sternocleidomastoid and scalene according to the functional classification of respiratory muscle) and expiratory muscle (intercostal muscle abdominal muscle) according to the nature of the muscle fibers can be divided into red muscle fibers (also known as slow contraction fatigue resistant fibers or fiber type Ⅰ) and white muscle fibers (also known as fast contraction fibers or II class fiber ). The Class Ⅱ fibers can be divided into resistance to fatigue fast contraction fibers (Ⅱ A fibers) and fast contraction fast fatigue fiber (II)The main function of the respiratory muscles is complete breathing exercise followed by participation in the cough expectoration vomiting. 2/3 of the diaphragm about the most important role shoulder throughout the respiratory function of 3% to 90% of the tidal volume of diaphragmatic contraction. When the auxiliary respiratory muscles involved in the contraction increased minute ventilation or presence of diaphragmatic fatigue. In quiet breathing expiratory muscle does not participate in the contraction in respiratory function increases intercostal muscle and abdominal expiratory muscle contraction, squeezing the diaphragm to the chest cavity, the diaphragm muscle fiber is the best bit early long tension.
1.COPD patients with skeletal muscle dysfunction (including respiratory muscles) in patients with COPD decreased exercise tolerance has a direct relationship. COPD patients with skeletal muscle structure changes showed a decline in muscle weight, changes in the structure of the muscle fibers (I class fiber reducing the proportion of the increase in the proportion of class II fibers, fiber atrophy of class Ⅰ and Ⅱ A I class and II class fiber diameter decreases) reduce the number of capillaries in skeletal muscle per unit area of the tree (oxidase activity decreased) function to change the performance of muscle strength reduced the partial oxygen uptake and oxygen transport significantly limited maximal exercise decreased endurance and metabolic changes. The main reason for the above structural and functional changes the: ① long-term hypoxemia, hypercapnia infection and chronic malnutrition; ② accompanied by electrolyte disorders (hypokalemia, hypophosphatemia, low magnesium) heart failure muscle disuse atrophy; ③ glucocorticoid-induced acute and chronic myopathy. Due to lung hyperinflation in COPD patients with severe airway obstruction, so that the mechanical characteristics of the respiratory system were to change significantly, significantly negative contraction of the diaphragm in the beginning of a long position shrink the efficiency significantly reduce health search combined with the various factors can easily lead to diaphragmatic fatigue and failure.
Characteristics of sepsis in patients with sepsis (Sepsis) system blood flow is normal or increased tissue oxygen uptake capacity decreased local perfusion reduction and tissue hypoxemia. Respiratory muscle, sepsis and shock the total perfusion increased Zhui but barriers to local microvascular perfusion and increased work of breathing can still cause respiratory muscle hypoxia and respiratory muscle dysfunction.
Mechanical ventilation on respiratory muscle mechanical ventilation for respiratory muscle function has two sides alternative or auxiliary respiratory muscles acting on the one hand fatigue of respiratory muscles to rest on the other hand lead to respiratory muscle disuse atrophy, respiratory muscle strength decreased and endurance produces ventilator dependent. Skeletal muscle atrophy major changes include:
(1) muscle weight was significantly reduced.
(2) the decline in protein synthesis.
(3) muscle fiber mesh diameter reduction.
(4) reduces the number of anti-fatigue fiber slow contraction.
Respiratory muscle fatigue (5) decreased mitochondrial glucose oxidation and decomposition. Although the respiratory muscles have unique characteristics different from ordinary skeletal muscle network, but can be found in the long-term controlling mechanical ventilation reduce the activity of the diaphragmatic EMG, transdiaphragmatic pressure decreased respiratory muscle endurance, reduce. Brochard et al healthy baboons for 11 days the controlling ventilation discovered a 25% reduction in Pdi Stamina reduced by 36% mechanical ventilation health search whether another major determinants of respiratory muscle atrophy muscle fiber length muscle fibers length of long-term fixed Zhui under its normal length, it is very easy to produce fatigue can avoid the occurrence of muscle atrophy; rather more than the length of its base.4, over a period of time in mechanically ventilated patients, respiratory muscle function in the process of weaning, respiratory muscle function is to determine whether weaning one of the key factors. Most difficult weaning patients in the clinical respiratory muscle fatigue Cohen et al found 12 cases of patients with difficult weaning study 7 patients EMG spectrum changed and prompts diaphragmatic fatigue, six cases of the six patients had abnormal abdominal breathing breathing Frequency faster, some patients with frequent cause of failure and respiratory muscle fatigue diaphragmatic fatigue weaning accelerate faster and PaCO2 increased suggesting that these patients breathing frequency and PaCO2 increased EMG spectral changes in breathing frequency.
5 the polyneuropathy sepsis in critically ill patients, multiple organ failure (MOF) can occur in patients with polyneuropathy main sensory - motor nerve damage, called critical illness polyneuropathy in ICU about more than 70% of patients with varying degrees of neuropathy. Bolton electrophysiological studies of 43 patients with sepsis and MOF patients, 30 patients have abnormal axonal degeneration associated with sensory and motor potential, 15 patients with clinical manifestations weakness weaning failure, critical illness multiple neural reflex diminished or disappeared The main clinical manifestations of lesions extremities weakness with atrophy, weakening or disappearance of sensory dysfunction deep reflection cranial nerve function is normal Zhui critical illness polyneuropathy self-limiting, and can be fully restored after a period of time, but the EMG there is a surviving abnormal Zhui now think this secondary neuromuscular disease is caused by the difficulty of weaning and prolong the ICU stay an important factor in 62% of patients with weaning difficulties relating.
Critical illness polyneuropathy mechanism is not yet clear, nutritional disorders poisoning, metabolic abnormalities, and vascular factors might be involved in the occurrence of neuropathy has also been suggested that the hypoxic edema caused by ischemia in the nerve and blood - nerve barrier damage nerve damage the main reason for the diagnosis of critical illness polyneuropathy mainly by electrophysiological studies, peripheral nerve axon injury is the main electrophysiological changes typical performance for seven days after the onset of resting EMG fibrillation potential incubation period of change and positive sharp wave neural potential map manifests itself in the segment of the proximal and distal nerve impulse conduction velocity normal reduce mixed muscle action potential amplitude. Typical change of primary demyelination of nerve conduction velocity decreased significantly extend the distal latency of compound muscle action potential scattering, block and F-wave potential of increased little in critical illness polyneuropathy patients appear.
6. Drugs on respiratory muscle function
Respiratory muscle fatigue (1) corticosteroids: high-dose or long-term use of glucocorticoids can cause a variety of side effects, including myopathy. Animal experiments confirmed that health search corticosteroids can significantly reduce the force of contraction of the diaphragm hormone induced myopathy pathological basis may reduce the fast contraction fibers (I type) protein synthesis, increased catabolism lead to the type of muscle fiber atrophy. Currently, corticosteroids induced myopathy the exact mechanism is not yet clear, but fast contraction fibers atrophy inevitably lead to muscle contraction capacity decreased when accompanied by application of muscle relaxants or patients are prone to increased work of breathing, diaphragmatic fatigue tissue blood perfusion can be further deterioration of the function of the respiratory muscles. Studies have reported that the incidence of corticosteroid-induced acute severe asthma myopathy up to 10%(2) neuromuscular blocker: application of mechanical ventilation, neuromuscular blocking agents (NBA) the health search of purpose is to help the smooth implementation of mechanical ventilation, improve the coordination of human - machine to reduce oxygen consumption in patients with intracranial hypertension avoid intracranial pressure fluctuations in the late 1970s, a British survey showed that 90% health search ICU patients routine application of muscle relaxants. For nearly 20 years, due to the emergence of powerful sedatives, the ventilator performance improvement and in-depth understanding of the pharmacological properties of NBA, especially NBA can cause muscle relaxation delay and myopathy there is a decreasing trend in the application of muscle relaxants NBA direct toxic effect on the muscle is not yet clear but it can enhance muscle function already exists an abnormal increase in the role of muscle toxicity of drugs or drug metabolites, the muscle relaxant effect continued to extend and can cause acute myopathy. At the same time, the application of certain drugs to prolong and enhance the role of the NBA.
Respiratory muscle fatigue - symptomsClinical manifestations: respiratory rate, breathing out of sync (such as periodic abdominal pressure and chest pressure breathing alternately, confusion, and not parallel abdominal pressure breathing abdominal bimodal breathing exercise) and paradoxical abdominal respiration.
Complications: concurrent diaphragmatic fatigue.
Respiratory muscle fatigue - CheckLaboratory tests
Respiratory muscle fatigue drug, maximum inspiratory pressure (MIP) with the greatest effort in the residual gas bit (RV) or functional residual air-bit (FRC) http://www.huoguan.com blocked airway suction can maximum inspiratory mouth pressure. The MIP measured clinical significance is: inspiratory muscle function in neuromuscular disease evaluation and diagnosis of the disease and the severity of the judgment parameters when MIP <normal expected value of 30%, and prone to respiratory failure; (2) evaluation of pulmonary disease (COPD) patients with respiratory muscle function in the thoracic deformity and drug intoxication; (3) used to predict weaning is generally believed that the MIP <-30cmH20 the likelihood of successful weaning. But with MIP predict weaning false negative rate is very high, mainly due to patients is not well with the measurements.Maximal expiratory pressure (MEP) in total lung capacity (TLC) airway blocked with maximum efforts to breath can generate maximum oral expiratory pressure they reflect all indicators of respiratory muscle strength is not entirely representative of the diaphragm function. Near the mouth end of the endotracheal tube with a pressure sensor value as the measurement value determination of MIP and MEP measurements repeated several times, take good reproducibility of mechanically ventilated patients when When obvious Zhui the airflow obstruction, the measurement of these indicators be affected, each measurement variability increases Moreover, the results also influenced by the patient's subjective efforts the normal MIP is no unified standard laboratory reports a very different health search, and certainly there are differences between Asians and Westerners kinds.
Transdiaphragmatic pressure (Pdi) Pdi is the diaphragmatic contraction of the diaphragm chest, ventral pressure difference on behalf of the diaphragmatic contractility largest transdiaphragmatic pressure (Pdimax) of means in functional residual air-bit (or residual gas bits), airway blocking state the utmost to inhale the Zhui Pdi max Pdimax, reflects pressure when the diaphragm for maximum contraction is not a reliable indicator of diaphragmatic fatigue evaluation of respiratory muscle strength Zhui Pdi the Pdimax lower when Pdi maintained at 40% level of http://www.huoguan.com of Pdimax suggesting diaphragmatic fatigue. Determination of transdiaphragmatic pressure more complex subject esophageal balloon and intragastric balloon pressure of the esophagus and gastric pressure were measured the inspiratory phase difference between the two shall Pdi
3, the diaphragm tension - time index (TTdi) of the indicators reflect good indicator of respiratory muscle endurance in terms of evaluation of respiratory muscle endurance is more important than strength muscle endurance depends on the energy supplied to the muscle fiber composition and the size of the work is done. Acting the size depends on the power of muscle contraction and sustained Zhui time. Diaphragmatic strength of individual differences, in order to reduce individual differences, diaphragmatic contraction the Pdi average of Pdimax ratio is used to reflect the strength of contraction, the Zhui the ratio of inspiratory time (Ti) and total respiratory cycle time (Ttot) reflect the product of the duration of both diaphragmatic contractility is TTdi. Formula: TTdi = Pdi / Pdimax, x Ti / Ttot. When TTdi value <0.15 in the case of the presence of inspiratory resistance load prone fatigue, while when TTdi value> 0.15 diaphragmatic fatigue time will be significantly shortened. It should be noted that the Determination of TTdi is completed in the case of artificial resistance, there may be a wide gap between how to determine respiratory muscle fatigue in various disease states, domain values need to be further explored with spontaneous breathing.
Other laboratory examinations
Respiratory muscle fatigue drugs. Diaphragmatic EMG EMG can be used for the detection of diaphragmatic intercostal muscle and physiological activity of the abdominal muscles during mechanical ventilation in critically ill patients is difficult to conventional for electromyography physiological examination carried out, and check interfering factors. repeatability and accuracy of the results are poor thin needle through the skin to the diaphragmatic percutaneous electrode than percutaneous electrode obtained data are accurate and reliable. EMG different Zhui frequency spectrum mainly between 20 ~ 250Hz, the spectral distribution of the change Zhui increase fatigue early in the process performance of the first diaphragm muscle Zhui reduce fatigue EMG spectrum of low-frequency component (L), high-frequency reduce health search component (H), H / L than the decline in the underlying value of 20% means that the spectrum significantly change the high frequency components from the accumulation of the metabolic toxic substances in the muscle caused a short recovery period (a few minutes) and the low-frequency components by muscle structural changes caused by the recovery takes more than 24h dynamic observation of EMG can be early detection of the presence of respiratory muscle fatigue. Clinically, such as the low-frequency components in the process of withdrawal of mechanical ventilation increase prompted at least 24 ~ 48h to the fatigue of respiratory muscle contractile function was restored.Phrenic nerve electrical stimulation of phrenic nerve stimulation of the diaphragmatic contraction is mainly dominated by the phrenic nerve with Pdi observed after stimulation of the phrenic nerve of the body surface or needle electrodes or the EMG diaphragmatic function may reflect the advantages of the method is to objectively evaluate diaphragmatic Zhui contractile properties and mechanical characteristics of the chest wall without self-effort or breathing affect shortcomings is to stimulate local pain, electrodes accurate positioning difficult, especially in patients with irritability postural change will affect the accuracy of the measurement. COPD and obese patients if there is the sternocleidomastoid muscle hypertrophy is difficult to accurately stimulate the phrenic nerve diaphragmatic stimulation been the restrictions mainly used for patients with stable disease research in the application of critically ill patients. Recently, someone using electromagnetic stimulation of the phrenic nerve to study the function of the diaphragm, found that magnetic stimulation and direct stimulation of the phrenic nerve, can be effective in stimulating the diaphragm contraction to overcome the shortcomings of direct stimulation of, for critically ill patients the diaphragmatic function studies have achieved good results.
Respiratory muscle fatigue - Differential Diagnosis1, according to a history of the respiratory underlying disease history.
2, the clinical manifestations of respiratory rate, respiratory synchronization.
Blood creatine increased phospholipid kinase, can be diagnosed under 3.
Extend the treatment of respiratory muscle fatigue instrument muscle relaxant effect more common in long-term application of a large number of patients with muscle relaxants or application of drugs affecting neuromuscular function at the same time, about 5% incidence in the ICU, extend the length of ICU stay. NBA induced acute myopathy incidence than the muscle relaxant effect extended the most low incidence seen in acute asthma exacerbation and large doses of hormones and NBA. In a prospective clinical study, Leatherman 25 cases accepted of Vecuronium and the cortex hormone treatment of asthma patients to observe found 19 cases of patients with increased creatine phosphokinase (CPK) 19 patients had clinical signs of myopathy, its severity related with the duration of mechanical ventilation. The major clinical manifestations of NBA-related myopathy the long sustained muscle weakness, muscle relaxants is disabled critical illness induced neuropathy and hormone-induced myopathy is difficult to identify. Some acute myopathy patients serum CPK increased, but some patients did not CPK increased with the severity of the myopathy, blood collection to check the timing of periodically dynamic review CPK helpful to determine the incidence of myopathy various etiologies The muscle weakness characteristics for clinicians Reference.Respiratory muscle fatigue - treatment and preventionDrug treatment of respiratory muscle fatigue is still very controversial experiments show that aminophylline can increase the force of contraction of the diaphragm muscle and endurance, but the accuracy of the method used to evaluate diaphragmatic function experiments concluded poor reliability. Experiments showed that the digoxin, β2 agonists, caffeine can increase diaphragmatic strength, but its exact effect needs to be further confirmed. In patients with COPD, recently been used anabolic hormones (growth hormone, testosterone, etc.) to increase muscle skeletal muscle strength to improve the quality of life of its exact effect and the price / benefit ratio needs further evaluation.
Prognosis: The prognosis of this disease and the incidence incentives disease duration, and age and physical condition.
Respiratory muscle fatigue prevention: If respiratory muscle fatigue or failure cupping network plays an important role in the incidence of respiratory failure and should be the first to correct and remove incentives that cause respiratory muscle dysfunction general principle: ensure adequate respiratory muscle energy supply , including nutritional supplements to correct electrolyte abnormalities, especially phosphorus and magnesium abnormalities, to correct hypoxemia and hypercapnia improve cardiac output. ② specific treatment for respiratory muscle fatigue, including nutritional supplements respiratory muscle function exercise such as respiratory muscle rest.1. Nutritional supplement research shows that the majority of COPD patients with nutritional and metabolic disorders mainly for patients at high metabolic state, when energy demand is greater than the energy supply of a variety of factors can affect the energy supply of patients with adverse effects such as loss of appetite and gastrointestinal nutrients eating hypoxemia consumption of high-carbohydrate, increased CO2 production beyond the ventilation capacity. Animal experiments and human studies have confirmed that malnutrition in type II muscle fiber atrophy can cause muscle weakness, vital capacity and maximum voluntary ventilation volume maximum oral suction pressure when the patient's actual body weight less than 71% of the average standard weight significantly lower than normal, nutritional supplements can increase the suction pressure and weight. Give enough heat to enhance the function of the respiratory muscles, improve the success rate of weaning course there are still some dispute the efficacy of nutritional supplementation on muscle fatigue, resulting in conclusions different reasons and the extent of malnutrition in patients with appropriate nutritional supplements in the weaning process, nutritional supplement, and time factors In addition, nutritional supplements ability to impact the prognosis of patients with COPD also need to be further confirmed.
Functional exercise on respiratory muscle function targeted exercise will not only improve the function of the respiratory muscles, can increase overall athletic ability that breathing exercises usually only applies to patients with moderate ventilatory dysfunction accompanied by shortness of breath, severe ventilatory dysfunction by should not be applied breathing exercise. Breathing exercises should follow three basic principles: load, targeted and reversible exercise should be gradual, and should not be anxious in a certain intensity of load for a particular long-term exercise main objective to increase respiratory muscle strength and endurance, and enhance the resistance to fatigue. Excessive exercise may aggravate respiratory muscle fatigue and lead to muscle damage.
Respiratory muscle training methods are mainly three kinds:
(1) resistance methods: Patients with small holes through the respirator to breathe, inhale increased load on the respiratory muscles, breath unaffected
Repeat breathing apparatus (2) over-breathing: patients through an indicative target ventilation level, autonomous rapid ventilation to maintain alveolar concentration of oxygen and carbon dioxide concentration within the physiological limits. The ventilation level should reach 70% to 90% of maximum voluntary ventilation in patients with COPD should reach the upper limit of the above range.
(3) the domain value load method: preset suction pressure, suction valve open when the patient's inspiratory pressure reaches the value of this domain, complete the suction if the suction pressure of cupping network is less than a preset pressure value can not breathe . Other methods include systemic exercise, abdominal breathing deep slow breathing, reduce lip breathing, external diaphragm pacing.
The exact effect of muscle function exercise also needs further evaluation cupping network, most studies suggest that a reasonable exercise can increase the strength and endurance of the respiratory muscles, improve exercise capacity of patients to relieve breathing difficulties, and improve the quality of life. But studies suggest that muscles after respiratory muscle function improved, but did not enhance the overall athletic ability.
Respiratory muscle fatigue after the rest of the rest of respiratory muscle fatigue of respiratory muscles can restore function. Commonly used positive pressure ventilation or partly replace the respiratory muscles to complete the ventilation of the fatigue of respiratory muscles rest. Ventilation can be selected through the nose and mouth mask non-invasive positive pressure ventilation on unconsciousness, the multiple hemodynamic instability due to the cooperation respiratory secretions should be taken in patients with endotracheal intubation establishment of artificial airway breathing in patients with chronic respiratory failure muscle dysfunction multi advocate the use of noninvasive positive pressure ventilation in patients with chronic respiratory failure in chronic neuromuscular disorders thoracic deformity has also made a good effect, but the effect of differences in COPD patients, the main problem is the non-invasive ventilation is really reduced the activities of the diaphragm so that the diaphragm really get adequate rest ventilation length of time, the size of the auxiliary ventilation pressure, the severity of the patient's underlying disease and drug use can affect the majority point of view of non-invasive ventilation efficacy judgments tend if correctly applied Noninvasive ventilation by reducing respiratory muscles acting good respiratory muscle function, could allow many patients to avoid endotracheal intubation. Of course, non-invasive ventilation to improve the condition there are other mechanisms, such as: re-tune to set the sensitivity of the respiratory center to carbon dioxide, hypoxia and CO2 retention respiratory muscle function by improving blood gas to reduce excessive rest cause respiratory muscle disuse atrophy caused respiratory machine dependent. Is difficult to determine the clinical respiratory muscle rest and be the ideal limit of the load, the general principles to get enough rest by 24 ~ 48h control ventilation or a high level of pressure support ventilation, respiratory muscle fatigue, reduce the intensity of ventilatory support in a timely manner gradually increase the load of the patient's breathing, and actively prepare for weaning.
