Respiratory muscle strength in hyperthyroidism before and after treatment.

We undertook this study to investigate respiratory muscle strength in relation to thyroid function in 20 thyrotoxic patients and in a group of 20 normal subjects matched for age and sex. Global respiratory muscle strength was assessed by measuring mouth pressure during maximal static inspiratory (PImax) and expiratory (PEmax) efforts. We also measured VC, FVC, and FEV1 as well as thyroid-related hormones (T3, T4, TSH). Measurements were made once in normal subjects and twice in thyrotoxic patients, before and 3 months after medical treatment. Our results showed that both maximal pressures were significantly reduced (p less than 0.0001) before treatment in thyrotoxic patients in relation to the mean values of the normal subjects (p less than 0.0001), and they increased significantly (p less than 0.0003) after treatment. Lung volumes were significantly reduced (p less than 0.0001) before and increased significantly (p less than 0.008) after treatment. The ratio FEV1/FVC did not change. A statistically significant linear relationship was found when PImax of patients with thyrotoxicosis before treatment and of normal subjects were plotted against thyroid hormones (T3, T4) (r = -0.746 and r = -0.745, respectively, p less than 0.001). Similarly, a statistically significant linear relationship was found between PEmax and T3 and T4 (r = -0.837 and r = -0.838, respectively, p less than 0.001). No relationship was found between maximal pressures and TSH. Finally, a significant linear relationship was found between PImax and PEmax (r = 0.872, p less than 0.001). Our results confirm that in thyrotoxicosis respiratory muscle weakness occurs that affects both inspiratory and expiratory muscles.(ABSTRACT TRUNCATED AT 250 WORDS)     

Respiratory muscle strength in congestive heart failure

In experimental animals, conditions which drastically decrease cardiac output may reduce the strength and endurance of respiratory muscles leading to hypercapnic respiratory failure. Because patients with chronic CHF have reduced cardiac output and vital capacity (FVC), we measured PImax and PEmax and maximal handgrip force in 16 patients with CHF and 18 AMNs. The patients with CHF had a mean left ventricular ejection fraction of 26 +/- 7 percent. Maximal respiratory pressures were significantly reduced; group mean values (+/- SD) for PImax at FRC were 41.4 +/- 5.6 cm H2O (CHF) and 102.1 +/- 27.4 cm H2O (AMN) (p less than 0.001), with PImax values in five patients with CHF as low as 20 to 30 cm H2O. In most patients, PEmax was comparably reduced. Handgrip force was less dramatically reduced, suggesting selective respiratory muscle weakness. Possible explanations include reduction in respiratory muscle blood flow or generalized muscular atrophy and weakness related to cardiac cachexia.     

Respiratory muscle strength, lung function, and dyspnea in patients with sarcoidosis.

BACKGROUND: Sarcoidosis is a systemic granulomatous disorder that is estimated to involve the skeletal muscles in up to 50% of patients. There is little information on the relationship among respiratory muscle strength, lung volumes, and the degree of dyspnea in patients with sarcoidosis. Design and patients: Lung function and maximal respiratory muscle force generation were measured in 36 patients with sarcoidosis (24 patients with pulmonary parenchymal infiltration) and 25 control subjects free of cardiorespiratory disease. Dyspnea in the sarcoidosis patients was quantitated by a score based on an activity tolerance assessment scale (ranging from rest to climbing hills or stairs). SETTING: Outpatient clinics of two teaching hospitals. RESULTS: Mean FVC, maximal voluntary ventilation, total lung capacity (TLC), functional residual capacity, residual volume (RV), and diffusing capacity of the lung for carbon monoxide (DLCO) were all at least 16% less than corresponding control values (in all cases, p < 0.001), while maximal inspiratory mouth pressure (PImax) and maximal expiratory mouth pressure (PEmax) were 37% and 39% less, respectively, than control values (both at p < 0.0001). PImax and PEmax declined with increasing dyspnea in a more graded, steady manner than did spirometric and DLCO values. For all measurements, however, the lowest mean values were found in patients with the most severe level of dyspnea. Strong inverse relationships were observed between PEmax and PImax with dyspnea level (p < 0.0001 and p < 0.01, respectively). Both PImax and PEmax correlated best with absolute values of FVC, while only PEmax correlated with RV (absolute and percent predicted) and percent predicted values of TLC. CONCLUSIONS: Maximal respiratory pressures correlate more closely with dyspnea level than lung volumes and DLCO. Since dyspnea is the most common presentation in early to moderately advanced sarcoidosis, respiratory pressures may be a more reliable index of functional work capacity and reflection of activities of daily living than standard tests of lung function.     

Respiratory muscle testing.

Respiratory muscles are a vital component of the respiratory system. Compromise in the function of respiratory muscles is assessed with a careful history, determination of the breathing frequency, and observation of the pattern of thoracoabdominal movements in the upright and supine positions. The most important diagnostic tools include measurement of lung volumes, FVC, oximetry, Pi(max) and Pe(max), and SNIP. Measurement of Pes and Pga pressures, Tw Pmo, phrenic nerve stimulation, magnetic stimulation, and EMG add new dimensions to the study of these muscles. These tools are helpful in understanding patients with acute and chronic disease that affects the respiratory muscles.     

Respiratory muscle strength and control of ventilation in patients with neuromuscular disease

To assess the relationship between respiratory mechanics and muscle strength and control of ventilation in patients with neuromuscular disease (NMD), we compared PImax and PEmax at RV, FRC and TLC, total respiratory elastance (Ers) with VT, TI, TT, VE, VT/TI, TI/TT, P.01, and P.01/(VT/TI) effective impedance in 21 patients with NMD and 21 healthy control (C) subjects, in seated position breathing room air. Ers in NMD patients was 79 percent higher than in the C subjects. While TI, TT, and VT in NMD were approximately half the corresponding C values, P.01 was 66 percent greater than in the C subjects (both p less than 0.001). NMD PImax and PEmax ranged from 37 to 52 percent of corresponding C values, respectively. Despite significant respiratory muscle weakness, only 7 of 16 patients demonstrated a PaCo2 greater than 45 mm Hg. Ventilatory output in NMD was modulated by respiratory mechanics as indicated by the increased P.01. In spite of muscle weakness, central drive in patients with NMD is not decreased, and in fact, is often increased. VE is not an accurate measure of central drive because of abnormal intrinsic respiratory mechanics and the effects of conscious responses or reflexes.     

Respiratory muscle involvement in multiple sclerosis.

Respiratory complications are common in the terminal stages of multiple sclerosis and contribute to mortality in these patients. When respiratory motor pathways are involved, respiratory muscle weakness frequently occurs. Although it is well established that weakness of the respiratory muscles produces a restrictive ventilatory defect, the degree of muscle weakness and pulmonary function are poorly related. Respiratory muscle weakness was observed in patients with normal or near normal pulmonary function. Expiratory muscle weakness is more prominent than inspiratory muscle weakness and may impair performance of coughing. Subsequently, in addition to bulbar dysfunction, respiratory muscle weakness may contribute to ineffective coughing, pneumonia, and sometimes even acute ventilatory failure may ensue. Respiratory muscle weakness may also occur early in the course of the disease. Recent studies suggest that the respiratory muscles can be trained for both strength and endurance in multiple sclerosis patients. Whether respiratory muscle training delays the development of respiratory dysfunction and subsequently improves exercise capacity and cough efficacy, prevents pulmonary complications or prolongs survival in the long-term remains to be determined.     

Respiratory muscle strength for discriminating frailty in community-dwelling elderly: a cross-sectional study

ObjectivesTo compare obtained and predicted inspiratory and expiratory muscle strength between frail, pre-frail, and non-frail older people; to examine the association between inspiratory and expiratory muscle strength and frailty in older people; and to determine cut-off points for inspiratory and expiratory muscle strength for discriminating frailty in older people.MethodsA cross-sectional study was conducted with 379 community-dwelling older adults. Frailty was assessed using Fried’s phenotype, while inspiratory and expiratory muscle strength were measured with maximum inspiratory and maximum expiratory pressures. Inferential analyses were performed using paired Student t-tests, one-way analysis of variance (ANOVA) tests, and a multinomial logistic regression model. ROC curves were constructed to establish cut-off points of maximum inspiratory and expiratory pressures for discriminating frailty and pre-frailty.ResultsFrail and pre-frail participants presented significantly lower mean inspiratory and expiratory pressures compared to non-frail participants; values were significantly lower than predicted. Inspiratory and expiratory muscle strength were inversely associated with frailty and pre-frailty. Cut-off points ≥-50cmH₂O and ≤60cmH₂O for maximum inspiratory and expiratory pressures, respectively, were established as optimal discriminators of frailty. The cut-off point ≤65cmH₂O for maximum expiratory pressure was established as a discriminant for the presence of pre-frailty.ConclusionsInspiratory and expiratory muscle strength were lower in frail than in pre-frail older adults, and lower in pre-frail than in non-frail peers. Frailty and pre-frailty were inversely associated with inspiratory and expiratory muscle strength. Cut-off points for inspiratory and expiratory muscle strength may be useful in clinical practice for discriminating frailty and pre-frailty in older adults.     

心力衰竭患者心脏康复应关注呼吸肌肌力

慢性心力衰竭(CHF)是各种心脏病的终末阶段,心脏康复治疗可以使CHF患者的症状减轻、生活质量及预后改善。近年来国外一些研究显示,CHF患者易合并存在吸气肌无力(IMW),可导致患者的运动耐量及生活质量的进一步下降,出现预后恶化。本文旨在总结国内外关于CHF患者合并IMW的相关研究报道,并阐明针对此类患者行吸气肌训练的益处。     

Reversible respiratory muscle weakness in hypothyroidism

Physiological studies performed 1 week after initiation of thyroid replacement showed persistence of significant respiratory muscle weakness in a patient presenting with hypothyroidism and hypercapnia. Repeat studies 12 months later demonstrated return of respiratory muscle strength to normal. Earlier reports on respiratory failure in hypothyroidism had postulated a critical role for respiratory muscle weakness in the genesis of hypercapnia. Since hypercapnia was rapidly reversed despite the persistence of severe respiratory muscle weakness, this explanation may not be always correct. It appears than in our patient thyroid replacement had its primary effect on the respiratory control system.     

Respiratory muscle strength but not BASFI score relates to diminished chest expansion in ankylosing spondylitis

Pulmonary function is altered in ankylosing spondylitis (AS) owing mainly to the restriction of chest wall involvement (limited chest expansion). The objective of this study was to investigate the relationship between chest expansion, respiratory muscle strength (MIP, MEP) maximum voluntary ventilation (MVV), and BASFI score in patients with AS. Twenty-three male patients with definite AS and 21 age-matched healthy male controls were recruited for the study. Patients with AS were assessed for functional status by BASFI. Measurement of chest expansion and lumbar spinal flexion (modified Schober) method was performed in all subjects. Pulmonary function tests were performed by spirometry. Respiratory muscle strength was evaluated by a mouth-pressure meter (MPM). Body mass index (kg/m²) was recorded in all individuals. Chest expansion and modified Schober measurement were significantly lower in AS patients (p<0.05). Pulmonary function tests revealed restrictive lung disease. The mean BASFI score suggested good functional capacity in the AS group. The respiratory muscle strength and MVV were also lower in AS (p<0.05). The chest expansion was correlated with MIP and MEP values (r=0.491; p=0.02, r=0.436; p=0.05). Chest expansion was also correlated negatively with disease duration (r=–0.502; p=0.03). In addition, there was no correlation between chest expansion and BASFI score (r=–0.076; p=0.773). This study demonstrates that functional status (BASFI) is not influenced by the limitation of chest wall movement. It may be as a result of the maintenance of moderate physical activity during active life in patients with AS.Abbreviations AS Ankylosing spondylitis - FEF Forced expiratory flow rate - FEV₁ Forced expiratory volume during the first second - FVC Forced vital capacity - MPM Mouth-pressure meter - MVV Maximum voluntary ventilation - VC Vital capacity     

Respiratory muscle training

The application of skeletal muscle training principles to the respiratory muscles is a relatively new field. Strength and endurance training of the respiratory muscles can be achieved in normal humans and in patients with neuromuscular and chronic obstructive pulmonary diseases. Careful monitoring is required throughout a training program to ensure that the respiratory muscles are, in fact, being trained. This is a promising area, although further research is necessary to determine the indications for respiratory muscle training. Furthermore, it is still necessary to determine the optimal mode of training.     

Respiratory muscle fatigue

Respiratory muscle fatigue is caused by excessive effort relative to the strength and endurance of the respiratory muscles. It can be manifested by reductions in respiratory drive (central fatigue), by impaired neuromuscular transmission (transmission fatigue), by decreased contractility (contractile fatigue), or by a combination of these factors. Respiratory muscle fatigue probably contributes to the difficulties some patients have with weaning from mechanical ventilation, the symptoms of exercise intolerance and dyspnea in chronic lung disease, and CO2 retention. Therapy depends on a reduction in the required level of respiratory effort and/or an improvement in respiratory muscle strength and endurance.     

Respiratory muscle function

The functional anatomy of the respiratory muscles has been reviewed. The diaphragm has been emphasized, since this is the most important inspiratory muscle, but the view has been presented that the intercostal, scaleni, and other accessory inspiratory muscles become increasingly important as airflow obstruction leads to hyperinflation. As work increases, the demand for energy and hence blood flow to those muscles has to increase. In spite of a large reserve there are situations in which demands may outstrip supply. This leads to local metabolic changes that result in muscle fatigue. We are now capable of detecting this change as alterations in EMG or in the ability to generate pressures. The latter leads to a decrease in the capacity of the respiratory pump to exchange gas, ultimately resulting in hypercapnia and hypoxemia. The true importance of respiratory muscle fatigue and its differentiation from weakness in patients with severe CAO requires more analysis. It is intuitively appropriate to address the overall decrement in the ability to maintain adequate ventilatory work at low energy cost with the different therapeutic modalities thought to be beneficial. A combination of a decrease in the load imposed on the respiratory muscles, an improvement in the contractility of those muscles, and, when there is absolute need, the resting of the fatigued muscles should result in a better chance to lead a meaningful life and perhaps to improve survival in these patients.     

Respiratory muscle fatigue

To estimate the effect of the increase in ventilation induced by exercise on the dynamics of respiratory muscle in normal subjects and cases of respiratory diseases, we measured the changes of transdiaphragmatic pressure (Pdi), gastric pressure (Pga), tension time index of the diaphragm (TTdi) and tension time index of the abdomen (TTab). To confirm the effect of oxygen on exercise endurance, we investigated changes of parameters measured during exercise under air breathing and oxygen inhalation. In normal subjects, we found the increase in diaphragmatic activity as a gradual increase of exercise level, but TTdi always stayed in the non-fatigue zone. On the contrary, patients with COPD showed that TTdi was near fatigue threshold during quiet breathing and crossed easily into fatigue zone during exercise. There was an increase in endurance time with oxygen for COPD patients. Breathing with oxygen was associated with a smooth increase in Pdi during the inspiratory phase which indicates efficient contraction of the diaphragm. During the expiratory phase, the degree of increase in Pga was markedly reduced by oxygen inhalation.