BACKGROUND:The functional status and outcomes in patients with prolonged mechanical ventilation (PMV) are often limited by poor endurance and pulmonary mechanics, which result from the primary diseases or prolonged time bedridden. We evaluate the impact of exercise training on pulmonary mechanics, physical functional status, and hospitalization outcomes in PMV patients. METHODS: Twenty-seven subjects with PMV in our respiratory care center (RCC) were divided randomly into an exercise training group (n ؍ 12) and a control group (n ؍ 15). The exercise program comprised 10 sessions of exercise training. The measurement of pulmonary mechanics and physical functional status (Functional Independence Measurement and Barthel index) were performed pre-study and post-study. The hospitalization outcomes included: days of mechanical ventilation, hospitalization days, and weaning and mortality rates during RCC stay. RESULTS: The training group had significant improvement in tidal volume (143.6 mL vs 192.5 mL, P ؍ .02) and rapid shallow breathing index after training (162.2 vs 110.6, P ؍ .009). No significant change was found in the control group except respiratory rate. Both groups had significant improvement in functional status during the study. However, the training group had greater changes in FIM score than the control group (44.6 vs 34.2, P ؍ .024). The training group also had shorter RCC stay and higher weaning and survival rates than the control group, although no statistical difference was found. CONCLUSIONS: Subjects with PMV in our RCC demonstrated significant improvement in pulmonary mechanics and functional status after exercise training. The application of exercise training may be helpful for PMV patients to improve hospitalization outcomes.
Mechanical ventilation (MV) is often used to maintain life in patients with sepsis and sepsis-related acute lung injury. However, controlled MV may cause diaphragm weakness due to muscle injury and atrophy, an effect termed ventilator-induced diaphragm dysfunction (VIDD). Toll-like receptor 4 (TLR4) and nuclear factor-κB (NF-κB) signaling pathways may elicit sepsis-related acute inflammatory responses and muscle protein degradation and mediate the pathogenic mechanisms of VIDD. However, the mechanisms regulating the interactions between VIDD and endotoxemia are unclear. We hypothesized that mechanical stretch with or without endotoxin treatment would augment diaphragmatic structural damage, the production of free radicals, muscle proteolysis, mitochondrial dysfunction, and autophagy of the diaphragm via the TLR4/NF-κB pathway. Male C57BL/6 mice, either wild-type or TLR4-deficient, aged between 6 and 8 weeks were exposed to MV (6 mL/kg or 10 mL/kg) with or without endotoxemia for 8 h. Nonventilated mice were used as controls. MV with endotoxemia aggravated VIDD, as demonstrated by the increases in the expression levels of TLR4, caspase-3, atrogin-1, muscle ring finger-1, and microtubule-associated protein light chain 3-II. In addition, increased NF-κB phosphorylation and oxidative loads, disorganized myofibrils, disrupted mitochondria, autophagy, and myonuclear apoptosis were also observed. Furthermore, MV with endotoxemia reduced P62 levels and diaphragm muscle fiber size (P < 0.05). Endotoxin-exacerbated VIDD was attenuated by pharmacologic inhibition with a NF-κB inhibitor or in TLR4-deficient mice (P < 0.05). Our data indicate that endotoxin-augmented MV-induced diaphragmatic injury occurs through the activation of the TLR4/NF-κB signaling pathway.
Common complications in PMV include changes in the airway clearance mechanism, pulmonary function, and respiratory muscle strength, as well as chest radiological changes such as atelectasis. Lung expansion therapy which includes IPPB and PEEP prevents and treats pulmonary atelectasis and improves lung compliance. Our study presented that patients with PMV have improvements in lung volume and oxygenation after receiving IPPB therapy. The combination of IPPB and PEEP therapy also results in increase in respiratory muscle strength. The application of IPPB facilitates the homogeneous gas distribution in the lung and results in recruitment of collapsed alveoli. PEEP therapy may reduce risk of respiratory muscle fatigue by preventing premature airway collapse during expiration. The physiologic effects of IPPB and PEEP may result in enhancement of pulmonary function and thus increase the possibility of successful weaning from mechanical ventilator during weaning process. For patients with PMV who were under the risk of atelectasis, the application of IPPB may be considered as a supplement therapy for the enhancement of weaning outcome during their stay in the hospital.
BACKGROUND: Muscle atrophy and deconditioning are common complications in patients on prolonged mechanical ventilation (PMV). There are few studies that reviewed the effects of electrical muscle stimulation in this population. The purpose of this study was to examine the effects of electrical muscle stimulation on muscle function and hospitalization outcomes in subjects with PMV. METHODS: Subjects on mechanical ventilation for >21 d were randomly assigned to the electrical muscle stimulation group (n ؍ 16) or the control group (n ؍ 17). The electrical muscle stimulation group received daily muscle electrical stimulation for 30 min/session for 10 d. The measurement of muscle strength (by medical research council [MRC] scale), leg circumference, and physical functional status (by Functional Independence Measure [FIM] scores) were performed before and after completion of the study. The length of stay in respiratory care center of subjects were recorded. RESULTS: After electrical muscle stimulation, there was no difference in pulmonary function between the electrical muscle stimulation and control groups. Significantly increased in MRC points was found in the electrical muscle stimulation group after intervention (2 [1-7] points vs 2 [1-3.5] points, respectively, P ؍ .034). No difference in MRC points was found between baseline and post-measurement in the control group (1[1-2] points vs 1[1-2.5] points, respectively, P > .99). At the end of the study, leg circumference in control group significantly decreased when compared with baseline (47.5 ؎ 8.3 cm vs 44.6 ؎ 5.7 cm, respectively, P ؍ .004) and remained unchanged in the EMS group. However, no significant differences were found between the electrical muscle stimulation and control groups. There was no difference in physical functional status and hospital stay between the electrical muscle stimulation and control groups. CONCLUSIONS: Electrical muscle stimulation enhanced muscle strength in subjects who received PMV. Electrical muscle stimulation can be considered a preventive strategy for muscle weakness in patients who receive PMV. (ClinicalTrials.gov registration NCT02227810.
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