Article

Sternomastoid, rib cage, and expiratory muscle activity during weaning failure

Division of Pulmonary and Critical Care Medicine, Edward Hines Jr. Veterans Administration Hospital, and Loyola University of Chicago Stritch School of Medicine, Hines, Illinois, USA.
Journal of Applied Physiology (Impact Factor: 3.06). 07/2007; 103(1):140-7. DOI: 10.1152/japplphysiol.00904.2006
Source: PubMed

ABSTRACT

We hypothesized that patients who fail weaning from mechanical ventilation recruit their inspiratory rib cage muscles sooner than they recruit their expiratory muscles, and that rib cage muscle recruitment is accompanied by recruitment of sternomastoid muscles. Accordingly, we measured sternomastoid electrical activity and changes in esophageal (DeltaPes) and gastric pressure (DeltaPga) in 11 weaning-failure and 8 weaning-success patients. At the start of trial, failure patients exhibited a higher DeltaPga-to-DeltaPes ratio than did success patients (P = 0.05), whereas expiratory rise in Pga was equivalent in the two groups. Between the start and end of the trial, failure patients developed additional increases in DeltaPga-to-DeltaPes ratio (P < 0.0014) and the expiratory rise in Pga also increased (P < 0.004). At the start of trial, sternomastoid activity was present in 8 of 11 failure patients contrasted with 1 of 8 success patients. Over the course of the trial, sternomastoid activity increased by 53.0 +/- 9.3% in the failure patients (P = 0.0005), whereas it did not change in the success patients. Failure patients recruited their respiratory muscles in a sequential manner. The sequence began with activity of diaphragm and greater-than-normal activity of inspiratory rib cage muscles; recruitment of sternomastoids and rib cage muscles approached near maximum within 4 min of trial commencement; expiratory muscles were recruited slowest of all. In conclusion, not only is activity of the inspiratory rib cage muscles increased during a failed weaning trial, but respiratory centers also recruit sternomastoid and expiratory muscles. Extradiaphragmatic muscle recruitment may be a mechanism for offsetting the effects of increased load on a weak diaphragm.

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Available from: Sairam Parthasarathy
    • "Its study reveals important impairments in the respiratory function. The electromyographic signal of the SMC muscle (EMGsc) has become evident in patients suffering from chronic pulmonary obstructive disease (COPD) [1] who present acute respiratory failure and undergo a weaning trial [2]. "
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    ABSTRACT: The use of non-invasive methods for the study of respiratory muscle signals can provide clinical information for the evaluation of the respiratory muscle function. The aim of this study was to evaluate the electrical activity of the sternocleidomastoid muscle recorded superficially by means of a concentric ring electrode (CRE) in bipolar configuration. This sensor enhances the spatial resolution of the signal recorded, attenuates interferences, as the cardiac activity, and also simplifies the orientation problem associated to the electrode location on the muscle under study. Five healthy subjects underwent a respiratory load test in which an inspiratory load was imposed during the inspiratory phase. During the test, the electromyographic signal of the sternocleidomastoid muscle (EMGsc) and the inspiratory mouth pressure (Pmouth) were acquired. The EMGsc signal was processed using the fixed sample entropy (fSampEn), a technique for the amplitude estimation of signals that is robust in presence of impulsive noise as cardiac activity. The agreement between the Pmouth and the fSampEn over the EMGsc signal showed a moderate Pearson’s correlation value at the lowest inspiratory load (0.46 ± 0.11) and a very strong value at the highest inspiratory load (0.84 ± 0.08). In conclusion, the surface recordings of the EMGsc signal using a CRE and the estimation of its amplitude using the fSampEn technique can be used for the study of muscle respiratory activity.
    No preview · Conference Paper · Nov 2015
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    • "Experimental evidence supports the existence of local protective mechanisms (Laghi et al., 2003; Mador et al., 1996; Eastwood et al., 1994). In patients who developed hypercapnia during a failed trial of weaning from mechanical ventilation, we observed sequential recruitment of the extradiaphragmatic muscles (Parthasarathy et al., 2007). The sequence began with greater-than-normal activity of inspiratory muscles followed by expiratory muscle recruitment. "
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    ABSTRACT: We hypothesized that improved diaphragmatic neuromechanical coupling during inspiratory loading is not sufficient to prevent alveolar hypoventilation and task failure, and that the latter results primarily from central-output inhibition of the diaphragm and air hunger rather than contractile fatigue. Eighteen subjects underwent progressive inspiratory loading. By task failure all developed hypercapnia. Tidal transdiaphragmatic pressure (ΔPdi) and diaphragmatic electrical activity (ΔEAdi) increased during loading–the former more than the latter; thus, neuromechanical coupling (ΔPdi/ΔEAdi) increased during loading. Progressive increase in extra-diaphragmatic muscle contribution to tidal breathing, expiratory muscle recruitment, and decreased end-expiratory lung volume contributed to improved neuromechanical coupling. At task failure, subjects experienced intolerable breathing discomfort, at which point mean ΔEAdi was 74.9 ± 4.9% of maximum, indicating that the primary mechanism of hypercapnia was submaximal diaphragmatic recruitment. Contractile fatigue was an inconsistent finding. In conclusion, hypercapnia during acute loading primarily resulted from central-output inhibition of the diaphragm suggesting that acute loading responses are controlled by the cortex rather than bulbopontine centers.
    Preview · Article · Jul 2014 · Respiratory Physiology & Neurobiology
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    • "To the authors' knowledge, this is the first reported study to assess musculoskeletal abnormalities of the rib cage in infants born prematurely. In this study, the measurement of angles associated with shoulder elevation was based on the respiratory physiology [25] and anatomy of the muscles responsible for thoracic abnormalities described previously in patients with asthma [10] [25] and chronic obstructive pulmonary disease [26] [27] [28]. For this reason, it is possible that the thoracic abnormalities found in the present study could be associated with impaired pulmonary function. "
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    ABSTRACT: To analyse the accuracy and reproducibility of photogrammetry in detecting thoracic abnormalities in infants born prematurely. Cross-sectional study. The Premature Clinic at the Federal University of São Paolo. Fifty-eight infants born prematurely in their first year of life. Measurement of the manubrium/acromion/trapezius angle (degrees) and the deepest thoracic retraction (cm). Digitised photographs were analysed by two blinded physiotherapists using a computer program (SAPO; http://SAPO.incubadora.fapesp.br) to detect shoulder elevation and thoracic retraction. Physical examinations performed independently by two physiotherapists were used to assess the accuracy of the new tool. Thoracic alterations were detected in 39 (67%) and in 40 (69%) infants by Physiotherapists 1 and 2, respectively (kappa coefficient=0.80). Using a receiver operating characteristic curve, measurement of the manubrium/acromion/trapezius angle and the deepest thoracic retraction indicated accuracy of 0.79 and 0.91, respectively. For measurement of the manubrium/acromion/trapezius angle, the Bland and Altman limits of agreement were -6.22 to 7.22° [mean difference (d)=0.5] for repeated measures by one physiotherapist, and -5.29 to 5.79° (d=0.75) between two physiotherapists. For thoracic retraction, the intra-rater limits of agreement were -0.14 to 0.18cm (d=0.02) and the inter-rater limits of agreement were -0.20 to -0.17cm (d=0.02). SAPO provided an accurate and reliable tool for the detection of thoracic abnormalities in preterm infants.
    Full-text · Article · Sep 2012 · Physiotherapy
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