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


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, Oct 06, 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.
    Respiratory Physiology & Neurobiology 07/2014; 198(1). DOI:10.1016/j.resp.2014.03.004 · 1.97 Impact Factor
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    • "In contrast, patients who have or are recovering from acute respiratory failure are characterized by very weak inspiratory muscles [47] and are not likely have enough reserve to alternate their inspiratory-pressure generation between different inspiratory muscle groups. Parthasarathy et al. [11] showed that the electrical activity of the rib cage and accessory inspiratory muscles increases early and more during a failing SBT. Although increased extradiaphragmatic muscle recruitment increases the amount of pressure and volume that will be delivered for a given EAdi, it is unlikely that the diaphragm activity remains constant. "
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    ABSTRACT: Introduction: Based on the hypothesis that failure of weaning from mechanical ventilation is caused by respiratory demand exceeding the capacity of the respiratory muscles, we evaluated whether extubation failure could be characterized by increased respiratory drive and impaired efficiency to generate inspiratory pressure and ventilation. Methods: Airway pressure, flow, volume, breathing frequency, and diaphragm electrical activity were measured in a heterogeneous group of patients deemed ready for a spontaneous breathing trial. Efficiency to convert neuromuscular activity into inspiratory pressure was calculated as the ratio of negative airway pressure and diaphragm electrical activity during an inspiratory occlusion. Efficiency to convert neuromuscular activity into volume was calculated as the ratio of the tidal volume to diaphragm electrical activity. All variables were obtained during a 30-minute spontaneous breathing trial on continuous positive airway pressure (CPAP) of 5 cm H2O and compared between patients for whom extubation succeeded with those for whom either the spontaneous breathing trial failed or for those who passed, but then the extubation failed. Results: Of 52 patients enrolled in the study, 35 (67.3%) were successfully extubated, and 17 (32.7%) were not. Patients for whom it failed had higher diaphragm electrical activity (48%; P < 0.001) and a lower efficiency to convert neuromuscular activity into inspiratory pressure and tidal volume (40% (P < 0.001) and 53% (P < 0.001)), respectively. Neuroventilatory efficiency demonstrated the greatest predictability for weaning success. Conclusions: This study shows that a mixed group of critically ill patients for whom weaning fails have increased neural respiratory drive and impaired ability to convert neuromuscular activity into tidal ventilation, in part because of diaphragm weakness.
    Critical care (London, England) 07/2012; 16(4):R143. DOI:10.1186/cc11451 · 4.48 Impact Factor
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    • "The clinical importance of monitoring the SCM in COPD patients may be most obvious in those who undergo weaning from mechanical ventilation after suffering from respiratory failure. COPD patients demonstrated greatly elevated electromyography (EMG) activation of the SCM in all " failed weaning " cases, and also showed SCM activity in the majority of breaths during the spontaneous breathing trials (83% vs. 19% of breaths during spontaneous breathing) compared to those who successfully weaned (Parthasarathy et al., 2007). Near infrared spectroscopy (NIRS) is a noninvasive, continuous, and direct method to study oxygenation and hemodynamics of living tissue in real time (Delpy and Cope, 1997; Ferrari et al., 2004). "
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    ABSTRACT: This study investigated the pattern of changes in muscle oxygenation, deoxygenation and blood volume in the sternocleidomastoid (SCM) in comparison with the parasternal (PS) and intercostal (IC) muscles during a bout of incremental inspiratory threshold loading (ITL) in healthy subjects using near-infrared spectroscopy. During progressive loading, the PS and IC showed a significant increase in oxygenated hemoglobin (5.9 ± 2.3 and 6.8 ± 2.4 μM, P<0.05) and the SCM showed an increase in deoxygenated hemoglobin (17.3 ± 3.8 μM, P<0.05). Total hemoglobin also steadily increased in the SCM whereas it decreased in the quiescent vastus lateralis muscle (20.7 ± 6.1μM vs. -6.6 ± 2.4 μM, P<0.05), which was used as the control muscle during the ITL. Our data suggests that the SCM is recruited progressively during progressive ITL and is accompanied by an increased blood volume and maintenance of O(2)Hb. Blood redistribution away from the nonactive limb muscles during the ITL may provide one source of maintaining inspiratory muscle blood volume and oxygenation during high respiratory motor output.
    Respiratory Physiology & Neurobiology 06/2011; 178(2):202-9. DOI:10.1016/j.resp.2011.06.001 · 1.97 Impact Factor
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