Inhibition of central activation of the diaphragm: a mechanism of weaning failure
| Autor: | Martin J. Tobin, Amal Jubran, Stephen W Littleton, Hameeda Shaikh, Franco Laghi, Daniel Morales |
|---|---|
| Rok vydání: | 2020 |
| Předmět: |
medicine.medical_specialty
Physiology medicine.medical_treatment mechanical ventilation 03 medical and health sciences neuromuscular coupling 0302 clinical medicine Physiology (medical) Internal medicine weaning from mechanical ventilation Humans Medicine Mechanical ventilation Muscle fatigue business.industry Mechanism (biology) Respiration Artificial Respiratory Muscles Diaphragm (structural system) 030228 respiratory system Exhalation diaphragm Weaning failure Cardiology muscle fatigue business Ventilator Weaning 030217 neurology & neurosurgery Research Article |
| Zdroj: | Journal of Applied Physiology |
| ISSN: | 1522-1601 8750-7587 |
| DOI: | 10.1152/japplphysiol.00856.2019 |
| Popis: | During a T-tube trial following disconnection of mechanical ventilation, patients failing the trial do not develop contractile diaphragmatic fatigue despite increases in inspiratory pressure output. Studies in volunteers, patients, and animals raise the possibility of spinal and supraspinal reflex mechanisms that inhibit central-neural output under loaded conditions. We hypothesized that diaphragmatic recruitment is submaximal at the end of a failed weaning trial despite concurrent respiratory distress. Tidal transdiaphragmatic pressure (ΔPdi) and electrical activity (ΔEAdi) were recorded with esophago-gastric catheters during a T-tube trial in 20 critically ill patients. During the T-tube trial, ∆EAdi was greater in weaning failure patients than in weaning success patients (P = 0.049). Despite increases in ΔPdi, from 18.1 ± 2.5 to 25.9 ± 3.7 cm H2O (P < 0.001), rate of transdiaphragmatic pressure development (from 22.6 ± 3.1 to 37.8 ± 6.7 cm H2O/s; P < 0.0004), and concurrent respiratory distress, ∆EAdi at the end of a failed T-tube trial was half of maximum, signifying inhibition of central neural output to the diaphragm. The increase in ΔPdi in the weaning failure group, while ∆EAdi remained constant, indicates unexpected improvement in diaphragmatic neuromuscular coupling (from 46.7 ± 6.5 to 57.8 ± 8.4 cm H2O/%; P = 0.006). Redistribution of neural output to the respiratory muscles characterized by a progressive increase in rib cage and accessory muscle contribution to tidal breathing and expiratory muscle recruitment contributed to enhanced coupling. In conclusion, diaphragmatic recruitment is submaximal at the end of a failed weaning trial despite concurrent respiratory distress. This finding signifies that reflex inhibition of central neural output to the diaphragm contributes to weaning failure. NEW & NOTEWORTHY Research into pathophysiology of failure to wean from mechanical ventilation has excluded several factors, including contractile fatigue, but the precise mechanism remains unknown. We recorded transdiaphragmatic pressure and diaphragmatic electrical activity in patients undergoing a T-tube trial. Diaphragmatic recruitment was submaximal at the end of a failed trial despite concurrent respiratory distress, signifying that inhibition of central neural output to the diaphragm is an important mechanism of weaning failure. |
| Databáze: | OpenAIRE |
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