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Inhibition of central activation of the diaphragm: a mechanism of weaning failure

Authors
  • Laghi, Franco1
  • Shaikh, Hameeda1
  • Littleton, Stephen W.1
  • Morales, Daniel1
  • Jubran, Amal1
  • Tobin, Martin J.1
  • 1 Loyola University Chicago Stritch School of Medicine, Maywood, Illinois
Type
Published Article
Journal
Journal of Applied Physiology
Publisher
American Physiological Society
Publication Date
Jul 16, 2020
Volume
129
Issue
2
Pages
366–376
Identifiers
DOI: 10.1152/japplphysiol.00856.2019
PMID: 32673161
PMCID: PMC7473953
Source
PubMed Central
Keywords
Disciplines
  • Research Article
License
Green

Abstract

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.

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