Laghi Franco, Shaikh Hameeda, Littleton Stephen W, Morales Daniel, Jubran Amal, Tobin Martin J
Division of Pulmonary and Critical Care Medicine, Hines Veterans Affairs Hospital, Hines, Illinois.
Division of Pulmonary and Critical Care Medicine, Loyola University Chicago Stritch School of Medicine, Maywood, Illinois.
J Appl Physiol (1985). 2020 Aug 1;129(2):366-376. doi: 10.1152/japplphysiol.00856.2019. Epub 2020 Jul 16.
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 (ΔP) and electrical activity (ΔEA) were recorded with esophago-gastric catheters during a T-tube trial in 20 critically ill patients. During the T-tube trial, ∆EA was greater in weaning failure patients than in weaning success patients ( = 0.049). Despite increases in ΔP, from 18.1 ± 2.5 to 25.9 ± 3.7 cm HO ( < 0.001), rate of transdiaphragmatic pressure development (from 22.6 ± 3.1 to 37.8 ± 6.7 cm HO/s; < 0.0004), and concurrent respiratory distress, ∆EA 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 ΔP in the weaning failure group, while ∆EA remained constant, indicates unexpected improvement in diaphragmatic neuromuscular coupling (from 46.7 ± 6.5 to 57.8 ± 8.4 cm HO/%; = 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. 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.
在机械通气断开后的T管试验期间,试验失败的患者尽管吸气压力输出增加,但并未出现膈肌收缩性疲劳。对志愿者、患者和动物的研究提出了脊髓和脊髓上反射机制的可能性,即在负荷条件下抑制中枢神经输出。我们假设,尽管同时存在呼吸窘迫,但在断奶试验失败结束时,膈肌的募集未达到最大程度。在20例危重症患者的T管试验期间,用食管胃导管记录潮气量跨膈压(ΔP)和电活动(ΔEA)。在T管试验期间,断奶失败患者的ΔEA高于断奶成功患者(P = 0.049)。尽管ΔP从18.1±2.5 cmH₂O增加到25.9±3.7 cmH₂O(P < 0.001),跨膈压发展速率(从22.6±3.1 cmH₂O/s增加到37.8±6.7 cmH₂O/s;P < 0.0004),且同时存在呼吸窘迫,但在T管试验失败结束时,ΔEA仅为最大值的一半,这表明中枢神经对膈肌的输出受到抑制。断奶失败组中ΔP增加,而ΔEA保持不变,这表明膈肌神经肌肉耦合意外改善(从46.7±6.5 cmH₂O/%增加到57.8±8.4 cmH₂O/%;P = 0.006)。神经输出重新分配到呼吸肌,其特征是胸廓和辅助肌对潮式呼吸的贡献逐渐增加以及呼气肌募集增加,这有助于增强耦合。总之,尽管同时存在呼吸窘迫,但在断奶试验失败结束时,膈肌的募集未达到最大程度。这一发现表明,中枢神经对膈肌输出的反射性抑制是断奶失败的一个原因。对机械通气断奶失败病理生理学的研究排除了包括收缩性疲劳在内的几个因素,但确切机制仍不清楚。我们记录了接受T管试验患者的跨膈压和膈肌电活动。尽管同时存在呼吸窘迫,但在试验失败结束时,膈肌的募集未达到最大程度,这表明中枢神经对膈肌输出的抑制是断奶失败的一个重要机制。