Rapid Disuse Atrophy of Diaphragm Fibers in Mechanically Ventilated Humans

Levine, Stephen B.; Nguyen, Taitan; Taylor, Nyali; Friscia, Michael E.; Budak, Murat T.; Rothenberg, Pamela; Zhu, Jie; Sachdeva, Rajeev; Sonnad, Seema S.; Kaiser, Larry R.; Rubinstein, Neal A.; Powers, Scott K.; Shrager, Joseph B.

doi:10.1056/nejmoa070447

Cited by 1,303 publications

(1,051 citation statements)

References 27 publications

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“…While animal studies consistently indicated that prolonged MV promotes VIDD, the question of whether long-term ventilator support produces VIDD in humans remained unknown until a milestone study published in 2008 revealed that prolonged MV results in rapid diaphragmatic atrophy in humans (58). These seminal findings have now been confirmed by other groups, and together, these studies clearly demonstrate that prolonged MV results in the rapid development of both diaphragmatic atrophy and contractile dysfunction in humans (39,42,47).…”

Section: Ventilator-induced Diaphragm Dysfunction: Historical Overviewsupporting

confidence: 71%

“…To date, three independent studies have evaluated the impact of prolonged MV on diaphragmatic atrophy in humans. The first report demonstrated that 18 -69 h of full support MV results in significant diaphragmatic atrophy (ϳ50% reduction in fiber cross sectional area) of both type I (slow) and type II (fast) muscle fibers in the costal diaphragm (58). This original finding was recently confirmed in another study indicating that diaphragmatic fiber atrophy occurs in humans exposed to full support MV for Ն24 h with the magnitude of the diaphragmatic atrophy being significantly correlated with the duration of MV (47).…”

Section: Mv-induced Diaphragm Atrophymentioning

confidence: 99%

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Ventilator-induced diaphragm dysfunction: cause and effect

Powers

Wiggs

Sollanek

et al. 2013

American Journal of Physiology-Regulatory, Integrative and Comp

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Powers SK, Wiggs MP, Sollanek KJ, Smuder AJ. Ventilator-induced diaphragm dysfunction: cause and effect. Am J Physiol Regul Integr Comp Physiol 305: R464 -R477, 2013. First published July 10, 2013 doi:10.1152/ajpregu.00231.2013 is used clinically to maintain gas exchange in patients that require assistance in maintaining adequate alveolar ventilation. Common indications for MV include respiratory failure, heart failure, drug overdose, and surgery. Although MV can be a life-saving intervention for patients suffering from respiratory failure, prolonged MV can promote diaphragmatic atrophy and contractile dysfunction, which is referred to as ventilator-induced diaphragm dysfunction (VIDD). This is significant because VIDD is thought to contribute to problems in weaning patients from the ventilator. Extended time on the ventilator increases health care costs and greatly increases patient morbidity and mortality. Research reveals that only 18 -24 h of MV is sufficient to develop VIDD in both laboratory animals and humans. Studies using animal models reveal that MV-induced diaphragmatic atrophy occurs due to increased diaphragmatic protein breakdown and decreased protein synthesis. Recent investigations have identified calpain, caspase-3, autophagy, and the ubiquitin-proteasome system as key proteases that participate in MV-induced diaphragmatic proteolysis. The challenge for the future is to define the MV-induced signaling pathways that promote the loss of diaphragm protein and depress diaphragm contractility. Indeed, forthcoming studies that delineate the signaling mechanisms responsible for VIDD will provide the knowledge necessary for the development of a pharmacological approach that can prevent VIDD and reduce the incidence of weaning problems. respiratory muscle; atrophy; mechanical ventilation; weaning; muscle wasting MECHANICAL VENTILATION (MV) is used clinically to achieve sufficient pulmonary gas exchange in patients unable to sustain adequate alveolar ventilation on their own. Common indications for MV include respiratory failure due to chronic obstructive pulmonary disease, status asthmaticus, and/or heart failure. In addition, MV is often an essential intervention in patients suffering from acute drug overdose, neuromuscular diseases, sepsis, and during surgery along with postsurgical recovery.The number of patients receiving prolonged MV in the United States exceeds more than 300,000 each year in the intensive care unit (ICU) (20). Although MV can be a lifesaving measure, prolonged MV results in the rapid development of diaphragmatic weakness due to both atrophy and contractile dysfunction. This detrimental impact of prolonged MV on the diaphragm has been termed ventilator-induced diaphragmatic dysfunction (VIDD) and VIDD is predicted to be a major contributor to problems in weaning patients from the ventilator (26, 114). Although previous reports describing the impact of prolonged MV on the diaphragm have appeared in the literature, advances in our understanding of the mechanisms responsible for VIDD h...

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Section: Ventilator-induced Diaphragm Dysfunction: Historical Overviewsupporting

confidence: 71%

Section: Mv-induced Diaphragm Atrophymentioning

confidence: 99%

Ventilator-induced diaphragm dysfunction: cause and effect

Powers

Wiggs

Sollanek

et al. 2013

American Journal of Physiology-Regulatory, Integrative and Comp

Self Cite

139

156

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“…In a previous study, diaphragm dysfunction in ICU‐AW patients was observed in 80% of patients, and 50% had a failed extubation and died during the ICU stay 6. A range of 18‐69 hours of complete diaphragmatic inactivity and MV support results in marked diaphragm myofiber atrophy 7. In our patient, the diaphragm dysfunction might be due to ICU‐AW, which in turn led to extubation failure.…”

Section: Discussionsupporting

confidence: 53%

Recovery of muscle weakness and physical function in a patient with severe ICU‐acquired weakness following pulmonary embolism: A case report

Morimoto

Sekino

Eishi

et al. 2018

Clinical Case Reports

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“…Kann die geschonte und bereits atrophierte Atemmuskulatur [6] am Beatmungsgerät wieder trainiert und gleichzeitig die Belastungsgrenze der Atempumpe so frühzeitig erkannt werden, dass es nicht zu einer Erschöpfung der Atemmuskeln kommt? Aus den großen Studien Mitte der 1990er Jahre wissen wir, dass ein respiratorunterstützter Weaning-Modus, näm-lich der "Synchronized-intermittentmandatory-ventilation"(SIMV)-Modus, einem simplen T-Stück-Versuch oder der einfachen Druckunterstützung ("pressure support ventilation", PSV) bezüglich der erfolgreichen Entwöhnung unterlegen war [5].…”

Section: Die Entwöhnung Oder Das Weaning Beginnt Mit Der Intubationunclassified

Augmentierte Spontanatmung im Entwöhnungsprozess

Ragaller

2014

Anaesthesist

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Rapid Disuse Atrophy of Diaphragm Fibers in Mechanically Ventilated Humans

Abstract: The combination of 18 to 69 hours of complete diaphragmatic inactivity and mechanical ventilation results in marked atrophy of human diaphragm myofibers. These findings are consistent with increased diaphragmatic proteolysis during inactivity.

Cited by 1,303 publications

References 27 publications

Ventilator-induced diaphragm dysfunction: cause and effect

Ventilator-induced diaphragm dysfunction: cause and effect

Recovery of muscle weakness and physical function in a patient with severe ICU‐acquired weakness following pulmonary embolism: A case report

Augmentierte Spontanatmung im Entwöhnungsprozess

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