Intermittent spontaneous breathing protects the rat diaphragm from mechanical ventilation effects*

Gayan‐Ramirez, Ghislaine; Testelmans, Dries; Maes, Karen; Rácz, Gábor; Cadot, Pascal; Zádor, Ernö; Wuytack, Frank; Decramer, Marc

doi:10.1097/01.ccm.0000191250.32988.a3

Cited by 130 publications

(108 citation statements)

References 26 publications

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“…Importantly, these results suggest that the MV-induced diaphragm contractile dysfunction occurs at the level of the peripheral muscle (91). Indeed, numerous animal studies consistently report that prolonged MV results in a rapid and time-dependent decrease in diaphragmatic specific force production measured in vitro using electrical stimulation of diaphragmatic muscle strips (9,16,19,33,35,56,87,93,98). A recent report suggests that as few as 6 h of MV results in diaphragmatic contractile dysfunction in mice (73).…”

Section: Mv-induced Diaphragmatic Contractile Dysfunctionmentioning

confidence: 96%

“…Investigations using both rodent (113) and porcine (78) models indicate that MV-induced contractile dysfunction occurs in all muscle fiber types. This ventilator-induced impairment in diaphragmatic contractile function in animals appears to be directly linked to diaphragm contractile inactivity because ventilator modes that provide partial ventilator support or short periods of intermittent spontaneous breathing during prolonged MV can reduce the magnitude of full ventilator support-induced contractile dysfunction (35,44,49,94). Furthermore, a recent study reveals that short periods of bilateral phrenic nerve stimulation (10 min/h) protects the diaphragm against full support MV-induced diaphragm contractile dysfunction (118).…”

Section: Mv-induced Diaphragmatic Contractile Dysfunctionmentioning

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

143

156

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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: Mv-induced Diaphragmatic Contractile Dysfunctionmentioning

confidence: 96%

Section: Mv-induced Diaphragmatic Contractile Dysfunctionmentioning

confidence: 99%

Ventilator-induced diaphragm dysfunction: cause and effect

Powers

Wiggs

Sollanek

et al. 2013

American Journal of Physiology-Regulatory, Integrative and Comp

143

156

View full text Add to dashboard Cite

show abstract

“…A full discussion of VIDD is beyond the scope of this article and the condition has been reviewed recently elsewhere (e.g. in [74]); at this point, it is sufficient to note only that diaphragm weakness is common among intubated patients [75,76] and may increase with duration of ventilation [77], and that modes of ventilation that require continued [78] (or at least in rodents, even intermittent [79]) phrenic activity may prevent or attenuate VIDD.…”

Section: Neuropathy and Nerve Activitymentioning

confidence: 99%

Molecular mechanisms of intensive care unit-acquired weakness

Bloch¹,

Polkey²,

Griffiths³

et al. 2011

Eur Respir J

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Intensive care unit-acquired weakness (ICUAW) is an increasingly recognised and important clinical consequence of critical illness. It is associated with significant morbidity and mortality. The aetiology of this disease is not well understood. The purpose of this article is to review our understanding of the molecular pathogenesis of ICUAW in the context of current knowledge of clinical risk factors and aetiology.Key features of the disease are loss of muscle mass resulting from a shift in the dynamic balance of muscle protein synthesis and breakdown and a reduction in force-generating capacity. These alternations are secondary to neuropathy, disruption of the myofilament structure and function, a disrupted sarcoplasmic reticulum, electrical inexcitability and bioenergenetic failure.As knowledge and understanding of ICUAW grows, potential therapeutic targets will be identified, hopefully leading to multiple strategies for prevention and treatment of this important condition.

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“…El primer protocolo debe iniciar con limpieza de las vías aéreas, posicionamiento a 45° de la cabecera, utilizando un dispositivo que ofrece una resistencia en el momento de la inspiración, realizando de 6 a 8 repeticiones, con pausa de 5 a 10 minutos una vez al día, de 6 a 7 veces por semana, progresivamente se aumenta la resistencia de 1 a 2 cmH2O, acompañado de actividades funcionales, el segundo protocolo consiste en trabajar en posición semiflower con un dispositivo de umbral inspiratorio con una carga de 40% de presión inspiratoria máxima del paciente, realizando 5 series de 10 repeticiones 2 veces al día acompañado de terapia convencional. Estas técnicas muestran una disminución de hasta 8 horas en procesos de destete ventilatorio, hubo mejoría significativa en presiones espiratorias y en volumen corriente secundaria al incremento de la fuerza muscular de la musculatura ventilatoria (Levine, et al, 2008, Sassoon, Zhu, y Caiozzo, 2004Gayan et al, 2005). …”

Section: Tabla 1 Distribución De Artículos Según El Tipo De Estudiounclassified

Acción De Los Fisioterapeutas en Situaciones De Desacondicionamiento en Unidades De Cuidado Intensivo

Cuellar

2017

Rev. Colomb. Rehabil.

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El desacondicionamiento físico es una situación de pérdida de condiciones fisiológicas y metabólicas de diversos sistemas ocasionada por la permanencia en reposo, afecta los desempeños y posibilidades funcionales de la persona, y se presenta de manera frecuente en personas en Unidades de Cuidado Intensivo (UCI). En dicho contexto se puede intervenir por programas de acción Fisioterapéutica. Objetivo: Revisar en la literatura reciente los aspectos que orientan la intervención del Fisioterapeuta en situaciones de desacondicionamiento en Unidades de Cuidado Intensivo. Método: Se realizó un estudio de revisión, de alcance descriptivo, a partir de consultas en bases de datos entre junio de 2014 y febrero de 2015 con artículos de texto completo. Resultados: Se encontraron 32 artículos que cumplieron los criterios de inclusión y de ellos el 53% correspondieron a estudios de carácter experimental. Los enfoques de intervención se concentraron en estrategias dirigidas al entrenamiento de la capacidad aeróbica , la fuerza y resistencia muscular, el 25% de los artículos mostraron que pacientes que se intervenían Fisioterapéuticamente en Cuidados Intensivos tenían una mejoría significativa en la función pulmonar, el rendimiento muscular y en particular en el entrenamiento efectivo de la fuerza explosiva. Conclusiones: Producto de la revisión adelantada se encuentra que las intervenciones tempranas realizadas por profesionales en Fisioterapia permiten revertir las complicaciones generadas por la inmovilidad prolongada y estas se deben instaurar en las primeras 24 horas de internación del paciente

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Intermittent spontaneous breathing protects the rat diaphragm from mechanical ventilation effects*

Abstract: The data demonstrated that intermittent spontaneous breathing during the course of mechanical ventilation may minimize the deleterious effect of controlled mechanical ventilation on diaphragm force, fiber dimensions, and expression of transcription factors.

Cited by 130 publications

References 26 publications

Ventilator-induced diaphragm dysfunction: cause and effect

Ventilator-induced diaphragm dysfunction: cause and effect

Molecular mechanisms of intensive care unit-acquired weakness

Acción De Los Fisioterapeutas en Situaciones De Desacondicionamiento en Unidades De Cuidado Intensivo

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