Ventilator-induced diaphragm dysfunction: cause and effect.

@article{Powers2013VentilatorinducedDD,
  title={Ventilator-induced diaphragm dysfunction: cause and effect.},
  author={Scott K Powers and Michael P Wiggs and Kurt J Sollanek and Ashley J. Smuder},
  journal={American journal of physiology. Regulatory, integrative and comparative physiology},
  year={2013},
  volume={305 5},
  pages={
          R464-77
        }
}
  • S. Powers, M. Wiggs, +1 author A. Smuder
  • Published 1 September 2013
  • Medicine
  • American journal of physiology. Regulatory, integrative and comparative physiology
Mechanical ventilation (MV) 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… 
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115 Citations

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Citation Type

Ventilator-induced diaphragm dysfunction in critical illness
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Several major cellular mechanisms associated with autophagy, apoptosis, and mitochondrial biogenesis—including toll-like receptor 4, nuclear factor-κB, Src, class O of forkhead box, signal transducer and activator of transcription 3, and Janus kinase—are reviewed and discussed.
Ventilator-Induced Diaphragm Dysfunction (Review)
TLDR
The search for an optimal strategy for lung ventilation, development of diagnostic and physiotherapeutic methods, as well as the consolidation of the work of a multidisciplinary team of specialists can help in solving this serious problem.
Disturbances in Calcium Homeostasis Promotes Skeletal Muscle Atrophy: Lessons From Ventilator-Induced Diaphragm Wasting
TLDR
The emerging evidence that increased mitochondrial production of reactive oxygen species promotes oxidation of the ryanodine receptor/calcium release channel, resulting in calcium release from the sarcoplasmic reticulum, accelerated proteolysis, and VIDD is discussed.
Partial Support Ventilation and Mitochondrial-Targeted Antioxidants Protect against Ventilator-Induced Decreases in Diaphragm Muscle Protein Synthesis
TLDR
Treatment with mitochondrial-targeted antioxidants or the use of partial-support MV are potential strategies to preserve diaphragm protein synthesis during prolonged MV.
AT1 receptor blocker losartan protects against mechanical ventilation-induced diaphragmatic dysfunction.
TLDR
These experiments provide the first evidence that the Food and Drug Administration-approved drug losartan may have clinical benefits to protect against ventilator-induced diaphragm weakness in humans.
Mechanical Ventilation for Duchenne Muscular Dystrophy: Sinner or Saint?
TLDR
The impact of MV is investigated in the context of an underlying neuromuscular disease, where the widely used dystrophic mouse model was subjected to a brief 6-hour period of MV, and diaphragms from ventilated mdx mice demonstrated a nearly 20% reduction in maximal diphragmatic force.
Hydrogen sulfide donor protects against mechanical ventilation‐induced atrophy and contractile dysfunction in the rat diaphragm
TLDR
Results confirm that sodium sulfide was sufficient to protect the diaphragm against both MV‐induced fiber atrophy and contractile dysfunction and provide the first evidence that H2S has therapeutic potential to protect against MV‐ induced diaphragem weakness and to reduce difficulties in weaning patients from the ventilator.
The JAK-STAT Pathway Is Critical in Ventilator-Induced Diaphragm Dysfunction
TLDR
It is reported here that the JAK-STAT pathway is activated in MV in the human diaphragm, as evidenced by significantly increased phosphorylation of JAK and STAT and is central to the downstream pathogenesis of clinical VIDD.
Diaphragm Dysfunction in Mechanically Ventilated Patients.
Diaphragm Dysfunction in Mechanically Ventilated Patients
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References

SHOWING 1-10 OF 122 REFERENCES
Ventilator-induced diaphragmatic dysfunction.
TLDR
This Critical Care Perspective defines the phenomenon, henceforth referred to as ventilatorinduced diaphragmatic dysfunction (VIDD), as a loss of diaphRAGmatic force-generating capacity that is specifically related to the use of mechanical ventilation.
Clinical review: Ventilator-induced diaphragmatic dysfunction - human studies confirm animal model findings!
TLDR
The large body of evidence demonstrating the existence of VIDD in animal models is summarized, the major cellular mechanisms that have been implicated in this process are outlined, and the methods that can be used in the clinical setting to diagnose and/or monitor the development ofVIDD in critically ill patients are reviewed.
Pressure support ventilation attenuates ventilator-induced protein modifications in the diaphragm
TLDR
Developing methods to protect against mechanical ventilation-induced diaphragmatic weakness is important because the most frequent cause of weaning difficulty is respiratory muscle failure due to inspiratory muscle weakness and/or a decline in inspiratory Muscle endurance.
Effects of mechanical ventilation on diaphragm function and biology
TLDR
These animal studies show that early alterations in diaphragm function develop after short-term mechanical ventilation and these alterations may contribute to the difficulties in weaning from mechanical ventilation seen in patients.
Endurance exercise attenuates ventilator-induced diaphragm dysfunction.
TLDR
Compared with sedentary animals, exercise training before MV protected the diaphragm against MV-induced oxidative damage, protease activation, myofiber atrophy, and contractile dysfunction and provided the first evidence that exercise can provide protection against MV -induced diaphRAGm weakness.
Rapid Onset of Specific Diaphragm Weakness in a Healthy Murine Model of Ventilator-induced Diaphragmatic Dysfunction
TLDR
Controlled mechanical ventilation for 6 h in the mouse is associated with significant diaphragmatic but not limb muscle weakness without atrophy or sarcolemmal injury and activates proteolysis.
Mechanical ventilation-induced diaphragmatic atrophy is associated with oxidative injury and increased proteolytic activity.
TLDR
The hypothesis that MV is associated with atrophy of all diaphragmatic fiber types, increased diaphagmatic protease activity, and augmented diaphRAGmatic oxidative stress is supported.
Prolonged mechanical ventilation alters diaphragmatic structure and function
TLDR
Prolonged mechanical ventilation can promote diaphragmatic atrophy and contractile dysfunction and the scientific challenge for the future is to delineate the mechanical ventilation-induced signaling pathways that activate these proteases and depress protein synthesis in thediaphragm.
Short-duration mechanical ventilation enhances diaphragmatic fatigue resistance but impairs force production.
TLDR
Testing the hypothesis that 18 h of controlled MV will diminish diaphragmatic maximal tetanic specific tension (force per cross-sectional area of muscle) without impairing diaphagmatic fatigue resistance indicates that 18h of MV enhances diaph Ragemates fatigue resistance but impairs diaphRAGmatic specific tension.
Mitochondrial dysfunction and lipid accumulation in the human diaphragm during mechanical ventilation.
TLDR
The data suggest that mitochondrial dysfunction lies at the nexus between oxidative stress and the impaired diaphragmatic contractility that develops during MV, and energy substrate oversupply relative to demand, resulting from diaphragematic inactivity during MV could play an important role in this process.
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