Dysfunction of the Diaphragm

McCool, F. Dennis; Tzelepis, George E.

doi:10.1056/nejmra1007236

Cited by 403 publications

(344 citation statements)

References 66 publications

Supporting

Mentioning

320

Contrasting

Unclassified

Order By: Relevance

“…9 Th at study confi rmed the fi ndings of prior smaller studies and provided normal values for future comparative studies; however, we did not know whether these values could be applied to the population of patients with COPD. 5,[12][13][14][15] We hypothesized that patients with moderate COPD would demonstrate compensatory overuse hypertrophy of the diaphragm and that patients with severe air trapping would have impaired diaphragm contractility because of the displacement of the muscle and subsequent suboptimal length-tension relationship of the muscle fi bers, resulting in a decreased thickening ratio. Contrary to our hypotheses, our results show that patients with COPD have comparable diaphragm thickness and contraction to that of normal subjects.…”

Section: Discussionmentioning

confidence: 99%

B-Mode Ultrasound Assessment of Diaphragm Structure and Function in Patients With COPD

Baria

Shahgholi

Sorenson

et al. 2014

Chest

112

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 99%

B-Mode Ultrasound Assessment of Diaphragm Structure and Function in Patients With COPD

Baria

Shahgholi

Sorenson

et al. 2014

Chest

112

View full text Add to dashboard Cite

show abstract

“…As the diaphragm has a central role in facilitating the unfolding of the lung and supporting breathing after birth 28 , we followed this observation closer. Electron microscopy revealed hypercontracted regions within the diaphragm in the absence of Ebf3 and a shortening of Z-stacks (Fig.…”

Section: Expression Of Ebf3mentioning

confidence: 99%

Ebf factors and MyoD cooperate to regulate muscle relaxation via Atp2a1

et al. 2014

View full text Add to dashboard Cite

Myogenic regulatory factors such as MyoD and Myf5 lie at the core of vertebrate muscle differentiation. However, E-boxes, the cognate binding sites for these transcription factors, are not restricted to the promoters/enhancers of muscle cell-specific genes. Thus, the specificity in myogenic transcription is poorly defined. Here we describe the transcription factor Ebf3 as a new determinant of muscle cell-specific transcription. In the absence of Ebf3 the lung does not unfold at birth, resulting in respiratory failure and perinatal death. This is due to a hypercontractile diaphragm with impaired Ca 2 þ efflux-related muscle functions. Expression of the Ca 2 þ pump Serca1 (Atp2a1) is downregulated in the absence of Ebf3, and its transgenic expression rescues this phenotype. Ebf3 binds directly to the promoter of Atp2a1 and synergises with MyoD in the induction of Atp2a1. In skeletal muscle, the homologous family member Ebf1 is strongly expressed and together with MyoD induces Atp2a1. Thus, Ebf3 is a new regulator of terminal muscle differentiation in the diaphragm, and Ebf factors cooperate with MyoD in the induction of muscle-specific genes.

show abstract

“…Diaphragm dysfunction can be confirmed by a number of invasive and noninvasive tests. 8 However, most of the studies available have been conducted on healthy volunteers or subjects breathing spontaneously, and only a few recent papers have focused attention on the function of respiratory muscles during the weaning process in mechanically ventilated subjects.…”

Section: Introductionmentioning

confidence: 99%

Ultrasonographic Assessment of Diaphragm Function in Critically Ill Subjects

Umbrello

Formenti

2016

Respir Care

View full text Add to dashboard Cite

The majority of patients admitted to the ICU require mechanical ventilation as a part of their process of care. However, mechanical ventilation itself or the underlying disease can lead to dysfunction of the diaphragm, a condition that may contribute to the failure of weaning from mechanical ventilation. However, extended time on the ventilator increases health-care costs and greatly increases patient morbidity and mortality. Nevertheless, symptoms and signs of muscle disease in a bedridden (or bed rest-only) ICU patient are often difficult to assess because of concomitant confounding factors. Conventional assessment of diaphragm function lacks specific, noninvasive, time-saving, and easily performed bedside tools or requires patient cooperation. Recently, the use of ultrasound has raised great interest as a simple, noninvasive method of quantification of diaphragm contractile activity. In this review, we discuss the physiology and the relevant pathophysiology of diaphragm function, and we summarize the recent findings concerning the evaluation of its (dys)function in critically ill patients, with a special focus on the role of ultrasounds. We describe how to assess diaphragm excursion and diaphragm thickening during breathing and the meaning of these measurements under spontaneous or mechanical ventilation as well as the reference values in health and disease. The spread of ultrasonographic assessment of diaphragm function may possibly result in timely identification of patients with diaphragm dysfunction and to a potential improvement in the assessment of recovery from diaphragm weakness.

show abstract

Dysfunction of the Diaphragm

Cited by 403 publications

References 66 publications

B-Mode Ultrasound Assessment of Diaphragm Structure and Function in Patients With COPD

B-Mode Ultrasound Assessment of Diaphragm Structure and Function in Patients With COPD

Ebf factors and MyoD cooperate to regulate muscle relaxation via Atp2a1

Ultrasonographic Assessment of Diaphragm Function in Critically Ill Subjects

Contact Info

Product

Resources

About