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Ultrasound Assessment of the Diaphragm in Patients With COPDUltrasound of Diaphragm in Patients With COPD FREE TO VIEW

Sachin Kumar, MD, DM, FCCP; Sandipan Chandra, MD
Author and Funding Information

From the Department of Pulmonary Medicine (Drs Kumar and Chandra), Institute of Liver & Biliary Sciences.

CORRESPONDENCE TO: Sachin Kumar, MD, DM, FCCP, Department of Pulmonary Medicine, Institute of Liver & Biliary Sciences, C-15, Delhi Govt. Residential complex, D-2 pocket, Vasant Kunj, New Delhi, PIN: 110070, New Delhi, India; e-mail: sachin.drk@gmail.com.


FINANCIAL/NONFINANCIAL DISCLOSURES: The authors have reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2014;146(4):e146. doi:10.1378/chest.14-1095
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To the Editor:

We read with great interest the article by Baria et al1 in a recent issue of CHEST (September 2014). In this article, the authors have studied diaphragm thickness (Tdi) and thickening ratio using B-mode ultrasound in patients with COPD. However, a few pertinent points should be highlighted before these values are accepted into clinical practice.

First, the authors have hypothesized that in COPD with moderate airflow obstruction, the diaphragm would show physiologic, compensatory overuse hypertrophy. Contradicting this view, it has been shown that oxidative stress and sarcomeric injury in COPD activate proteolytic machinery, leading to contractile protein wasting and, consequently, loss of force-generating capacity of diaphragm fibers.2 This accelerated protein degradation actually leads to diaphragmatic atrophy and not hypertrophy. Indeed, loss of myosin in the diaphragm fibers occurs even in mild to moderate COPD. However, despite the chronically reduced muscle length of the diaphragm in COPD, the pressure-generating ability is largely preserved at functional residual capacity (FRC). During tidal breathing, the firing rate of diaphragmatic motor units in patients with COPD is 70% greater than that of matched control subjects.2

Second, the authors have measured Tdi both at end-expiration (Tmin) and at maximal inspiration (Tmax), and the thickening ratio was calculated as Tmax / Tmin. However, Tdi measurements during spontaneous breathing may be influenced by lung volume in a nonlinear relationship. The Tdi is more pronounced above 50% of the vital capacity, and there is a large increase in thickness between relaxation and 10% of the inspiratory effort.3

In this context, Gottesman and McCool4 found that Tdi alone cannot distinguish between a chronically paralyzed atrophic diaphragm and a functioning diaphragm in patients with generalized muscle wasting or in small individuals. Change in thickness during inspiration or thickening fraction (TF or ΔTdi), calculated as TF = (thickness at peak inspiration or total lung capacity − thickness at end expiration or FRC)/thickness at end expiration or FRC, might be more definitive. The function, TF vs lung volume, for a range of volumes is linear.5 Moreover, as the diaphragm shortens during contraction, it thickens, and measures of ΔTdi are inversely related to changes in diaphragm length (Ldi) (ΔTdi is approximately 1/ΔLdi). Hence, it is intriguing to compare a diaphragm with chronically reduced length, as in COPD, with that of a normal population by measuring ΔTdi with respect to per unit change in Ldi. This might shed some light on the pathophysiologic differences in diaphragm between COPD and normal population.

References

Baria MR, Shahgholi L, Sorenson EJ, et al. B-mode ultrasound assessment of diaphragm structure and function in patients with COPD. Chest. 2014;146(3):680-685. [CrossRef] [PubMed]
 
Ottenheijm CA, Heunks LM, Dekhuijzen PN. Diaphragm muscle fiber dysfunction in chronic obstructive pulmonary disease: toward a pathophysiological concept. Am J Respir Crit Care Med. 2007;175(12):1233-1240. [CrossRef] [PubMed]
 
Cohn D, Benditt JO, Eveloff S, McCool FD. Diaphragm thickening during inspiration. J Appl Physiol (1985). 1997;83(1):291-296. [PubMed]
 
Gottesman E, McCool FD. Ultrasound evaluation of the paralyzed diaphragm. Am J Respir Crit Care Med. 1997;155(5):1570-1574. [CrossRef] [PubMed]
 
Wait JL, Nahormek PA, Yost WT, Rochester DP. Diaphragmatic thickness-lung volume relationship in vivo. J Appl Physiol (1985). 1989;67(4):1560-1568. [PubMed]
 

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Tables

References

Baria MR, Shahgholi L, Sorenson EJ, et al. B-mode ultrasound assessment of diaphragm structure and function in patients with COPD. Chest. 2014;146(3):680-685. [CrossRef] [PubMed]
 
Ottenheijm CA, Heunks LM, Dekhuijzen PN. Diaphragm muscle fiber dysfunction in chronic obstructive pulmonary disease: toward a pathophysiological concept. Am J Respir Crit Care Med. 2007;175(12):1233-1240. [CrossRef] [PubMed]
 
Cohn D, Benditt JO, Eveloff S, McCool FD. Diaphragm thickening during inspiration. J Appl Physiol (1985). 1997;83(1):291-296. [PubMed]
 
Gottesman E, McCool FD. Ultrasound evaluation of the paralyzed diaphragm. Am J Respir Crit Care Med. 1997;155(5):1570-1574. [CrossRef] [PubMed]
 
Wait JL, Nahormek PA, Yost WT, Rochester DP. Diaphragmatic thickness-lung volume relationship in vivo. J Appl Physiol (1985). 1989;67(4):1560-1568. [PubMed]
 
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