| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Guest Access | Sign In via User Name/Password
|
|
|
|||||||
Guest Access | Sign In via User Name/Password |
|||||||||
SARAH Network of Rehabilitation Hospitals, Brasilia, Brazil
Correspondence to: Paulo Sergio Beraldo, MD, PhD, SARAH Network-University SARAH, SMPW Q18, Conj 5, Lote 3, Casa H (Park-Way) 71, Brasilia, Brazil DF71741-80; e-mail beraldo8{at}terra.com.br
To the Editor:
Schoenhofer et al (June 2004)1 brought an important contribution to the understanding of water immersion effects on respiratory parameters in subjects with severe diaphragm weakness. Seven patients with neuromuscular diseases and seven healthy control subjects were studied out of the water (sitting erect) and in the water (standing up at neck level) by spirometry, maximal static inspiratory pressure (PImax), and mouth occlusion pressure measurements. The patients and control subjects showed mean drops in vital capacity of 30% and 3%, respectively, while showing mouth occlusion pressure increases of 191% and 29%, respectively. There is evidence that some factors not mentioned by the authors could have influenced the changes observed between the groups. Water temperature and time of immersion are examples. Specifically, a time of immersion between 20 and 30 min can minimize the enlarged plasma volume, which is the most important factor for the decrease in vital capacity.2 Thus, it would be important to know in the study of Schoenhofer et al1 the length of time of immersion, and whether this time was the same for both groups.
In addition, water temperature ranging from 33 to 35°C (thermoneutral) is the most appropriate way to study immersion effects, since it prevents significant changes in the core temperature of the body.3 Moreover, water temperature induces different changes on pulmonary volumes.4 On the other hand, patients with amyotrophic lateral sclerosis (three of seven patients studied) usually present a different pattern of FVC change, compared to subjects with no disability, between the supine and erect seated positions.5 To avoid these potential biases, patients and control subjects in the research of Schoenhofer et al1 should have been studied in the erect seated position, both out of the pool and in it.
Finally, we wonder about the low mean (± SD) value of the PImax (60 ± 26% predicted) observed in the control group by Schoenhofer et al.1 Besides the small number of subjects enrolled in the study (type II error), the low mean PImax may also justify the lack of difference between the groups. Overall, it remains to be elucidated whether the group differences observed by Schoenhofer et al1 were due per se to the effects of immersion.
References
Klinikum Hannover Oststadt, Hannover, Germany Royal Brompton Hospital, National Heart & Lung Institute, London, United Kingdom
Correspondence to: B. Schönhofer, MD, PhD, FCCP, Pneumologie und Internistische Intensivemedizen, Klinikum Hannover Oststadt, Hannover, Germany; e-mail: bernd.schoenhofer{at}t-online.de
To the Editor:
We thank Dr. Leal and colleagues for their interest in our article. In response to their questions we can report that, although we did not measure it specifically, the time from immersion to measurement was similar for patients and control subjects (typically 15 min). The swimming pool temperature was 27°C. Although this is less than is recommended by Leal et al, it was of course the same for patients and control subjects. Likewise, although it might have been better to use the seated erect position both in and out of the pool, we did not consider this to the practical, so patients in the pool were studied erect and straight. Since this was not the same for patients and control subjects, we doubt that this influenced our results.
Finally, in our article we acknowledged that the difference in maximum inspiratory pressure (PImax) between patients and control subjects just failed to reach the 0.05 significance level. We believe that the small number of enrolled patients may be associated with a type II error. Nevertheless, based on clinical criteria, our control subjects were healthy; therefore, if anything, this serves to support our conclusion that the differences in PImax between the groups are due to respiratory muscle weakness.
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
