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Surgery and respiratory muscles
  1. G DRUMMOND
  1. Department of Anaesthetics
  2. The University of Edinburgh
  3. Royal Infirmary
  4. Lauriston Place
  5. Edinburgh EH3 9YW
  6. UK
    1. N M SIAFAKAS,
    2. I MITROUSKA,
    3. D BOUROS,
    4. D GEORGOPOULOS
    1. Pulmonary Department
    2. University of Crete Medical School
    3. 71110 Heraklion, Crete, Greece

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      In their review of the effects of surgery on the respiratory muscles Siafakas and co-workers have cited my work incorrectly on two occasions.1 We reported a study of respiratory mechanics after abdominal surgery with measurements of the pressure-volume characteristics of the rib cage and abdomen.2 This report has been cited to support statements on the effects of surgery on gas exchange efficiency of the lung and of general anaesthesia on the thorax. On neither occasion is this citation appropriate. We found evidence that the abdominal muscles were active in patients after abdominal surgery, that this activity was variable, and that it could possibly explain the patterns of movement otherwise considered to represent “diaphragmatic dysfunction”. These observations, along with a short review of the published work on the subject, formed an editorial3 in which I argued that the concept of diaphragmatic dysfunction was outmoded. This work has been cited in support of the effects of laparoscopic chole cystectomy, which is incorrect. Indeed, there is remarkably little direct evidence that the intercostal inspiratory muscles become more active in the patient after surgery. There is also little direct evidence in humans that the diaphragm is the respiratory muscle most affected by surgery.

      Many of the changes in the shape of the thorax caused by the induction of anaesthesia can be attributed to a loss of skeletal muscle tone, with a change in the shape of the vertebral column. If this is prevented, then the changes in thoracic dimensions during induction of anaesthesia are small, variable, and do not require the hypothesis of major movements of intravascular volume as indicated in fig 1 of their review.4 This is supported by direct measurements of intravascular volume, which do not show these shifts.5

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      authors' reply We wish to thank Dr Drummond for pointing out the incorrect citation of his work in our recent review.1-1 We apologise for this, especially for quoting his editorial1-2 for the effects of laparoscopic cholecystectomy on the respiratory muscles. However, we have extensively discussed the semantics of the term “diaphragmatic dysfunction” in the methodological part of our review, sharing some of Dr Drummond's views.1-2 Furthermore, we have cited the work of Dr Drummond and colleagues in the general discussion of the function of respiratory muscles during surgery, arguing that respiratory muscle dysfunction, in the general sense of the term, could influence functional residual capacity. We believe that this is in agreement with Dr Drummond's findings that upper abdominal surgery alters the relative activity of respiratory muscles (including the abdominal muscles) leading to changes in the rib cage abdominal configuration (fig 1, Nimmo and Drummond1-3).

      Similarly, we have cited his work to support the argument that general anaesthesia causes volume displacement between the thoracic and abdominal cavities. Dr Drummond argues that this could be due to the loss of skeletal muscle tone. We have no objection to this since the respiratory muscles are skeletal muscles too. Furthermore, the changes seen in the pattern of breathing after upper abdominal surgery and the relative contributions of the rib cage and abdomen during quiet breathing have been attributed by most investigators to dysfunction of the diaphragm.1-4-1-6 Dr Drummond's experiments offer another explanation, pointing out the role of the abdominal muscles (the major expiratory muscles). Our own experiments have shown that upper abdominal surgery impairs the global strength of the inspiratory and expiratory muscles to produce maximum pressure.1-7 1-8 It is well known that the major contributor to the maximum inspiratory pressure (MIP) is the pressure produced by the diaphragm. Thus, it is logical to suggest that, if MIP is grossly reduced after surgery, this is primarily due to diaphragmatic dysfunction. We believe that the above differences may be due to the different experimental conditions (quiet breathing versus maximum static pressures).

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