Respiratory Dysfunction in Ventilated Patients: Can Inspiratory Muscle Training Help?

Author:

Bissett B.12,Leditschke I. A.13,Paratz J. D.14,Boots R. J.15

Affiliation:

1. Physiotherapy Department and Intensive Care Unit, Canberra Hospital, Canberra, Australian Capital Territory and University of Queensland, Brisbane, Queensland, Australia

2. Physiotherapy Department, Canberra Hospital and PhD Candidate, University of Queensland.

3. Intensive Care Unit, Canberra Hospital and Australian National University.

4. Department of Intensive Care Medicine, Royal Brisbane and Women's Hospital and University of Queensland.

5. Deputy Director, Intensive Care Unit, Department of Intensive Care Medicine, Royal Brisbane and Women's Hospital and University of Queensland.

Abstract

Respiratory muscle dysfunction is associated with prolonged and difficult weaning from mechanical ventilation. This dysfunction in ventilator-dependent patients is multifactorial: there is evidence that inspiratory muscle weakness is partially explained by disuse atrophy secondary to ventilation, and positive end-expiratory pressure can further reduce muscle strength by negatively shifting the length-tension curve of the diaphragm. Polyneuropathy is also likely to contribute to apparent muscle weakness in critically ill patients, and nutritional and pharmaceutical effects may further compound muscle weakness. Moreover, psychological influences, including anxiety, may contribute to difficulty in weaning. There is recent evidence that inspiratory muscle training is safe and feasible in selected ventilator-dependent patients, and that this training can reduce the weaning period and improve overall weaning success rates. Extrapolating from evidence in sports medicine, as well as the known effects of inspiratory muscle training in chronic lung disease, a theoretical model is proposed to describe how inspiratory muscle training enhances weaning and recovery from mechanical ventilation. Possible mechanisms include increased protein synthesis (both Type 1 and Type 2 muscle fibres), enhanced limb perfusion via dampening of a sympathetically-mediated metaboreflex, reduced lactate levels and modulation of the perception of exertion, resulting in less dyspnoea and enhanced exercise capacity.

Publisher

SAGE Publications

Subject

Anesthesiology and Pain Medicine,Critical Care and Intensive Care Medicine

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