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Mechanisms of improvement of respiratory failure in patients with restrictive thoracic disease treated with non-invasive ventilation
  1. A H Nickol1,
  2. N Hart1,
  3. N S Hopkinson1,
  4. J Moxham2,
  5. A Simonds1,
  6. M I Polkey1
  1. 1Respiratory Muscle Laboratory, Royal Brompton Hospital, London SW3 6NP, UK
  2. 2Respiratory Muscle Laboratory, Guy’s King’s and St Thomas’ School of Medicine, King’s College Hospital, London SE5 9PJ, UK
  1. Correspondence to:
    Dr A Nickol
    Osler Chest Unit, Churchill Hospital, Headington, Oxford OX4 7LJ, UK;


Background: Nocturnal non-invasive ventilation (NIV) is an effective treatment for hypercapnic respiratory failure in patients with restrictive thoracic disease. We hypothesised that NIV may reverse respiratory failure by increasing the ventilatory response to carbon dioxide, reducing inspiratory muscle fatigue, or enhancing pulmonary mechanics.

Methods: Twenty patients with restrictive disease were studied at baseline (D0) and at 5–8 days (D5) and 3 months (3M).

Results: Mean (SD) daytime arterial carbon dioxide tension (Paco2) was reduced from 7.1 (0.9) kPa to 6.6 (0.8) kPa at D5 and 6.3 (0.9) kPa at 3M (p = 0.004), with the mean (SD) hypercapnic ventilatory response increasing from 2.8 (2.3) l/min/kPa to 3.6 (2.4) l/min/kPa at D5 and 4.3 (3.3) l/min/kPa at 3M (p = 0.044). No increase was observed in measures of inspiratory muscle strength including twitch transdiaphragmatic pressure, nor in lung function or respiratory system compliance.

Conclusions: These findings suggest that increased ventilatory response to carbon dioxide is the principal mechanism underlying the long term improvement in gas exchange following NIV in patients with restrictive thoracic disease. Increases in respiratory muscle strength (sniff oesophageal pressure and sniff nasal pressure) correlated with reductions in the Epworth sleepiness score, possibly indicating an increase in the ability of patients to activate inspiratory muscles rather than an improvement in contractility.

  • ESS, Epworth sleepiness score
  • FEV1, forced expiratory volume in 1 second
  • FRC, functional residual capacity
  • FVC, forced vital capacity
  • HCVR, hypercapnic ventilatory response
  • NIV, non-invasive ventilation
  • Paco2, arterial carbon dioxide tension
  • Pao2, arterial oxygen tension
  • PeMax, maximum expiratory mouth pressure
  • Pga, cough gastric pressure
  • PiMax, maximum inspiratory mouth pressure
  • Ptcco2, transcutaneous CO pressure
  • SNIP, sniff nasal inspiratory pressure
  • Sniff Pdi, sniff transdiaphragmatic pressure
  • Sniff Poes, sniff oesophageal pressure
  • TwPdi, twitch transdiaphragmatic pressure
  • hypercapnic respiratory failure
  • neuromuscular weakness
  • kyphoscoliosis
  • non-invasive ventilation

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  • Published Online First 6 June 2005

  • AHN and this work was funded by a project grant from the British Lung Foundation, NH by the Dorothy Osbourne Legacy, NSH by the Wellcome Trust, and MIP’s group from the European Union (QLK6-CT-2002-02285).

  • Competing interests: AHN has received contributions from GlaxoWellcome, Astra Pharmaceuticals, Cephalon, Medic-Aid and Breas Medical towards the cost of attending professional meetings (ERS, ATS). AS has received research grants from Breas Medical (£75 000) and ResMed (£62 000) to investigate the appropriate time to initiate non-invasive ventilation and inpatient versus outpatient initiation, and the use of a ventilator in patients with congestive heart failure, respectively. These projects are unrelated to the current study. She has received financial support from Cephalon to attend a scientific meeting. MIP has received fees for lecturing from the following companies totalling £2674 between 2003 and 2004: Astra Zeneca, GlaxoSmithKline, Nutricia and Cephalon. He has also attended professional meetings (ERS, ATS, APSS) as a guest of GlaxoWellcome, Astra Zeneca, Cephalon, 3M and Ciba. NH, NSH and JM have no competing financial interests.

  • Some of the data presented here have been presented previously in abstract form.

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