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Clinical aspects of NIV
P159 HOT HMV UK: sleep disruption following initiation of domiciliary NIV in hypercapnic COPD
  1. P Murphy1,
  2. M I Polkey2,
  3. N Hart3
  1. 1Lane Fox Respiratory Unit, Guy's & St Thomas’ NHS Foundation Trust, London, UK
  2. 2Sleep & Ventilation Unit, Royal Brompton & Harefield NHS Foundation Trust, London, UK
  3. 3Guy's & St Thomas’ NHS Foundation Trust and Kings College London NIHR Biomedical Research Centre, London, UK


Introduction The use of domiciliary NIV for the treatment of chronic hypercapnic respiratory failure (CHRF) in COPD remains controversial. Previous data from randomised controlled trials do not show a sustained clinical benefit, but to date there has been no RCT that has titrated NIV to nocturnal oximetry and capnometry. Although one randomised cross-over trial has shown that high intensity NIV produced greater improvements in health-related quality of life (HRQL) compared to low intensity set up (Dreher et al Thorax 2010) concern remains that this strategy may cause significant sleep disruption that would be expected to adversely effect the clinical benefits.

Method Patient who remained persistently hypercapnic (PaCO2 >7 kPa) following acute exacerbations of COPD requiring NIV were offered participation in the home oxygen therapy versus home mechanical ventilation in COPD trial (HOT-HMV Trial). Baseline arterial blood gas analysis, HRQL and lung function parameters were performed prior to randomisation. Patients had nasal oxygen therapy or NIV established over a 3 day in-patient hospital stay. Sleep disruption and daytime activity was monitored for 7 days following HMV or HOT set up using a sleep diary and actigraphy (Actiwatch spectrum, Phillips-Respironics, Murrysville, PA, USA).

Results 7 patients were enrolled (4 HMV, 3 HOT). Mean ± SD age of 65 ± 11 years, BMI 25.5 ± 6.4 kg/m2, FEV1 30 ± 12%, FVC 58 ± 14%, FEV1/FVC 39 ± 12%, PaCO2 8.22 ± 0.72 kPa, PaO2 6.65 ± 0.58 kPa and MRC dyspnoea score of 4 ± 1. Actigraphy analysis showed HMV patients total sleep time (TST) was 241 ± 29 min with wake after sleep onset (WASO) time of 111 ± 41 min and a mobile time of 709 ± 119 min. Patients in the HOT arm had a TST of 373 ± 143 min with a WASO 116 ± 87 min and a mobile time 674 ± 132 min. No significant between group differences could be demonstrated in the sleep or activity variables. HMV settings Ipap 26 ± 3 cm H2O, Epap 5 ± 1 cm H2O, back up rate 15 ± 1 bpm.

Conclusion Although these data must be interpreted with caution, as the number of patients currently enrolled in this trial is small, there was no difference between the HOT and HMV groups. These data support the view that high pressure HMV does not cause significant sleep disruption when compared with HOT.

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