Neural respiratory drive predicts clinical deterioration and safe discharge in exacerbations of COPD

Abstract

Rationale: Hospitalised patients with acute exacerbation of COPD may deteriorate despite treatment, with early readmission being common.

Objectives: To investigate whether neural respiratory drive, measured using second intercostal space parasternal muscle electromyography (EMGpara), would identify worsening dyspnoea and physician-defined inpatient clinical deterioration, and predict early readmission.

Methods: Patients admitted to a single-site university hospital with exacerbation of COPD were enrolled. Spirometry, inspiratory capacity (IC), EMGpara, routine physiological parameters, modified early warning score (MEWS), modified Borg scale for dyspnoea and physician-defined episodes of deterioration were recorded daily until discharge. Readmissions at 14 and 28 days post discharge were recorded.

Measurements and main results: 120 patients were recruited (age 70 ± 9 years, forced expiratory volume in 1 s (FEV1) of 30.5 ± 11.2%). Worsening dyspnoea, defined as at least one-point increase in Borg scale, was associated with increases in EMGpara%max and MEWS, whereas an increase in EMGpara%max alone was associated with physician-defined inpatient clinical deterioration. Admission-to-discharge change (Δ) in the normalised value of EMGpara (ΔEMGpara%max) was inversely correlated with ΔFEV1 (r = -0.38, p < 0.001) and ΔIC (r = -0.44, p < 0.001). ΔEMGpara%max predicted 14-day readmission (OR 1.13, 95% 1.03 to 1.23) in the whole cohort and 28-day readmission in patients under 85 years (OR 1.09, 95% CI 1.01 to 1.18). Age (OR 1.08, 95% CI 1.03 to 1.14) and 12-month admission frequency (OR 1.29, 1.01 to 1.66), also predicted 28-day readmission in the whole cohort.

Conclusions: Measurement of neural respiratory drive by EMGpara represents a novel physiological biomarker that may be helpful in detecting inpatient clinical deterioration and identifying the risk of early readmission among patients with exacerbations of COPD.

Trial registration: NCT01361451.

Keywords: COPD Exacerbations; Lung Physiology; Respiratory Muscles.

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Figures

Figure 1

Representative trace of nasal pressure and second intercostal space parasternal electromyogram during tidal breathing in a patient with COPD during an exacerbation. Pnp, nasal pressure; EMGpara, parasternal electromyogram; RMSpara, root mean square of EMGpara.

Figure 2

Relationship between admission-to-discharge change in EMGpara%max, and changes in (A) FEV1, (B) FVC and (C) IC. EMGpara%max, 1 min mean magnitude of rectified inspiratory parasternal EMG activity normalised to a maximal manoeuvre; IC, inspiratory capacity.

Figure 3

Receiver-operator curves for prediction of 14-day readmission for (A) ΔEMGpara%max, (B) ΔFEV1, and (C) ΔIC. EMGpara%max, 1 min mean magnitude of rectified inspiratory parasternal EMG activity normalised to a maximal manoeuvre; IC, inspiratory capacity; ROC, receiver-operator curve; AUC, area under the receiver-operator curve.

Figure 4

Time-to-readmission Kaplan–Meier plots for patients whose EMGpara%max fell by more than 3.1% between admission and discharge (solid line), and those whose EMGpara%max fell by less than 3.1% (dotted line). EMGpara%max, 1 min mean magnitude of rectified inspiratory parasternal EMG activity normalised to a maximal manoeuvre.