Introduction Patients with idiopathic persistent exertional dyspnoea are often labelled as having a breathing pattern disorder (BPD). There are no agreed objective diagnostic measures for BPD, which complicates its characterisation and response to therapy. Approximate entropy (ApEn) is a measure of unpredictability, based on chaos theorem, which quantifies the degree of irregularity in time-series data.
Objectives To measure ApEn of ventilatory variables during a cardiopulmonary exercise test (CPET) in patients referred with unexplained dyspnoea. We hypothesised that ApEn of tidal volume and breathing frequency would be greater (i.e. more irregular) in patients with BPD than healthy controls.
Methods We studied 20 adults (14 female) with unexplained dyspnoea referred for CPET and diagnosed with BPD (by a senior respiratory physiotherapist blinded to ApEn data) and 15 age- gender- and BMI-matched healthy controls. Underlying cardiorespiratory disease was excluded using various investigations (e.g. imaging and echocardiography) prior to referral, in addition to tests performed on the day of CPET; namely pulmonary function and blood gas analysis. ApEn of various ventilatory parameters including tidal volume, breathing frequency and minute ventilation was calculated at rest and during a cycle-ergometer CPET.
Results BPD patients had greater dyspnoea (modified BORG) at rest (1.4 ± 1.2 vs 0.2 ± 0.6; P < 0.01) and lower peak oxygen uptake (VO2) (P < 0.01; Table 1). Peak exercise respiratory exchange ratio was similar between groups (1.14 ± 0.17 vs 1.13 ± 0.08, P = 0.84) as were nadir values for ventilatory equivalent for CO2 (28.5 ± 5.2 vs 25.5 ± 3.6, P = 0.07) and end-exercise arterial PCO2 (4.21 ± 0.68 vs 4.1 ± 0.67, P = 0.68). ApEn was significantly greater in the BPD cohort for the duration of the test (Table 1); however differences were not apparent at rest. There was no relationship between ApEn and baseline symptom scores.
Conclusion Measurement of ventilatory ApEn in patients referred with unexplained dyspnoea quantified irregularity of breathing pattern and was significantly greater (more irregular) in BPD than controls. These differences were not apparent from resting phase analysis. Quantifying increased dys-regulation in exercise hyperpnoea using ApEn can be applied to ventilatory variables collected during standard CPET, and thus could aid in diagnosis and evaluating treatment response in BPD. Further work should explore how ventilatiory ApEn relates to perception of symptoms.