Non-linear statistical interrogation of CPET-acquired ventilatory data has utility in the detection of BPD. A simple calculation of approximate entropy of ventilation, during an incremental cardiopulmonary exercise test, provides a quantitative method to detect BPD.
IntroductionPatients 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.ObjectivesTo 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.MethodsWe 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.ResultsBPD 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.Abstract S49 Table 1Participant characteristics and exercise responsesBPD (N = 20)Healthy Controls (N = 15)Age (years)49 (14)50 (18)BMI (kg/m2)26.0 (5.0)24.5 (3.7)FEV1 (% predicted)107 (18)95 (18)*FEV1/FVC0.78 (0.06)0.75 (0.12)VO2/kg Peak (ml/min/kg)20.7 (7.1)37.9 (14.9)**VO2 Peak (% Predicted)79.8 (17.5)124.8 (27.3)**ApEn Tidal Volume 1.31 (0.23)1.04 (0.28)**ApEn Breathing Frequency1.42 (0.22)1.24 (0.24)*ApEn Minute Ventilation1.01 (0.29)0.64 (0.22)**ConclusionMeasurement 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.
Background: Acute pulmonary embolism (PE) results in approximately 150,000 deaths per year in the United States. Massive PE results in haemodynamic instability. Patients with a sub-massive PE have a large embolus burden with evidence of right ventricular dysfunction (RV/LV ratio >0.9) but are haemodynamically stable. A Lancet review estimates the 3-month mortality rate for sub-massive PE is 21%. The treatment for massive PE is systemic intravenous tissue plasminogen activator (tPA) therapy. A beneficial reduction in all-cause mortality in these patients is attenuated by the 3-5% risk of catastrophic intracerebral haemorrhage. For haemodynamically stable patients with sub-massive PE, the current standard of care is anticoagulation. Our institution presents three patients with acute sub-massive PE managed with EkoSonic (EKOS) acoustic pulse thrombolysis, a form of ultrasound-enhanced catheter-directed thrombolysis (UE-CDTR). This combines conventional catheter directed tPA thrombolysis with high-frequency ultrasound, which increases thrombus permeability via acoustic cavitation for increased tPa efficacy. Methods: Three patients with CT pulmonary angiography (CTPA) confirmed sub-massive PE with RV dysfunction and a positive biomarker of cardiac strain (BNP/ Troponin) underwent EKOS. Under local anaesthetic and via common femoral vein approach, EKOS endovascular systems were placed in either one or both lower lobe pulmonary arteries. A tPA bolus followed by infusion (0.5 mg/hr tPA) was commenced according to protocol. Results: At 4 hours, all patients had a reduction in resting heart rate and a reciprocal improvement in oxygen requirements. Repeat CTPA at 24 hours following initiation of EKOS-directed thrombolysis demonstrated significantly decreased thrombus burden (up to 75%) and radiographic resolution of RV dysfunction with no episodes of major haemorrhage. Conclusions: Our institution has successfully employed EKOS-directed thrombolysis in three patients with sub-massive PE. All patients had clinical and radiological improvement with reduced inpatient stay compared to patients treated with anticoagulation alone.
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