Abstract

COPD exacerbation is a life-threatening condition with acute dyspnoea caused by respiratory or circulatory distress. The significance and co-presence of lung hyperinflation, bronchial obstruction, and changes in haemodynamics in the course of COPD exacerbation treatment have not been well described yet in course of a single study. Our aim was to evaluate the influence of COPD exacerbation treatment on bronchial obstruction, pulmonary hyperinflation, and possible changes of right and left ventricle haemodynamics in relation to the patient's clinical status. A total of 40 patients (90% males), 67 ± 8 years old, with COPD were assessed pre- and post-exacerbation treatment by the following: respiratory function tests, transthoracic echocardiography, 6MWT, endothelin-1 (ET-1) and NT-proBNP serum concentrations, and MRC scale. A significant decrease in RV%TLC (%) and mean pulmonary artery pressure (PAPmean) [mm Hg] was observed: pre -RV%TLC: 64.3 ± 9.0; post-RV%TLC 60.6 ± 11.1; p = 0.03; pre-PAPmean: 41.2 ± 11.2; post-PAPmean: 39.1 ± 12.1; p = 0.029, coupled with a significant increase of FEV1 [L]-preFEV1: 1.0 ± 0.4, post-FEV1: 1.2 ± 0.5; p < 0.001. A trend for reduced right ventricle systolic pressure (RVSP) [mm Hg]: pre-treatment: 44.5 ± 12.9; post-treatment: 36.3 ± 14.3; p = 0.068 and ET-1 [fmol/ml]: pre-treatment: 1.7 ± 2.8; post-treatment: 1.3 ± 1.9; p = 0.076, but not for NT-proBNP was noticed. Improvement of both, 6MWT [m]: pre-treatment: 294 ± 132; post-treatment: 415 ± 102; p < 0.001 and MRC [pts.]: pre-treatment: 3.3 ± 0.8; post-treatment: 1.8 ± 0.9; p < 0.001, were noticed. 6MWT correlated with RV%TLC (p < 0.05; r = -0.46; r = -0.53; respectively) and FEV1 (p < 0.05; r = 0.55; r = 0.60, respectively) on admission as well as on discharge. There was no such correlation with RVSP or PAPmean. Pulmonary hyperinflation and bronchial obstruction may be reduced by effective COPD exacerbation treatment and are accompanied by clinical improvement. The mPAP reduction observed in the course of treatment was not correlated with the results of 6MWT and MRC score.

Highlights

  • Chronic obstructive pulmonary disease (COPD) exacerbation is a life-threatening condition with acute dyspnoea caused by respiratory or circulatory distress

  • The purpose of this study was to examine the relationship between exercise capacity and dyspnoea with respiratory function parameters, echocardiographic indexes of cardiac function, and trends of serum markers related to cardiac decompensation in patients undergoing COPD exacerbation treatment

  • Hyperinflation [intra thoracic gas volume (ITGV) > 140%N and residual volume percentage total lung capacity (RV%TLC) > 140%N] was present in 60% of the 40 subjects included in the study

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Summary

Introduction

COPD exacerbation is a life-threatening condition with acute dyspnoea caused by respiratory or circulatory distress. Our aim was to evaluate the influence of COPD exacerbation treatment on bronchial obstruction, pulmonary hyperinflation, and possible changes of right and left ventricle haemodynamics in relation to the patient’s clinical status. Static hyperinflation is caused by distal airway collapsing on exhalation and subsequent air trapping It can result in an increase in the RV%TLC ratio, if total lung capacity (TLC) exceeds normal values. In patients with COPD, during exercise, dynamic hyperinflation increases expiratory flow limitation, and has haemodynamic consequences resulting from more rapid, shallow breathing and progressive reduction in dynamic lung compliance. That explains both exercise intolerance and gas exchange disturbances [6]. In most severe COPD stages hyperinflation may develop on mild exercise [9], and this results in inspiratory capacity (IC) decline and dyspnoea

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