Pulmonary haemodynamic changes in patients with severe COPD

Hanaoka, Masayuki; Ideura, Gen; Ito, Michiko; Urushihata, Kazuhisa; Koizumi, Tomonobu; Kubo, Keishi

doi:10.1111/j.1440-1843.2008.01318.x

Cited by 9 publications

(10 citation statements)

References 16 publications

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“…According to pulmonary hypertension guidelines [10] and as suspected, moderately increased PAP on admission was found and then was partially reduced by the exacerbation treatment [4] (Table 4). Similarly to Hanaoka et al [33], but engaging a larger number of patients, we showed that PAP increases during COPD exacerbation. The results of both studies raise the unresolved question of whether there is a need for a larger study with pulmonary artery pressure PAP assessed by right heart catheterisation (RHC).…”

Section: Discussionsupporting

confidence: 88%

“…The observed post-treatment PAPmean and RVSP reduction were independent of dyspnoea, exercise capacity, and blood gasses, which might be the result of oxygen supplementation [32]. In the study by Weitzenblum et al [33] changes of right heart haemodynamics were observed during an episode of peripheral oedema. However, an episode like this could also have been related to right ventricle decompensation, independent of COPD exacerbation.…”

Section: Discussionmentioning

confidence: 81%

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Lung-Heart Clinical Crosstalk in the Course of Copd Exacerbation

Skoczyński

Mizia-Stec

Semik-Orzech

et al. 2015

Advances in Respiratory Medicine

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Introduction: 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. Materials and Methods: 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. Results: 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. Conclusions: 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.

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Section: Discussionsupporting

confidence: 88%

Section: Discussionmentioning

confidence: 81%

Lung-Heart Clinical Crosstalk in the Course of Copd Exacerbation

Skoczyński

Mizia-Stec

Semik-Orzech

et al. 2015

Advances in Respiratory Medicine

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“…Data are mean ± SD with exception of symptoms (median and range) BMI body mass index; FVC forced vital capacity; IC inspiratory capacity; TLC total lung capacity; RV residual volume; D L CO lung diffusing capacity for carbon monoxide; Pa arterial partial pressure; EF ejection fraction (by echo-Doppler cardiography); _ VO 2 oxygen consumption; _ VE minute ventilation; MVV maximal voluntary ventilation; HR heart rate end-inspiratory lung volumes (Chabot et al 2001), and (3) higher pulmonary vascular resistance due to compression of juxta-alveolar vessels (Whittemberger et al 1960;Hanaoka et al 2008).…”

Section: Discussionmentioning

confidence: 99%

Influence of respiratory pressure support on hemodynamics and exercise tolerance in patients with COPD

et al. 2010

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Inspiratory pressure support (IPS) plus positive end-expiratory pressure (PEEP) ventilation might potentially interfere with the "central" hemodynamic adjustments to exercise in patients with chronic obstructive pulmonary disease (COPD). Twenty-one non- or mildly-hypoxemic males (FEV(1) = 40.1 +/- 10.7% predicted) were randomly assigned to IPS (16 cmH(2)O) + PEEP (5 cmH(2)O) or spontaneous ventilation during constant-work rate (70-80% peak) exercise tests to the limit of tolerance (T (lim)). Heart rate (HR), stroke volume (SV), and cardiac output (CO) were monitored by transthoracic cardioimpedance (Physioflow, Manatec, France). Oxyhemoglobin saturation was assessed by pulse oximetry (SpO(2)). At similar SpO(2), IPS(16) + PEEP(5) was associated with heterogeneous cardiovascular effects compared with the control trial. Therefore, 11 patients (Group A) showed stable or increased Delta "isotime" - rest SV [5 (0-29) mL], lower DeltaHR but similar DeltaCO. On the other hand, DeltaSV [-10 (-15 to -3) mL] and DeltaHR were both lower with IPS(16) + PEEP(5) in Group B (N = 10), thereby reducing DeltaCO (p < 0.05). Group B showed higher resting lung volumes, and T (lim) improved with IPS(16) + PEEP(5) only in Group A [51 (-60 to 486) vs. 115 (-210 to 909) s, respectively; p < 0.05]. We conclude that IPS(16) + PEEP(5) may improve SV and exercise tolerance in selected patients with advanced COPD. Impaired SV and CO responses, associated with a lack of enhancement in exercise capacity, were found in a sub-group of patients who were particularly hyperinflated at rest.

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“…Probably the only relevant clinical feature to define constancy is whether it is ever reported to disappear once it has developed; intuitively one would imagine that it is as constant as the degree of respiratory failure though this is not supported by published evidence. One small study has shown that pulmonary artery pressure varies with exacerbations and exercise [105]; animal studies also imply phases of remission [106]. There have been few published studies detailing longitudinal changes in sputum bacterial content in stable COPD.…”

Section: Constancy Of Copd Subgroupsmentioning

confidence: 99%

Clinically relevant subgroups in COPD and asthma

Turner

Tamási

Schleich³

et al. 2015

Eur Respir Rev

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As knowledge of airways disease has grown, it has become apparent that neither chronic obstructive pulmonary disease (COPD) nor asthma is a simple, easily defined disease. In the past, treatment options for both diseases were limited; thus, there was less need to define subgroups. As treatment options have grown, so has our need to predict who will respond to new drugs. To date, identifying subgroups has been largely reported by detailed clinical characterisation or differences in pathobiology. These subgroups are commonly called "phenotypes"; however, the problem of defining what constitutes a phenotype, whether this should include comorbid diseases and how to handle changes over time has led to the term being used loosely.In this review, we describe subgroups of COPD and asthma patients whose clinical characteristics we believe have therapeutic or major prognostic implications specific to the lung, and whether these subgroups are constant over time. Finally, we will discuss whether the subgroups we describe are common to both asthma and COPD, and give some examples of how treatment might be tailored in patients where the subgroup is clear, but the label of asthma or COPD is not. @ERSpublications Summary of subgroups of airways disease that can be found in COPD and asthma, and their management

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Pulmonary haemodynamic changes in patients with severe COPD

Cited by 9 publications

References 16 publications

Lung-Heart Clinical Crosstalk in the Course of Copd Exacerbation

Lung-Heart Clinical Crosstalk in the Course of Copd Exacerbation

Influence of respiratory pressure support on hemodynamics and exercise tolerance in patients with COPD

Clinically relevant subgroups in COPD and asthma

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