scholarly journals An official European Respiratory Society statement: pulmonary haemodynamics during exercise

2017 ◽  
Vol 50 (5) ◽  
pp. 1700578 ◽  
Author(s):  
Gabor Kovacs ◽  
Philippe Herve ◽  
Joan Albert Barbera ◽  
Ari Chaouat ◽  
Denis Chemla ◽  
...  

There is growing recognition of the clinical importance of pulmonary haemodynamics during exercise, but several questions remain to be elucidated. The goal of this statement is to assess the scientific evidence in this field in order to provide a basis for future recommendations.Right heart catheterisation is the gold standard method to assess pulmonary haemodynamics at rest and during exercise. Exercise echocardiography and cardiopulmonary exercise testing represent non-invasive tools with evolving clinical applications. The term “exercise pulmonary hypertension” may be the most adequate to describe an abnormal pulmonary haemodynamic response characterised by an excessive pulmonary arterial pressure (PAP) increase in relation to flow during exercise. Exercise pulmonary hypertension may be defined as the presence of resting mean PAP <25 mmHg and mean PAP >30 mmHg during exercise with total pulmonary resistance >3 Wood units. Exercise pulmonary hypertension represents the haemodynamic appearance of early pulmonary vascular disease, left heart disease, lung disease or a combination of these conditions. Exercise pulmonary hypertension is associated with the presence of a modest elevation of resting mean PAP and requires clinical follow-up, particularly if risk factors for pulmonary hypertension are present. There is a lack of robust clinical evidence on targeted medical therapy for exercise pulmonary hypertension.

2020 ◽  
Vol 2020 (1) ◽  
Author(s):  
Martin Wilkins

The plasma proteome is rich in information. It comprises proteins that are secreted or lost from cells as they respond to their local environment. Changes in the constitution of the plasma proteome offer a relatively non-invasive report on the health of tissues. This is particularly true of the lung in pulmonary hypertension, given the large surface area of the pulmonary vasculature in direct communication with blood. So far, this is relatively untapped; we have relied on proteins released from the heart, specifically brain natriuretic peptide and troponin, to inform clinical management. New technology allows the measurement of a larger number of proteins that cover a broad range of molecular pathways in a single small aliquot. The emerging data will yield more than just new biomarkers of pulmonary hypertension for clinical use. Integrated with genomics and with the help of new bioinformatic tools, the plasma proteome can provide insight into the causative drivers of pulmonary vascular disease and guide drug development.


2019 ◽  
Vol 7 ◽  
pp. 2050313X1984780
Author(s):  
Geeshath Jayasekera ◽  
Martin Johnson ◽  
Keith Hussey ◽  
Colin Church

Pulmonary hypertension is a disease process affecting the pulmonary circulation and is defined by an increase in pulmonary artery pressure subsequently causing right ventricular failure. Vascular complications, including arteriovenous fistulae, are recognised, but are uncommon complications of spinal surgery. Arteriovenous fistulae increase venous return to the right heart and can induce a high-output cardiac state, mimicking pulmonary arterial hypertension and right heart failure. We present a 47-year-old man with a 1 year history of worsening dyspnoea, exertional pre-syncope and leg swelling presenting with severe right heart failure. The previous year, he had complex spinal surgery, which included discectomy, laminectomy and bilateral nerve reconstruction at L5-S1 level. Initial non-invasive investigations including echocardiography and chest imaging raised the possibility of right heart failure presumed secondary to pulmonary vascular disease. Clinical examination and right heart catheterisation were in keeping with a high cardiac output state, and invasive saturation monitoring was suggestive of a sub-diaphragmatic shunt. Subsequent imaging confirmed the presence of an iatrogenic ilio-iliac arteriovenous fistula. The patient underwent urgent endovascular repair, which resulted in resolution of his symptoms and haemodynamics. We describe the case and present a review of the relevant literature.


2019 ◽  
Vol 21 (Supplement_K) ◽  
pp. K4-K8 ◽  
Author(s):  
Gérald Simonneau ◽  
Marius M Hoeper

Abstract At the 6th World Symposium on Pulmonary Hypertension (PH), it was proposed that the mean pulmonary arterial pressure (mPAP) threshold used to define PH should be lowered from ≥25 mmHg to &gt;20 mmHg. The rationale for this change is that the ≥25 mmHg threshold is arbitrary, whereas the revised threshold is based on scientific evidence. For the definition of all forms of pre-capillary PH, the inclusion of a pulmonary vascular resistance (PVR) ≥3 Wood Units was also proposed, placing greater emphasis on an elevated PVR to identify pulmonary vascular disease. Here, we discuss the possible impact of the revised definition of PH on future clinical management. This change may facilitate earlier PH detection, particularly in at-risk patient groups that are already undergoing screening programmes, e.g. those with systemic sclerosis or mutations associated with PH. As an mPAP above the upper limit of normal (&gt;20 mmHg) but &lt;25 mmHg is associated with increased risk of morbidity and mortality compared with a normal mPAP, early identification of patients in this group is important to enable close monitoring and timely treatment initiation once clinically indicated. Treatments currently approved for PH are not necessarily suitable for patients with an mPAP 21–24 mmHg, as the management of this group has not been widely examined. The revised definition may facilitate inclusion of these patients in prospective trials, allowing the evaluation of appropriate management strategies.


2015 ◽  
Vol 46 (3) ◽  
pp. 738-749 ◽  
Author(s):  
Luiza H. Degani-Costa ◽  
Barbara Levarge ◽  
Subba R. Digumarthy ◽  
Aaron S. Eisman ◽  
R. Scott Harris ◽  
...  

When overt pulmonary hypertension arises in interstitial lung disease (ILD), it contributes to exercise intolerance. We sought to determine the functional significance of abnormal pulmonary arterial pressure (PAP) responses to exercise in ILD.27 ILD patients and 11 age-matched controls underwent invasive cardiopulmonary exercise testing (iCPET). Mean PAP (mPAP) was indexed to cardiac output (Q´T) during exercise, with a mPAP–Q´Tslope ≥3 mmHg·min·L−1defined as an abnormal pulmonary vascular response.All control subjects had mPAP–Q´Tslopes <3 mmHg·min·L−1(mean±sem1.5±0.1 mmHg·min·L−1). 15 ILD patients had mPAP–Q´Tslopes ≥3 mmHg·min·L−1(4.1±0.2 mmHg·min·L−1) and were labelled as having ILD plus pulmonary vascular dysfunction (PVD). Subjects without pulmonary hypertension and with mPAP–Q´Tslopes <3 mmHg·min·L−1(1.9±0. 2 mmHg·min·L−1) were labelled as ILD minus PVD (n=12). ILD+PVD and ILD−PVD patients did not differ in terms of age, sex, body mass index, pulmonary function testing or degree of exercise oxygen desaturation. Peak oxygen consumption was lower in ILD+PVD than in ILD−PVD (13.0±0.9versus17±1.1 mL·kg−1·min−1, p=0.012) and controls (19.8±1.7 mL·kg−1·min−1, p=0.003). ILD+PVD patients had increased dead space volume (VD)/tidal volume (VT) and minute ventilation/carbon dioxide production at the anaerobic threshold.In ILD, mPAP–Q´Tslope ≥3 mmHg·min·L−1is associated with lower peak oxygen consumption, increasedVD/VTand inefficient ventilation. While noninvasive parameters were unable to predict those with abnormal pulmonary vascular responses to exercise, iCPET-derived mPAP–Q´Tslope may aid in identifying physiologically significant, early pulmonary vascular disease in ILD.


2021 ◽  
Vol 13 (1) ◽  
pp. 68-78
Author(s):  
Simon Wernhart ◽  
Jürgen Hedderich ◽  
Eberhard Weihe

Introduction: Exercise pulmonary hypertension (exPH) has been defined as total pulmonary resistance (TPR) >3 mm Hg/L/min and mean pulmonary artery pressure (mPAP) >30 mm Hg, albeit with a considerable risk of false positives in elderly patients with lower cardiac output during exercise. Methods:We retrospectively analysed patients with unclear dyspnea receiving right heart catheterisation at rest and exercise (n=244) between January 2015 and January 2020. Lung function testing, blood gas analysis, and echocardiography were performed. We elaborated a combinatorial score to advance the current definition of exPH in an elderly population (mean age 67.0 years±11.9). A stepwise regression model was calculated to non-invasively predict exPH. Results: Analysis of variables across the achieved peak power allowed the creation of a model for defining exPH, where three out of four criteria needed to be fulfilled: Peak power ≤100 Watt, pulmonary capillary wedge pressure ≥18 mm Hg, pulmonary vascular resistance >3 Wood Units, and mPAP ≥35 mm Hg. The new scoring model resulted in a lower number of exPH diagnoses than the current suggestion (63.1% vs. 78.3%). We present a combinatorial model with vital capacity (VCmax) and valvular dysfunction to predict exPH (sensitivity 93.2%; specificity 44.2%, area under the curve 0.73) based on our suggested criteria. The odds of the presence of exPH were 2.1 for a 1 l loss in VCmax and 3.6 for having valvular dysfunction. Conclusion: We advance a revised definition of exPH in elderly patients in order to overcome current limitations. We establish a new non-invasive approach to predict exPH by assessing VCmax and valvular dysfunction for early risk stratification in elderly patients.


2019 ◽  
Vol 4 (3) ◽  
pp. 225-237
Author(s):  
Faisal Shaikh ◽  
Zafia Anklesaria ◽  
Tasneam Shagroni ◽  
Rajeev Saggar ◽  
Luna Gargani ◽  
...  

In general, pulmonary vascular disease has important negative prognostic implications, regardless of the associated condition or underlying mechanism. In this regard, systemic sclerosis is of particular interest as it is the most common connective tissue disease associated with pulmonary hypertension, and a well-recognized at-risk population. In the setting of systemic sclerosis and unexplained dyspnea, the concept of using exercise to probe for underlying pulmonary vascular disease has acquired significant interest. In theory, a diagnosis of systemic sclerosis–associated exercise pulmonary hypertension may allow for earlier therapeutic intervention and a favorable alteration in the natural history of the pulmonary vascular disease. In the context of underlying systemic sclerosis, the purpose of this article is to provide a comprehensive review of the evolving definition of exercise pulmonary hypertension, the current role and methodologies for non-invasive and invasive exercise testing, and the importance of the right ventricle.


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
P Xanthouli ◽  
N Milde ◽  
A M Marra ◽  
N Benjamin ◽  
C Nagel ◽  
...  

Abstract Background Patients with systemic sclerosis (SSc) are at high risk of developing concomitant pulmonary hypertension (PH) which has a crucial impact on the patients' symptoms, quality of life and prognosis. Purpose The aim of this study was to analyse the impact of the new hemodynamic definition of precapillary PH as proposed at the 2018 World Symposium on PH in Nice in patients with SSc. Although recent data suggest that PVR >2 WU could be considered as abnormal in the new definition a conservative cut-off value of PVR ≥3 WU has been used. Methods SSc-patients were screened for PH using clinical assessments as WHO-functional class, 6 minute walking distance and right heart catheterisation. Patients were divided into hemodynamic subgroups according to their mean pulmonary arterial pressure (mPAP) values with mPAP ≤20 mmHg, 21–24 mmHg and ≥25 mmHg. These subgroups were further divided according to their pulmonary vascular resistance (PVR) with PVR <3 WU or ≥3 WU. Results One-hundred-twenty-two patients (79% female, age 57.6±12.7 years, 6MWD 439.5±98.1 meters, 70% diffuse cutaneous SSc, 30% limited cutaneous SSc, 53% WHO-FC II, 25% WHO-FC III) who were prospectively screened for PH were included in the analysis (Figure 1). Among them 26 had a symptomatic manifest PH using the cut-off value of mPAP ≥25 mmHg. Only half of this group presented with PVR ≥3 WU, the others had PVR <3 WU. Eight of these 26 PH-patients presented with PH due to left heart disease. Out of 21 patients with mildly elevated mPAP 21–24 mmHg, two (10%) met the new definition criteria of PH (pulmonary arterial wedge pressure <15 mmHg, mPAP 23 and 24 mmHg, PVR 3.0 and 3.2 WU, CI 2.2 L/min/m2 both, WHO-FC II both, respectively). Out of 75 patients with mPAP <21 mmHg, three presented with PVR ≥3 WU. Overview of systemic sclerosis patients Conclusions The new definition of precapillary pulmonary hypertension may on the one hand allow detecting an additional 10% of PH patients with mild elevated mPAP. On the other hand, eight of 13 patients (62%), who met the former definition of pulmonary arterial hypertension, would be classified as “normal” due to a lack of increase in PVR according to the new definition. The data of this study suggest that for SSc-patients the cut-off value of mPAP >20 mmHg is useful, but the criteria of PVR ≥3 WU may be too strict. Further studies with larger sample sizes will be needed to better characterise these hemodynamic subgroups and to define the extent of pulmonary vascular disease and treatability.


Sign in / Sign up

Export Citation Format

Share Document