Dyspnea in Pulmonary Arterial Hypertension (original) (raw)
Related papers
Exercise-induced Pulmonary Hypertension
American Journal of Respiratory and Critical Care Medicine, 2013
Exercise stresses the pulmonary circulation through increases in cardiac output (_ Q) and left atrial pressure. Invasive as well as noninvasive studies in healthy volunteers show that the slope of mean pulmonary artery pressure (mPAP)-flow relationships ranges from 0.5 to 3 mm Hg$min$L 21. The upper limit of normal mPAP at exercise thus approximates 30 mm Hg at a _ Q of less than 10 L$min 21 or a total pulmonary vascular resistance at exercise of less than 3 Wood units. Left atrial pressure increases at exercise with an average upstream transmission to PAP in a close to one-for-one mm Hg fashion. Multipoint PAP-flow relationships are usually described by a linear approximation, but present with a slight curvilinearity, which is explained by resistive vessel distensibility. When mPAP is expressed as a function of oxygen uptake or workload, plateau patterns may be observed in patients with systolic heart failure who cannot further increase _ Q at the highest levels of exercise. Exercise has to be dynamic to avoid the increase in systemic vascular resistance and abrupt changes in intrathoracic pressure that occur with resistive exercise and can lead to unpredictable effects on the pulmonary circulation. Postexercise measurements are unreliable because of the rapid return of pulmonary vascular pressures and flows to the baseline resting state. Recent studies suggest that exercise-induced increase in PAP to a mean higher than 30 mm Hg may be associated with dyspnea-fatigue symptomatology.
Pulmonary arterial pressure during rest and exercise in healthy subjects: a systematic review
European Respiratory Journal, 2009
According to current guidelines, pulmonary arterial hypertension (PAH) is diagnosed when mean pulmonary arterial pressure (Ppa) exceeds 25 mmHg at rest or 30 mmHg during exercise. Issues that remain unclear are the classification of Ppa values <25 mmHg and whether Ppa >30 mmHg during exercise is always pathological. We performed a comprehensive literature review and analysed all accessible data obtained by right heart catheter studies from healthy individuals to determine normal Ppa at rest and during exercise. Data on 1,187 individuals from 47 studies in 13 countries were included. Data were stratified for sex, age, geographical origin, body position and exercise level. Ppa at rest was 14.0+/-3.3 mmHg and this value was independent of sex and ethnicity. Resting Ppa was slightly influenced by posture (supine 14.0+/-3.3 mmHg, upright 13.6+/-3.1 mmHg) and age (<30 yrs: 12.8+/- 3.1 mmHg; 30-50 yrs: 12.9+/-3.0 mmHg; > or = 50 yrs: 14.7+/-4.0 mmHg). Ppa during exercise was dependent on exercise level and age. During mild exercise, Ppa was 19.4+/-4.8 mmHg in subjects aged <50 yrs compared with 29.4+/-8.4 mmHg in subjects > or = 50 yrs (p<0.001). In conclusion, while Ppa at rest is virtually independent of age and rarely exceeds 20 mmHg, exercise Ppa is age-related and frequently exceeds 30 mmHg, especially in elderly individuals, which makes it difficult to define normal Ppa values during exercise.
Resting pulmonary artery pressure of 21-24 mmHg predicts abnormal exercise haemodynamics
The European respiratory journal, 2016
A resting mean pulmonary artery pressure (mPAP) of 21-24 mmHg is above the upper limit of normal but does not reach criteria for the diagnosis of pulmonary hypertension (PH). We sought to determine whether an mPAP of 21-24 mmHg is associated with an increased risk of developing an abnormal pulmonary vascular response during exercise.Consecutive patients (n=290) with resting mPAP <25 mmHg who underwent invasive exercise haemodynamics were analysed. Risk factors for pulmonary vascular disease or left heart disease were present in 63.4% and 43.8% of subjects. An abnormal pulmonary vascular response (or exercise PH) was defined by mPAP >30 mmHg and total pulmonary vascular resistance >3 WU at maximal exercise.Exercise PH occurred in 74 (86.0%) out of 86 versus 96 (47.1%) out of 204 in the mPAP of 21-24 mmHg and mPAP <21 mmHg groups, respectively (OR 6.9, 95% CI: 3.6-13.6; p<0.0001). Patients with mPAP of 21-24 mmHg had lower 6-min walk distance (p=0.002) and higher New Yo...
Exercise pulmonary haemodynamics: a test in search of purpose
European Respiratory Journal, 2016
Ever since the entity of "exercise induced pulmonary hypertension" was banned from the pulmonary hypertension (PH) dictionary in 2008, during the World Symposium on Pulmonary Hypertension at Dana Point (CA, USA) [1], there has been a concern that by just measuring pulmonary haemodynamics at rest, many patients with subclinical pulmonary vascular disease go unrecognised. This could be harmful, if subjects with an abnormal pulmonary haemodynamic response to exercise are at particular risk of developing PH and that early recognition of PH in these patients would improve their outcome. It may even be that the presence of an abnormal pulmonary haemodynamic response to exercise represents a treatable condition. To date, there is no proof to validate any of these assumptions. The plea in favour of invasive exercise testing so far has failed to overcome several important obstacles. First, there has been a lack of standardisation of invasive cardiopulmonary exercise testing, while the mode of testing and intensity of exercise may certainly affect outcomes. For example, particularly elderly patients may fulfil criteria of an abnormal haemodynamic response at submaximal exercise levels, but no longer at maximal exercise [2]. Second, there remains uncertainty about the physiological limits of a normal response to exercise of pulmonary artery pressure, cardiac output and pulmonary vascular resistance. Third, there is no evidence that treatment of subjects with an abnormal pulmonary haemodynamic response but without PH would improve their outcome. An additional question, to the usefulness of invasive exercise testing, is whether the population of subjects with an abnormal pulmonary haemodynamic response to exercise overlaps with another population that physicians are struggling with, i.e. those with resting mean pulmonary artery pressures (Ppa) below the definition of PH, but clearly higher than the normal physiological limits. Just like patients with abnormal exercise pulmonary haemodynamics, these subjects suffer from increased mortality and hospitalisation [3]. In this issue of the European Respiratory Journal LAU et al. [4] report on exercise pulmonary haemodynamics in 290 consecutive patients at risk for PH with a resting mean Ppa of ⩽25 mmHg. They found that an "abnormal" response was common in those with borderline elevation of resting pressures (86%) and further that the likelihood of an "abnormal" response increased progressively as resting mean pressure increased from 13 mmHg upwards. There was no systematic follow-up, thus we have no direct insight into the prognostic significance of these observations. However, patients with exercise PH were more symptomatic and had reduced exercise tolerance. We must, therefore, consider whether the proposed definition of an "abnormal" exercise response is valid, whether the population investigated includes biases that would increase the
Advances in Pulmonary Hypertension, 2014
During the Fifth World Symposium on Pulmonary Hypertension, the working group on diagnosis and assessment was charged with evaluating the definition of pulmonary arterial hypertension (PAH) as it was established at the Fourth World Symposium. The group also covered related topics such as “borderline PAH,” exercise-induced PAH, and issues surrounding the measurement of pulmonary capillary wedge pressure (PCWP). The working group's discussion specifically addressed the following questions:Should pulmonary hypertension (PH) continue to be defined by a resting mean pulmonary artery pressure (MPAP) ≥25 mm Hg, and should the term “borderline PH” be introduced?Should exercise-induced PH be included as a subset of PH?Should pulmonary vascular resistance (PVR) be reintroduced in the definition of PAH?Is pulmonary artery wedge pressure (PAWP) of 15 mm Hg adequate to distinguish between pre- and post-capillary PH, and how should it be measured?Should fluid or exercise challenge be used to ...
Dynamic respiratory mechanics and exertional dyspnoea in pulmonary arterial hypertension
The European respiratory journal, 2013
Patients with pulmonary arterial hypertension (PAH) may exhibit reduced expiratory flows at low lung volumes, which could promote exercise-induced dynamic hyperinflation (DH). This study aimed to examine the impact of a potential exercise-related DH on the intensity of dyspnoea in patients with PAH undergoing symptom-limited incremental cardiopulmonary cycle exercise testing (CPET). 25 young (aged mean±sd 38±12 yrs) nonsmoking PAH patients with no evidence of spirometric obstruction and 10 age-matched nonsmoking healthy subjects performed CPET to the limit of tolerance. Ventilatory pattern, operating lung volumes (derived from inspiratory capacity (IC) measurements) and dyspnoea intensity (Borg scale) were assessed throughout CPET. IC decreased (i.e. DH) progressively throughout CPET in PAH patients (average 0.15 L), whereas it increased in all the healthy subjects (0.45 L). Among PAH patients, 15 (60%) exhibited a decrease in IC throughout exercise (average 0.50 L), whereas in the ...
Criteria for diagnosis of exercise pulmonary hypertension
European Respiratory Journal, 2015
The previous definition of exercise pulmonary hypertension (PH) with a mean pulmonary artery pressure (mPAP) >30 mmHg was abandoned because healthy individuals can exceed this threshold at high cardiac output (CO). We hypothesised that incorporating assessment of the pressure–flow relationship using the mPAP/CO ratio, i.e. total pulmonary resistance (TPR), might enhance the accuracy of diagnosing an abnormal exercise haemodynamic response.Exercise haemodynamics were evaluated in 169 consecutive subjects with normal resting mPAP ≤20 mmHg. Subjects were classified into controls without heart or lung disease (n=68) versus patients with pulmonary vascular disease (PVD) (n=49) and left heart disease (LHD) (n=52).TPR and mPAP at maximal exercise produced diagnostic accuracy with area under the receiver operating curve of 0.99 and 0.95, respectively, for discriminating controls versus patients with PVD and LHD. The old criterion of mPAP >30 mmHg had sensitivity of 0.98 but specificit...
ERJ Open Research, 2020
The contemporary population of patients with pulmonary arterial hypertension (PAH) are older, with a high prevalence of cardiovascular risk factors [1], and potentially at risk for left ventricular diastolic dysfunction [2]. Accordingly, the effect of exercise or volume expansion may elicit augmented increases in pulmonary artery wedge pressure (PAWP) [3, 4], in addition to abnormal behaviour of pulmonary artery pressures. In healthy older subjects, exercise-associated increases in PAWP are predictably coupled to decreases in pulmonary arterial compliance (PAC) and pulmonary vascular resistance (PVR), thereby systematically lowering the product of the resistance-compliance relationship (RC-time) [5]. We prospectively examined this physiology in older patients with PAH. Exercise and volume expansion were compared with respect to the response of the PAWP and relationships to pulmonary artery pressures and RC-time. Adults with PAH aged >45 years referred for right heart catheterisation were recruited. Exclusion criteria included left ventricular systolic dysfunction (left ventricular ejection fraction <50%) or ⩾ moderate left-sided valvular heart disease. The local research ethics board approved the study protocol. Participants provided written informed consent. A balloon-tipped fluid-filled catheter was positioned in the pulmonary artery via internal jugular venous access. Right atrial pressure (RAP), pulmonary artery pressures (PAP) and PAWP were recorded at baseline in the supine position and heart rate (HR) was monitored continuously. After baseline, Volume consisted of volume expansion challenge by intravenous infusion of 15 mL•kg −1 of 0.9% sodium chloride solution at 100 mL•min −1. Haemodynamic data were recorded 1 min after completing Volume. Afterwards, participants were transferred to a cycle ergometer in a semi-upright position. Haemodynamic data were acquired at 1, 3 and 5 min at rest (Control) and averaged. Participants then pedalled at self-selected cadence between 60 and 80 xg at constant a work-rate of 15 watts. Haemodynamic data were obtained at 3 min after onset of cycling (Exercise). Analysis intervals consisted of ⩾10 consecutive beats free from premature beats. Calculations included: pulmonary pulse pressure (pulmonary PP; mmHg) = pulmonary artery systolic pressure (PASP) − pulmonary artery diastolic pressure (PADP); transpulmonary gradient (TPG; mmHg) = mean pulmonary artery pressure (mPAP) − PAWP; diastolic pressure difference (DPD; mmHg) = PADP-PAWP; RC-time is calculated as the product of PVR (TPG/(stroke volume×HR)) and PAC (stroke volume/PP), which can be simplified to TPG/(HR×PP). Changes in RAP and PAWP, relative to volume infused, were assessed by the slopes of RAP/volume infused and PAWP/volume infused relations. Data were analysed using SPSS, version 21 (IBM Corp., Armonk, NY, USA) and presented as median and interquartile ranges (IQR). Comparisons of continuous variables between conditions were analysed using related-samples Wilcoxon signed rank test. Two-tailed α level of 0.05 was considered statistically significant. @ERSpublications In this study, among patients with pulmonary arterial hypertension, exercise was more potent in eliciting pulmonary vascular abnormalities and demonstrated paradoxical increase in RC-time https://bit.ly/35Mb0dv