Exertional dyspnea increases when the mechanical output of the respiratory muscles becomes uncoupled from increases in neural respiratory drive. Combining measurements of inspiratory constraints and ...ventilatory inefficiency may better uncover the role of mechanical-ventilatory abnormalities on exertional dyspnea than the currently-recommended approach, i.e., a low breathing reserve.
We determined the presence of a low breathing reserve (1-(peak ventilation (V̇E)/estimated maximal voluntary ventilation) x 100 < 15%), critical inspiratory constraints (tidal volume (VT)/exercise inspiratory capacity (ICdyn) > 0.7) and ventilatory inefficiency (V̇E/CO2 output (V̇CO2) nadir>34) in 284 subjects (161 males) with “disproportionate dyspnea” (N = 148), “dyspnea with multiple potential causes” (N = 93) and “dyspnea without an apparent cause.
The agreement between breathing reserve and assessment of inspiratory constraints was only “fair” (kappa confidence interval (CI) = 0.264 0.169–0.358). Attainment of critical inspiratory constraints and an upward inflection in dyspnea ratings systematically preceded a low breathing reserve. Of note, ~55% (93/167) of subjects with normal breathing reserve showed critical inspiratory constraints despite largely preserved lung function. Regardless of the breathing reserve, subjects showing critical inspiratory constraints and/or poor ventilatory efficiency reported higher dyspnea and more impaired exercise tolerance compared to their counterparts (p < 0.05). Poor ventilatory efficiency strongly predicted a high dyspnea/work rate in subjects without critical inspiratory constraints regardless of the breathing reserve (odds ratio 95% CI = 4.21 2.01–6.42; p < 0.001).
An integrated analysis of inspiratory constraints and ventilatory inefficiency is key to uncover physiological abnormalities germane to dyspnea in clinical populations in whom the origins of this distressing symptom are uncertain.
•~55% of subjects with dyspnea of unclear origin showed inspiratory constraints.•These subjects, however, had normal breathing reserve.•Inspiratory constraints plus ventilatory inefficiency predicted dyspnea burden and exercise intolerance.•These measurements should be routinely used in the assessment of dyspnea of unclear origin.
Dyspnea is a common, distressing symptom of cardiopulmonary and neuromuscular diseases. Since the ATS published a consensus statement on dyspnea in 1999, there has been enormous growth in knowledge ...about the neurophysiology of dyspnea and increasing interest in dyspnea as a patient-reported outcome.
The purpose of this document is to update the 1999 ATS Consensus Statement on dyspnea.
An interdisciplinary committee of experts representing ATS assemblies on Nursing, Clinical Problems, Sleep and Respiratory Neurobiology, Pulmonary Rehabilitation, and Behavioral Science determined the overall scope of this update through group consensus. Focused literature reviews in key topic areas were conducted by committee members with relevant expertise. The final content of this statement was agreed upon by all members.
Progress has been made in clarifying mechanisms underlying several qualitatively and mechanistically distinct breathing sensations. Brain imaging studies have consistently shown dyspnea stimuli to be correlated with activation of cortico-limbic areas involved with interoception and nociception. Endogenous and exogenous opioids may modulate perception of dyspnea. Instruments for measuring dyspnea are often poorly characterized; a framework is proposed for more consistent identification of measurement domains.
Progress in treatment of dyspnea has not matched progress in elucidating underlying mechanisms. There is a critical need for interdisciplinary translational research to connect dyspnea mechanisms with clinical treatment and to validate dyspnea measures as patient-reported outcomes for clinical trials.
•Patients with coexistent heart failure (HF)-chronic obstructive pulmonary disease (COPD) are frequently unable to sustain prolonged exercise due to intolerable dyspnea.•In the present study, ...bi-level positive airway pressure (BiPAP™) successfully decreased the operating lung volumes and improved exertional dyspnea and endurance exercise tolerance in these patients.•The consequent increase in exercise capacity with BiPAP™ might allow these patients to train at higher exercise intensities thereby deriving greater benefit from cardiopulmonary rehabilitation.
This study tested the hypothesis that, by increasing the volume available for tidal expansion (inspiratory capacity, IC), bi-level positive airway pressure (BiPAP™) would lead to greater beneficial effects on dyspnea and exercise intolerance in comorbid heart failure (HF)-chronic obstructive pulmonary disease (COPD) than HF alone. Ten patients with HF and 9 with HF−COPD (ejection fraction = 30 ± 6% and 35 ± 7%; FEV1 = 83 ± 12% and 65 ± 15% predicted, respectively) performed a discontinuous exercise protocol under sham ventilation or BiPAP™. Time to intolerance increased with BiPAP™ only in HF−COPD (p < 0.05). BiPAP™ led to higher tidal volume and lower duty cycle with longer expiratory time (p < 0.05). Of note, BiPAP™ improved IC (by ∼0.5 l) across exercise intensities only in HF−COPD. These beneficial consequences were associated with lower dyspnea scores at higher levels of ventilation (p < 0.05). By improving the qualitative” (breathing pattern and operational lung volumes) and sensory (dyspnea) features of exertional ventilation, BiPAP™ might allow higher exercise intensities to be sustained for longer during cardiopulmonary rehabilitation in HF−COPD.
Reduced exercise capacity has been reported previously in patients with OSA hypopnea syndrome (OSAHS), although the underlying mechanisms are unclear.
What are the underlying mechanisms of reduced ...exercise capacity in untreated patients with OSAHS? Is there a role for systemic or pulmonary vascular abnormalities?
This was a cross-sectional observational study in which 14 patients with moderate to severe OSAHS and 10 control participants (matched for age, BMI, smoking history, and FEV
) underwent spirometry, incremental cycle cardiopulmonary exercise test (CPET) with arterial line, resting echocardiography, and assessment of arterial stiffness (pulse wave velocity PWV and augmentation index AIx).
Patients (age, 50 ± 11 years; BMI, 30.5 ± 2.7 kg/m
; smoking history, 2.4 ± 4.0 pack-years; FEV
to FVC ratio, 0.78 ± 0.04; FEV
, 85 ± 14% predicted, mean ± SD for all) had mean ± SD apnea hypopnea index of 43 ± 19/h. At rest, PWV, AIx, and mean pulmonary artery pressure (PAP) were higher in patients vs control participants (P < .05). During CPET, patients showed lower peak work rate (WR) and oxygen uptake and greater dyspnea ratings compared with control participants (P < .05 for all). Minute ventilation (V·
), ventilatory equivalent for CO
output (V·
/V·CO
), and dead space volume (V
) to tidal volume (V
) ratio were greater in patients vs control participants during exercise (P < .05 for all). Reduction in V
to V
ratio from rest to peak exercise was greater in control participants compared with patients (0.24 ± 0.08 vs 0.04 ± 0.14, respectively; P = .001). Dyspnea intensity at the highest equivalent WR correlated with corresponding values of V·
/V·CO
(r = 0.65; P = .002), and dead space ventilation (r = 0.70; P = .001). Age, PWV, and mean PAP explained approximately 70% of the variance in peak WR, whereas predictors of dyspnea during CPET were rest-to-peak change in V
to V
ratio and PWV (R
= 0.50; P < .001).
Patients with OSAHS showed evidence of pulmonary gas exchange abnormalities during exercise (in the form of increased dead space) and resting systemic vascular dysfunction that may explain reduced exercise capacity and increased exertional dyspnea intensity.
Background: This consensus statement was developed based on the understanding that patients with advanced lung or heart disease are not
being treated consistently and effectively for relief of ...dyspnea.
Methods: A panel of experts was convened. After a literature review, the panel developed 23 statements covering five domains that
were considered relevant to the topic condition. Endorsement of these statements was assessed by levels of agreement or disagreement
on a five-point Likert scale using two rounds of the Delphi method.
Results: The panel defined the topic condition as âdyspnea that persists at rest or with minimal activity and is distressful despite
optimal therapy of advanced lung or heart disease.â The five domains were: measurement of patient-reported dyspnea, oxygen
therapy, other therapies, opioid medications, and ethical issues. In the second round of the Delphi method, 34 of 56 individuals
(61%) responded, and agreement of at least 70% was achieved for 20 of the 23 statements.
Conclusions: For patients with advanced lung or heart disease, we suggest that: health-care professionals are ethically obligated to treat
dyspnea, patients should be asked to rate the intensity of their breathlessness as part of a comprehensive care plan, opioids
should be dosed and titrated for relief of dyspnea in the individual patient, both the patient and clinician should reassess
whether specific treatments are serving the goal of palliating dyspnea without causing adverse effects, and it is important
for clinicians to communicate about palliative and end-of-life care with their patients.
Individuals with COPD and preserved ratio impaired spirometry (PRISm) findings in clinical settings have an increased risk of cardiovascular disease (CVD).
Do individuals with mild to moderate or ...worse COPD and PRISm findings in community settings have a higher prevalence and incidence of CVD compared with individuals with normal spirometry findings? Can CVD risk scores be improved when impaired spirometry is added?
The analysis was embedded in the Canadian Cohort Obstructive Lung Disease (CanCOLD). Prevalence of CVD (ischemic heart disease IHD and heart failure HF) and their incidence over 6.3 years were compared between groups with impaired and normal spirometry findings using logistic regression and Cox models, respectively, adjusting for covariables. Discrimination of the pooled cohort equations (PCE) and Framingham risk score (FRS) in predicting CVD were assessed with and without impaired spirometry.
Participants (n = 1,561) included 726 people with normal spirometry findings and 835 people with impaired spirometry findings (COPD Global Initiative for Chronic Obstructive Lung Disease GOLD stage 1 disease, n = 408; GOLD stage ≥ 2, n = 331; PRISm findings, n = 96). Rates of undiagnosed COPD were 84% in GOLD stage 1 and 58% in GOLD stage ≥ 2 groups. Prevalence of CVD (IHD or HF) was significantly higher among individuals with impaired spirometry findings and COPD compared with those with normal spirometry findings, with ORs of 1.66 (95% CI, 1.13-2.43; P = .01∗) (∗ indicates statistical significane with P < .05) and 1.55 (95% CI, 1.04-2.31; P = .033∗), respectively. Prevalence of CVD was significantly higher in participants having PRISm findings and COPD GOLD stage ≥ 2, but not GOLD stage 1. CVD incidence was significantly higher, with hazard ratios of 2.07 (95% CI, 1.10-3.91; P = .024∗) for the impaired spirometry group and 2.09 (95% CI, 1.10-3.98; P = .024∗) for the COPD group compared to individuals with normal spirometry findings. The difference was significantly higher among individuals with COPD GOLD stage ≥ 2, but not GOLD stage 1. The discrimination for predicting CVD was low and limited when impaired spirometry findings were added to either risk score.
Individuals with impaired spirometry findings, especially those with moderate or worse COPD and PRISm findings, have increased comorbid CVD compared with their peers with normal spirometry findings, and having COPD increases the risk of CVD developing.
Chronic obstructive pulmonary disease (COPD) is a major respiratory illness in Canada that is both preventable and treatable. Our understanding of the pathophysiology of this complex condition ...continues to grow and our ability to offer effective treatment to those who suffer from it has improved considerably. The purpose of the present educational initiative of the Canadian Thoracic Society (CTS) is to provide up to date information on new developments in the field so that patients with this condition will receive optimal care that is firmly based on scientific evidence. Since the previous CTS management recommendations were published in 2003, a wealth of new scientific information has become available. The implications of this new knowledge with respect to optimal clinical care have been carefully considered by the CTS Panel and the conclusions are presented in the current document. Highlights of this update include new epidemiological information on mortality and prevalence of COPD, which charts its emergence as a major health problem for women; a new section on common comorbidities in COPD; an increased emphasis on the meaningful benefits of combined pharmacological and nonpharmacological therapies; and a new discussion on the prevention of acute exacerbations. A revised stratification system for severity of airway obstruction is proposed, together with other suggestions on how best to clinically evaluate individual patients with this complex disease. The results of the largest randomized clinical trial ever undertaken in COPD have recently been published, enabling the Panel to make evidence-based recommendations on the role of modern pharmacotherapy. The Panel hopes that these new practice guidelines, which reflect a rigorous analysis of the recent literature, will assist caregivers in the diagnosis and management of this common condition.
Symptom perception and respiratory sensation in asthma BANZETT, Robert B; DEMPSEY, Jerome A; O, Denis E ...
American journal of respiratory and critical care medicine,
09/2000, Letnik:
162, Številka:
3
Journal Article
Division of Respiratory and Critical Care Medicine, Department of
Medicine, Queen's University, Kingston, Ontario, Canada K7L 2V7
We compared
qualitative and quantitative aspects of perceived ...exertional dyspnea in
patients with interstitial lung disease (ILD) and normal subjects and
sought a physiological rationale for their differences. Twelve patients
with ILD forced vital capacity = 64 ± 4 (SE)
%predicted and 12 age-matched normal subjects performed
symptom-limited incremental cycle exercise tests with measurements of
dyspnea intensity (Borg scale), ventilation, breathing pattern,
operational lung volumes, and esophageal pressures (Pes). Qualitative
descriptors of dyspnea were selected at exercise cessation. Both groups
described increased "work and/or effort" and
"heaviness" of breathing; only patients with ILD described
"unsatisfied inspiratory effort" (75%), "increased
inspiratory difficulty" (67%), and "rapid breathing" (58%)
( P < 0.05 patients with ILD vs.
normal subjects). Borg-O 2 uptake
( O 2 ) and Borg-ventilation
slopes were significantly greater during exercise in patients with ILD
( P < 0.01). At peak exercise, when
dyspnea intensity and inspiratory effort (Pes-to-maximal inspiratory
pressure ratio) were similar, the distinct qualitative perceptions of
dyspnea in patients with ILD were attributed to differences in dynamic
ventilatory mechancis, i.e., reduced inspiratory capacity, heightened
Pes-to-tidal volume ratio, and tachypnea. Factors contributing to
dyspnea intensity in both groups were also different: the best
correlate of the Borg- O 2
slope in patients with ILD was the resting tidal volume-to-inspiratory
capacity ratio ( r = 0.58, P < 0.05) and in normal subjects was
the slope of Pes-to-maximal inspiratory pressure ratio over
O 2
( r = 0.60, P < 0.05).
respiratory sensation; respiratory mechanics; exercise
Chronic obstructive pulmonary disease (COPD) is a heterogeneous disorder characterized by dysfunction of the small and large airways, as well as by destruction of the lung parenchyma and vasculature, ...in highly variable combinations. Breathlessness and exercise intolerance are the most common symptoms in COPD and progress relentlessly as the disease advances. Exercise intolerance is multifactorial, but in more severe disease, ventilatory limitation is often the proximate exercise-limiting event. Multiple factors determine ventilatory limitation and include integrated abnormalities in ventilatory mechanics and ventilatory muscle function as well as increased ventilatory demands (as a result of gas exchange abnormalities) and alterations in the neuroregulatory control of breathing. Despite its heterogeneity, the pathophysiological hallmark of COPD is expiratory flow limitation. When ventilation increases in flow-limited patients during exercise, air trapping is inevitable and causes further dynamic lung hyperinflation (DH) above the already increased resting volumes. DH causes elastic and inspiratory threshold loading of inspiratory muscles already burdened with increased resistive work. It seriously constrains tidal volume expansion during exercise. DH compromises the ability of the inspiratory muscles to generate pressure, and the positive intrathoracic pressures likely contribute to cardiac impairment during exercise. Progressive DH hastens the development of critical ventilatory constraints that limit exercise and, by causing serious neuromechanical uncoupling, contributes importantly to the quality and intensity of breathlessness. The corollary of this is that therapeutic interventions that reduce operational lung volumes during exercise, by improving lung emptying or by reducing ventilatory demand (which delays the rate of DH), result in clinically meaningful improvement of exercise endurance and symptoms in disabled COPD patients.
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