Heart, lungs, and muscle interplay in worsening activity-related breathlessness in advanced cardiopulmonary disease.

PURPOSE OF REVIEW: Activity-related breathlessness is a key determinant of poor quality of life in patients with advanced cardiorespiratory disease. Accordingly, palliative care has assumed a prominent role in their care. The severity of breathlessness depends on a complex combination of negative cardiopulmonary interactions and increased afferent stimulation from systemic sources. We review recent data exposing the seeds and consequences of these abnormalities in combined heart failure and chronic obstructive pulmonary disease (COPD). RECENT FINDINGS: The drive to breathe increases ('excessive breathing') secondary to an enlarged dead space and hypoxemia (largely COPD-related) and heightened afferent stimuli, for example, sympathetic overexcitation, muscle ergorreceptor activation, and anaerobic metabolism (largely heart failure-related). Increased ventilatory drive might not be fully translated into the expected lung-chest wall displacement because of the mechanical derangements brought by COPD ('inappropriate breathing'). The latter abnormalities, in turn, negatively affect the central hemodynamics which are already compromised by heart failure. Physical activity then decreases, worsening muscle atrophy and dysfunction. SUMMARY: Beyond the imperative of optimal pharmacological treatment of each disease, strategies to lessen ventilation (e.g., walking aids, oxygen, opiates and anxiolytics, and cardiopulmonary rehabilitation) and improve mechanics (heliox, noninvasive ventilation, and inspiratory muscle training) might mitigate the burden of this devastating symptom in advanced heart failure-COPD.

Differences in respiratory muscle activity during cycling and walking do not influence dyspnea perception in obese patients with COPD.

In patients with combined obesity and chronic obstructive pulmonary disease (COPD), dyspnea intensity at matched work rates during weight-supported cycling and weight-bearing walking is similar, despite consistent metabolic differences between test modalities. The present study examined the influence of differences in activity of the diaphragm and abdominal muscles during cycling and walking on intensity and quality of dyspnea at matched ventilation in obese patients with COPD. We compared respiratory muscle activity patterns and dyspnea ratings during incremental cycle and treadmill exercise tests, where work rate was matched, in 12 obese (body mass index 36.6 ± 5.4 kg/m(2); mean ± SD) patients with moderate COPD. We used a multipair electrode-balloon catheter to compare electromyography of the diaphragm and esophageal, gastric, and transdiaphragmatic pressures during the two exercise tests. Ventilation, breathing pattern, operating lung volumes, global respiratory effort, and electrical activation of the diaphragm were similar across exercise modalities for a given work rate. The cycling position was associated with greater neuromuscular efficiency of the diaphragm (P < 0.01), greater diaphragm use (P < 0.01) measured by the ventilatory muscle recruitment index, and less expiratory muscle activity compared (P < 0.01) with treadmill walking. However, intensity and quality of dyspnea were similar between exercise modalities. In obese patients with COPD, altered respiratory muscle activity due to body position differences between cycling and walking did not modulate perceived dyspnea when indirect measures of respiratory neural drive were unchanged.

Should mild COPD be treated? Evidence for early pharmacological intervention.

Chronic obstructive pulmonary disease (COPD) is a common and often progressive inflammatory disease of the airways that is both preventable and treatable. It is well established that those with mild-to-moderate disease severity represent the majority of patients with COPD, yet this subpopulation is relatively under-studied. Because of an insidious pre-clinical phase, COPD is both under-diagnosed and under-treated. Recent studies have confirmed that even patients with mild, grade 1 COPD [i.e. those with a reduced forced expiratory volume in one second (FEV1)/forced vital capacity ratio but normal FEV1], have measurable physiological impairment with increased morbidity and a higher risk of mortality compared with non-smoking healthy controls. Beyond the imperative of smoking cessation-the pivotal intervention in all COPD stages-the role of pharmacotherapy for prevention of disease progression has yet to be established. The main objective of this review is to provide a concise overview of the heterogeneous pathophysiology of COPD with only mild airway obstruction on spirometry and obstacles for early diagnosis. We emphasize that the absence of sufficiently powered trials involving a large number of patients precludes definitive recommendations in support of (or against) long-term pharmacological treatment in mild COPD. Despite these limitations, we present a rationale for earlier pharmacological intervention derived from recent physiological studies performed in symptomatic patients with mild COPD.

Effects of bicarbonate on oxyhaemoglobin desaturation and exercise performance in athletes.

AIM: Decrease in peripheral oxygen delivery may impact exercise performance in athletes with exercise-related arterial oxygen desaturation (ERD). We evaluated whether sodium bicarbonate ingestion would be effective to reduce ERD and what is the consequences upon exercise performance. METHODS: Seventy highly trained athletes performed an incremental treadmill cardiopulmonary exercise test (incCPX) and a high intensity constant speed test (ctCPX) on separate days. Subjects who developed ERD by pulse oximetry were randomly allocated to oral sodium bicarbonate or placebo during 5 days. At the end of treatment subjects repeated both tests. RESULTS: ERD prevalence was 33% during the incCPX (17 % severe, 48% moderate and 35% mild) and 34% (5 % severe, 37% moderate and 58% mild) in the ctCPX. Athletes who developed ERD have greater aerobic capacity (incCPX) and endurance time (ctCPX). Active treatment, but not placebo, reduced ERD during ctCPX (P<0.05). However, there were no significant positive effects on main parameters of aerobic function and endurance exercise capacity (P>0.05). CONCLUSION: Sodium bicarbonate was effective in lessening ERD during ctCPX in athletes. However, this intervention failed to improve maximal and submaximal exercise capacity in these subjects.

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

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.