Heart failure worsens leg muscle strength and endurance in coexistence patients with COPD and heart failure reduced ejection fraction.

PURPOSE: Exercise intolerance and dyspnoea are clinical symptoms in both heart failure (HF) reduced ejection fraction (HFrEF) and chronic obstructive pulmonary disease (COPD), which are suggested to be associated with musculoskeletal dysfunction. We tested the hypothesis that HFrEF + COPD patients would present lower muscle strength and greater fatigue compared to compared to the COPD group. METHODS: We included 25 patients with HFrEF + COPD (100% male, age 67.8 ± 6.9) and 25 patients with COPD alone (100% male, age 66.1 ± 9.1). In both groups, COPD severity was determined as moderate-to-severe according to the GOLD classification (FEV1/FVC < 0.7 and predicted post-bronchodilator FEV1 between 30%-80%). Knee flexor-extensor muscle performance (torque, work, power and fatigue) were measured by isokinetic dynamometry in age and sex-matched patients with HFrEF + COPD and COPD alone; Functional capacity was assessed by the cardiopulmonary exercise test, the 6-min walk test (6MWT) and the four-minute step test. RESULTS: The COPD group exhibited reduced lung function compared to the HFrEF + COPD group, as evidenced by lower FEV1/FVC (58.0 ± 4.0 vs. 65.5 ± 13.9; p < 0.0001, respectively) and FEV1 (51.3 ± 17.0 vs. 62.5 ± 17.4; p = 0.026, respectively) values. Regarding musculoskeletal function, the HFrEF + COPD group showed a knee flexor muscles impairment, however this fact was not observed in the knee extensors muscles. Power peak of the knee flexor corrected by muscle mass was significantly correlated with the 6MWT (r = 0.40; p < 0.05), number of steps (r = 0.30; p < 0.05) and work ratepeak (r = 0.40; p < 0.05) in the HFrEF + COPD and COPD groups. CONCLUSION: The presence of HFrEF in patients with COPD worsens muscular weakness when compared to isolated COPD.

Exertional oscillatory ventilation in subjects without heart failure reporting chronic dyspnoea.

Oscillatory ventilation detected on incremental cardiopulmonary exercise testing might be found in subjects without heart failure reporting exertional dyspnoea despite the best available therapy for their underlying cardiopulmonary disease https://bit.ly/3Tyl7bE.

Rib cage distortion and dynamic hyperinflation during two exercise intensities in people with COPD.

BACKGROUND: The relationship between rib cage (RC) motion abnormalities, dynamic hyperinflation (DH), and exercise capacity in people with COPD is controversial. AIM: To investigate RC distortion and operational chest wall volumes during moderate and high constant-rate exercises in people with COPD. METHODS: Seven male participants [median(Q1-Q3) age: 63(60.0-66.0) years; FEV1: 39.0(38.0-63.0)% of predicted] performed a symptom-limited incremental exercise testing on cycle ergometer, followed by constant-rate tests (60 % and 80 % of peak work rate). Optoelectronic plethysmography was used to evaluate RC distortion: phase angle-PhAng, inspiratory phase ratio-PhRIB, expiratory phase ratio-PhREB; and chest wall volumes: end-inspiratory volume-Vei and end-expiratory volume-Vee. RESULTS: PhRIB and PhREB significantly increased during both constant-rate exercise tests, without difference between them. In general, Vei of the chest wall significantly increased in both exercise intensities while Vee did not change. CONCLUSIONS: The occurrence of RC distortion seemed not to limit the exercise capacity in people with COPD evaluated, and it was present even in the absence of DH.

Noninvasive Ventilation Accelerates Oxygen Uptake Recovery Kinetics in Patients With Combined Heart Failure and Chronic Obstructive Pulmonary Disease.

PURPOSE: Oxygen uptake (V˙o2) recovery kinetics appears to have considerable value in the assessment of functional capacity in both heart failure (HF) and chronic obstructive pulmonary disease (COPD). Noninvasive positive pressure ventilation (NIPPV) may benefit cardiopulmonary interactions during exercise. However, assessment during the exercise recovery phase is unclear. The purpose of this investigation was to explore the effects of NIPPV on V˙o2, heart rate, and cardiac output recovery kinetics from high-intensity constant-load exercise (CLE) in patients with coexisting HF and COPD. METHODS: Nineteen males (10 HF/9 age- and left ventricular ejection fraction-matched HF-COPD) underwent 2 high-intensity CLE tests at 80% of peak work rate to the limit of tolerance (Tlim), receiving either sham ventilation or NIPPV. RESULTS: Despite greater V˙o2 recovery kinetics on sham, HF-COPD patients presented with a faster exponential time constant τ (76.4 ± 14.0 sec vs 62.8 ± 15.2 sec, P < .05) and mean response time (MRT) (86.1 ± 19.1 sec vs 68.8 ± 12.0 sec, P < .05) with NIPPV and greater ΔNIPPV-sham (τ: 5.6 ± 19.5 vs -25.2 ± 22.4, P < .05; MRT: 4.1 ± 32.2 vs -26.0 ± 19.2, P < .05) compared with HF. There was no difference regarding Tlim between sham and NIPPV in both groups (P < .05). CONCLUSION: Our results suggest that NIPPV accelerated the V˙o2 recovery kinetics following high-intensity CLE to a greater extent in patients with coexisting HF and COPD compared with HF alone. NIPPV should be considered when the objective is to apply high-intensity interval exercise training as an adjunct intervention during a cardiopulmonary rehabilitation program.

Effects of bi-level positive airway pressure on ventilatory and perceptual responses to exercise in comorbid heart failure-COPD.

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.

Exercise intolerance in comorbid COPD and heart failure: the role of impaired aerobic function.

Impaired aerobic function is a potential mechanism of exercise intolerance in patients with combined cardiorespiratory disease. We investigated the pathophysiological and sensory consequences of a low change in oxygen uptake (ΔV'O2 )/change in work rate (ΔWR) relationship during incremental exercise in patients with coexisting chronic obstructive pulmonary disease (COPD) and systolic heart failure (HF).After clinical stabilisation, 51 COPD-HF patients performed an incremental cardiopulmonary exercise test to symptom limitation. Cardiac output was non-invasively measured (impedance cardiography) in a subset of patients (n=18).27 patients presented with ΔV'O2 /ΔWR below the lower limit of normal. Despite similar forced expiratory volume in 1 s and ejection fraction, the low ΔV'O2 /ΔWR group showed higher end-diastolic volume, lower inspiratory capacity and lower transfer factor compared to their counterparts (p<0.05). Peak WR and peak V'O2 were ∼15% and ∼30% lower, respectively, in the former group: those findings were associated with greater symptom burden in daily life and at a given exercise intensity (leg discomfort and dyspnoea). The low ΔV'O2 /ΔWR group presented with other evidences of impaired aerobic function (sluggish V'O2 kinetics, earlier anaerobic threshold) and cardiocirculatory performance (lower oxygen pulse, lower stroke volume and cardiac output) (p<0.05). Despite similar exertional hypoxaemia, they showed worse ventilatory inefficiency and higher operating lung volumes, which led to greater mechanical inspiratory constraints (p<0.05).Impaired aerobic function due to negative cardiopulmonary-muscular interactions is an important determinant of exercise intolerance in patients with COPD-HF. Treatment strategies to improve oxygen delivery to and/or utilisation by the peripheral muscles might prove particularly beneficial to these patients.

Current challenges in managing comorbid heart failure and COPD.

INTRODUCTION: Heart failure (HF) with reduced ejection fraction and chronic obstructive pulmonary disease (COPD) frequently coexist, particularly in the elderly. Given their rising prevalence and the contemporary trend to longer life expectancy, overlapping HF-COPD will become a major cause of morbidity and mortality in the next decade. Areas covered: Drawing on current clinical and physiological constructs, the consequences of negative cardiopulmonary interactions on the interpretation of pulmonary function and cardiopulmonary exercise tests in HF-COPD are discussed. Although those interactions may create challenges for the diagnosis and assessment of disease stability, they provide a valuable conceptual framework to rationalize HF-COPD treatment. The impact of COPD or HF on the pharmacological treatment of HF or COPD, respectively, is then comprehensively discussed. Authors finalize by outlining how the non-pharmacological treatment (i.e. rehabilitation and exercise reconditioning) can be tailored to the specific needs of patients with HF-COPD. Expert commentary: Randomized clinical trials testing the efficacy and safety of new medications for HF or COPD should include a sizeable fraction of patients with these coexistent pathologies. Multidisciplinary clinics involving cardiologists and respirologists trained in both diseases (with access to unified cardiorespiratory rehabilitation programs) are paramount to decrease the humanitarian and social burden of HF-COPD.

Excess ventilation in COPD: Implications for dyspnoea and tolerance to interval exercise.

Interval exercise delays critical mechanical-ventilatory constraints with positive consequences on Dyspnoea and exercise tolerance in COPD. We hypothesized that those advantages of interval exercise would be partially off-set in patients showing excessive ventilation (V˙E) to metabolic demand (V˙CO2). Sixteen men (FEV1 = 42.3 ±â€¯8.9%) performed, on different days, 30 s and 60 s bouts at 100% peak (on) interspersed by moderate exercise at 40% (off). Nine patients did not sustain exercise for 30 min irrespective of on duration. They presented with higher V˙E/V˙CO2 nadir (35 ±â€¯3 vs. 30 ±â€¯5) and dead space/tidal volume (0.39 ±â€¯0.05 vs. 0.34 ±â€¯0.06) compared to their counterparts (p < 0.05). [Lactate], operating lung volumes and symptom burden (dyspnoea and leg effort) were also higher (p < 0.05). Unloading off decreased the metabolic-ventilatory demands, thereby allowing 7/9 patients to exercise for 30 min. Increased wasted ventilation accelerates the rate at which critical mechanical constraints and limiting dyspnoea are reached during interval exercise in patients with COPD.

Excess Ventilation in Chronic Obstructive Pulmonary Disease-Heart Failure Overlap. Implications for Dyspnea and Exercise Intolerance.

RATIONALE: An increased ventilatory response to exertional metabolic demand (high [Formula: see text]e/[Formula: see text]co2 relationship) is a common finding in patients with coexistent chronic obstructive pulmonary disease and heart failure. OBJECTIVES: We aimed to determine the mechanisms underlying high [Formula: see text]e/[Formula: see text]co2 and its impact on operating lung volumes, dyspnea, and exercise tolerance in these patients. METHODS: Twenty-two ex-smokers with combined chronic obstructive pulmonary disease and heart failure with reduced left ventricular ejection fraction undertook, after careful treatment optimization, a progressive cycle exercise test with capillary (c) blood gas collection. MEASUREMENTS AND MAIN RESULTS: Regardless of the chosen metric (increased [Formula: see text]e-[Formula: see text]co2 slope, [Formula: see text]e/[Formula: see text]co2 nadir, or end-exercise [Formula: see text]e/[Formula: see text]co2), ventilatory inefficiency was closely related to PcCO2 (r values from -0.80 to -0.84; P < 0.001) but not dead space/tidal volume ratio. Ten patients consistently maintained exercise PcCO2 less than or equal to 35 mm Hg (hypocapnia). These patients had particularly poor ventilatory efficiency compared with patients without hypocapnia (P < 0.05). Despite the lack of between-group differences in spirometry, lung volumes, and left ventricular ejection fraction, patients with hypocapnia had lower resting PaCO2 and lung diffusing capacity (P < 0.01). Excessive ventilatory response in this group was associated with higher exertional PcO2. The group with hypocapnia, however, had worse mechanical inspiratory constraints and higher dyspnea scores for a given work rate leading to poorer exercise tolerance compared with their counterparts (P < 0.05). CONCLUSIONS: Heightened neural drive promoting a ventilatory response beyond that required to overcome an increased "wasted" ventilation led to hypocapnia and poor exercise ventilatory efficiency in chronic obstructive pulmonary disease-heart failure overlap. Excessive ventilation led to better arterial oxygenation but at the expense of earlier critical mechanical constraints and intolerable dyspnea.

Are heart rate dynamics in the transition from rest to submaximal exercise related to maximal cardiorespiratory responses in COPD?

BACKGROUND: Poor exercise capacity is an important negative prognostic marker in patients with chronic obstructive pulmonary disease (COPD). Heart rate variability (HRV) responses can indicate alterations in cardiac autonomic control. Nevertheless, it remains unclear whether these abnormalities are related to cardiorespiratory responses to exercise in these patients. OBJECTIVE: To evaluate whether HRV at rest and submaximal exercise are related to impaired cardiopulmonary responses to exercise in COPD patients. METHODS: Fifteen men (66.2±8.7 years) with COPD (FEV1: 55.1±19.2%) were assessed. The R-R interval (RRi) data collection was performed at rest (stand position) and during the six-minute walk test (6MWT). All patients performed a symptom-limited cardiopulmonary exercise test on a cycle ergometer. The HRV changes from rest to submaximal exercise (Δ rest-6MWT) were calculated. RESULTS: We found significant correlations between low frequency (LF) and high frequency (HF) Δ rest-6MWT with Δ oxyhemoglobin saturation by pulse oximetry (r=-0.64 and r=0.65, respectively; p<0.05), minute ventilation/carbon dioxide output relationship from beginning to peak exercise (r=-0.52 and r=0.53, p<0.05), and exercise ventilatory power (r=0.52 and r=-0.53, p<0.05). Interestingly, there was a strong positive correlation (r=0.82, p<0.05) between six-minute walk distance (6MWD) and Δ LF/HF from rest to exercise. CONCLUSION: HRV analysis in the transition from rest to submaximal exercise is associated with exercise ventilatory and hemodynamic abnormalities in COPD patients. Rehabilitative strategies to improve HRV responses may provide an important tool to clinical practice in these patients.

Physiological and clinical relevance of exercise ventilatory efficiency in COPD.

Exercise ventilation (V'E) relative to carbon dioxide output (V'CO2 ) is particularly relevant to patients limited by the respiratory system, e.g. those with chronic obstructive pulmonary disease (COPD). High V'E-V'CO2 (poor ventilatory efficiency) has been found to be a key physiological abnormality in symptomatic patients with largely preserved forced expiratory volume in 1 s (FEV1). Establishing an association between high V'E-V'CO2 and exertional dyspnoea in mild COPD provides evidence that exercise intolerance is not a mere consequence of detraining. As the disease evolves, poor ventilatory efficiency might help explaining "out-of-proportion" breathlessness (to FEV1 impairment). Regardless, disease severity, cardiocirculatory co-morbidities such as heart failure and pulmonary hypertension have been found to increase V'E-V'CO2 In fact, a high V'E-V'CO2 has been found to be a powerful predictor of poor outcome in lung resection surgery. Moreover, a high V'E-V'CO2 has added value to resting lung hyperinflation in predicting all-cause and respiratory mortality across the spectrum of COPD severity. Documenting improved ventilatory efficiency after lung transplantation and lung volume reduction surgery provides objective evidence of treatment efficacy. Considering the usefulness of exercise ventilatory efficiency in different clinical scenarios, the V'E-V'CO2 relationship should be valued in the interpretation of cardiopulmonary exercise tests in patients with mild-to-end-stage COPD.

Influence of heart failure on resting lung volumes in patients with COPD.

OBJECTIVE:: To evaluate the influence of chronic heart failure (CHF) on resting lung volumes in patients with COPD, i.e., inspiratory fraction-inspiratory capacity (IC)/TLC-and relative inspiratory reserve-[1 - (end-inspiratory lung volume/TLC)]. METHODS:: This was a prospective study involving 56 patients with COPD-24 (23 males/1 female) with COPD+CHF and 32 (28 males/4 females) with COPD only-who, after careful clinical stabilization, underwent spirometry (with forced and slow maneuvers) and whole-body plethysmography. RESULTS:: Although FEV1, as well as the FEV1/FVC and FEV1/slow vital capacity ratios, were higher in the COPD+CHF group than in the COPD group, all major "static" volumes-RV, functional residual capacity (FRC), and TLC-were lower in the former group (p < 0.05). There was a greater reduction in FRC than in RV, resulting in the expiratory reserve volume being lower in the COPD+CHF group than in the COPD group. There were relatively proportional reductions in FRC and TLC in the two groups; therefore, IC was also comparable. Consequently, the inspiratory fraction was higher in the COPD+CHF group than in the COPD group (0.42 ± 0.10 vs. 0.36 ± 0.10; p < 0.05). Although the tidal volume/IC ratio was higher in the COPD+CHF group, the relative inspiratory reserve was remarkably similar between the two groups (0.35 ± 0.09 vs. 0.44 ± 0.14; p < 0.05). CONCLUSIONS:: Despite the restrictive effects of CHF, patients with COPD+CHF have relatively higher inspiratory limits (a greater inspiratory fraction). However, those patients use only a part of those limits, probably in order to avoid critical reductions in inspiratory reserve and increases in elastic recoil. OBJETIVO:: Avaliar a influência da insuficiência cardíaca crônica (ICC) nos volumes pulmonares de repouso em pacientes com DPOC, ou seja, fração inspiratória -capacidade inspiratória (CI)/CPT - e reserva inspiratória relativa - [1 - (volume pulmonar inspiratório final/CPT)]. MÉTODOS:: Após cuidadosa estabilização clínica, 56 pacientes com DPOC (24 alocados no grupo DPOC+ICC; 23 homens/1 mulher) e 32 (28 homens/4 mulheres) com DPOC isolada foram submetidos à espirometria forçada e lenta e pletismografia de corpo inteiro. RESULTADOS:: Os pacientes do grupo DPOC+ICC apresentaram maior VEF1, VEF1/CVF e VEF1/capacidade vital lenta; porém, todos os principais volumes "estáticos" - VR, capacidade residual funcional (CRF) e CPT - foram menores que aqueles do grupo DPOC (p < 0,05). A CRF diminuiu mais do que o VR, determinando assim menor volume de reserva expiratória no grupo DPOC+ICC que no grupo DPOC. Houve redução relativamente proporcional da CRF e da CPT nos dois grupos; logo, a CI também foi similar. Consequentemente, a fração inspiratória no grupo DPOC+ICC foi maior que no grupo DPOC (0,42 ± 0,10 vs. 0,36 ± 0,10; p < 0,05). Embora a razão volume corrente/CI fosse maior no grupo DPOC+ICC, a reserva inspiratória relativa foi notadamente similar entre os grupos (0,35 ± 0,09 vs. 0,44 ± 0,14; p < 0,05). CONCLUSÕES:: Apesar dos efeitos restritivos da ICC, pacientes com DPOC+ICC apresentam elevações relativas dos limites inspiratórios (maior fração inspiratória). Entretanto, esses pacientes utilizam apenas parte desses limites, com o provável intuito de evitar reduções críticas da reserva inspiratória e maior trabalho elástico.

Physiological and sensory consequences of exercise oscillatory ventilation in heart failure-COPD.

BACKGROUND: Exercise oscillatory ventilation (EOV) is associated with poor ventilatory efficiency and higher operating lung volumes in heart failure. These abnormalities may be particularly deleterious to dyspnea and exercise tolerance in mechanically-limited patients, e.g. those with coexistent COPD. METHODS: Ventilatory, gas exchange and sensory responses to incremental exercise were contrasted in 68 heart failure-COPD patients (12 EOV+). EOV was established by standard criteria. RESULTS: Compared to EOV-, EOV+ had lower exercise capacity, worse ventilatory inefficiency and higher peak dyspnea scores (p<0.05). Peak capillary PCO2 (PcCO2) was higher and end-tidal CO2 (PETCO2) was lower in EOV+. Thus, greater (i.e., more positive) P(c-ET)CO2 and dead space/tidal volume values were found in these patients compared to EOV- (p<0.05). Ventilatory inefficiency was related to increased dead space/tidal volume in EOV+ (r=0.74; p<0.01). Owing to higher operating lung volumes, inspiratory reserve volume (IRV) decreased to a greater extent in EOV+. Tidal volume oscillations consistently ceased when a "critical" IRV was reached (~0.3-0.5L); thereafter, PcCO2 stabilized or increased and dyspnea scores rose sharply. Exercise capacity was closely related to IRV decrements and peak dyspnea in EOV+ (r=-0.78 and 0.84, respectively; p<0.01). CONCLUSIONS: Dyspnea and exercise tolerance are negatively influenced by EOV in heart failure patients presenting with COPD as co-morbidity. Pharmacological and non-pharmacological interventions known to decrease EOV might prove particularly valuable to mitigate symptom burden and exercise intolerance in this specific heart failure group.

Does Exercise Ventilatory Inefficiency Predict Poor Outcome in Heart Failure Patients With COPD?

PURPOSE: To investigate whether the opposite effects of heart failure (HF) and chronic obstructive pulmonary disease (COPD) on exercise ventilatory inefficiency (minute ventilation [(Equation is included in full-text article.)E]-carbon dioxide output [(Equation is included in full-text article.)CO2] relationship) would negatively impact its prognostic relevance. METHODS: After treatment optimization and an incremental cardiopulmonary exercise test, 30 male patients with HF-COPD (forced expiratory volume in 1 second [FEV1] = 57% ± 17% predicted, ejection fraction = 35% ± 6%) were prospectively followed up during 412 ± 261 days for major cardiac events. RESULTS: Fourteen patients (46%) had a negative outcome. Patients who had an event had lower echocardiographically determined right ventricular fractional area change (RVFAC), greater ventilatory inefficiency (higher (Equation is included in full-text article.)E/(Equation is included in full-text article.)CO2 nadir), and lower end-tidal CO2 (PETCO2) (all P < .05). Multivariate Cox models revealed that (Equation is included in full-text article.)E/(Equation is included in full-text article.)CO2 nadir >36, ΔPETCO2(PEAK-REST)≥2 mm Hg, and PETCO2PEAK≤33 mm Hg added prognostic value to RVFAC≤45%. Kaplan-Meyer analyses showed that although 18% of patients with RVFAC>45% had a major cardiac event after 1 year, no patient with RVFAC>45% and (Equation is included in full-text article.)E/(Equation is included in full-text article.)CO2 nadir ≤36 (or PETCO2PEAK>33 mm Hg) had a negative event. Conversely, although 69% of patients with RVFAC≤45% had a major cardiac event after 1 year, all patients with RVFAC≤45% and ΔPETCO2(PEAK-REST)≥2 mm Hg had a negative event. CONCLUSION: Ventilatory inefficiency remains a powerful prognostic marker in HF despite the presence of mechanical ventilatory constraints induced by COPD. If these preliminary findings are confirmed in larger studies, optimal thresholds for outcome prediction are likely greater than those traditionally recommended for HF patients without COPD.

Cerebral microvascular blood flow and CO2 reactivity in pulmonary arterial hypertension.

Hypocapnia and endothelial dysfunction might impair microvascular cerebral blood flow (CBFmicr) and cerebrovascular reactivity to CO2 (CVRCO2). Pulmonary arterial hypertension (PAH) is characteristically associated with chronic alveolar hyperventilation and microvascular endothelial dysfunction. We therefore determined CBFmicr (pre-frontal blood flow index (BFI) by the indocyanine green-near infrared spectroscopy methodology) during hypocapnia and hypercapnia in 25 PAH patients and 10 gender- and age-matched controls. Cerebral BFI was lower in patients than controls at similar transcutaneous PCO2 (PtcCO2) levels in both testing conditions. In fact, while BFI increased from hypocapnia to hypercapnia in all controls, it failed to increase in 17/25 (68%) patients. Thus, BFI increased to a lesser extent from hypo to hypercapnia ("Δ") in patients, i.e., they showed lower Δ BFI/Δ PtcCO2 ratios than controls. In conclusion, CBFmicr and CVRCO2 are lessened in clinically stable, mildly-impaired patients with PAH. These abnormalities might be associated with relevant clinical outcomes (hyperventilation and dyspnea, cognition, cerebrovascular disease) being potentially amenable to pharmacological treatment.

Influence of heart failure on resting lung volumes in patients with COPD / Influência da insuficiência cardíaca nos volumes pulmonares de repouso em pacientes com DPOC

ABSTRACT Objective: To evaluate the influence of chronic heart failure (CHF) on resting lung volumes in patients with COPD, i.e., inspiratory fraction-inspiratory capacity (IC)/TLC-and relative inspiratory reserve-[1 − (end-inspiratory lung volume/TLC)]. Methods: This was a prospective study involving 56 patients with COPD-24 (23 males/1 female) with COPD+CHF and 32 (28 males/4 females) with COPD only-who, after careful clinical stabilization, underwent spirometry (with forced and slow maneuvers) and whole-body plethysmography. Results: Although FEV1, as well as the FEV1/FVC and FEV1/slow vital capacity ratios, were higher in the COPD+CHF group than in the COPD group, all major "static" volumes-RV, functional residual capacity (FRC), and TLC-were lower in the former group (p < 0.05). There was a greater reduction in FRC than in RV, resulting in the expiratory reserve volume being lower in the COPD+CHF group than in the COPD group. There were relatively proportional reductions in FRC and TLC in the two groups; therefore, IC was also comparable. Consequently, the inspiratory fraction was higher in the COPD+CHF group than in the COPD group (0.42 ± 0.10 vs. 0.36 ± 0.10; p < 0.05). Although the tidal volume/IC ratio was higher in the COPD+CHF group, the relative inspiratory reserve was remarkably similar between the two groups (0.35 ± 0.09 vs. 0.44 ± 0.14; p < 0.05). Conclusions: Despite the restrictive effects of CHF, patients with COPD+CHF have relatively higher inspiratory limits (a greater inspiratory fraction). However, those patients use only a part of those limits, probably in order to avoid critical reductions in inspiratory reserve and increases in elastic recoil.

RESUMO Objetivo: Avaliar a influência da insuficiência cardíaca crônica (ICC) nos volumes pulmonares de repouso em pacientes com DPOC, ou seja, fração inspiratória -capacidade inspiratória (CI)/CPT - e reserva inspiratória relativa - [1 − (volume pulmonar inspiratório final/CPT)]. Métodos: Após cuidadosa estabilização clínica, 56 pacientes com DPOC (24 alocados no grupo DPOC+ICC; 23 homens/1 mulher) e 32 (28 homens/4 mulheres) com DPOC isolada foram submetidos à espirometria forçada e lenta e pletismografia de corpo inteiro. Resultados: Os pacientes do grupo DPOC+ICC apresentaram maior VEF1, VEF1/CVF e VEF1/capacidade vital lenta; porém, todos os principais volumes "estáticos" - VR, capacidade residual funcional (CRF) e CPT - foram menores que aqueles do grupo DPOC (p < 0,05). A CRF diminuiu mais do que o VR, determinando assim menor volume de reserva expiratória no grupo DPOC+ICC que no grupo DPOC. Houve redução relativamente proporcional da CRF e da CPT nos dois grupos; logo, a CI também foi similar. Consequentemente, a fração inspiratória no grupo DPOC+ICC foi maior que no grupo DPOC (0,42 ± 0,10 vs. 0,36 ± 0,10; p < 0,05). Embora a razão volume corrente/CI fosse maior no grupo DPOC+ICC, a reserva inspiratória relativa foi notadamente similar entre os grupos (0,35 ± 0,09 vs. 0,44 ± 0,14; p < 0,05). Conclusões: Apesar dos efeitos restritivos da ICC, pacientes com DPOC+ICC apresentam elevações relativas dos limites inspiratórios (maior fração inspiratória). Entretanto, esses pacientes utilizam apenas parte desses limites, com o provável intuito de evitar reduções críticas da reserva inspiratória e maior trabalho elástico.

Exercise Ventilation in COPD: Influence of Systolic Heart Failure.

Systolic heart failure is a common and disabling co-morbidity of chronic obstructive pulmonary disease (COPD) which may increase exercise ventilation due to heightened neural drive and/or impaired pulmonary gas exchange efficiency. The influence of heart failure on exercise ventilation, however, remains poorly characterized in COPD. In a prospective study, 98 patients with moderate to very severe COPD [41 with coexisting heart failure; 'overlap' (left ventricular ejection fraction < 50%)] underwent an incremental cardiopulmonary exercise test (CPET). Compared to COPD, overlap had lower peak exercise capacity despite higher FEV1. Overlap showed lower operating lung volumes, greater ventilatory inefficiency and larger decrements in end-tidal CO2 (PETCO2) (P < 0.05). These results were consistent with those found in FEV1-matched patients. Larger areas under receiver operating characteristic curves to discriminate overlap from COPD were found for ventilation ([Formula: see text]E)-CO2 output [Formula: see text]CO2) intercept, [Formula: see text]E-[Formula: see text]CO2 slope, peak [Formula: see text]E/[Formula: see text]CO2 ratio and peak PETCO2. Multiple logistic regression analysis revealed that [Formula: see text]CO2 intercept ≤ 3.5 L/minute [odds ratios (95% CI) = 7.69 (2.61-22.65), P < 0.001] plus [Formula: see text]E-[Formula: see text]CO2 slope ≥ 34 [2.18 (0.73-6.50), P = 0.14] or peak [Formula: see text]E/[Formula: see text]CO2 ratio ≥ 37 [5.35 (1.96-14.59), P = 0.001] plus peak PETCO2 ≤ 31 mmHg [5.73 (1.42-23.15), P = 0.01] were indicative of overlapping. Heart failure increases the ventilatory response to metabolic demand in COPD. Variables reflecting excessive ventilation might prove useful to assist clinical interpretation of CPET responses in COPD patients presenting heart failure as co-morbidity.