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.

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.

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.

Exercise Ventilatory Inefficiency Adds to Lung Function in Predicting Mortality in COPD.

Severity of resting functional impairment only partially predicts the increased risk of death in chronic obstructive pulmonary disease (COPD). Increased ventilation during exercise is associated with markers of disease progression and poor prognosis, including emphysema extension and pulmonary vascular impairment. Whether excess exercise ventilation would add to resting lung function in predicting mortality in COPD, however, is currently unknown. After an incremental cardiopulmonary exercise test, 288 patients (forced expiratory volume in one second ranging from 18% to 148% predicted) were followed for a median (interquartile range) of 57 (47) months. Increases in the lowest (nadir) ventilation to CO2 output (VCO2) ratio determined excess exercise ventilation. Seventy-seven patients (26.7%) died during follow-up: 30/77 (38.9%) deaths were due to respiratory causes. Deceased patients were older, leaner, had a greater co-morbidity burden (Charlson Index) and reported more daily life dyspnea. Moreover, they had poorer lung function and exercise tolerance (p < 0.05). A logistic regression analysis revealed that ventilation/VCO2 nadir was the only exercise variable that added to age, body mass index, Charlson Index and resting inspiratory capacity (IC)/total lung capacity (TLC) ratio to predict all-cause and respiratory mortality (p < 0.001). Kaplan-Meier analyses showed that survival time was particularly reduced when ventilation/VCO2 nadir > 34 was associated with IC/TLC ≤ 0.34 or IC/TLC ≤ 0.31 for all-cause and respiratory mortality, respectively (p < 0.001). Excess exercise ventilation is an independent prognostic marker across the spectrum of COPD severity. Physiological abnormalities beyond traditional airway dysfunction and lung mechanics are relevant in determining the course of the disease.

Heart Failure Impairs Muscle Blood Flow and Endurance Exercise Tolerance in COPD.

Heart failure, a prevalent and disabling co-morbidity of COPD, may impair cardiac output and muscle blood flow thereby contributing to exercise intolerance. To investigate the role of impaired central and peripheral hemodynamics in limiting exercise tolerance in COPD-heart failure overlap, cycle ergometer exercise tests at 20% and 80% peak work rate were performed by overlap (FEV1 = 56.9 ± 15.9% predicted, ejection fraction = 32.5 ± 6.9%; N = 16), FEV1-matched COPD (N = 16), ejection fraction-matched heart failure patients (N = 15) and controls (N = 12). Differences (Δ) in cardiac output (impedance cardiography) and vastus lateralis blood flow (indocyanine green) and deoxygenation (near-infrared spectroscopy) between work rates were expressed relative to concurrent changes in muscle metabolic demands (ΔO2 uptake). Overlap patients had approximately 30% lower endurance exercise tolerance than COPD and heart failure (p < 0.05). ΔBlood flow was closely proportional to Δcardiac output in all groups (r = 0.89-0.98; p < 0.01). Overlap showed the largest impairments in Δcardiac output/ΔO2 uptake and Δblood flow/ΔO2 uptake (p < 0.05). Systemic arterial oxygenation, however, was preserved in overlap compared to COPD. Blunted limb perfusion was related to greater muscle deoxygenation and lactate concentration in overlap (r = 0.78 and r = 0.73, respectively; p < 0.05). ΔBlood flow/ΔO2 uptake was related to time to exercise intolerance only in overlap and heart failure (p < 0.01). In conclusion, COPD and heart failure add to decrease exercising cardiac output and skeletal muscle perfusion to a greater extent than that expected by heart failure alone. Treatment strategies that increase muscle O2 delivery and/or decrease O2 demand may be particularly helpful to improve exercise tolerance in COPD patients presenting heart failure as co-morbidity.

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.

Exercise ventilatory inefficiency in mild to end-stage COPD.

Ventilatory inefficiency during exercise is a key pathophysiological feature of chronic obstructive pulmonary disease. Currently, it is unknown how this physiological marker relates to clinically relevant outcomes as resting ventilatory impairment progresses across disease stages. Slope and intercept of the linear region of the ventilation-carbon dioxide output relationship and the ratio between these variables, at the lowest point (nadir), were contrasted in 316 patients with Global Initiative for Chronic Obstructive Lung Disease (GOLD) stages 1-4 (forced expiratory volume in 1 s, ranging from 148% pred to 12% pred) and 69 aged- and gender-matched controls, Compared to controls, slope and intercept were higher in GOLD stages 1 and 2, leading to higher nadirs (p<0.05). Despite even larger intercepts in GOLD stages 3 and 4, slopes diminished as disease evolved (from mean±sd 35±6 in GOLD stage 1 to 24±5 in GOLD stage 3, p<0.05). As a result, there were no significant differences in nadirs among patient groups. Higher intercepts, across all stages (p<0.01), and to a lesser extent lower slopes in GOLD stages 2-4 (p<0.05), were related to greater mechanical constraints, worsening pulmonary gas exchange, higher dyspnoea scores, and poorer exercise capacity. Increases in the ventilation intercept best indicate the progression of exercise ventilatory inefficiency across the whole spectrum of chronic obstructive pulmonary disease severity.

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.

Comparing hospital admissions, comorbidities, and biomarkers between severe asthma and Gold III-IV chronic obstructive pulmonary disease.

INTRODUCTION: In spite of difficulties in differentiating asthma from chronic obstructive pulmonary disease (COPD), physicians should strive for accurate diagnosis because outcomes may be different. OBJECTIVES: Our aims were to compare the frequency of hospital admissions (HA) between severe asthmatic (SA) and Gold III-IV COPD subjects receiving disease-specific guideline recommended therapy and to depict the frequency of prevalent chronic disorders and the laboratorial profile suggesting allergic and eosinophilic phenotypes. METHODS: This cross-sectional study comprises one group of SA subjects and another group of Gold III-IV COPD subjects. Subjects answered standard questionnaires, underwent spirometry, and provided a peripheral blood sample. We validated the HA that have occurred during the preceding year by review of the report emitted by the hospital. We detected comorbidities by review of current pharmacological therapies. RESULTS: We enrolled 160 SA and 41 Gold III-IV COPD subjects. As compared with Gold III-IV COPD subjects, SA subjects had lower odds of HA (odds ratio [OR] 0.19, 95% confidence interval [CI] 0.05-0.74) and higher odds of obesity (OR 9.17, 95%CI 2.68-31.37), hypertension (OR 2.54, 95%CI 1.16-5.57), and diabetes mellitus (OR 5.71, 95%CI 1.56-20.85). The frequency of atopic and eosinophilic phenotypes was similar between study groups. CONCLUSIONS: Our results demonstrated that Gold III-IV COPD subjects had worse outcomes as compared with SA subjects. We also observed that the frequency of atopy and high peripheral blood eosinophil count were similar between study groups. Finally, we exposed aspects of comorbidities related to asthma and COPD that indicate the need of close monitoring the cardiovascular risk in SA subjects above 40 years of age.

Modified BODE Index to Predict Mortality in Individuals With COPD: The Role of 4-Min Step Test.

BACKGROUND: The BODE (body mass index, air-flow obstruction, dyspnea, exercise capacity) index is a composite prognostic marker that predicts mortality in COPD. It includes body mass index, air-flow obstruction, dyspnea score, and exercise capacity by using the 6-min walk distance. However, a 30-m-long corridor is necessary to perform the test and this limits its use in clinical practice. Step tests may elicit distinct physiologic responses compared with the 6-min walk test but are easy to perform in the office setting. We sought to investigate whether a 4-min step test would be a suitable surrogate of the 6-min walk test, in a modified BODE step index (simplified BODE index), to predict mortality in COPD. METHODS: Individuals with COPD performed a self-paced 4-min step test, and the simplified BODE index was calculated by replacing the 6-min walk distance by the number of steps climbed. Cutoff values were determined by receiver operating characteristic curve analysis as follows: score 0 for >60 steps; score 1 for 50-60 steps; score 2 for 40-49 steps; and score 3 for <40 steps. RESULTS: A total of 186 individuals with COPD were enrolled from 2011 to 2016 (60% males; mean ± SD age, 65 ± 9 y; mean ± SD FEV1, 50 ± 17 L). There were 36 deaths among the study cohort. The simplified BODE index was a prognostic marker, independent of cardiovascular comorbidities and oxygen desaturation (HR 1.12, confidence interval (CI) [1.03-1.22]). Individuals with simplified BODE index scores ≥ 7 were at higher risk of death from any cause (P < .001, log-rank test). CONCLUSIONS: This was the first study, to our knowledge, to show that the 4-min step test as a surrogate of exercise capacity in the BODE index (simplified BODE index) is an independent predictor of mortality in COPD and may help to spread its use among practicing physicians.

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.

Risk factors for tuberculosis: diabetes, smoking, alcohol use, and the use of other drugs.

Tuberculosis continues to be a major public health problem. Although efforts to control the epidemic have reduced mortality and incidence, there are several predisposing factors that should be modified in order to reduce the burden of the disease. This review article will address some of the risk factors associated with tuberculosis infection and active tuberculosis, including diabetes, smoking, alcohol use, and the use of other drugs, all of which can also contribute to poor tuberculosis treatment results. Tuberculosis can also lead to complications in the course and management of other diseases, such as diabetes. It is therefore important to identify these comorbidities in tuberculosis patients in order to ensure adequate management of both conditions.

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.

Air pollution from biomass burning and asthma hospital admissions in a sugar cane plantation area in Brazil.

OBJECTIVE: To evaluate the association between the total suspended particles (TSPs) generated from preharvest sugar cane burning and hospital admission due to asthma (asthma hospital admissions) in the city of Araraquara. DESIGN: An ecological time-series study. Total daily records of asthma hospital admissions (ICD 10th J15) were obtained from one of the main hospitals in Araraquara, São Paulo State, Brazil, from 23 March 2003 to 27 July 2004. The daily concentration of TSP (microg/m(3)) was obtained using Handi-vol equipment (Energética, Brazil) placed in downtown Araraquara. The local airport provided the daily mean figures of temperature and humidity. The daily number of asthma hospital admissions was considered as the dependent variable in Poisson's regression models and the daily concentration of TSP was considered the independent variable. The generalised linear model with natural cubic spline was adopted to control for long-time trend. Linear terms were used for weather variables. RESULTS: TSP had an acute effect on asthma admissions, starting 1 day after TSP concentrations increased and remaining almost unchanged for the next four days. A 10 microg/m(3) increase in the 5-day moving average (lag1-5) of TSP concentrations was associated with an increase of 11.6% (95% CI 5.4 to 17.7) in asthma hospital admissions. CONCLUSION: Increases in TSP concentrations were definitely associated with asthma hospital admissions in Araraquara and, despite using sugar cane alcohol to reduce air pollution from automotive sources in large Brazilian urban centres, the cities where sugar cane is harvested pay a high toll in terms of public health.

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.

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.