Mayron F. Oliveira

Effects of oxygen supplementation on cerebral oxygenation during exercise in chronic obstructive pulmonary disease patients not entitled to long-term oxygen therapy.

Background:  The rate of change (Δ) in cerebral oxygenation (COx) during exercise is influenced by blood flow and arterial O2 content (CaO2). It is currently unclear whether ΔCOx would (i) be impaired during exercise in patients with chronic obstructive pulmonary disease (COPD) who do not fulfil the current criteria for long‐term O2 therapy but present with exercise‐induced hypoxaemia and (ii) improve with hyperoxia (FIO2 = 0·4) in this specific sub‐population.

Does impaired O2 delivery during exercise accentuate central and peripheral fatigue in patients with coexistent COPD-CHF?

Impairment in oxygen (O2) delivery to the central nervous system (“brain”) and skeletal locomotor muscle during exercise has been associated with central and peripheral neuromuscular fatigue in healthy humans. From a clinical perspective, impaired tissue O2 transport is a key pathophysiological mechanism shared by cardiopulmonary diseases, such as chronic obstructive pulmonary disease (COPD) and chronic heart failure (CHF). In addition to arterial hypoxemic conditions in COPD, there is growing evidence that cerebral and muscle blood flow and oxygenation can be reduced during exercise in both isolated COPD and CHF. Compromised cardiac output due to impaired cardiopulmonary function/interactions and blood flow redistribution to the overloaded respiratory muscles (i.e., ↑work of breathing) may underpin these abnormalities. Unfortunately, COPD and CHF coexist in almost a third of elderly patients making these mechanisms potentially more relevant to exercise intolerance. In this context, it remains unknown whether decreased O2 delivery accentuates neuromuscular manifestations of central and peripheral fatigue in coexistent COPD-CHF. If this holds true, it is conceivable that delivering a low-density gas mixture (heliox) through non-invasive positive pressure ventilation could ameliorate cardiopulmonary function/interactions and reduce the work of breathing during exercise in these patients. The major consequence would be increased O2 delivery to the brain and active muscles with potential benefits to exercise capacity (i.e., ↓central and peripheral neuromuscular fatigue, respectively). We therefore hypothesize that patients with coexistent COPD-CHF stop exercising prematurely due to impaired central motor drive and muscle contractility as the cardiorespiratory system fails to deliver sufficient O2 to simultaneously attend the metabolic demands of the brain and the active limb muscles.

Effects of heart failure on cerebral blood flow in COPD: Rest and exercise

Cerebral blood flow (CBF) and oxygenation (COx) are generally well-preserved in COPD. It is unknown whether prevalent cardiovascular co-morbidities, such as heart failure, may impair CBF and COx responses to exertion. Eighteen males with moderate-to-severe COPD (8 with and 10 without overlapping heart failure) underwent a progressive exercise test with pre-frontal CBF and COx measurements (indocyanine green and near-infrared spectroscopy). Mean arterial pressure and cardiac output were lower from rest to exercise in overlap. Only COPD patients demonstrated an increase in arterialized PCO2 towards the end of progressive exercise. CBF index was consistently higher and increased further by ∼40% during exercise in COPD whereas a ∼10% reduction was observed in overlap. COx was lower in overlap despite preserved arterial oxygenation. In conclusion, heart failure introduces pronounced negative effects on CBF and COx in COPD which may be associated with clinically relevant outcomes, including dyspnea, exercise intolerance, cerebrovascular disease and cognitive impairment.

Additive effects of non-invasive ventilation to hyperoxia on cerebral oxygenation in COPD patients with exercise-related O2 desaturation.

It is currently unknown whether potential haemodynamic improvements induced by non‐invasive ventilation (NIV) would positively impact upon cerebral oxygenation (COx) in patients with moderate‐to‐severe chronic obstructive pulmonary disease (COPD).

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

Abstract 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.

Heart failure impairs cerebral oxygenation during exercise in patients with COPD

To the Editor: Impaired systemic oxygen delivery, particularly during exertion, is the key pathophysiological feature shared by chronic obstructive pulmonary disease (COPD) and heart failure with reduced left ventricular ejection fraction (HFrEF). Unfortunately, COPD and HFrEF frequently coexist not only because of their high individual prevalence but also due to common risk factors, including cigarette smoking, advanced age, oxidative stress and systemic inflammation [1]. It is expected that any reduction in the rate of oxygen transfer due to COPD and/or HFrEF would be particularly deleterious to tissues heavily dependent upon constant oxygen flow, such as the central nervous system (as reviewed in [2]). Exercise cerebral oxygenation (Cox) (as noninvasively determined by near-infrared spectroscopy) depends upon the dynamic balance between the instantaneous rate of oxygen delivery and oxygen utilisation [3]. Koike et al . [4], for instance, reported that congestive heart failure (CHF) HFrEF was associated with appreciable decreases in COx during exertion. Our laboratory found that exercise COx might be impaired in some patients with more advanced COPD, even if not overtly hypoxaemic [5]. Moreover, improvement in cardiac output with noninvasive ventilation (under the same arterial oxygen content) had positive effects on COx in COPD [6]. These data suggest that reduced cerebral blood flow might be mechanistically linked to impaired exercise COx in some patients with moderate-to-severe COPD. It is conceivable that the presence of HFrEF would further deteriorate this scenario by adding components of dysfunctional cerebral autoregulation, lower cardiac output and hypocapnia-induced vasoconstriction [4]. The compound effects of HFrEF plus COPD on …

Dynamics of chest wall volume regulation during constant work rate exercise in patients with chronic obstructive pulmonary disease

This study evaluated the dynamic behavior of total and compartmental chest wall volumes [(VCW) = rib cage (VRC) + abdomen (VAB)] as measured breath-by-breath by optoelectronic plethysmography during constant-load exercise in patients with stable chronic obstructive pulmonary disease. Thirty males (GOLD stages II-III) underwent a cardiopulmonary exercise test to the limit of tolerance (Tlim) at 75% of peak work rate on an electronically braked cycle ergometer. Exercise-induced dynamic hyperinflation was considered to be present when end-expiratory (EE) VCW increased in relation to resting values. There was a noticeable heterogeneity in the patterns of VCW regulation as EEVCW increased non-linearly in 17/30 “hyperinflators” and decreased in 13/30 “non-hyperinflators” (P < 0.05). EEVAB decreased slightly in 8 of the “hyperinflators”, thereby reducing and slowing the rate of increase in end-inspiratory (EI) VCW (P < 0.05). In contrast, decreases in EEVCW in the “non-hyperinflators” were due to the combination of stable EEVRC with marked reductions in EEVAB. These patients showed lower EIVCW and end-exercise dyspnea scores but longer Tlim than their counterparts (P < 0.05). Dyspnea increased and Tlim decreased non-linearly with a faster rate of increase in EIVCW regardless of the presence or absence of dynamic hyperinflation (P < 0.001). However, no significant between-group differences were observed in metabolic, pulmonary gas exchange and cardiovascular responses to exercise. Chest wall volumes are continuously regulated during exercise in order to postpone (or even avoid) their migration to higher operating volumes in patients with COPD, a dynamic process that is strongly dependent on the behavior of the abdominal compartment.

Influência da insuficiência cardíaca nos volumes pulmonares de repouso em pacientes com DPOC

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.

Alternatives to Aerobic Exercise Prescription in Patients with Chronic Heart Failure

Background Exercise is essential for patients with heart failure as it leads to a reduction in morbidity and mortality as well as improved functional capacity and oxygen uptake (⩒O2). However, the need for an experienced physiologist and the cost of the exam may render the cardiopulmonary exercise test (CPET) unfeasible. Thus, the six-minute walk test (6MWT) and step test (ST) may be alternatives for exercise prescription. Objective The aim was to correlate heart rate (HR) during the 6MWT and ST with HR at the anaerobic threshold (HRAT) and peak HR (HRP) obtained on the CPET. Methods Eighty-three patients (58 ± 11 years) with heart failure (NYHA class II) were included and all subjects had optimized medication for at least 3 months. Evaluations involved CPET (⩒O2, HRAT, HRP), 6MWT (HR6MWT) and ST (HRST). Results The participants exhibited severe ventricular dysfunction (ejection fraction: 31 ± 7%) and low peak ⩒O2 (15.2 ± 3.1 mL.kg-1.min-1). HRP (113 ± 19 bpm) was higher than HRAT (92 ± 14 bpm; p < 0.05) and HR6MWT (94 ± 13 bpm; p < 0.05). No significant difference was found between HRP and HRST. Moreover, a strong correlation was found between HRAT and HR6MWT (r = 0.81; p < 0.0001), and between HRP and HRST (r = 0.89; p < 0.0001). Conclusion These findings suggest that, in the absence of CPET, exercise prescription can be performed by use of 6MWT and ST, based on HR6MWT and HRST

Pre-Frailty Increases the Risk of Adverse Events in Older Patients Undergoing Cardiovascular Surgery

Background Frailty is identified as a major predictor of adverse outcomes in older surgical patients. However, the outcomes in pre-frail patients after cardiovascular surgery remain unknown. Objective To investigate the main outcomes (length of stay, mechanical ventilation time, stroke and in-hospital death) in pre-frail patients in comparison with no-frail patients after cardiovascular surgery. Methods 221 patients over 65 years old, with established diagnosis of myocardial infarction or valve disease were enrolled. Patients were evaluated by Clinical Frailty Score (CFS) before surgery and allocated into 2 groups: no-frailty (CFS 1~3) vs. pre-frailty (CFS 4) and followed up for main outcomes. For all analysis, the statistical significance was set at 5% (p < 0.05). Results No differences were found in anthropometric and demographic data between groups (p > 0.05). Pre-frail patients showed a longer mechanical ventilation time (193 ± 37 vs. 29 ± 7 hours; p<0.05) than no-frail patients; similar results were observed for length of stay at the intensive care unit (5 ± 1 vs. 3 ± 1 days; p < 0.05) and total time of hospitalization (12 ± 5 vs. 9 ± 3 days; p < 0.05). In addition, the pre-frail group had a higher number of adverse events (stroke 8.3% vs. 3.9%; in-hospital death 21.5% vs. 7.8%; p < 0.05) with an increased risk for development stroke (OR: 2.139, 95% CI: 0.622-7.351, p = 0.001; HR: 2.763, 95%CI: 1.206-6.331, p = 0.0001) and in-hospital death (OR: 1.809, 95% CI: 1.286-2.546, p = 0.001; HR: 1.830, 95% CI: 1.476-2.269, p = 0.0001). Moreover, higher number of pre-frail patients required homecare services than no-frail patients (46.5% vs. 0%; p < 0.05). Conclusion Patients with pre-frailty showed longer mechanical ventilation time and hospital stay with an increased risk for cardiovascular events compared with no-frail patients.