Inspiratory resistance decreases limb blood flow in COPD patients with heart failure

Hosp Clin Porto Alegre, Exercise Pathophysiol Res Lab, BR-90035007 Porto Alegre, RS, BrazilHosp Clin Porto Alegre, Div Cardiol, BR-90035007 Porto Alegre, RS, BrazilSerra Gaucha Coll, Phys Therapy Dept, Caxias Do Sul, RS, BrazilHosp Clin Porto Alegre, Pulmonary Div, Porto Alegre, RS, BrazilFed Univ Rio Grande, Fac Med, Dept Med, Porto Alegre, RS, BrazilUniversidade Federal de São Paulo, Dept Med, Div Resp Dis, Pulmonary Funct & Clin Exercise Physiol Unit, São Paulo, BrazilQueens Univ, Dept Med, Div Respirol, LACEP, Kingston, ON, CanadaKingston Gen Hosp, Kingston, ON K7L 2V7, CanadaUniversidade Federal de São Paulo, Dept Med, Div Resp Dis, Pulmonary Funct & Clin Exercise Physiol Unit, São Paulo, BrazilWeb of Scienc

Sildenafil improves microvascular O-2 delivery-to-utilization matching and accelerates exercise O-2 uptake kinetics in chronic heart failure

Sperandio PA, Oliveira MF, Rodrigues MK, Berton DC, Treptow E, Nery LE, Almeida DR, Neder JA. Sildenafil improves microvascular O-2 delivery-to-utilization matching and accelerates exercise O-2 uptake kinetics in chronic heart failure. Am J Physiol Heart Circ Physiol 303: H1474-H1480, 2012. First published September 28, 2012; doi:10.1152/ajpheart.00435.2012.-Nitric oxide (NO) can temporally and spatially match microvascular oxygen (O-2) delivery (QO(2mv)) to O-2 uptake (VO2) in the skeletal muscle, a crucial adjustment-to-exercise tolerance that is impaired in chronic heart failure (CHF). To investigate the effects of NO bioavailability induced by sildenafil intake on muscle QO(2mv)-to-O-2 utilization matching and VO2 kinetics, 10 males with CHF (ejection fraction = 27 +/- 6%) undertook constant work-rate exercise (70-80% peak). Breath-by-breath VO2, fractional O-2 extraction in the vastus lateralis {similar to deoxy-genated hemoglobin + myoglobin ([deoxy-Hb + Mb]) by near-infrared spectroscopy}, and cardiac output (CO) were evaluated after sildenafil (50 mg) or placebo. Sildenafil increased exercise tolerance compared with placebo by similar to 20%, an effect that was related to faster on-and off-exercise VO2 kinetics (P 0.05). On-exercise [deoxy-Hb + Mb] kinetics were slowed by sildenafil (similar to 25%), and a subsequent response overshoot (n = 8) was significantly lessened or even abolished. in contrast, [deoxy-Hb + Mb] recovery was faster with sildenafil (similar to 15%). Improvements in muscle oxygenation with sildenafil were related to faster on-exercise VO2 kinetics, blunted oscillations in ventilation (n = 9), and greater exercise capacity (P < 0.05). Sildenafil intake enhanced intramuscular QO(2mv)-to-VO2 matching with beneficial effects on VO2 kinetics and exercise tolerance in CHF. the lack of effect on CO suggests that improvement in blood flow to and within skeletal muscles underlies these effects.Universidade Federal de São Paulo, Dept Med, Div Resp Dis, Pulm Funct & Clin Exercise Physiol Unit, BR-04020050 São Paulo, BrazilQueens Univ, Dept Med, Div Resp & Crit Care Med, Kingston, ON K7L 3N6, CanadaUniversidade Federal de São Paulo, Dept Med, Div Cardiol, BR-04020050 São Paulo, BrazilUniversidade Federal de São Paulo, Dept Med, Div Resp Dis, Pulm Funct & Clin Exercise Physiol Unit, BR-04020050 São Paulo, BrazilUniversidade Federal de São Paulo, Dept Med, Div Cardiol, BR-04020050 São Paulo, BrazilWeb of Scienc

Proportional Assist Ventilation Improves Leg Muscle Reoxygenation After Exercise in Heart Failure With Reduced Ejection Fraction

BackgroundRespiratory muscle unloading through proportional assist ventilation (PAV) may enhance leg oxygen delivery, thereby speeding off-exercise oxygen uptake (V.⁢O2) kinetics in patients with heart failure with reduced left ventricular ejection fraction (HFrEF).MethodsTen male patients (HFrEF = 26 ± 9%, age 50 ± 13 years, and body mass index 25 ± 3 kg m2) underwent two constant work rate tests at 80% peak of maximal cardiopulmonary exercise test to tolerance under PAV and sham ventilation. Post-exercise kinetics of V.⁢O2, vastus lateralis deoxyhemoglobin ([deoxy-Hb + Mb]) by near-infrared spectroscopy, and cardiac output (QT) by impedance cardiography were assessed.ResultsPAV prolonged exercise tolerance compared with sham (587 ± 390 s vs. 444 ± 296 s, respectively; p = 0.01). PAV significantly accelerated V.⁢O2 recovery (τ = 56 ± 22 s vs. 77 ± 42 s; p &lt; 0.05), being associated with a faster decline in Δ[deoxy-Hb + Mb] and QT compared with sham (τ = 31 ± 19 s vs. 42 ± 22 s and 39 ± 22 s vs. 78 ± 46 s, p &lt; 0.05). Faster off-exercise decrease in QT with PAV was related to longer exercise duration (r = −0.76; p &lt; 0.05).ConclusionPAV accelerates the recovery of central hemodynamics and muscle oxygenation in HFrEF. These beneficial effects might prove useful to improve the tolerance to repeated exercise during cardiac rehabilitation

Ventilatory Inefficiency and Exertional Dyspnea in Early Chronic Obstructive Pulmonary Disease

Exertional dyspnea is present across the spectrum of chronic obstructive pulmonary disease (COPD) severity. However, without realizing it themselves, patients may decrease daily physical activity to avoid distressing respiratory sensations. Dyspnea also may be associated with deconditioning. Cardiopulmonary exercise testing can uncover exertional dyspnea and its physiological determinants in patients with preserved or only mildly-reduced FEV1. Dyspnea in mild COPD can largely be explained by increased "wasted" ventilation in the physiological dead space which heightens the drive to breathe and worsens the inspiratory mechanical constraints. During incremental exercise testing, this is readily identified as an excessive ventilation-tometabolic demand, that is a high ventilation (V̇E) to carbon dioxide output (V̇CO2) relationship. Linking increases in V̇E/V̇CO2 to exertional dyspnea may provide objective evidence that patient's poor exercise tolerance is not just a consequence of deconditioning. This information should prompt a proactive therapeutic approach to increase the available ventilatory reserve, by, for example, giving inhaled bronchodilators. Considering that the structural determinants of ventilatory inefficiency (early emphysema, ventilation-perfusion mismatching, and microvascular disease) may progress despite only modest changes in FEV1, serial V̇E/V̇CO2 measurements might also prove valuable to track disease progression in these symptomatic 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