Oliveira Mayron F, Arbex Flavio F, Alencar Maria Clara, Souza Aline, Sperandio Priscila A, Medeiros Wladimir M, Mazzuco Adriana, Borghi-Silva Audrey, Medina Luiz A, Santos Rita, Hirai Daniel M, Mancuso Frederico, Almeida Dirceu, O'Donnell Denis E, Neder J Alberto
a Pulmonary Function and Clinical Exercise Physiology Unit (SEFICE), Respiratory Division , Federal University of São Paulo (UNIFESP) , São Paulo , Brazil.
b Department of Physiotherapy , Federal University of São Carlos (UFSCAR) , São Carlos , Brazil.
COPD. 2016 Aug;13(4):407-15. doi: 10.3109/15412555.2015.1117435. Epub 2016 Jan 20.
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.
心力衰竭是慢性阻塞性肺疾病（COPD）常见且导致功能障碍的合并症，可能会损害心输出量和肌肉血流量，从而导致运动耐力下降。为了研究在COPD-心力衰竭重叠患者中，中枢和外周血流动力学受损在限制运动耐力方面的作用，对重叠患者（FEV1 = 56.9 ± 15.9%预计值，射血分数 = 32.5 ± 6.9%；N = 16）、FEV1匹配的COPD患者（N = 16）、射血分数匹配的心力衰竭患者（N = 15）和对照组（N = 12）进行了峰值工作率20%和80%时的蹬车测力计运动试验。工作率之间的心输出量（阻抗心动图）、股外侧肌血流量（吲哚菁绿）和脱氧情况（近红外光谱）差异（Δ）相对于肌肉代谢需求的同时变化（ΔO2摄取）表示。重叠患者的耐力运动耐力比COPD和心力衰竭患者低约30%（p < 0.05）。所有组中，Δ血流量与Δ心输出量密切相关（r = 0.89 - 0.98；p < 0.01）。重叠患者在Δ心输出量/ΔO2摄取和Δ血流量/ΔO2摄取方面受损最大（p < 0.05）。然而，与COPD相比，重叠患者的全身动脉氧合得以保留。重叠患者肢体灌注不足与更大程度的肌肉脱氧和乳酸浓度相关（分别为r = 0.78和r = 0.73；p < 0.05）。仅在重叠患者和心力衰竭患者中，Δ血流量/ΔO2摄取与运动不耐受时间相关（p < 0.01）。总之，COPD和心力衰竭共同导致运动时的心输出量和骨骼肌灌注减少，其程度比仅由心力衰竭导致的预期程度更大。增加肌肉氧输送和/或减少氧需求的治疗策略可能对改善合并心力衰竭的COPD患者的运动耐力特别有帮助。
