Moreno A M, Castro R R T, Silva B M, Villacorta H, Sant'Anna Junior M, Nóbrega A C L
Procordis Hospital Cardiológico, Niterói, RJ, Brasil.
Programa de Pós-graduação em Ciências Cardiovasculares, Universidade Federal Fluminense, Niterói, RJ, Brasil.
Braz J Med Biol Res. 2014 Nov;47(11):972-6. doi: 10.1590/1414-431X20143896. Epub 2014 Aug 29.
The purpose of this study was to determine the effect of respiratory muscle fatigue on intercostal and forearm muscle perfusion and oxygenation in patients with heart failure. Five clinically stable heart failure patients with respiratory muscle weakness (age, 66 ± 12 years; left ventricle ejection fraction, 34 ± 3%) and nine matched healthy controls underwent a respiratory muscle fatigue protocol, breathing against a fixed resistance at 60% of their maximal inspiratory pressure for as long as they could sustain the predetermined inspiratory pressure. Intercostal and forearm muscle blood volume and oxygenation were continuously monitored by near-infrared spectroscopy with transducers placed on the seventh left intercostal space and the left forearm. Data were compared by two-way ANOVA and Bonferroni correction. Respiratory fatigue occurred at 5.1 ± 1.3 min in heart failure patients and at 9.3 ± 1.4 min in controls (P<0.05), but perceived effort, changes in heart rate, and in systolic blood pressure were similar between groups (P>0.05). Respiratory fatigue in heart failure reduced intercostal and forearm muscle blood volume (P<0.05) along with decreased tissue oxygenation both in intercostal (heart failure, -2.6 ± 1.6%; controls, +1.6 ± 0.5%; P<0.05) and in forearm muscles (heart failure, -4.5 ± 0.5%; controls, +0.5 ± 0.8%; P<0.05). These results suggest that respiratory fatigue in patients with heart failure causes an oxygen demand/delivery mismatch in respiratory muscles, probably leading to a reflex reduction in peripheral limb muscle perfusion, featuring a respiratory metaboreflex.
本研究的目的是确定呼吸肌疲劳对心力衰竭患者肋间肌和前臂肌肉灌注及氧合的影响。五名临床稳定的呼吸肌无力的心力衰竭患者(年龄66±12岁;左心室射血分数34±3%)和九名匹配的健康对照者接受了呼吸肌疲劳方案,即他们以最大吸气压力的60%对抗固定阻力进行呼吸,持续尽可能长的时间以维持预定的吸气压力。通过将传感器置于左第七肋间和左前臂,利用近红外光谱法持续监测肋间肌和前臂肌肉的血容量及氧合情况。数据采用双向方差分析和Bonferroni校正进行比较。心力衰竭患者在5.1±1.3分钟时出现呼吸疲劳,对照组在9.3±1.4分钟时出现呼吸疲劳(P<0.05),但两组间的主观用力程度、心率变化和收缩压变化相似(P>0.05)。心力衰竭患者的呼吸疲劳会降低肋间肌和前臂肌肉的血容量(P<0.05),同时肋间肌(心力衰竭组为-2.6±1.6%;对照组为+1.6±0.5%;P<0.05)和前臂肌肉(心力衰竭组为-4.5±0.5%;对照组为+0.5±0.8%;P<0.05)的组织氧合均下降。这些结果表明,心力衰竭患者的呼吸疲劳会导致呼吸肌出现氧需求/输送不匹配,可能会导致外周肢体肌肉灌注反射性降低,其特征为呼吸代谢反射。