Mechanism of augmented exercise hyperpnea in chronic heart failure and dead space loading.
Mechanism of augmented exercise hyperpnea in chronic heart failure and dead space loading.
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DOI：
10.1016/j.resp.2012.12.004
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发表时间：
2013-03-01
影响因子：
2.3
通讯作者：
Tin, Chung
中科院分区：
文献类型：
--
作者：
Poon, Chi-Sang;Tin, Chung
关键词：
慢性心力衰竭（CHF）患者的肺泡VD/VT（死腔潮气量比）增加，但他们表现出肺通气增强，使得动脉PCO 2（PaCO 2）从休息到适度运动保持显著正常。这种矛盾的效应表明，控制运动呼吸过度的控制律不仅由代谢CO2产生（V今CO2）本身决定，而且对表观（真实感觉）代谢CO2负荷有反应 还包括生理性VD/VT对肺CO2清除的不利影响。相比之下，受到死腔负荷的健康个体在休息时和运动期间也经历了增强的通气，如CHF中的肺泡VD/VT增加，但所得的反应是高碳酸血症而不是正常碳酸血症，如CO2呼吸。因此，死腔负荷的缓解作用类似于肺泡VD/VT和CO2呼吸联合增加的缓解作用。这些观察结果与假设一致，即死腔负载中VD/VT系列增加， 与CHF中增加的肺泡VD/VT一样，但这是通过在死腔气体中再呼吸CO2，从而在每次吸气中产生虚拟（虚幻）气道CO2负荷，而不是在CO2呼吸期间阻塞通过肺通气消除CO2的机制的真实气道CO2负荷。因此，呼吸控制器处的化学传感机制可以响应于由呼吸内PaCO 2振荡介导的推定驱动信号，该呼吸内PaCO 2振荡独立于平均PaCO 2水平的呼吸到呼吸波动。虽然骨骼肌传入反馈对早期运动心脏动力学很重要，但对晚期运动呼吸过度似乎无关紧要。
Patients with chronic heart failure (CHF) suffer increased alveolar VD/VT (dead-space-to-tidal-volume ratio), yet they demonstrate augmented pulmonary ventilation such that arterial PCO2 (PaCO2) remains remarkably normal from rest to moderate exercise. This paradoxical effect suggests that the control law governing exercise hyperpnea is not merely determined by metabolic CO2 production (V̇CO2) per se but is responsive to an apparent (real-feel) metabolic CO2 load that also incorporates the adverse effect of physiological VD/VT on pulmonary CO2 elimination. By contrast, healthy individuals subjected to dead space loading also experience augmented ventilation at rest and during exercise as with increased alveolar VD/VT in CHF, but the resultant response is hypercapnic instead of eucapnic, as with CO2 breathing. The ventilatory effects of dead space loading are therefore similar to those of increased alveolar VD/VT and CO2 breathing combined. These observations are consistent with the hypothesis that the increased series VD/VT in dead space loading adds to as with increased alveolar VD/VT in CHF, but this is through rebreathing of CO2 in dead space gas thus creating a virtual (illusory) airway CO2 load within each inspiration, as opposed to a true airway CO2 load during CO2 breathing that clogs the mechanism for CO2 elimination through pulmonary ventilation. Thus, the chemosensing mechanism at the respiratory controller may be responsive to putative drive signals mediated by within-breath PaCO2 oscillations independent of breath-to-breath fluctuations of the mean PaCO2 level. Skeletal muscle afferents feedback, while important for early-phase exercise cardioventilatory dynamics, appears inconsequential for late-phase exercise hyperpnea.
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DOI：
10.1016/0034-5687(80)90060-2
发表时间：
1980-01-01
期刊：
RESPIRATION PHYSIOLOGY
影响因子：
--
作者：
BECH, C;JOHANSEN, K
通讯作者：
JOHANSEN, K
影响因子：
3.3
作者：
Amann, Markus;Blain, Gregory M.;Dempsey, Jerome A.
通讯作者：
Dempsey, Jerome A.
影响因子：
5.5
作者：
Amann, Markus;Runnels, Sean;Richardson, Russell S.
通讯作者：
Richardson, Russell S.
影响因子：
5.5
作者：
CROSS, BA;DAVEY, A;STIDWILL, R
通讯作者：
STIDWILL, R
影响因子：
5.5
作者：
BERKENBOSCH, A;BOVILL, JG;OLIEVIER, ICW
通讯作者：
OLIEVIER, ICW