Mitrouska Ioanna, Bolaki Maria, Vaporidi Katerina, Georgopoulos Dimitris
Department of Pulmonary Medicine, University Hospital of Heraklion, Medical School University of Crete Heraklion Crete Greece.
Department of Intensive Care Medicine, University Hospital of Heraklion, Medical School University of Crete Heraklion Crete Greece.
Pulm Circ. 2022 Mar 23;12(1):e12060. doi: 10.1002/pul2.12060. eCollection 2022 Jan.
Dyspnea on exertion is a devastating symptom, commonly observed in patients with pulmonary hypertension (PH). The pathophysiology of dyspnea in these patients has been mainly attributed to cardiovascular determinants and isolated abnormalities of the respiratory system during exercise, neglecting the contribution of the control of the breathing system. The aim of this review is to provide a novel approach to the interpretation of dyspnea in patients with PH, focused on the impact of the control of the breathing system during exercise. Exercise through multiple mechanisms affects the (1) ventilatory demands, as dictated by respiratory center activity, (2) actual ventilation, and (3) metabolic hyperbola. In patients with PH, exertional dyspnea can be explained by exercise-induced alterations in these variables. Compared to healthy subjects, at a given CO production during exercise, ventilatory demands in patients with PH are higher due to metabolic acidosis (early reaching the anaerobic threshold), hypoxemia, and excessive upward movement of metabolic hyperbola owing to abnormal exercise response of dead space to tidal volume ratio. Simultaneously, dynamic hyperinflation and respiratory muscles weakness decreases the actual ventilation for a given respiratory center activity, creating a dissociation between demands and ventilation. Consequently, a progressive increase in ventilatory demands and respiratory center activity occurs during exercise. The forebrain projection of high respiratory center activity causes exertional dyspnea despite the relatively low ventilation and significant ventilatory reserve. This type of analysis suggests that the respiratory system is the main determinant of exertional dyspnea in patients with PH, with the cardiovascular system being an indirect contributor.
劳力性呼吸困难是一种严重的症状，常见于肺动脉高压（PH）患者。这些患者呼吸困难的病理生理学主要归因于心血管因素以及运动期间呼吸系统的孤立异常，而忽视了呼吸系统控制的作用。本综述的目的是提供一种新的方法来解释PH患者的呼吸困难，重点关注运动期间呼吸系统控制的影响。运动通过多种机制影响：（1）由呼吸中枢活动决定的通气需求；（2）实际通气量；（3）代谢双曲线。在PH患者中，劳力性呼吸困难可以通过运动引起的这些变量的改变来解释。与健康受试者相比，在运动期间给定的CO产生量下，由于代谢性酸中毒（早期达到无氧阈值）、低氧血症以及由于无效腔与潮气量比值的异常运动反应导致代谢双曲线过度上移，PH患者的通气需求更高。同时，动态肺过度充气和呼吸肌无力会降低给定呼吸中枢活动时的实际通气量，导致需求与通气之间的分离。因此，运动期间通气需求和呼吸中枢活动会逐渐增加。尽管通气量相对较低且有显著的通气储备，但高呼吸中枢活动的前脑投射仍会导致劳力性呼吸困难。这种分析表明，呼吸系统是PH患者劳力性呼吸困难的主要决定因素，而心血管系统是间接因素。
