REMODELING OF THE EXTERNAL RESPIRATORY SYSTEM IN CHRONIC HEART FAILURE - A FACTOR OF PATHOGENESIS AND A THERAPEUTIC TARGET

During the development of chronic heart failure (CHF), the lungs and the external respiratory system (ERS) as a whole undergo significant remodeling. These changes are most clearly manifested during physical exercise (PE), when the requirement for ventilation increases, and the ERS works under stress. Patients with CHF during exercise are characterized by the so-called pattern of frequent shallow breathing, when minute ventilation increases mainly due to an increase in the respiratory rate, and the depth of breathing increases to a much lesser extent than in individuals without CHF. The pattern of frequent shallow breathing is an adaptive response that prevents rapid exhaustion of the respiratory muscles (RM) due to the decreased compliance of the lung tissue and airways, and, accordingly, increased work of breathing typical of patients with CHF. In such conditions, tachypnea becomes the only available mechanism for maintaining the required ventilation volume. As the exercise load increases, the inability to adequately increase the depth of breathing contributes to the growth of physiological dead space, and the ventilation efficiency drops. The progressive decrease in the ventilation efficiency is evident as a paradoxically low level of carbon dioxide released relative to the ventilated volume. Such << working conditions >> lead to hyperactivation of the inspiratory metaboreflex, which causes a whole pathogenetic cascade, including sympathicotonia, deterioration of the blood supply to the motor muscles and hyperactivation of their metaboreflex, which leads to further limitation of exercise tolerance. Sympathicotonia characteristic of CHF enhances the activation of carotid chemoreceptors. Along with hypocapnia, this can lead to the development of periodic breathing and central sleep apnea to further worsen the prognosis. Progressive sympathicotonia, hypoxia, endothelial dysfunction, and chronic inflammation result in aggravation of skeletal muscle myopathy. Thus, the condition of RM is at least an important, if not the leading factor in the pathogenesis of impaired exercise tolerance, which requires continuous therapeutic treatment. Such treatment cannot be of a << rehabilitation >> nature, i.e., be used for a limited time, but must be performed on a permanent basis. The search for optimal methods of the respiratory and skeletal muscle training in order to weaken the mutually reinforcing connection between the carotid chemoreflex and muscle metaboreflex, as well as the search for such forms of their implementation, in which they will become a permanent part of the treatment, is extremely important for successful management of CHF patients.