Description:
Dyspnea and fatigue are cardinal symptoms of both cardiac and lung diseases. Frequently, these pathologies coexist, worsening clinical condition and making it difficult for physicians to correctly identify the cause of dyspnea and reduced exercise capacity. A wide amount of evidence suggests that CPET, in conjunction with PFT, is a useful clinical tool to identify cardiac and/or pulmonary causes of dyspnea of unclear or multifactorial origin. In fact, lung function evaluation is pivotal in the diagnostic assessment of heart failure, as lung disease comorbidities influence both prognosis and therapy. The close relationship between cardiac and pulmonary pathophysiology was first described in 1785 by Withering and in 1883 by Hope, who coined the term “cardiac asthma.” Moreover, several studies showed a reduction in FEV1, FVC and DLCO in heart failure. Several factors may be responsible for restrictive lung pattern in heart failure, such as increased lung stiffness due to alveolar effusion, reduction of working alveolar–capillary units, respiratory muscle fatigue, cardiac enlargement, and constriction of under-perfused alveoli leading to reduced lung compliance in a low cardiac output state. However, evidence in this field is not extensive and pathophysiology regulating heart-lung interactions is complex and not completely cleared.
Learning Objectives:
• Mechanisms in heart failure that can induce a restrictive lung pattern
• Which variables of the CPET are important to evaluate a lung-restrictive pattern
• Clinical strategies in the treatment of lung/heart pathological interactions