Pathophysiology Of Pulmonary And Systemic Hemodynamics In Chronic Obstructive Pulmonary Disease

Abstract

This scientific review systematizes and analyzes current evidence regarding the mechanisms underlying pulmonary and systemic hemodynamic disturbances in patients with chronic obstructive pulmonary disease (COPD). The cardiopulmonary continuum is examined, within which chronic hypoxia, systemic inflammation (the “spill-over” phenomenon of cytokines such as IL-6, TNF-α, and C-reactive protein [CRP]), and oxidative stress initiate a cascade of pathological changes ranging from hypoxic pulmonary vasoconstriction to structural remodeling of the pulmonary vasculature, generalized endothelial dysfunction, and anatomical reduction of the pulmonary capillary network associated with emphysema. The review provides a detailed description of the pathophysiological mechanisms involved in the development of cor pulmonale, left ventricular diastolic dysfunction resulting from interventricular interaction and fluctuations in intrathoracic pressure, as well as the formation of an arrhythmogenic substrate. A critical analysis is presented of contemporary diagnostic approaches, including echocardiography, computed tomography pulmonary angiography (CTPA), cardiac magnetic resonance imaging (MRI), biomarkers such as N-terminal pro-B-type natriuretic peptide (NT-proBNP), and current therapeutic strategies, with particular emphasis on the limitations of pulmonary hypertension-specific therapies in COPD patients. The authors highlight the necessity of transitioning toward precision medicine through the identification of the vascular phenotype of COPD and the integration of artificial intelligence and radiomics technologies for the early subclinical detection of hemodynamic abnormalities.