Pulmonary vascular resistance

Pulmonary vascular resistance reflects the opposition encountered by blood as it flows through the pulmonary circulation. Elevated resistance increases the workload on the right ventricle, contributing to pulmonary hypertension and subsequent right heart strain. Various factors influence pulmonary vascular resistance, including structural changes in the pulmonary arteries, hypoxic vasoconstriction, thromboembolic events, and inflammatory or fibrotic remodeling of the vascular bed. Chronic elevation can lead to right ventricular hypertrophy, reduced exercise tolerance, and progressive cardiopulmonary compromise. Assessment of pulmonary vascular resistance involves both non-invasive and invasive techniques. Echocardiography provides initial insights into right heart pressures and pulmonary artery function, while right heart catheterization offers direct measurement of pulmonary arterial pressures and cardiac output, allowing calculation of resistance. Advanced imaging modalities, such as CT pulmonary angiography or MRI, can further delineate structural abnormalities contributing to elevated resistance and assist in treatment planning.

Management strategies focus on addressing the underlying cause and reducing vascular strain. Vasodilator therapy, including endothelin receptor antagonists, phosphodiesterase-5 inhibitors, and prostacyclin analogs, is central in pulmonary arterial hypertension. Anticoagulation, thrombolysis, or surgical intervention may be indicated for thromboembolic disorders. Supportive measures, such as oxygen therapy and supervised exercise programs, enhance functional capacity and quality of life. Ongoing research explores novel molecular targets and regenerative approaches to reduce pulmonary vascular remodeling. By combining precise hemodynamic evaluation, targeted pharmacologic therapy, and supportive interventions, management of pulmonary vascular resistance aims to improve circulation, preserve right heart function, and optimize patient outcomes.