BPD - Cardiovascular
Introduction Pathogenesis Clinical Prevention Management Prognosis Growth Cardiovascular Pulmonary Neurodevelopmental Mortality References Abbreviations Other Lectures		Cardiovascular complications of BPD include systemic hypertension, left ventricular hypertrophy (LVH), pulmonary hypertenson and cor pulmonale. Systemic hypertension has been reported in 10-40% of patients with BPD. Although its exact cause is unknown, it is usually mild, responding well to therapy. Onset is between 2 and 4 months of age and can even be after NICU discharge, so serial blood pressure measurements on follow up are required to detect this late onset hypertension. The duration is usually less than 1 year. Left ventricular hypertrophy can occur in the absence of hypertension. The stiff hypertrophic left ventricle then requires high filling pressures, which means increased hydrostatic pressures in the pulmonary vessels, which in turn favors the development of pulmonary edema. LVH has also been associated with the reports in the older literature of sudden unexpected deaths in BPD. Presurfactant data indicates that severe BPD can be associated with the destruction of pulmonary vessels leading to increased pulmonary vascular resistance, increased pulmonary artery pressure, right ventricular hypertrophy and cor pulmonale. Cor pulmonale, in turn, is associated with pulmonary edema, worsening of gas exchange and death. There is also an abnormal pulmonary vascular bed in BPD, characterized by a marked pulmonary vasoconstrictive response to hypoxia. Many patients respond to nasal cannula oxygen with a marked decrease in pulmonary artery pressure. These pulmonary vascular abnormalities have not been reported in the postsurfactant era. Return to top of page