Open AccessGas Exchange and Pulmonary Hypertension following Acute Pulmonary Thromboembolism: Has the Emperor Got Some New Clothes Yet?
Author(s) -
Tsang John Y. C.,
Hogg James C.
Publication year - 2014
Publication title -
pulmonary circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.791
H-Index - 40
ISSN - 2045-8940
DOI - 10.1086/675985
Subject(s) - medicine , hypoxic pulmonary vasoconstriction , hypoxemia , vasoconstriction , cardiology , pulmonary hypertension , pulmonary vasculature , perfusion , vascular resistance , vasoactive , hemodynamics
Patients present with a wide range of hypoxemia after acute pulmonary thromboembolism (APTE). Recent studies using fluorescent microspheres demonstrated that the scattering of regional blood flows after APTE, created by the embolic obstruction unique in each patient, significantly worsened regional ventilation/perfusion (V/Q) heterogeneity and explained the variability in gas exchange. Furthermore, earlier investigators suggested the roles of released vasoactive mediators in affecting pulmonary hypertension after APTE, but their quantification remained challenging. The latest study reported that mechanical obstruction by clots accounted for most of the increase in pulmonary vascular resistance, but that endothelin‐mediated vasoconstriction also persisted at significant level during the early phase.