Pulmonary vasodilation in acute pulmonary embolism – a systematic review

Acute pulmonary embolism is the third most common cause of cardiovascular death. Pulmonary embolism increases right ventricularafterload, which causes right ventricular failure, circulatory collapse and death. Most treatments focus on removal of themechanical obstruction caused by the embolism, but pulmonary vasoconstriction is a significant contributor to the increased rightventricular afterload and is often left untreated. Pulmonary thromboembolism causes mechanical obstruction of the pulmonaryvasculature coupled with a complex interaction between humoral factors from the activated platelets, endothelial effects, reflexesand hypoxia to cause pulmonary vasoconstriction that worsens right ventricular afterload. Vasoconstrictors include serotonin,thromboxane, prostaglandins and endothelins, counterbalanced by vasodilators such as nitric oxide and prostacyclins. Exogenousadministration of pulmonary vasodilators in acute pulmonary embolism seems attractive but all come with a risk of systemicvasodilation or worsening of pulmonary ventilation-perfusion mismatch. In animal models of acute pulmonary embolism, modulatorsof the nitric oxide-cyclic guanosine monophosphate-protein kinase G pathway, endothelin pathway and prostaglandinpathway have been investigated. But only a small number of clinical case reports and prospective clinical trials exist. The aim ofthis review is to give an overview of the causes of pulmonary embolism-induced pulmonary vasoconstriction and of experimentaland human investigations of pulmonary vasodilation in acute pulmonary embolism.