Pulmonary arterial hypertension and sepsis: prothrombotic profile and inflammation can changes pulmonary mechanics?

Abstract

Pulmonary arterial hypertension (PAH) is associated to cellular and structural alterations of lung vasculature. Endothelial dysfunction promotes vasoconstriction, smooth muscle hypertrophy, intimal proliferation, angioproliferative plexiform lesions, and in situ thrombosis increasing pulmonary vascular resistance and arterial stiffness. Indeed, an inflammatory component has been defined in PAH on the last years. Sepsis is a systemic complex syndrome, of infectious origin. The presence of inflammation is well established in this condition and it is also considered a risk factor for acute lung injury. Thrombotic events play important role in sepsis pathophysiology. The association between PAH and sepsis potentiate the metabolic oxygen consumption/offer imbalance, with very high mortality risk. Furthermore, it is possible that the association of these two conditions should intensify thrombotic events on pulmonary microcirculation, reducing area of pulmonary vascular bed available for blood flow. For the other side, an inflammation synergism observed on these two conditions should increase the respiratory system impedance.