Mechanisms of Hypoxemia in the Acute Respiratory Distress Syndrome

Acute respiratory distress syndrome (ARDS) is characterized by hypoxemia and bilateral infiltrates due to non-cardiogenic pulmonary edema. In the context of growing awareness of the considerable heterogeneity of this syndrome, differences in the pathophysiology of hypoxemia might help characterize ARDS phenotypes and guide treatment. In this chapter we focus on the mechanisms involved in the onset and persistence of hypoxemia in patients with ARDS. Intrapulmonary shunt due to perfusion of non-ventilated areas, associated with loss of aeration and low compliance, is the main mechanism of hypoxemia in the classical “baby lung” model of ARDS. Alternative/additional causes of hypoxemia originate from overperfusion of poorly ventilated areas due to redistribution of pulmonary blood flow in the presence of increased dead space and/or impairment of hypoxic pulmonary vasoconstriction. Moreover, low mixed oxygen venous saturation, due to an imbalance between oxygen delivery and peripheral oxygen consumption, may be a ‘metabolic’ cause of hypoxemia. Finally, intra-cardiac or intra-pulmonary anatomical shunts contribute to hypoxemia in the presence of patent foramen ovale or massive pulmonary vasodilation or neoangiogenesis. Bedside physiological reasoning aimed at identification of the prevalent mechanisms of hypoxemia in ARDS could represent a novel personalized approach to management of this deadly syndrome.