Purpose of review: To summarize what is currently known about the relationship between single-lung ventilation (SLV), oxidative stress, and postoperative disruption of organ function.
Recent findings: SLV produces progressive alelectasis that is associated with hypoxic pulmonary vasoconstriction and redistribution of blood flow away from the nonventilated lung. This local tissue hypoxia induces the generation of reactive oxygen and reactive nitrogen species, an effect subsequently amplified by lung re-expansion consistent with well described hypoxia/reperfusion responses. Both experimental and clinical data indicate that the magnitude of oxidative and nitrosative stress is related to the duration of SLV and that these stresses affect not only the collapsed/re-expanded lung, but other organs as well.
Summary: SLV and subsequent re-expansion of atelectatic lung are associated with the generation of reactive oxygen and nitrogen species that may modulate persistent systemic effects.