An anesthesiologist's guide to hypoxic pulmonary vasoconstriction: implications for managing single-lung anesthesia and atelectasis

Abstract

Hypoxic pulmonary vasoconstriction is the pulmonary circulation's homeostatic mechanism for matching regional perfusion to ventilation and optimizing systemic PaO2. The role of hypoxic pulmonary vasoconstriction in anesthesiology is reviewed. In hypoxic pulmonary vasoconstriction, airway hypoxia causes resistance pulmonary arteries to constrict, diverting blood to better-oxygenated alveoli. Hypoxic pulmonary vasoconstriction optimizes O2 uptake in atelectasis, pneumonia, asthma, and adult respiratory distress syndrome. During single-lung anesthesia, hypoxic pulmonary vasoconstriction helps maintain systemic oxygenation. When hypoxic pulmonary vasoconstriction is weak, systemic hypoxemia is exacerbated. Although not widely used, the peripheral chemoreceptor agonist almitrine enhances hypoxic pulmonary vasoconstriction and improves PaO2 during single-lung anesthesia. The mechanism of hypoxic pulmonary vasoconstriction involves a redox-based O2 sensor within pulmonary artery smooth muscle cells. Pulmonary artery smooth muscle cells mitochondria vary production of reactive O2 species in proportion to PaO2. Hypoxic withdrawal of these redox second messengers inhibits voltage-gated potassium channels, depolarizing the pulmonary artery smooth muscle cells. Depolarization activates L-type calcium channels, increasing cytosolic calcium and triggering hypoxic pulmonary vasoconstriction. An understanding of hypoxic pulmonary vasoconstriction is clinically relevant for anesthesiologists. Randomized clinical trials with robust endpoints are required to assess strategies for enhancing hypoxic pulmonary vasoconstriction in thoracic surgery patients.