An anesthesiologist's guide to hypoxic pulmonary... : Current Opinion in Anesthesiology (original) (raw)

Thoracic anaesthesia

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

Nagendran, Jayana,b; Stewart, Kenb; Hoskinson, Mikec; Archer, Stephen L.a,d

aVascular Biology Group, Division of Cardiology, University of Alberta, Edmonton, Canada

bDepartment of Surgery, University of Alberta, Edmonton, Canada

cDepartment of Radiology, University of Alberta, Edmonton, Canada

dDepartment of Physiology, University of Alberta, Edmonton, Canada

Correspondence to Stephen L. Archer, MD, Heart and Stroke Chair in Cardiovascular Research, Cardiology Division, University of Alberta, WMC 2C2.36, 8440 112th Street, Edmonton, Alberta, Canada, T6G 2B7 Tel: +780 407 6353, fax: +780 407 6032; E-mail: [email protected]

Abstract

Purpose of the review

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.

Recent findings

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.

Summary

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.