How are pulmonary perfusion and ventilation altered during one-lung ventilation?
During two-lung ventilation in the lateral decubitus position, ventilation is preferentially diverted to the non-dependent lung and perfusion is primarily directed to the dependent lung. Once the nondependent lung is collapsed, ventilation to that side is eliminated, but some perfusion persists.
Blood passing through the deflated lung does not exchange gas with alveoli and is called shunted blood. This unoxygenated (shunted) blood mixes with oxygenated blood from the dependent lung in the pulmonary vein and left atrium. Shunted blood dilutes oxygenated blood, resulting in a significant overall reduction in oxygen ten-sion. In cases where the nondependent lung was mostly healthy preoperatively, its contribution to overall oxygena-tion is important and loss of its function produces major reductions in oxygenation. When the nondependent lung was significantly impaired preoperatively, its contribution to overall oxygenation is not as great. When its contribu-tion to oxygenation is lost during one-lung anesthesia, expected falls in oxygen tension are not as great. Consequently, one might expect greatest hypoxemia asso-ciated with one-lung anesthesia in patients without pul-monary disease, such as during esophageal surgery.
CO2 exchange is not affected by one-lung ventilation to the same extent as oxygenation.
Fortunately, there is a reduction in pulmonary blood flow to the nondependent lung during one-lung anesthesia, which tends to decrease the shunt fraction. Gravity, surgical com-pression, and ligation of nondependent pulmonary vessels decrease blood flow to the nondependent lung. Alveolar hypoxia in the nondependent lung from atelectasis stimulates hypoxic pulmonary vasoconstriction (HPV), which leads to further diversion of blood to the dependent (ventilated) lung.
HPV is a local mechanism that constricts pulmonary vessels and diverts blood flow to the better-oxygenated (ventilated) portions of the lung. Continued blood flow to hypoxic lung constitutes true shunt. The stimulus for HPV appears to be related to PO2 in the mixed venous (Pv) blood, and the alveolar PO2 (PAO2). Active HPV can decrease blood flow to hypoxic lung by 50%, thereby decreasing shunt and improving PaO2.
In numerous in vitro and in vivo animal studies, HPV has been shown to be inhibited by potent inhaled anesthetics; vasodilators (nitroglycerin, nitroprusside, and β2-agonists such as isoproterenol); surgical manipulation; calcium channel blockers; cold; positive end-expiratory pressure (PEEP); vasoconstrictors (phenylephrine, epinephrine, and dopamine); high PvO2; increased cardiac output; hypocarbia; and certain granulomatous infections.
Intravenous agents such as ketamine, opioids, and benzo-diazepines do not appear to inhibit HPV. These effects on HPV are difficult to demonstrate in the clinical situation because of the many confounding variables present in patients undergoing surgery. Thus, whether inhaled anes-thetics inhibit HPV in humans remains controversial. Cyclo-oxygenase inhibitors (aspirin, ibuprofen, etc.) appear to potentiate HPV in some animal studies, but they have not been evaluated for their possible side-effects on HPV in humans. A potential disadvantage of such agents in the clinical situation is their adverse effect on coagulation.