What are the effects of anesthetic agents on HPV and their clinical implications?
Answer:
Any medication that causes vasodilation may inhibit hypoxic vasoconstriction. Several clinical studies have failed to demonstrate a decrease in HPV during single-lung ventilation and total intravenous anesthesia. Intravenous anesthetics, such as thiopental, ketamine, morphine, and fentanyl, have no direct effect on HPV. In contrast, inhalational anesthetics have been shown to inhibit HPV in a dose-related fashion but usually at concentrations much higher than clinically used. Other nonanesthetic drugs such as -agonists and antagonists, calcium channel blockers, nitrovasodilators, and theophylline may influence the effects of inhalation anesthetics on shunting and arterial oxygenation during single-lung ventilation. There is no good evidence that neuraxial blockade affects HPV, unless causing a decrease in cardiac output or systemic vasodilation.
The result of an increased shunt on PaO2 depends on the absolute level of the initial shunt and the inspired oxygen concentration used. Even when shunt is increased, PaO2 usually remains well above 100 mmHg, with minimal changes in oxygen saturation and content.
Inhalational agents inhibit HPV, but they also decrease cardiac output, oxygen consumption, and may cause a decrease in mixed oxygen venous tension (PVO2). If cardiac output decreases and oxygen consumption does not change, there will be a decrease in PVO2, which is a potent stimulus for HPV. A low cardiac output will result in a decreased perfusion of the collapsed lung (where there is an increase in pulmonary vascular resistance as a result of HPV). Nevertheless, the presence of chronic and irreversible vascular disease in the nondependent lung may impair HPV response.
The presence of disease in the dependent lung will decrease the ability of accepting blood flow redistribution, thereby decreasing the local HPV effect.
Direct surgical manipulation may cause the release of vasoactive substances, such as thromboxane and prostacyclin (PGI2), promoting local vasodilatation and blunting HPV, with a subsequent increase in shunt.
Metabolic or respiratory acidosis and hypothermia are also associated with an impairment in HPV.