**7.2 Anesthetic drugs**

Numerous studies (Fischer et al., 2003; Blaise et al., 2003) investigate the effect of anesthetic drugs on pulmonary vascular tone. In general, it appears that the effect of anesthetic agents on the pulmonary circulation is different from their effect on the systemic circulation, often resulting in an increase in PVR.

*Propofol* decreases PAP, PVR as well as mean arterial pressure (MAP) after CPB. Propofol infusion to children undergoing cardiac catheterization decreased SVR significantly and cardiac contractility mildly. In addition, patients with cardiac shunts and fixed elevated PVR (Eisenmenger syndrome) may experience oxygen desaturation because the decrease in SVR will augment right-to-left shunt.

*Etomidate* is known for its lack of systemic hemodynamic effects on patients with heart disease, but its pulmonary vascular effects have not been investigated adequately.

*Thiopental* has been reported to increase PVR in adults, but in children a decrease of PVR by thiopental has been reported. However, thiopental is a less desirable choice for patient with PH, because it can cause significant myocardial depression and systemic hypotension.

An increase in PVR has been observed with *Ketamine* during spontaneous ventilation, but decreases in PVR have been reported during controlled ventilation. This effect makes ketamine the drug of choice for the anesthetic management of patients with PH, particularly of children with congenital heart diseases.

*Benzodiazepines* are associated with minimal hemodynamic effects and are considered useful for preanesthetic premedication.

*Fentanyl and sufentanil* have minimal pulmonary and systemic effects and attenuate pulmonary and vascular response to noxious stimuli in adults as well as in children.

*Volatile anesthetics* have variable effects on pulmonary vascular tone. Isoflurane and halothane potentiate the vasodilator response to β1 adrenoceptor activation. Isoflurane, halothane, enflurane and desflurane (but not sevoflurane) inhibit endothelium-dependent relaxation by inhibiting the activity of the adenosine triphosphate-sensitive potassium channels, which mediate the vasodilator effect of many endogenous mediators such as adenosine, PGI2 and nitric oxide. In general, isoflurane and sevoflurane are associated with clinical pulmonary vasodilatation and are accepted components of a balanced anesthetic technique in patients with PH.

However, volatile anesthetic agents can lead to dose-dependent depression of cardiac contractility and reduction of SVR, which may be problematic. Moreover, volatile anesthetics, when administered in high minimal alveolar concentrations, attenuate hypoxic pulmonary vasoconstriction, thereby exacerbating ventilation-perfusion mismatching.

*Nitrous oxide* increases the pulmonary vascular tone in adult patients undergoing valve surgery preoperatively and postoperatively. In children, it has shown to have little effect on pulmonary hemodynamics.
