KEY POINTS

1. Volatile anesthetics produce dose-related depression of LV, RV, and LA myocardial contractility, LV diastolic function, and LV-arterial coupling in the normal heart.
2. Negative inotropic effects of volatile anesthetics are related to alterations in intracellular Ca²⁺ homeostasis within the cardiac myocyte.
3. Volatile anesthetics affect the determinants of LV afterload to varying degrees in the presence of normal and dysfunctional myocardium.
4. Systemic hemodynamic effects of volatile anesthetics are complex and determined by the interaction of myocardial effects, direct actions on the arterial and venous vasculature, and alterations in autonomic nervous system activity.
5. Volatile anesthetics sensitize myocardium to the arrhythmogenic effects of epinephrine to varying degrees and may prevent or facilitate the development of atrial or ventricular arrhythmias during myocardial ischemia or infarction, depending upon the concentration of the agent, the extent of the injury, and the location affected within the conduction pathway.
6. Volatile anesthetics are relatively weak coronary vasodilators that are not capable of producing coronary steal at typically used clinical concentrations, even in patients with steal-prone coronary anatomy.
7. Volatile anesthetics exert important cardioprotective effects against reversible and irreversible myocardial ischemia in experimental animals and humans by activating intracellular signal transduction pathways involving A₁ receptors, PKC, G_i proteins, mitochondrial or sarcolemmal K_ATP channels, and ROS.
8. Volatile agents depress baroreceptor reflex control of arterial pressure to varying degrees.
9. Nitrous oxide causes direct negative inotropic effects, does not substantially affect LV diastolic function, and produces modest increases in pulmonary and systemic arterial pressure via a sympathomimetic effect. These actions are dependent to some degree upon the baseline anesthetic.
10. Xenon is essentially devoid of cardiovascular effects.