Hypoxic conditions are rapidly sensed by the carotid body initiating the hypoxic ventilatory response (HVR) pathways. TASK-1/3 K+ channels are responsible for this and a decrease in PO2 causes them to rapidly close, depolarizing the cell and initiating synaptic transmission. Adequate O2 pressures and Volatile Anesthetics (VA) activate these channels preventing the HVR. After years of research, the precise molecular mechanisms for hypoxic effects are still poorly understood. The exact VA binding site and mechanism of action is also unknown. Here it is shown, with the use of molecular electrostatic potentials (MEP), that O2 and VA weakly H-bond to an uncharged Arginine guanidinium group (Arg-245) within the X-gate, breaking other H-bonds and forming δ-charges in the hydrophobic region which opens the pore allowing K+ to flow out. The current flow for a number of channel activators, including VA and O2, is highly correlated with H-bond strength and resulting δ-charge magnitude (R2 = 0.998). The sequence of molecular changes is explored in detail explaining the significance of current outflow "flickering" from open to closed. O2 modulates these channels directly.The role of H2S in this and other related systems is explored. VA and O2 share a number of mutual sites of action, shedding additional light on jet fighter pilot rapid +Gz loss-of-consciousness and subsequent convulsive episodes - also poorly understood after years of research.