How does saltatory conduction work?

Most axons in the human nervous system are myelinated, meaning they are enclosed in a myelin sheath, a fatty deposit created and maintained by Schwann cells that acts as an electrical insulator. There are small gaps in the sheath around 1-2 micrometers apart. These gaps are known as the nodes of Ranvier.
Because the myelin sheath prevents the flow of current, and ion channels are only present in high densities in the membrane at the nodes of Ranvier, action potentials are generated only at nodes. During an action potential when Na+ ions rush into the neuron, the intracellular environment at the node becomes more positively charged relative to the next node along the axon. As such, the positive ions within the already-depolarised section of the axon are ‘pushed’ along the electrical gradient towards the more negative environment at the next node. The arrival of positive ions at this node depolarises this section of the axon as well, initiating another action potential. This process is repeated, allowing the action potential to propagate rapidly along the axon, effectively ‘jumping’ between nodes.
This ‘jumping’ mechanism is known as saltatory conduction. It minimises the length of the axon that needs to depolarise in order for an action potential to propagate. This reduces energy used and makes action potentials travel much faster than in unmyelinated axons, which (in most situations) is preferable to minimise the delay between the initiation of the electrical signal and the response of the next neuron or the effector, as many of our axons have to be very long (the motor neuron that travels from your spinal cord all the way down to the muscles in your foot, for example!). However, there are still some unmyelinated axons within the human nervous system. For example, the axons of the pain receptors in your skin that are responsible specifically for that delayed but longer-lasting ‘dull’ pain after you’re hurt are unmyelinated.