Mechanism of Action of Spinal Anesthesia
Spinal anesthesia works by local anesthetic drugs stabilizing neuronal membranes and inhibiting the ionic fluxes required for initiation and conduction of nerve impulses, thereby blocking sensory, motor, and autonomic nerve transmission in the subarachnoid space. 1
Primary Mechanism
Local anesthetics injected into the subarachnoid space directly interact with nerve structures, primarily nerve roots and the spinal cord itself, blocking sodium channels and preventing action potential propagation. 1, 2
The drugs stabilize neuronal membranes by inhibiting sodium ion flux, which is essential for nerve impulse initiation and conduction. 1
This blockade affects three types of nerve fibers: sensory (pain and temperature), motor (muscle movement), and autonomic (sympathetic nervous system control of blood vessels). 3, 4
Distribution Pathways
Local anesthetics reach their sites of action through direct diffusion from the cerebrospinal fluid into neural tissue, with the highest drug concentrations occurring in the periphery of the spinal cord near the injection site. 5
The drugs diffuse into subperineural spaces of mixed spinal nerves and pass centripetally along spinal roots into both the cerebrospinal fluid and spinal cord parenchyma. 5
Distribution is independent of active circulation and occurs primarily through passive diffusion across concentration gradients. 5
Dose-Response Relationship
The total dose of local anesthetic injected into the subarachnoid space is the most important determinant of both therapeutic effects (extent and duration of block) and unwanted effects (hypotension, high block). 4
Small doses of local anesthetic (less than 10 mg bupivacaine) provide adequate surgical anesthesia while significantly reducing cardiovascular side effects, particularly hypotension. 3, 6
Spinal anesthesia requires much lower doses than epidural anesthesia because the drug is placed directly into the cerebrospinal fluid where nerve roots are located, rather than having to penetrate the dura and diffuse through epidural tissues. 2
Cardiovascular Effects
The sympathetic blockade that accompanies spinal anesthesia causes vasodilation and venous pooling, resulting in decreased venous return, cardiac output, and blood pressure—these are attributable to blockade of autonomic fibers rather than direct cardiac depression. 1
Hypotension is the most common side effect and results from the block of sympathetic nerve fibers (T1-L2 levels) that normally maintain vascular tone. 4
Lower doses of intrathecal local anesthetic (particularly bupivacaine less than 10 mg) significantly reduce the incidence and severity of hypotension while maintaining adequate surgical anesthesia. 3, 6
Pharmacokinetics in the Subarachnoid Space
Initial absorption rates from the subarachnoid space are slower than from the epidural space, but late-phase absorption rates are similar between the two routes. 2
Local anesthetics cross the blood-brain barrier and are metabolized primarily in the liver (for amide-type agents like bupivacaine and lidocaine), with elimination half-lives typically 1.5 to 2 hours for lidocaine. 1
Because of the low doses required for spinal anesthesia, systemic toxicity is rarely a problem, unlike epidural anesthesia where the safety margin is much smaller. 2