General & Local Anesthetics

“Anesthetic” covers two distinct tasks. A local anesthetic (the “-caine” drugs) is injected or applied to one area to block sensation there while the patient stays awake. A general anesthetic (propofol, ketamine, inhaled sevoflurane) acts on the whole brain to produce unconsciousness. The distinction matters because their dangers are completely different.

A crucial safety point that recurs across this class: anesthesia is not analgesia, and it is not muscle relaxation. Propofol, for instance, produces deep sedation but provides no pain relief — a paralyzed or sedated patient can still be in agony if analgesia is not given separately. Nurses reason about anesthesia as three separable goals — unconsciousness, analgesia, and immobility — and a given drug may not supply all three (propofol, for example, gives no analgesia).

Local anesthetics work by blocking voltage-gated sodium channels in the nerve membrane. Without sodium influx the nerve cannot fire an action potential, so the pain signal never leaves the area. Lidocaine has a medium duration and a long safety record; bupivacaine is long-acting but the most cardiotoxic of the group.

The feared complication is local anesthetic systemic toxicity (LAST) — too much drug reaching the bloodstream (accidental IV injection or overdose), where the same sodium-channel block now hits the brain and heart. It presents as a progression: early perioral numbness, metallic taste, tinnitus, agitation, then seizures, then cardiovascular collapse (arrhythmia, arrest — bupivacaine is notoriously hard to resuscitate). The specific antidote is IV 20% lipid emulsion ("lipid rescue"), first explained as a "lipid sink" that pulls the drug out of the heart (it likely works in several ways) — it must be immediately available wherever large-dose local anesthesia is done.

Propofol is the workhorse IV general anesthetic: it potentiates GABA-A (the brain’s main inhibitory brake), giving fast, smooth unconsciousness that wears off quickly. Its trade-offs: hypotension (vasodilation + myocardial depression), respiratory depression/apnea, pain on injection, and no analgesia. Its lipid emulsion (soybean oil, egg lecithin) supports bacterial growth, so tubing/vials are discarded within 12 hours. Prolonged high-dose infusion (roughly > 4 mg/kg/hr for > 24–48 h) risks propofol infusion syndrome (PRIS) — metabolic acidosis, rhabdomyolysis, hyperkalemia, and cardiac/renal failure — a rare but lethal ICU emergency.

Ketamine is the opposite in almost every way: a dissociative anesthetic (NMDA-receptor blocker) that is sympathomimetic — it raises heart rate and blood pressure, preserves airway reflexes and breathing, and bronchodilates (useful in asthma and hemodynamically unstable patients). Its signature downside is emergence reactions — vivid hallucinations, delirium, and nightmares on waking — reduced by a quiet recovery and a benzodiazepine.

The volatile inhaled anesthetics (sevoflurane, isoflurane, desflurane) maintain general anesthesia through the case. Their catastrophic complication is malignant hyperthermia (MH) — a genetic (RYR1) trait in which volatile agents, or the depolarizing paralytic succinylcholine, trigger uncontrolled calcium release from skeletal-muscle sarcoplasmic reticulum. The muscle goes into runaway metabolism: rising end-tidal CO₂ (often the first sign), muscle rigidity, tachycardia, a steep temperature rise, rhabdomyolysis, and hyperkalemia.

This is where anesthetics tie back to the Neuromuscular Blockers class — succinylcholine is the paralytic that shares this trigger. The specific antidote is dantrolene, which blocks the ryanodine receptor to stop the calcium release; it must be stocked wherever triggering agents are used, alongside stopping the agent, hyperventilating with 100% oxygen, and active cooling.