Pharmacology  ·  General Anesthesia

Intravenous Anesthetic Agents and Total Intravenous Anesthesia

Mechanisms, key advantages, critical adverse effects, and total intravenous anesthesia indications

• All the agents in the first table share the goal of unconsciousness but differ in mechanism, and the mechanism predicts nearly everything clinically important about each drug. Five of the seven potentiate the gamma-aminobutyric acid type A receptor; ketamine is the N-methyl-D-aspartate outlier, which is why it alone increases blood pressure and heart rate instead of lowering them.
• The "Key Advantage" column is a clinical routing signal: which specific situation is this drug the right answer for? Etomidate's advantage is hemodynamic stability; ketamine's is that it sustains the circulation when everything else would drop it. Those are different problems, and the drugs are not interchangeable even though both are called induction agents.
• The "Critical Adverse Effect" column maps to the situations where each drug is contraindicated or demands monitoring. Etomidate's adrenal suppression is safe for a single induction dose but disqualifies it for infusion. Propofol infusion syndrome does not occur with short-term use but is predictable above certain dose-duration thresholds.
• The four total intravenous anesthesia indication cards are arranged by strength of preference: the first is obligatory (malignant hyperthermia susceptibility — all volatile agents prohibited), and the next three are strong clinical indications where volatile maintenance would either be hazardous or technically incompatible with the monitoring being used.
• Remifentanil's pharmacokinetics are explained in the rule box because they are the reason propofol-remifentanil total intravenous anesthesia works at all. A context-sensitive half-time of 3 to 5 minutes regardless of infusion length means offset is predictable — but it also means there is no residual analgesia at emergence, and that transition must be planned before waking the patient.