What does a general anaesthetic need to achieve?
General anaesthesia is a controlled state in which a patient can undergo a procedure without awareness or intolerable pain, with appropriate control of movement and physiological responses. It is usually produced by a combination of drugs rather than expecting a single agent to provide every component. A hypnotic may produce unconsciousness while an opioid or another analgesic addresses nociception, and a neuromuscular blocker facilitates conditions for surgery or airway management.
The high-yield distinction is hypnosis versus analgesia. Propofol is an effective hypnotic but does not provide analgesia. Etomidate also lacks analgesic properties. Ketamine is different: its dissociative state includes analgesia, amnesia and sedation. Neuromuscular paralysis must never be interpreted as evidence of unconsciousness; an immobile patient still needs an appropriate anaesthetic plan.
| Component | Purpose | Revision example |
|---|---|---|
| Hypnosis | Loss of consciousness | Propofol or etomidate |
| Amnesia | Reduced formation of procedural memories | Hypnotic agents or benzodiazepines |
| Analgesia | Control of painful stimulation | Opioid or ketamine |
| Immobility/relaxation | Suitable operating conditions | Anaesthetic effect and, when needed, neuromuscular blockade |
How do the main intravenous agents differ?
Start IV-agent revision with the receptor mechanism and dominant physiological effect, then add its characteristic adverse event. Propofol and etomidate enhance GABA-mediated inhibition. Barbiturates such as thiopental also act through GABA-related mechanisms. Ketamine instead blocks NMDA-mediated excitation. These differences explain why agents with the same broad role in anaesthesia can behave very differently in a hypotensive patient or a painful procedure.
| Agent | Principal mechanism | Useful discriminator | Important limitation |
|---|---|---|---|
| Propofol | GABA-mediated inhibition | Rapid hypnosis; antiemetic action | Hypotension, respiratory depression; no analgesia |
| Etomidate | Positive modulation of GABA-A | Relatively stable haemodynamics | Adrenal suppression, myoclonus; no analgesia |
| Ketamine | NMDA antagonism | Dissociation with analgesia; bronchodilation | Emergence reactions, secretions, laryngospasm risk |
| Thiopental | Barbiturate enhancement of GABA-A | Single-bolus effect ends largely through redistribution | Cardiorespiratory depression; porphyria concern |
| Midazolam | Benzodiazepine sedative action | Anxiolysis and amnesia as an adjunct | No analgesia; sedation can deepen with other depressants |
Thiopental is a classic examination agent even though propofol has largely replaced it for routine IV induction. A short clinical effect after a single bolus does not imply that the drug has already been eliminated. Redistribution lowers the concentration in the brain as drug moves to other tissues. Repeated doses or infusions can behave differently because those tissue compartments accumulate drug.
Choose an agent in context. Blood pressure, airway risk, comorbidity and whether the procedure is painful all influence the plan. A comparison table summarises tendencies rather than establishing an unconditional best drug. Separate general-anaesthesia induction from procedural-sedation regimens; a dose or monitoring assumption from one setting cannot simply be copied into the other.
What makes propofol distinctive?
Propofol is a widely used IV hypnotic that potentiates inhibitory GABA-mediated signalling. Its characteristic milky appearance comes from a lipid emulsion. It can be used for induction and for maintenance by infusion, but analgesia must be provided separately when the procedure is painful. Its antiemetic action is a useful distinguishing property in a comparison with agents that are more likely to cause nausea or vomiting.
The main immediate concerns are hypotension and respiratory depression. Vasodilation and reduced myocardial contractility contribute to the fall in blood pressure, particularly in hypovolaemia or catecholamine depletion. Apnoea can occur, especially after a bolus. Pain on injection is another common recognition clue. Administration therefore requires appropriate monitoring and immediate airway-support capability.
After a single bolus, redistribution is a major reason the hypnotic effect ends quickly. An infusion can continue the effect, but prolonged administration introduces different risks. Propofol infusion syndrome is a rare serious syndrome associated with prolonged high-dose exposure, featuring metabolic acidosis, rhabdomyolysis, hyperkalaemia and cardiac or renal dysfunction. It should not be reduced to one universally safe dose or time threshold.
Why are ketamine and etomidate common comparison questions?
Ketamine produces dissociative anaesthesia through NMDA antagonism and has clinically useful analgesic activity. It generally increases heart rate and blood pressure through sympathetic effects and has bronchodilatory properties. These tendencies help explain its use in selected painful procedures or patients with bronchospasm. They do not make it an automatic choice whenever a stem mentions shock or respiratory disease.
The characteristic adverse effects are emergence phenomena such as vivid dreams, hallucinations or agitation, increased respiratory secretions and occasional laryngospasm. Respiratory drive and airway reflexes may be relatively preserved compared with some other agents, but airway protection is not guaranteed. Rapid administration, large doses or co-administered sedatives can produce respiratory problems. Airway equipment and trained support remain necessary.
Etomidate is a short-acting hypnotic with relatively little depression of blood pressure at induction. Its exam association is adrenal steroid synthesis inhibition, particularly inhibition of 11-beta-hydroxylase. Myoclonus and injection discomfort are additional clues. Myoclonic movements during administration do not necessarily represent an epileptic seizure. Because etomidate has no analgesic effect, painful stimulation requires a separate analgesic strategy.
A stem asking for an NMDA antagonist points towards ketamine. A stem asking for an IV agent associated with adrenal suppression points towards etomidate. A milky emulsion with antiemetic action suggests propofol. These mechanism-to-property links are more dependable than treating an agent as universally suitable for a broad clinical category.
What is MAC and how does it compare anaesthetic potency?
Minimum alveolar concentration (MAC) is the alveolar concentration of an inhaled anaesthetic at which 50% of people do not move in response to a surgical stimulus. Conventional MAC values are referenced to one atmosphere. It is an inhalational potency measure: if less agent is needed to reach the same defined effect, that agent is more potent. Therefore a lower MAC corresponds to greater potency.
MAC is a population endpoint rather than a personalised prescription. Age, temperature, pregnancy and co-administered drugs change anaesthetic requirements. Increasing age after infancy, decreasing body temperature and pregnancy generally reduce the MAC requirement. Opioids, benzodiazepines and other sedative agents also reduce it. Acute alcohol exposure and chronic alcohol use have different effects, so the time course in the stem matters.
| Measure | What it describes | Common trap |
|---|---|---|
| MAC | Potency for immobility after a surgical stimulus | Higher MAC does not mean greater potency |
| Blood–gas partition coefficient | Solubility in blood and equilibration behaviour | It is not the principal potency measure |
| Oil–gas partition coefficient | Lipid solubility associated with potency | Do not substitute it for blood–gas solubility |
| MAC-awake | Response to verbal command | It is a different endpoint from surgical immobility |
The MAC effects of inhaled agents are approximately additive when agents are combined. Their delivered volume percentages cannot simply be added and called a combined MAC because each agent has a different potency. Likewise, MAC does not directly describe a total intravenous anaesthetic technique. Anaesthetic adequacy still requires assessment of the patient and the complete drug regimen.
How does blood–gas solubility affect induction and recovery?
An inhaled agent reaches the alveoli, enters pulmonary blood and equilibrates with the brain. Blood that dissolves a large amount of agent acts as a reservoir. With a higher blood–gas partition coefficient, more uptake is required before alveolar partial pressure rises towards the inspired partial pressure. Equilibration is therefore slower. Lower blood solubility generally allows a faster change in alveolar and brain partial pressures.
The central exam distinction is speed versus potency. A low blood–gas coefficient favours rapid adjustment and washout; a low MAC identifies a potent agent. These are different properties. An agent can be relatively weak yet fast acting. Concentration, ventilation, circulation and the duration of administration also affect the observed speed, so solubility is an important determinant rather than the only determinant.
Volatile anaesthetics such as sevoflurane, isoflurane, desflurane and halothane are liquids at room temperature and are delivered through suitable vaporising equipment. Nitrous oxide is a gas under ordinary ambient conditions. The delivery system must match the agent and be checked before use. Concentration monitoring and ventilation monitoring help relate the intended anaesthetic to what the patient actually receives.
Which inhalational-agent properties are most useful for revision?
Compare volatile agents by airway tolerability, cardiovascular effects and characteristic toxicity. Sevoflurane is less pungent and suitable for inhalational induction in selected patients. Desflurane and isoflurane can irritate the airway; desflurane can also produce tachycardia and hypertension when its concentration is increased rapidly. Volatile agents can reduce systemic vascular resistance and cause hypotension, particularly in a hypovolaemic patient.
| Agent | Useful property | Adverse-effect clue |
|---|---|---|
| Sevoflurane | Less pungent; used for inhalational induction | Volatile-agent hypotension and malignant-hyperthermia susceptibility |
| Desflurane | Pungent agent requiring appropriate delivery equipment | Airway irritation; rapid concentration rise can cause sympathetic responses |
| Isoflurane | Volatile maintenance agent | Airway irritation and vasodilation |
| Halothane | Classic volatile agent in exam comparisons | Rare severe hepatotoxicity; malignant-hyperthermia trigger |
| Nitrous oxide | Analgesic inhaled adjunct with high MAC | Closed-gas-space expansion and diffusion hypoxia |
| Agent | MAC | Blood–gas coefficient |
|---|---|---|
| Desflurane | ~6% | 0.42 (fastest onset/offset) |
| Nitrous oxide | ~104% | 0.47 |
| Sevoflurane | ~2% | 0.65 |
| Isoflurane | ~1.2% | 1.4 |
| Halothane | ~0.75% | 2.4 (most potent, slowest) |
Nitrous oxide enters closed gas spaces and can expand them. Pneumothorax, intraocular gas and other trapped-gas settings are therefore important contraindication clues. On discontinuation, rapid movement of nitrous oxide from blood back into the alveoli can dilute alveolar oxygen, producing diffusion hypoxia. Oxygen administration during recovery addresses this risk. It is distinct from expansion of a trapped gas space.
Halothane-associated liver injury is a classic adverse-event pairing, particularly after prior exposure. Its inclusion here is for drug recognition rather than a statement that it is routinely preferred in current practice. For all agents, useful revision asks what property explains a specific stem, not which drug occupies a memorised rank without clinical context.
Which adverse effects and exam traps need a final check?
Malignant hyperthermia can be triggered by volatile anaesthetics and by succinylcholine in susceptible patients. It is a skeletal-muscle calcium-regulation emergency associated with hypermetabolism, rising carbon dioxide, rigidity and later temperature rise. Management includes removing triggering agents, administering dantrolene and supporting oxygenation, cooling and correction of metabolic disturbances. Nitrous oxide is not itself a malignant-hyperthermia trigger.
- Propofol: hypnosis, antiemetic action, hypotension and respiratory depression; provide analgesia separately.
- Ketamine: NMDA antagonism and analgesia; do not assume the airway is protected.
- Etomidate: relative haemodynamic stability plus adrenal suppression.
- Thiopental: redistribution ends the single-bolus effect; porphyria is a major caution.
- MAC: lower value means greater potency, and its endpoint is population immobility.
- Blood–gas solubility: lower value generally favours faster equilibration.
A patient who cannot move because of a neuromuscular blocker needs continued assessment of anaesthetic delivery; movement cannot serve as a reliable warning of insufficient hypnosis. Similarly, stable blood pressure does not establish adequate analgesia. Drug selection, airway planning and physiological monitoring belong together. Revise the properties as connected mechanisms rather than as interchangeable labels for a single anaesthetic state.