"General Anesthesia Drugs & Protocols" — Practice

Question 1

The induction agent of choice in a hypotensive trauma patient is

Accepted Answer

C

Question 2

In a patient with combined hepatic and renal failure, the preferred neuromuscular blocker is

Accepted Answer

B

Question 3

Why does a single dose of propofol wear off in minutes when its elimination half-life is hours?

Accepted Answer

Because recovery from a single dose is caused by redistribution rather than by elimination.

Propofol is highly lipid soluble, so after injection it reaches the brain within one arm-brain circulation time, since the brain is a vessel-rich organ receiving a large share of cardiac output. Unconsciousness follows almost immediately.

Concentration in the brain then falls as the drug moves down its gradient into muscle and, more slowly, into fat, both of which are large reservoirs. Once brain concentration falls below the threshold for unconsciousness the patient wakes, within minutes.

The drug has not left the body, and hepatic metabolism proceeds over hours.

The consequences follow directly. Repeated doses progressively saturate the peripheral compartments, so redistribution can no longer terminate the effect and recovery becomes dependent on metabolism. This is the basis of the context-sensitive half-time concept.

Question 4

Why is nitrous oxide contraindicated in a patient with a pneumothorax?

Accepted Answer

Because it expands closed gas-filled spaces.

Nitrous oxide is approximately 34 times more soluble in blood than nitrogen. When delivered, it diffuses from blood into any air-filled cavity far faster than the nitrogen already there can diffuse out.

In a compliant space such as bowel, volume increases. In a non-compliant space such as the middle ear or an eye containing intraocular gas, pressure increases instead. In a pneumothorax the volume expands, and under positive pressure ventilation this can convert a simple pneumothorax into a tension pneumothorax.

The same reasoning applies to bowel obstruction, middle ear surgery where a raised pressure can displace a tympanoplasty graft, and after intraocular gas injection.

The separate hazard is worth recalling alongside: nitrous oxide irreversibly oxidises the cobalt in vitamin B12, inactivating methionine synthase, so prolonged or repeated exposure causes megaloblastic anaemia and subacute combined degeneration.

Question 5

Which factors lower minimum alveolar concentration, and which raise it?

Accepted Answer

Minimum alveolar concentration is the alveolar concentration at which half of patients do not move to a standard surgical stimulus, and it measures potency, so a lower value means a more potent agent.

It falls with increasing age, hypothermia, pregnancy, opioids and sedatives, and acute alcohol intoxication, all of which reduce the anaesthetic requirement.

It rises with chronic alcohol use, hyperthermia, and sympathomimetics including amphetamines and cocaine, all of which increase the requirement.

The alcohol distinction is examined directly, since acute intoxication lowers it through additive central depression while chronic use raises it through tolerance and enzyme induction.

The practical significance is that it is additive between agents, so nitrous oxide contributes and allows the volatile concentration to be reduced, and that a fixed dial setting appropriate for a young patient may be excessive for an elderly one.

Question 6

A patient remains paralysed two hours after a single dose of suxamethonium. Explain and manage.

Accepted Answer

Suxamethonium apnoea, caused by an inherited abnormality of plasma cholinesterase, also called butyrylcholinesterase or pseudocholinesterase.

Suxamethonium is normally hydrolysed within minutes by this enzyme, which is why its action is so brief. In the homozygous atypical form, hydrolysis is dramatically slowed and paralysis persists for hours rather than minutes.

The specific danger is awareness. The induction agent wears off within minutes while the paralysis continues, so the patient is fully conscious and completely paralysed unless sedation is maintained.

Management is therefore supportive with two components. Continue ventilation until neuromuscular function returns, monitored objectively with a nerve stimulator. And continue sedation throughout, which is the part most often omitted.

No reversal agent exists, since this is depolarising blockade and neostigmine would prolong it.

Afterwards the patient is informed, given written documentation, and the family is tested, since the trait is inherited and the diagnosis protects relatives from the same event.

Question 7

Why is a paralysed patient under total intravenous anaesthesia at particular risk of awareness, and what safeguards apply?

Accepted Answer

Because the routine safeguard used during inhalational anaesthesia does not exist, and the usual clinical signs are abolished.

During inhalational anaesthesia, end-tidal agent concentration is measured continuously, so any failure of delivery is immediately visible and depth can be inferred from a value related to minimum alveolar concentration. Total intravenous anaesthesia has no equivalent measurement of effect-site concentration, only an assumption based on the pump setting and a pharmacokinetic model.

That assumption fails in specific ways. A disconnected or tissued cannula delivers no drug while the pump continues to run and alarms nothing. Pump programming errors, wrong drug concentrations and occluded lines produce the same result.

Neuromuscular blockade removes the safeguard of last resort, since an aware patient cannot move, and heart rate and blood pressure are unreliable in the presence of opioids or beta blockade.

Safeguards are procedural and technological: a dedicated cannula kept visible and checked, processed electroencephalographic depth monitoring, and avoiding paralysis where it is not needed.

Question 8

Compare neostigmine and sugammadex, and state when each is appropriate.

Accepted Answer

They work by opposite strategies, and that difference determines when each can be used.

Neostigmine inhibits acetylcholinesterase, raising acetylcholine concentration at the neuromuscular junction so that it competes more effectively with the blocking agent. Because it works by competition, it requires some spontaneous recovery to have occurred, and it has a ceiling: once all cholinesterase is inhibited, no further effect is possible. It also raises acetylcholine at muscarinic sites, causing bradycardia, bronchoconstriction and secretions, so an antimuscarinic such as glycopyrrolate is given with it. It works against any non-depolarising agent.

Sugammadex is a modified cyclodextrin that physically encapsulates aminosteroid molecules, forming a complex that is renally excreted. Because it removes drug rather than competing with it, it reverses even profound blockade within minutes and does not depend on spontaneous recovery, and it has no muscarinic effects.

Its limitation is specificity. It binds rocuronium and vecuronium but has no useful effect on atracurium, cisatracurium or suxamethonium, so neostigmine remains the agent for benzylisoquinolinium blockade.

Question 9

A patient becomes hypoxic during anaesthesia and the anaesthetist suspects a gas supply problem. Which machine safety features should have prevented this, and how do they work?

Accepted Answer

Several layers exist, each introduced after a fatality, and knowing them directs the search.

The pin index safety system for cylinders and non-interchangeable screw threads for pipelines make it mechanically impossible to connect a cylinder or hose to the wrong yoke, preventing nitrous oxide being delivered from an oxygen inlet.

The oxygen failure alarm sounds when oxygen supply pressure falls, and it is powered by the oxygen supply itself, so it cannot fail silently in the event that matters.

The hypoxic guard links nitrous oxide and oxygen flow control mechanically or electronically so that a mixture containing less than about 25 per cent oxygen cannot be set, preventing a hypoxic mixture being delivered by error.

The inspired oxygen analyser measures what actually reaches the patient rather than what was set, which is the final safeguard and the one that detects problems downstream of the flowmeters.

If all these are intact, the fault is more likely a disconnection or an airway problem, and capnography together with hand ventilation distinguishes them within seconds.

Practice — "General Anesthesia Drugs & Protocols"

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