ANZCA Primary key terms

The alveolar concentration of an inhaled anaesthetic at which 50% of patients do not move in response to a standard surgical stimulus. It allows comparison of potency between volatile agents and is reduced by age, hypothermia, pregnancy and opioids.

The ratio of anaesthetic concentration in blood to that in gas at equilibrium. A low value means the agent equilibrates quickly, giving fast induction and recovery; a high value slows both.

The transient rise in alveolar concentration of a co-administered gas caused by rapid uptake of a high-volume gas such as nitrous oxide, which concentrates the remaining gases and accelerates induction.

The phenomenon whereby a high inspired fraction of an inhaled agent is taken up so rapidly that further inspired gas is drawn in, raising the alveolar concentration faster than predicted by simple mixing.

The time for plasma concentration of a drug given by infusion to fall by half after the infusion stops. It lengthens as infusion duration increases for lipophilic drugs, reflecting accumulation in peripheral compartments.

The estimated concentration of a drug at its site of action, linked to plasma concentration by a rate constant describing delayed equilibration. It better predicts clinical effect than plasma concentration and underpins target-controlled infusion.

A pharmacokinetic description in which a drug distributes between a central plasma compartment and two peripheral tissue groups, with elimination from the central compartment. It explains rapid distribution then slower redistribution and elimination phases.

The apparent volume in which the total amount of drug in the body would need to be dissolved to give the observed plasma concentration. A large value indicates extensive tissue uptake or high lipid solubility.

The volume of plasma from which a drug is completely removed per unit time. It determines maintenance dose rate needed to sustain a target steady-state concentration, independent of volume of distribution.

The reversible attachment of drug molecules to plasma proteins such as albumin and alpha-1-acid glycoprotein. Only unbound drug exerts effect and is available for metabolism, so displacement can increase free active fraction.

Metabolism of an orally absorbed drug during its passage through gut wall and liver before reaching systemic circulation. It reduces oral bioavailability and can be saturated, causing disproportionate rises in plasma concentration.

The fraction of an administered dose that reaches systemic circulation unchanged. It is 100% for intravenous dosing and lower for other routes because of incomplete absorption and first-pass metabolism.

Elimination of drug by the liver, determined by hepatic blood flow and intrinsic enzyme activity. For high-extraction drugs clearance is flow-limited; for low-extraction drugs it depends mainly on enzyme capacity and protein binding.

Elimination at a constant rate independent of drug concentration, because metabolising enzymes are saturated. Small dose increases can then produce large and unpredictable rises in plasma level.

Elimination in which a constant fraction of the drug is removed per unit time, so plasma concentration falls exponentially. Most anaesthetic drugs follow this pattern at therapeutic concentrations.

The time taken for plasma concentration to fall by half during elimination. It depends on both volume of distribution and clearance, so a large distribution volume prolongs half-life even when clearance is normal.

A rapid decrease in response to a drug after repeated doses over a short period, distinct from tolerance developing over longer exposure. It is seen with indirectly acting sympathomimetics such as ephedrine.

A reduced effect of a drug after prolonged exposure, requiring higher doses for the same response. It may be pharmacokinetic, pharmacodynamic or learned, and is important in opioid and benzodiazepine prescribing.

Increased sensitivity to painful stimuli paradoxically caused by opioid exposure, distinct from tolerance and withdrawal. It presents as pain spreading beyond the original site or worsening with dose escalation.

The combined use of analgesic drugs and techniques acting at different points in the pain pathway to improve relief and reduce individual drug doses and side effects. It is central to enhanced recovery protocols.

Analgesia given before a painful stimulus with the aim of preventing central sensitisation and reducing subsequent pain. Evidence for benefit beyond treating established pain is limited.

An increase in excitability of spinal and higher neurones after repeated noxious input, producing amplified pain responses and spread of tenderness. It underlies chronic postsurgical and neuropathic pain states.

A progressive increase in the response of dorsal horn neurones during repeated low-frequency C-fibre stimulation. It is a short-lived activity-dependent form of plasticity, distinct from longer-lasting central sensitisation.

The concept that nociceptive signals in the dorsal horn can be inhibited by concurrent input from large myelinated afferents and by descending pathways from the brain. It explains why rubbing an injury reduces pain.

Delivery of low-intensity electrical current through skin electrodes to activate large afferents and reduce pain via segmental and descending inhibitory mechanisms. Evidence of benefit is modest and technique-dependent.

The neural encoding of actual or threatened tissue damage by specialised sensory endings. It is not equivalent to pain, which is a conscious experience shaped by context and emotion.

Pain caused by a lesion or disease of the somatosensory nervous system, often described as burning or shooting with altered sensation. Standard analgesics are less effective than gabapentinoids or tricyclics.

A structured perioperative pathway combining evidence-based elements such as carbohydrate loading, opioid-sparing analgesia, early feeding and mobilisation to reduce complications and shorten hospital stay.

Systematic evaluation of a patient's comorbidity, functional capacity and planned procedure to estimate perioperative risk and guide optimisation, monitoring and level of postoperative care.

Measurement of gas exchange during graded exercise to derive peak oxygen consumption and anaerobic threshold. Poor values predict complications after major surgery and can inform shared decision-making.

Myocardial damage occurring around surgery, detected by raised troponin with or without ischaemic symptoms or ECG changes. It is common after major surgery and associated with increased mortality.

Nausea or vomiting occurring after surgery, driven by patient, anaesthetic and surgical risk factors. Prophylaxis with multiple agents is guided by validated risk scores and reduces length of stay.

A clinical situation in which trained personnel experience difficulty with ventilation, laryngoscopy, intubation or supraglottic rescue. Prediction is unreliable, so a preformed strategy and backup plans are always required.

A technique for urgent airway control that minimises the interval between induction and intubation to reduce aspiration risk. It typically uses a fast-acting induction agent, neuromuscular blocker and cricoid force.

A modified gamma-cyclodextrin that encapsulates aminosteroid neuromuscular blockers such as rocuronium, reversing even deep blockade rapidly. It does not reverse benzylisoquinolinium agents and can cause anaphylaxis.

Assessment of neuromuscular block using peripheral nerve stimulation and evoked responses such as train-of-four. Quantitative monitoring is recommended to confirm adequate recovery before extubation.

Persisting weakness after anaesthesia due to incomplete reversal of neuromuscular blockers. It increases aspiration and respiratory complications, so extubation should await a train-of-four ratio above 0.9.

Aching pain arising during limb surgery under tourniquet despite an apparently adequate regional block, mediated by unmyelinated fibres that continue to conduct. It often needs systemic analgesia or lighter tourniquet duration.

The balance of hydrostatic and oncotic pressures across a capillary membrane that governs fluid movement between plasma and interstitium. Changes in these forces explain oedema formation and the rationale for fluid therapy.

The osmotic pressure exerted by large molecules, mainly albumin, across a semipermeable membrane. It draws fluid into the vascular space and is a key determinant of intravascular volume retention.

The total oxygen transported to tissues per minute, calculated as cardiac output multiplied by arterial oxygen content. Content depends mainly on haemoglobin concentration and saturation rather than dissolved oxygen.

The sigmoid relationship between oxygen partial pressure and haemoglobin saturation. It shifts right with acidosis, hypercapnia, raised temperature and 2,3-DPG, favouring oxygen unloading to tissues.