HKCA Final MCQ 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 guides dosing.

A liquid halogenated agent, such as sevoflurane, desflurane or isoflurane, vaporised for inhalation to produce general anaesthesia. Uptake depends on blood and tissue solubility, cardiac output and alveolar ventilation.

The transient rise in alveolar concentration of a second gas caused by rapid uptake of a concurrently administered high-volume gas, usually nitrous oxide. It accelerates induction when a potent agent is given simultaneously.

The phenomenon whereby a high inspired concentration of a soluble anaesthetic is taken up so rapidly that it raises the fractional concentration of the remaining gas mixture in the alveoli and speeds equilibration with blood.

An inherited pharmacogenetic reaction to volatile anaesthetics or depolarising muscle relaxants, producing uncontrolled skeletal muscle hypermetabolism, hypercapnia, rigidity and hyperthermia. Treatment is dantrolene plus supportive cooling and correction of hyperkalaemia and acidosis.

A depolarising neuromuscular blocker of rapid onset and very short duration, used for rapid sequence induction. It may cause hyperkalaemia, bradycardia, raised intraocular or intragastric pressure, and triggers malignant hyperthermia.

An induction technique for patients at risk of aspiration, using preoxygenation, a fast-acting induction agent and neuromuscular blocker, with cricoid pressure and early intubation, avoiding positive-pressure ventilation before the airway is secured.

External pressure applied to the cricoid cartilage to compress the oesophagus against the vertebral body and reduce passive regurgitation during induction. Effectiveness is debated and it can impair laryngoscopy and ventilation.

A peripheral nerve stimulation pattern delivering four supramaximal twitches, used to assess the depth of neuromuscular blockade. A ratio of four responses indicates recovery, and a train-of-four count of one to two indicates moderate block.

Persisting neuromuscular weakness after anaesthesia due to incomplete reversal of muscle relaxants. It increases aspiration, hypoxaemia and airway obstruction risk, so quantitative monitoring and adequate reversal with sugammadex or neostigmine are recommended.

A modified gamma-cyclodextrin that encapsulates rocuronium and vecuronium, reversing even deep aminosteroid-induced neuromuscular blockade within minutes. It cannot reverse benzylisoquinolinium agents and may cause bradycardia or anaphylaxis.

Reflex closure of the vocal cords triggered by stimulation of the larynx during light anaesthesia or airway irritation. It causes partial or complete airway obstruction, and treatment includes deepening anaesthesia, continuous positive airway pressure and small-dose suxamethonium.

Chemical lung injury from inhalation of acidic gastric contents, causing bronchospasm, hypoxaemia and pulmonary infiltrates, typically within hours of the event. Management is supportive, with airway clearance, oxygen and ventilation as needed; antibiotics are reserved for infection.

Injection of local anaesthetic into the subarachnoid space to block spinal nerve roots, producing surgical anaesthesia and often hypotension from sympathetic blockade. It is commonly used for lower abdominal, pelvic and lower limb surgery.

Injection of local anaesthetic, usually with an opioid, into the epidural space to block nerve roots. It allows catheter-based titration for labour analgesia or postoperative pain, but carries risks of dural puncture, patchy block and epidural haematoma.

A postural headache, worse upright and relieved lying flat, caused by cerebrospinal fluid leakage through a dural puncture. It is treated initially with hydration, caffeine and an epidural blood patch for persistent cases.

Adverse effects of excessive local anaesthetic in the circulation, ranging from perioral tingling and tinnitus to seizures, arrhythmias and cardiac arrest. Management includes airway support, benzodiazepines for seizures and intravenous lipid emulsion.

A clinical situation in which trained personnel have difficulty with facemask ventilation, supraglottic device placement, laryngoscopy, intubation or front-of-neck access. Anticipation, planning and a declared failed-airway algorithm reduce harm.

Emergency front-of-neck airway access through the cricothyroid membrane, used in a cannot-intubate, cannot-oxygenate situation. It provides rapid oxygenation and ventilation when other airway techniques have failed.

Life-threatening organ dysfunction caused by a dysregulated host response to infection. It is identified clinically by suspected infection plus an acute rise in organ dysfunction scores, and requires early antibiotics, source control and haemodynamic support.

Sepsis with persisting hypotension requiring vasopressors to maintain a mean arterial pressure of at least 65 mmHg and a raised serum lactate despite adequate fluid resuscitation. Mortality is high and management includes fluids, noradrenaline and source control.

Prompt physical removal or drainage of the focus of infection, such as abscess drainage, debridement of necrotic tissue or removal of an infected line. Antibiotics alone often fail without it, and delay worsens outcomes in sepsis.

A product of anaerobic and accelerated aerobic glucose metabolism, used as a marker of tissue hypoperfusion and illness severity. Serial lactate clearance guides resuscitation in sepsis and shock.

A first-line vasopressor in septic shock, acting mainly on alpha-adrenergic receptors to raise vascular tone and mean arterial pressure. It is titrated to a target pressure, and vasopressin is commonly added when requirements are high.

A vasoconstrictor acting on V1 receptors via a catecholamine-independent pathway, used as a second-line agent in septic shock and for variceal bleeding. It is usually started at a fixed dose when noradrenaline requirements escalate.

Acute hypoxaemic respiratory failure with bilateral pulmonary infiltrates not fully explained by cardiac failure, arising within a week of a known insult. Management uses lung-protective ventilation, prone positioning and careful fluid balance.

The volume of gas moved into or out of the lungs with each breath. In ARDS, a low tidal volume of about 6 mL/kg predicted body weight reduces ventilator-induced lung injury and mortality compared with higher volumes.

The airway pressure maintained above atmospheric at the end of expiration during mechanical ventilation. It recruits collapsed alveoli, improves oxygenation and reduces atelectrauma, but can impair venous return and raise intrathoracic pressure.

The difference between plateau pressure and positive end-expiratory pressure, reflecting the cyclic stress applied to the lung. It is calculated as tidal volume divided by respiratory system compliance, and raised values are associated with worse outcomes in ARDS.

Turning a ventilated patient face down to improve dorsal lung recruitment and ventilation-perfusion matching. Used for several hours per day in moderate to severe ARDS, it reduces mortality when performed early.

An abrupt decline in kidney function, defined by a rise in serum creatinine or fall in urine output over hours to days. It is staged by severity, and management focuses on treating the cause, optimising perfusion and avoiding nephrotoxins.

Extracorporeal removal of solute and fluid in kidney failure, by haemodialysis, haemofiltration or peritoneal dialysis. Continuous forms are preferred in haemodynamically unstable intensive care patients, and indications include refractory acidosis, hyperkalaemia and fluid overload.

A breakdown product of muscle creatine cleared mainly by glomerular filtration, used to estimate kidney function. Serum levels lag behind acute injury, and interpretation depends on muscle mass, age and sex.

A score from 3 to 15 based on eye, verbal and motor responses, used to grade impaired consciousness. It guides airway decisions, neurological monitoring and prognosis after brain injury.

The pressure within the rigid skull, normally around 5 to 15 mmHg in adults. Raised pressure reduces cerebral perfusion and can cause herniation, so it is managed with head elevation, sedation, osmotherapy and controlled ventilation.

The pressure gradient driving blood flow through the brain, calculated as mean arterial pressure minus intracranial pressure. Targets are usually 60 to 70 mmHg in brain-injured patients, balancing perfusion against bleeding risk.

A planned daily pause in sedative infusion to reassess neurological status and readiness for extubation. It shortens ventilation and intensive care stay and reduces delirium when combined with spontaneous breathing trials.

An acute fluctuating disturbance of attention and awareness, common in critically ill patients and associated with longer stays and cognitive decline. Prevention uses orientation, sleep hygiene, early mobilisation and avoidance of unnecessary sedatives.

Pain caused by a lesion or disease of the somatosensory nervous system, often described as burning, shooting or electric-shock-like with allodynia. Anticonvulsants and tricyclic antidepressants are first-line treatments.

Pain elicited by a stimulus that normally does not provoke pain, such as light touch on sunburnt or neuropathic skin. It reflects central sensitisation and altered sensory processing rather than simple nociceptor activation.

An increased pain response to a stimulus that is normally painful. It can occur at the site of injury from sensitised nociceptors or more widely from central sensitisation, and is a feature of neuropathic and opioid-induced pain states.

An activity-dependent increase in the excitability of spinal and higher nociceptive neurons after persistent noxious input, producing amplified pain and enlarged receptive fields. It underlies chronic postsurgical pain and is targeted by multimodal and pre-emptive analgesia.

Combining analgesic drugs and techniques with different mechanisms, such as paracetamol, NSAIDs, opioids and regional blocks, to improve pain relief while reducing opioid dose and adverse effects. It is central to enhanced recovery pathways.

Reducing total opioid consumption by adding non-opioid drugs or regional techniques, thereby limiting sedation, respiratory depression, constipation and tolerance. It is a key goal of multimodal analgesic regimens.

A system allowing patients to self-administer small intravenous opioid doses on demand, usually with a lockout interval and background infusion optional. It improves satisfaction and titration but requires monitoring for respiratory depression.

A reduced analgesic response to an opioid after repeated exposure, requiring higher doses for the same effect. It is distinct from dependence and addiction and complicates acute pain management in patients on long-term opioids.

A paradoxical increase in pain sensitivity caused by opioid exposure, distinct from tolerance and withdrawal. It presents as diffuse pain worsening with dose escalation, and management involves dose reduction or rotation.

A non-invasive technique applying low-voltage electrical current through surface electrodes to modulate pain, thought to act via gate control and endogenous opioids. Evidence is limited but it is low-risk as an adjunct.

Injection of local anaesthetic near a peripheral nerve or plexus to produce targeted anaesthesia or analgesia. Ultrasound guidance improves success and safety, and catheter techniques allow prolonged postoperative pain relief.