General Anaesthetics - Neuromuscular blockade, Induction agents, Malignant hyperthermia

Question 1

Why are neuromuscular blockades used?

Answer 1

Used during GA to block transmission of signals between motor nerve endings and skeletal muscle, reducing tone

Relaxed vocal cords => easier intubation
Relaxed diaphragm => easier to ventilate
Optimise surgical conditions

Question 2

Depolarising NMB - suxamethonium
-MOA
-onset and duration
-reversal
-adverse effects

Answer 2

Inhibits Ach binding to receptor at NMJ
-initial depolarisation => muscular contraction
-receptor becomes desensitised => muscle relaxes and paralysed

Fastest onset (1min) and shortest duration (10mins) of all muscle relaxants

Muscle relaxant of choice for rapid sequence induction in intubation

No reversal agent, must wait for plasma cholinesterases of AChesterase to break it down

Hyperkalemia
Malignant hyperthermia
Not enough AChesterase
Not used in
-penetrating eye injuries
-acute angle glaucoma
Due to increase in IOP

Question 3

Non depolarising NMB - atacurium
-MOA
-onset and duration
-reversal
-adverse effects

Answer 3

Competitive antagonist of Ach receptor at NMJ

Onset 2mins
Duration 30-45mins
Broken down by tissues

Reversed by neostigmine

Generalised histamine release => facial flushing, tachycardia, HYPOTENSION

Question 4

Non depolarising NMB - vecuronium
-MOA
-onset and duration
-reversal
-adverse effects

Answer 4

Competitive antagonist of Ach receptor at NMJ

Onset 2mins
Duration 30-40mins
Broken down by liver and kidney

Reversed by sugammadex
May be reversed by neostigmine

Duration may be greater if liver or kidney dysfunction
Generalised histamine release => facial flushing, tachycardia, HYPOTENSION

Question 5

Non depolarising NMB - pancuronium
-MOA
-onset and duration
-reversal
-adverse effects

Answer 5

Competitive antagonist of ACh receptor at NMJ

Onset 2-3mins
Duration 2hrs

Reversed by sugammadex

Generalised histamine release => facial flushing, tachycardia, HYPOTENSION

Question 6

Inhaled anaesthetics - volatile liquids (isoflurane, desflurane, sevoflurane)
-uses
-MOA
-adverse effects

Answer 6

Induction and maintenance of anaesthesia

MOA unknown - combination of GABA, glycine, NDMA?

MALIGNANT HYPERTHERMIA

Question 7

Inhaled anaesthetics - nitrous oxide
-uses
-MOA
-adverse effects

Answer 7

Maintenance (when mixed with other drugs) and analgesia
-can’t be used alone as minimal alveolar concentration is 105%

MOA unknown - combination of GABA, glycine, NDMA?

Can diffuse into gas filled body compartments
-avoid in pneumothorax

Question 8

IV anaesthetics - propofol
-MOA
-adverse effects
-positive effects

Answer 8

Potentiates GABA
Induction and maintenance

Pain on injection
No analgesic effects
Low BP

Antiemetic effects

Question 9

IV anaesthetics - etomidate
-MOA
-adverse effects
-positive effects

Answer 9

Potentiates GABA
Not for maintenance

Primary adrenal suppression
Myoclonus
No analgesic effects

Less hypotension, so often used in cases of hemodynamic instability
Ultrafast induction

Question 10

IV anaesthetics - ketamine
-MOA
-adverse effects
-positive effects

Answer 10

Blocks NMDA receptors
Induction and maintenance

Disorientation
Hallucination

Dissociative anaesthetic
Profound analgesia
Does not affect BP, good in trauma

Question 11

Malignant hyperthermia
-pathophysiology
-causative agents
-investigations
-management

Answer 11

Excessive release of Ca from sarcoplasmic reticulum => sustained muscle contraction, breakdown, hypermetabolic state

Linked to genetic mutation in ryanodine receptors

Inhaled volatile liquids
Suxamethonium

High CK

Dantrolene - prevent Ca release from sarcoplasmic reticulum
Supportive therapy
STOP CAUSATIVE AGENT