Anaesthetics Flashcards
(49 cards)
what are the rules on fasting pre-op?
6hrs = no food or solids
2 hrs = no clear fluids
What is the purpose of preoxygenation?
Patient given a few mins of 100% O2
- provides reserve O2 while insetting tube
What is the triad of anaesthetics?
- Hypnotics
- Muscle relaxation
- Analgesia
What are the types of hypnotics?
- propofol
- sevoflurane
- ketamine
- thiopental
- etomidate
Types of muscle relaxants?
- depolarising e.g. suxamethonim
- non-depolarising e.g. rocuronium
What are the pros and cons of TIVA vs volatile gas?
Gas
- bad for environment, greenhouse gases
- more nausea and vomiting
- take longer to wake up and out to sleep
- can cause rigidity first and then floppiness
TIVA
- wake up more immediately
- Less nausea and vomiting
When is a muscle relaxant used?
- to intubate
- laparotomy
- big surgeries
(in paeds spray local on vocal cords instead)
How does a depolarising muscle relaxant work? example?
- mimics acetylcholine and binds to nicotine Ash receptors
- causes initial depolarisation of the muscle membrane -> muscle fasciculations
- not broken down by acetylcholinesterase –> stays bound –> receptor stay depolarised -> muscle cannot depolarise -> lead to flaccid paralysis
example: suxamethonium
When is suxamethonium used and risks?
in emergencies = quick onset and short duration
Risks:
- hyperkalemia
- malignant hyperthermia
- bradycardia
- fasciculations
- increased intraocular pressure
- suxamethonium apnoea
What is malignant hyperthermia?
genetic disorder of skeletal muscle that causes massive, uncontrolled release of calcium from the sarcoplasmic reticulum in muscle cells.
leads to:
- sustained muscle contraction
- hyper metabolism
- massive heat production
- cell damage and death
cause
- due to RYR1 gene
What are the triggers of malignant hyperthermia?
- suxamethonium
- volatile anaesthetic agents e.g. halothane, sevoflurane, isoflurane
What are the clinical features of malignant hyperthermia?
Usually starts within minutes of induction, but can be delayed:
Rapid rise in end-tidal CO₂ (early sign)
Muscle rigidity (especially masseter spasm)
Hyperthermia (can exceed 41°C/105.8°F)
Tachycardia, arrhythmias
Acidosis (metabolic and respiratory)
Hyperkalemia
Rhabdomyolysis → myoglobinuria → renal failure
Management: malignant hyperthermia
- stop triggering agents
- administer IV dantrolene
- active cooling - ice packs, cold IV fluids
- treat complications - acidosis, hyperkalaemia, arrhythmias
- supportive care in ICU
Diagnosis + prevention: malignant hyperthermia
Definitive diagnosis via muscle biopsy and in vitro contracture test (IVCT)
Genetic testing for RYR1 or CACNA1S mutations
High-risk individuals should wear medical alert tags
Use safe anesthesia protocols (e.g., TIVA – total intravenous anesthesia)
How do non-depolarising muscle relaxants work?
- competitive antagonist at nicotinic acetylcholine receptors at neuromuscular junction
- bind to receptor without activating it, blocking acetylcholine from binding
- prevents depolarisation of muscle membrane –> no action potential –> no muscle contraction
- result = flaccid paralysis
Types and features of non-depolarising muscle relaxants used?
- rocuronium
- vecuronium
- atracurium
- pancuronium
slower onset and duration varies
- do NOT cause fasciculations
- onset and recovery are slower and more controlled
- cardiovascular side effects
How does reversal for non-depolarising muscle relaxants work?
can be reversed with acetylcholinesterase inhibitors e.g. neostigmine
(these increase EACh levels, which outcompete the NDMR at the receptor)
OR with sugammadex = binds directly to drug and inactivates it
What are the emergency anaesthetic drugs?
- suxamethonium = laryngospasm
- atropine = bradycardia
- glycopyrronium = bradycardia
- ephedrine = hypotension
- metaraminol = hypotension
- adrenaline = suspected anaphylaxis
What local anaesthetic toxicity?
- excessive dose or accidental intravascular injection of local anaesthetic
- slow metabolic or accumulation in patients with liver issues
Presentation: local anaesthetic toxicity
CNS toxicity
early sx
- perioral numbness
- metallic taste
- tinnitus
- light headed
- visual disturbances
late
- tremors, muscle twitching
- seizures
- CNS depression
Cardiovascular toxicity
- myocardial depression
- bradycardia
- conduction blocks
- ventricular arrhythmias
- cardiac arrest
Management: local anaesthetic toxicity
1.Stop injecting LA immediately
- Call for help & secure ABCs
- Give 100% oxygen, maintain airway
- Control seizures:
- Benzodiazepines (e.g., midazolam)
- Avoid large doses of propofol if cardiovascular collapse is suspected - 20% intralipid emulsion therapy
- initial = 1.5ml/kg IV over 1 min
- then = 0.25ml/kg/min for least 10 mins
How can you prevent local anaesthetic toxicity?
Use lowest effective dose
Aspirate before injecting
Inject slowly with frequent aspiration
Use ultrasound guidance when available
Be especially cautious with bupivacaine and ropivacaine
what is the process of emergence from anaesthetic?
- check muscle relaxant has worn off
- ulnar nerve = thumb twitch
- facial nevre = obicularis oculi
(need 4 twitches) - Hypnotic agent stopped
- extubated when breathing themselves
MOA of local anaesthetics
Inhibit excitation of nerve endings
- reversibly bind to and inactivate sodium channels
- stop influx of sodium through channels so NO depolarisation of nerve cell membranes
- no depolarisation = loss of sensation