What is the triad of anaesthesia and what types can you get
- General
- Regional - epidural / spinal
- Local
Analgesia
Relaxation
Hypnosis
Balanced anaesthesia has contribution from all 3 but doesn’t require all 3
Allows flexibility
Can titrate doses so more accurate
Avoid overdosage
What provides analgesia
LA
Regional block
Opiates
What provides relaxation
LA
Muscle relaxants
General anaesthetics
Why is relaxation needed
Provide immobility for procedures and allow ventilation
What provides hypnosis / unconsciousness
GA
Opiates - small affect (lessen pain so less GA needeD)
What is always needed with a GA
Hyponosis
What is a GA
Central acting drugs which cause whole body unconsciousness except ketamine
What is regional anaesthesia
Insensbility in an area or region
Applied to nerves supplying area
Nerve and plexus block including spinal and epidural
What is a LA
Insensibility in relevant part of body
Applied directly to tissues
How can GA be given
Inhaled or IV
What does GA lead too
Hypnosis
Small degree of relaxation
Neglible analgesia except for ketamine
What does GA require
Airway management
How does GA work
Hyperpolarise neuronal ion channels
Less likely to fire
More complex processes lost first e.g. cerebral function and reflexes relatively spared
What is halothane and what are SE
Inhaled GA
Hepatotoxity - NO LONGER USED DUE TO THIS
Myocardial depression
Malignant hyperthermia
What is thiopental and what are SE
IV GA Cause laryngospasm Rapid onset Quickly affects brain Use if short procedure or risk of ICP Reduces CO so not in truama/. hypovolaemia
What is propofol used for
Rapid onset Rapid loss of reflexes No obvious planes of GA Widely used to maintain sedation / total IV anaesthesia and day case Radidly metabolised Anti-emetic
SE
Pain on IV injection so use with LA
Moderate myocardial and resp depression
What is agent of choice for rapid induction
Sodium thiopentone
SE / disadvantages
Metaoblites build up quick
Little analgesia
Marked myocardial depression
What is used in young children and why
Sevoflurane gas
Slow
More obvious planes of anaesthesia
When is ketamine useful for
Can be used for induction
Little myocardial depression and does not cause hypo so better if haemodynaimcally unstable / polytrauma
Also has mod-strong analgesic properties
Can increase BP so avoid in HTN or ICP
What has most favourable cardiac safety
Etomidate
What is it unsuitable for
Maintaining sedation as risk of adrenal suppression
Also high post-op vomiting
What is the sequence of GA
Pre-op - Premeds - Pre-oxygen Preparation Induction Maintenance Emergencies Recovery Post op care and pain management
What is IV induction
Rapid onset with rapid recovery
What is inhalation induction
WHAT IS MAC
Slow and prolonged duration
Minimum alveolar conc = minimum drug to produce anaesthesia
Low MAC = very potent
What is most common
IV induction with inhalation maintenance
What are planes of anaesthesia
Analgesia
Excitation
Anaesthesia - light then deep
Overdose
What is needed during GA
Careful monitoring of conscious - Loss of verbral - Movement - RR - EEG - Planes Airway maintenance
What is minimum monitoring with GA
SpO2, FiO2, ETCO2 NIBP - non-invasive BP ECG Temp / UO / NMG Invasive venous / arterial
What happens when awakening
Change inspired gas to 100% O2 only Discontinue anaesthetic Use nerve stimulator to check some reversal has occurs Muscle relaxation wears of Anaesthetic wears of Can give anti-cholinesterase to reverse Return of airway reflex Remove ET once breathing spontaneous Adminster O2 via facemask Transfer to recovery
What happens in recovery
Dedicated area
Many may still be unconscious or requiring airway control
Pain control
- Pain ladder
- Have naloxone written up PRN incase of opiate overdose
N+V management
What is the physiology of GA
Depress CVS
- Reduced sympathetic
- -ve inotrope
- Vasdilaton so decreased resistance
- Ventilation so decreased return and CO
- Decreased MAP
Depress Resp
- Reduced hypoxic and hypercarbic drive
- Reduced TV and increased RR (opiates opposite)
- Decreased FRC
What can be prolonged after GA
Decreased FRC
Lower lung volume / V/Q mismatch
May need post op O2
How do muscle relaxants work
Paralyse skeletal muscle by blocking NMJ
Affects resp and airway muscles
What are indications for muscle relaxant
Ventilation and intubation
Microscopic surgery
Neurosurgery
Body cavity surgery
What are problems with relaxant
Awaerness
Incomplete reversal leading to obstrcution
Apnoea so need airway support
What is used to reverse muscle relaxant
Neostigmine if non-depolarisation
What are types of muscle relaxant
Depolarizing
Non-depolarizing
Example of depolarising
Suxamethonium
How do they work
Bind to Ach receptors and first activates
Cause fasciculation then paralysis
Deactivated by acetylcholinesterase
Rapid onset and short acting
What happens if cholinesterase deficiency / myasthenia graves Rx
Prolonged action leading to resp arrest
Keep ventilated whilst drug degrades
What are SE
Malignant hyperthermia
Hyperkalaemia
What is muscle relaxant of choice for rapid
Suxamethonium
What are CI to suxamethonium
Penetrating eye injury
Acute narrow angle glaucoma as increased pressure
Causes a transient rise in IOP
FH suxamethonium apnoea
What are examples of non-depolarising
Tubcurarine
Vecuronium
Pancuronium
How do they work and what is used to reverse
Antagonise Ach receptor
Neostigmine
Longer onest and longer lasting
No fasciculation
AE
Hypotension
Why is intraoperative analgesia used
Prevent arousal
Suppress reflex responses to painful stimuli e.g. tachy and hypertension
Opiates can contribute to hypnosis of GA
Why are regional good
Less GA needed as eliminates pan
Has no sedative effects itself
Physiology of local and regional anaesthetic
Retain awareness and consciousness Affects CVS proportional to size of area Veno and vasodilation Decreased FRC Increased V/Q mismatch
How does lidocaine work
Blocks Na channels so no AP is sent
Hepatic metabolism
Protein bound
Renal excretion
What does lidocaine interact with
BB
Ciprofloxacin
Phenytoin
What is it useful for
Local wounds
Fast acting
Doesn’t last long
What may be added to LA and what does it do
Adrenaline
Prolongs duration of action
Permits uses of higher doses as limits systemic absorption as vasoconstriction
When is adrenaline CI
MAOI
TCA
Procedures where risk of digital ishaemia
Max safe dose of lidocaine
3mg / kg
7mg / kg if 1% or 2% adrenaline 1 in200,000
Max safe dose of bupivacaine
2mg / kg
Max sae dose of prilocaine
6mg / kg
What is buivacaine good for
Topical wound infiltration at end of surgery as longer duration
When is it CI
Regional as cardiotoxic so if tourniquet fails will affect heart
What is 1st line in regional
Prilocaine as less cardiotoic
How is cocaine applied
Paste in conc of 4% + 10%
Causes vasoconstriction
Lipophillic and cross BBB causing arrhythmia / tachy
When is cocaine used
ENT
Nasal mucosa
Otherwise not used
What must you do if injecting LA
Aspirate to make sure not in blood vessel as would constrict the heart
Calculations = important for exam
1% lidocaine = 10mg in 1 ml
If max dose worked out as 180mg then this is 18ml (move decimal point)
If 2% = 20mg in 1ml
If given 20ml = 40mg of drug
If 20ml of 2% lidocaine given what is the mg
= 400mg
2g in 100ml
20ml = 400mg
What are signs of lidocaine toxicity
Tingling Light head Tinnitus Visual disturbance Muscle twitching Confusion Agitation Drowsy CVS depression Seizure Collapse Abnormal ECG
What increases risk of toxicity
Liver issue
Low protein
How do you monitor
ABCDE
Help - ICU / anaethestist
IV intra-lipid
Benzo - midalazam to prevent seizure
What level of care does LA require
Same
IV access
Anaesthesist
If need more than LA what can you do
Regional nerve block
Epidural or spinal
What are indications for spinal
Avoid a GA
Severe respiratory disease / cardio
Allergy to GA
What are CI
Fixed CO due to stenosis Infection Bleeding Anti-caog Technical difficulties Spinal problem
What is a TIVA
Total IV anaesthesia
What is malignant hyperthermia
AD condition following administration of anaesthetic
Often FH
What happens
Excessive release of Ca2 from SER of skeletal muscle Sudden increase in O2 requirement Hyperpyrexia - can be a late sign Muscle rigdity Tachycardia CK raised
What causes
Halothane
Suzemthonium
Anti-psychotics= NMS
How do you Rx
Stop offending agent
Hyperventilate
Dantrole - prevents Ca2 release
Take to ITU
Why is analgesia used in maintenance
Body still response to pain i.e. BP and HR increase
What should you always have written up with opiates
Naloxone PRN incase of overdose
What are complications of GA
Anaphylaxis Oesophageal intubation / airway management Temp control Loss o protective reflexes VTE Atelectasis Awareness - Careul monitoring of sedation Bronchospasm Laryngospasm Malignant hyperthermia Suxamethonium apnoea Unable to consent
What do you do for bronchospasm
100% O2 Salbutamol Steroid Mg Same as asthma
What causes laryngospasm
Irritation with vapour
Make sure patient paralysed fully
What is suxamethonium apnoea
Pseudo-cholinesterase definceicny
AD
What happens
Prolonged muscle relaxation
Lasts 24 hours
Have to keep in ITU ventilated till it wears of as nothing to reverse
What are signs of anaphylaxis if under GA
Hypotension + tachycardia = 1st signs
Desaturation = later sign
Rash + angioedema = late sign
Won’t have cough or resp distress as under GA
What are signs of oesophageal intubation instead of tracheal
Desaturation
CO2 trace diminishes
Unable to hear air entry despite being able to hand ventilate
