UNSW School of Medicine
Liverpool Clinical School
Year VI Critical Care Rotation
Anaesthetics Study Guide
Blair Munford, BMedSc, MB,ChB, FFARACS, FANZCA
Senior Specialist Anaesthetist, Liverpool Hospital
Aims of Anaesthetic Attachment
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To understand the scope of the practice of anaesthesia.
To understand the role of the anaesthetist as part of the surgical or
procedural team.
To gain exposure to airway management and other procedural skills
To understand the importance of the perioperative process including
pre-anaesthetic assessment, investigations, and optimisation.
To understand post anaesthetic care including pain management, and
the indications for specialised postanaesthetic monitoring & support.
To revise/enhance key concepts & simple competencies in emergency
assessment and resuscitation, including CPR/BLS/ALS.
For those interested, to acquire insight into anaesthetics as a medical
career option.
Introductory Case Study
“Don’t play with that!” …
A simple paediatric case - NOT
My first ever weekend on duty as an
anaesthetics registrar . . .
Case transferred from country hospital for theatre:
 3 year old girl, previously well
 Mixed total/partial toe amputation
(From playing with grandfather’s axe!)
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18 hours ago, fasted since
IV in situ, IV fluids running.
Has had antibiotics/narcotic analgesics.
No problem, even for a junior registrar, right?
What happened next . . .
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To OT as scheduled.
Rapid sequence induction, uneventful anaesthesia.
Extubated near awake at end (in hindsight, too
soon)
Vomited undigested food, developed
laryngospasm, desaturated.
Re-paralysed, intubated, pharynx sucked out,
suction down ET tube – no evidence aspiration
Awoken & re-extubated uneventfully.
The lessons from this:
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1.
2.
Specific: Beware occult delayed gastric emptying
– predictable in hindsight.
General:
There is minor surgery but there is no minor
anaesthesia!
Anaesthetic practice is more than just being able
to give an anaesthetic – just like being a 747
captain is more than just holding the controls!
Part I:
Scope & Development of
Anaesthetic Practice
Imagine a world without
anaesthesia . . .
What medicine was like prior to the
invention of anaesthesia:

Surgical operations performed rarely & only as a last
resort. Death was the expected and usual outcome,
from shock, haemorrhage, or infection.
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When surgery unavoidable, patient was held down by
assistants & surgeons operated as fast as possible. The
first incision was often deliberately brutal in the hope
that the patient would faint, allowing less haste.
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No analgesia in labour & interventional/operative
obstetrics essentially unknown – except post mortem
(original meaning of Caesarean Section)
Without anaesthesia . . .
Surgical advances would have been
minimal.
 Childbirth would remain a major risk for
baby and/or mother.
 Concepts of intensive care & resuscitation
would not have developed.
 Pain - acute and chronic - would have
remained an inevitable part of life.
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Without doubt the development of anaesthesia
has been one of the top ten medical advances
of all time.
Some have even ranked it as the most important
medical invention ever.
Others rank it amongst greatest discoveries of
any type in human history.
But what is anaesthesia?
A state that encompasses (1)analgesia plus (2)
arreflexia (muscle relaxation or lack of
movement) and (in the case of general
anaesthesia) (3) hypnosis; enabling painful
or distressing procedures to be performed
humanely.
This is the “Triad of Anaesthesia”
The other triad of anaesthesia
1.
THE MISSION IS (in order of importance):
Preserve life
2.
Relieve suffering
3.
Provide optimum conditions for procedure
(Any fool can do the third by ignoring the first. Doing the
second by ignoring the first is called euthanasia. The
art is in being able to provide all three.)
Anaesthesia can be:
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Cerebral
 Sedation/analgesia
 General
 Inhalational/spontaneous ventilating
 Balanced/controlled ventilation
Neuro-interruptive
(Or some combination of
 Local
two or more of these)
 Regional
 Neuraxial
Classification of Anaesthetics
Anaesthesia
General
Alternative
Regional
Dissociative
Surface/topical
Controlled
ventilation
Intubated
Spontaneous
ventilation
Intubated
infiltration
Auditory
Nerve/plexus
block
Electrical
Spinal blocks
Hypnosis
LMA
Epidural:
Manual
Mechanical
Mask
Subarachnoid cervical, thoracic,
lumbar, caudal
Acupuncture
Single shot, intermittent, continuous
Local anaesthetic, narcotic/adjuvant, combination
But wait . . . there’s more:
Scope of Anaesthetic Practice
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Anaesthesia for surgery
Sedation/anaesthesia for other procedures
Obstetric analgesia/anaesthesia services
Pre-anaesthetic assessment & perioperative medicine
Acute & Chronic Pain Services
Vascular access services: Central venous lines, et al.
Resuscitation: Trauma team/MET/Prehospital
Teaching: Procedural skills/resuscitation/analgesia
Intensive Care practice/cover/support
Operating theatre management/coordination
Critical care transport
(It’s a broad church!)
Part II:
Perioperative Medicine
“The way of the future”
What is perioperative medicine?
“Integrated multidisciplinary
management of the surgical or
procedural patient’s hospital
admission & stay.”
Perioperative system includes:
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Identification of patient requiring procedure
Referral to perioperative service
Screening for level of workup required
Pre-anaesthetic assessment/plan
Referral & investigations as required.
Admission at appropriate pre-op interval
Post-operative drug/fluid/other therapy
Appropriate post op level of care & stay
Discharge at earliest appropriate point
But why?
Minimize unnecessary pre-op bed days.
 Minimize preoperative cancellations
 Enable more predictable bed occupancy
 Minimize pseudo-urgent blood tests & other
investigations
 Improve post operative care & shorten post
operative stay
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The Pre-anaesthetic Consultation
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What? Targeted history & examination, &
formulation of anaesthetic/perioperative plan.
Who? Ideally by the anaesthetist for the procedure
(not always possible).
Whom? All patients should have some form of this.
When? At the earliest appropriate opportunity
(Obviously this varies on a case by case basis)
Why? To enable optimimum pre-anaesthetic
preparation, risk minimisation, informed consent,
and allaying of anxiety.
Pre-operative preparation may
include premedication
Use if required, not “one size fits all”
Aims:
1.
2.
Ameliorate anxiety
Usually with a benzodiazepine such as temazepam
Relieve pain – predominantly in the acute setting –
usually with narcotics.
3.
4.
Prevent reflux/aspiration - in at risk patient
Usually (a) H2 blocker or PPI 6-8 hrs preop if
possible, then (b) non particulate antacid
immediately preop.
Treat other medical conditions
e.g. asthma prophylaxis.
Most regular medications are continued,
including on the day of surgery
(b)
Exceptions include:
(a) Oral hypoglycaemics
Antithrombotic agents (mostly)
ASA Physical Status
ASA 1 – Healthy patient
 ASA 2 – Mild or controlled systemic disease
 ASA 3 – Significant systemic disease
 ASA 4 – Severe systemic disease – current
or constant threat to life
 ASA 5 – Moribund patient unlikely to
survive with or without procedure
 ASA 6 – Brain dead patient (organ donor)
+/- E = Emergency procedure
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Relevance of this?
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Risk stratification
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Workload/resource utilisation planning
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Remuneration aspects
Perioperative (Preanaesthetic) Clinic
Surgical clinic
Nurse Clinic
Checked up, satisfied
as fit & suitable
Decides to proceed
with planned time,
date & procedure
Surgeon refers case
Satisfied with it;
decides to send
it back to her
for mx
Not certain;sends
only case notes to
anaesthetist to review it
Decides to further
investigate. May cancel,
postpone, refer case or
decide to do it
Not quite satisfied;
takes over review & mx
Preanaesthetic Clinic
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The Doctor takes a quick history, leading
questions are allowed as major diagnoses
should already be known
Asks for hypertension, diabetes,
asthma,epilepsy, previous anaesthetics,
allergies, complications, medications
being used
A quick examination is done, Ix like Xray,
ECG, UES & Blood ix are done
ASA categorised, anaesthesia decided
Explained to patient about anaesthetics,
risks, PCA & possible complications
Preanaesthetic Clinic
Based on:
History
Examination, Investigation . . .
Decision:
To do the
planned
procedure
To postpone the
procedure till fully
investigated
optimised
To cancel the
procedure
CASE STUDY II
Perioperative management
Diabetic patient for
vascular surgery
History
65 year old man, BMI 35
 Type II DM, 15 yrs, on OHGs, poor control
 Smoker 60+ pack years
 Hypertension
 Hypercholesterolaemia
 Ischaemic heart disease
 Diabetic nephropathy, (eGFR ~ 30mls/min)
For (R) femoro-popliteal bypass
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What are the issues and risks here?
1.What are the issues and risks here?
2. How can we optimise him preoperatively?
1. What are the issues and risks here?
2. How can we optimise him preoperatively?
3. What are our anaesthetic options &
problems?
1. What are the issues and risks here?
2. How can we optimise him preoperatively?
3. What are our anaesthetic options & problems?
4. How do we manage him postoperatively?
Part III:
Safety & Monitoring
in Anaesthesia
Safety in anaesthesia is
paramount
“When it goes right, no-one remembers. . .
When it goes wrong, no-one forgets”
. . . So the aim is to make anaesthesia as
forgettable as possible!
Safety Initiatives in Anaesthesia
Anaesthetists have been the leaders in safety initiatives in
medicine – e.g. :
 Privileged reporting & investigation of deaths under or
associated with anaesthesia in most states.
 Systematic reporting of incidents and near misses
 Collegial policies on minimum standards for facilities,
equipment, monitoring, staffing, & training.
 Publication of algorithms – e.g: difficult airway
management; malignant hyperthermia
 Simulation & contingency training e.g. difficult airway
workshops, emergency management of anaesthetic
crises (EMAC) course.
Principles of Safety
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Recognise risk – pre anaesthetic consultation
Avoid risk if possible – e.g. can procedure be done
under LA?
Mitigate risk – optimise patient condition, select
safest technique/agents/resources – e.g “cardiac”
anaesthetic & postop ventilation.
Plan & be prepared for emergencies – e.g.
predrawn emergency drugs, backup airway plan.
Observe/monitor for deviations & crises.
Respond in a timely& appropriate fashion.
Call for help/backup if required.
“The price of safety is eternal vigilance”
“Clinical observation is the cornerstone of
patient monitoring”
-
ANZCA Policy statements (several)
OR . . .
“The best patient monitor is still the one
between your ears – so make sure it’s
switched on”
– my take on the above.
Monitoring in anaesthesia
Basic (all/most patients)
 Pulse oximetry
 ECG
 Noninvasive (cuff) BP
 Capnography
 Oxygen concentration
 Agent monitoring
 Airway pressures
 Temperature
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Others as indicated
Invasive arterial BP
Precordial stethescope
Ventilator alarm(s)
Nerve stimulator
BIS/entropy
Spirometry
CVP
“Swann Ganz” (PAP)
Transoesophageal echo
Pulse oximetry
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First monitor I put on most patients & first I
usually look at.
If this is OK, then patient has a pulse, a survivable
blood pressure (at least 60/) and is oxygenating
their blood.
But if it’s not right, it’s not very specific – i.e. it
may be as simple as a dislodged probe, or as
serious as a cardiac arrest.
Doesn’t guarantee tissue oxygenation – may be
relatively normal in extreme anaemia, carboxyhaemoglobinaemia, cyanide posoning, etc.
Electrocardiogram
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Good monitor for:
 Arrhythmias/ectopics
 Some electrolyte abnormalities (K+ & Ca++)
 Ischaemic/strain changes
(Provided leads are placed correctly!)
Does not monitor:
 Volume status
 Cardiac output
 Blood pressure
Remember: it is entirely possible to die
with a relatively normal ECG!
Noninvasive arterial blood
pressure (NIBP) monitoring
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Usually automated
Convenient but not reliable:
Dependant on correct cuff size & position
Not continuous
Usually under-estimates true hyper-& overestimates true hypotensive values.
Interferes with IV infusions & pulse oximetry
Should not be placed on limb with AV fistula or
lymphoedema.
Capnography
“Gold standard” for verification of ETT placement.
Can also give information on:
 Dead space/V-Q mismatching
 Adequacy of ventilation
 Spontaneous respiratory effort during controlled
vent’n.
 Rebreathing: circuit problems or inadequate gas flow.
 Venous return, RV function & pulmonary blood flow
e.g. thrombotic, gas or fat embolism
Oxygen monitoring
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Monitors machine rather than patient.
The only specific monitor of oxygen supply
(Other safety features assume/depend on the gas
from O2 outlets & cylinders actually being
oxygen)
N.B. Before adoption/mandating of oxygen
monitoring, all reported (& thankfully very
rare) “wrong gas” anaesthetic incidents
(misconnected pipelines or incorrectly filled
cylinders) resulted in the death of the first
patient exposed in every case.
Anaesthetic agent monitoring
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Identifies (hopefully confirms!) anaesthetic agent
being used
Measures inspiratory & expiratory concentrations
Expiratory (alveolar) concentration enables
calculation of MAC fraction or multiple – i.e.
estimation of anaesthetic depth.
Now mandatory when inhalational anaesthetic agents
are used.
Temperature monitoring
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Anaesthesia promotes hypothermia by:
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Patients may need temperature support
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Decreased metabolic rate -> decreased heat production
Redistribution of blood flow -> increased heat loss
Passive (prevent heat loss)
Active warming: forced air/ heated IV fluids
What you support you must monitor
Ideally monitor core temperature:
Nasopharyngeal/oesophageal/bladder/PV
Better than
Skin/axillary/oral/rectal
Airway manometry
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Usually analogue
gauge on circle circuit
Monitors inflation
pressure
With IPPV can help
identify:
Airway obstruction
Bronchospasm
Circuit leaks/faults
Ventilator monitor
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Mandatory when
mechanical IPPV
employed.
Usually integrated into
ventilator w/automatic
activation.
High (overpressure) &
low (disconnect)
functions
Precordial stethescope
“Traditional” monitor
 Still used in some
paediatric cases
 Can monitors:
Heart & respiratory rate
Breath sounds presence
& quality.
Only as good as the person
listening to it!
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Direct arterial pressure
monitoring
Invasive procedure, but:
 Gold standard for real
time haemodynamic
assessment
 Accurate, reliable.
 Immediate warning of
hypo/hypertension of
any aetiology.
Depth of Anaesthesia
monitoring
Nerve stimulator
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Used with muscle relaxants
(neuromuscular blockers):
Electrical stimulus to nerve then
observation of innervated
muscle.
Commonest site: Ulnar nerve
Nondepolarising block
characterised by “fade” –
weakening of contraction with
(4) successive impulses “train
of four.”
Assesses:
- Density of block
- Return of function
- Point of safe reversal
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Uses simplified EEG recording
& algorithm to produce number
related to level of conciousness
(lower no=deeper anaesthesia)
Two methods: bispectral edge
(“BIS”) and entropy.
Role/value still controversial
Probably indicated for:
 TIVA (as no MAC to
monitor)
 Patient with a history of
awareness
 Where lightest possible
plane of anesthesia essential
Other monitors
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Central venous line.
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- Mostly used for drug
infusions but can also
measure CVP as a (not very
accurate) guide to volume
status.
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Has become the gold standard
cardiac function monitor.
Able to estimate:
Ejection fraction/stroke
volume/cardiac output
LV & RV Preload/pressures
Diastolic dysfunction (early
index of ischaemia)
Pulmonary artery (Swann
Ganz) catheter
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Can estimate LV filling
pressure (preload) – a better
guide to functional volume
status than CVP
Also can measure cardiac
output by thermodilution.
Trans-Oesphageal Echocardiography (TOE)
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Spirometry
Measurement of pressure
volume loops & hence work
of breathing in controlled,
spont. & ass’t’d ventilation
CASE STUDY III
Gynaecological laparoscopy
Patient with polycystic ovaries
for laparoscopic cystotomies as
day case procedure
History
25 year old woman
 Height 165cm, weight 80kg
 BMI 29.5
 Typical PCOS history/findings.
 Allergies nil
 Rx: Metformin 0.5G b.d.
 Previous GA – E/O wisdom teeth – OK
 O/Ex: Overweight, otherwise
unremarkable.
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Common lies told by surgeons
- number 2: “Just a quick
laparoscopy”!
What are the issues and risks here?
Anaesthetic issues
Medical condition
 Prolonged surgery
 Laparoscopy/pneumoperitoneum
 Trendellenberg
 Analgesia
 PONV
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“Quiet victory”
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Largely uneventful anaesthesia/surgery
Problems maintaining normocarbia without excessive
airway pressures when head down
Mild permissive hypercapnoea, corrected at end
Polymodal antiemetic therapy – no PONV
Comfortable on combined analgesia
Home as day case.
A typical “straightforward” case that was expected to go
well - & did - so is not memorable to anyone but the
anaesthetist who worked hard to make it that way.
“There are a million stories in the naked
city, this is one of them.”
- The Naked City, US crime drama series
The practice, safety & reputation of anaesthesia is
built on thousands of such cases – far more so than
the glamorous emergency cases & heroic saves.
Part IV:
Anaesthetic Equipment
& Airway Management
Introduction to/overview of the
Anaesthetic Machine
Consists of three main parts:
1.
“A cocktail bar”
This is the backbar – which blends piped &/or bottle gasses: O2,
N2O & air, and the vapour of (usually one only) volatile
anaesthetic agent (liquid) to produce the desired blend.
2.
“A delivery service”
This is the breathing circuit – which delivers the fresh gas mixture
to the patient and removes carbon dioxide. (There are three main
classes of circuits – discussed later)
3.
“A bunch of hangers on”
These are all the ancillaries attached to the anaesthetic machine
but not part of its core function: typically suction system,
patient monitors, drawers/trays for airway equipment, and a
mechanical ventilator for hands-free controlled ventilation.
A Note of Caution:
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Modern anaesthetic machines are complex devices that
require special knowledge to operate.
In particular, knowledge of the pharmacology of inhaled
anaesthetic agents is essential.
Undetected mishaps can be rapidly fatal.
A thorough check prior to use, appropriate for the
particular machine, by an experienced person, is vital.
Some parts of the circuit e.g. filters & hoses, need to be
changed after every or certain cases, or a different type of
circuit may be selected & attached. An abbreviated recheck must be carried out after any such change.
Anaesthetic Circuits
Three principal types:
1.
2.
3.
Drawover or “semi-open” systems: where non-rebreathing valves are
used to ensure unidirectional flow of gas. Principally now used in
resuscitation & field anaesthetic systems, because of the ability to use
ambient air instead of (some or even all) pressurised gas supply.
Simple or “semi-closed” systems with pressurised fresh gas inflow,
reservoir tube & bag in one of several different configurations.
(Sometimes called Maplesen systems, after the man who classified &
evaluated the different configurations). The patient breathes ‘to & fro’
through the reservoir tube & bag & the system relies on an adequate
fresh gas flow to minimise rebreathing. Commonest example: the
“Jackson-Rees T-piece (Maplesen “F”)” paediatric circuit.
Circle, or closed circuit systems which use one way valves to direct
expired gas through a carbon dioxide absorber. This gas can then be
supplemented with only enough fresh gas mix to replenish the oxygen
and anaesthetic agents taken up, and then rebreathed. This is the
commonest type of anaesthetic circuit in modern practice.
Remember:
The commonest anaesthetic circuit most
medical & nursing staff will ever use is the
non-rebreathing resuscitation bag (“Laerdal
bag” or similar) . . .
. . . to give the commonest anaesthetic and
resuscitation drug of all: Oxygen
Another rule of three:
The triad of resuscitation
A – AIRWAY
B – BREATHING
C – CIRCULATION
Or . . . Alternatively:
(The triad of resuscitation – my own version)
1.
2.
3.
Air goes in & out
Blood goes round & round
Variations on the first two are a BAD THING
Note that airway always comes first
Airway isn’t everything . . .
. . . but without it everything else is nothing.
This is why anaesthetists are good people to
have around at a resuscitation – and why a
grounding in anaesthesia is good training
for emergencies.
Airway Control – Why?
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Prevent obstruction
Anatomical/foreign body
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Protect against aspiration
Vomit/blood/secretions
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Permit controlled ventilation
With paralysis/deep anaesthesia
Where ventilatory support required
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Enable special manoeuvres
e.g IPPV & PEEP for thoracotomy, laryngeal surgery
with microlaryngeal tube, single lung deflation with
double lumen ET tube.
Classification of airways
SUPRAGLOTTIC TRANSGLOTTIC SUBGLOTTIC
Oropharyngeal
airway
Nasopharyngeal
airway
Laryngeal Mask
Airways (various)
Combitube/PTL *
Orotracheal tube
(85% of placements
oesophageal)
- if one of the 15%
placed tracheally
Cricothyrotomy
Nasotracheal tube Transtracheal jet
catheter
Intubating LMA Tracheostomy
(w/ETT placed thru it)
(Combitube/PTL)
The winner, and still champion:
Endotracheal intubation
(usually oral), remains the
gold standard for airway
management, . . . but . . .
It is also the most difficult to
master and carries the
highest risk.
Remember: An unrecognised
oesophageal intubation has a
100% mortality
Emergency Airway Management
(in anaesthesia & resuscitation)
>90%
<10%
Rapid sequence
intubation
Other techniques:
[or unmodified (“cold”)
intubation if apnoeic &
arreflexic]
Supraglottic airway
Fibreoptic intubation
Surgical airway
Rapid Sequence Intubation:
How to do it properly
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Preoxygenation: 3mins or 5 VC breaths.
IV induction agent – titrated to effect
Cricoid pressure – 30N.
Suxamethonium 1.5mg/kg (IBW).
 or Modified RSI: 0.9mg/kg rocuronium
No bag mask ventilation (unless hypoxic)
Intubation & confirmation of placement
(then & only then) Cricoid pressure released.
Remember (1) : every intubation attempt is a
potential failed intubation.
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You should always have a backup plan
- i.e. a failed intubation drill.
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Backup begins even before you start - with
preoxygenation for every IV induction
Remember (2): People don’t die of failure to
intubate, but of failure to oxygenate
FAILED INTUBATION DRILL
FIRSTLY MAINTAIN
OXYGENATION!
CAN YOU MASK VENTILATE?
[With Geudels &/or nasopharyngeal
airway if necessary]
YES
1. Bag mask ventilation
2. Repeat attempt &/or
alternate technique to
intubate
NO
NO
Supraglottic rescue
airway e.g. LMA
SUCCESSFUL?
NO
SUCCESSFUL?
Subglottic (surgical)
airway
Non endotracheal airways
There’s more to anaesthetic airways than just ET tubes!
Laryngeal masks (of various types) are the most widely
used airways in modern anaesthetic practice:
 Classic (original) & its various copies – reuseable or single
use.
 Reinforced – kink resistant & more flexible upper lumen
to permit alternative positioning after insertion for
oral/facial procedures.
 Proseal - second lumen to communicate with oesophagus
& allow drainage of gastric contents or placement of
gastric tube.
 Intubating – modified shape, more rigid, & lacking
apeture bars – to enable passage of a special ET tube
through it.
Non endotracheal airways II
Advantages of laryngeal masks:
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Hands free (compared to face
mask/oral airway)
Easier to insert & become
proficient at compared to ETT
Tolerated at lighter plane of
anaesthesia than ETT.
Good protection against “top”
aspiration - of saliva/mucus.
Pressure support & in some
cases IPPV can be given.
Disadvantages of laryngeal masks
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Less secure airway - more prone to
dislodgement than ETT
No protection against
laryngospasm
Poor protection against “bottom”
aspiration – of gastric contents
(Except “Proseal”)
Not guaranteed to permit
satisfactory IPPV – especially
where high pressures required.
Remember, the traditional facemask/chin lift +/- Geudel’s airway is still an
acceptable – possibly even underutilised – technique for short simple cases.
Part V:
Anaesthetic Drugs:
Pharmacology, Use &
Related Issues
Classification of drugs used for anaesthesia
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“The Big Five “
Inhalation anaesthetic agents – gasses/vapours
IV anaesthetic agents alias “Hypnotics” or “induction
agents”
Narcotic (& other) analgesics
Muscle relaxants – neuromuscular blocking agents
Local anaesthetic agents
Other agents are often given as part of anaesthesia – e.g.
antiemetics & autonomic agents, but are not
conventionally regarded as anaesthetic agents per se.
Pharmacology 1:
Inhalational Anaesthetic Agents
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Inhaled – therefore delivered via apparatus
Gasses or volatile liquids
Moderate to high lipid solubility – “solvents”
Effects related to physical properties
(rather than to a generic chemical structure)
Effects on multiple organ systems
Actual mode of action not yet fully elucidated, but thought
to be by dissolving into cell membranes & causing
secondary changes in configuration of ion channels.
Currently Used Inhalational Anaesthetics
(shown in their international colour codes):

Nitrous oxide (N20)– a gas. Insufficiently potent
to produce full anaesthesia on its own, but is rapid
acting, pleasant to inhale & is the only currently
used agent that is also analgesic.
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Sevoflurane
Desflurane
Isoflurane
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all liquids that are flourinated ethers
Earlier volatile agents such as ether, chloroform &
halothane have been superceded due to issues such
as flammability, slow recovery, & toxicity.
Practical Pharmacology of
Inhalational Agents
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Used for induction sometimes (predominantly in children) &
maintenance of anaesthesia in the majority of cases - either
alone, or in combination with narcotics & muscle relaxants.
Modern flourinated agents are good hypnotics, & provide a
degree of muscle relaxation at high doses, but not analgesia.
In contrast, nitrous oxide is analgesic, but doesn’t decrease
muscle tone, and is a poor hypnotic except at very high (i.e.
hypoxic) concentrations.
The combination of a volatile agent, e.g. sevoflurane, with a
50:50 nitrous oxide/oxygen mix is a useful combination that
combines the attributes of both agents.
Practical Pharmacology of
Inhalational Agents (2)
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Sevoflurane has superceded isoflurane as probably the most
widely used agent, & has also superceded halothane as the
agent of choice for inhalational induction in children.
All currently used agents have relatively low solubility in
blood & tissue – meaning that their partial pressures rise &
fall quickly, producing more rapid induction & emergence.
The classical stages of anaesthesia are still seen with
modern agents – including the delerium phase –
characterised by restlessness & risk of laryngospasm. This
stage is usually seen on emergence, or with inhalational
inductions in children.
Practical Pharmacology of
Inhalational Agents (3)
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Nitrous oxide, as a gas is delivered by a flowmeter (as are O2
& air – the 3 flowmeters on a typical modern anaesthetic
machine). A linkage between the N20 & oxygen flowmeters
stops the delivery of any mixture <25%O2. Most anaesthetic
machines also only allow delivery of either N20/O2 or air/O2,
not all 3 & none allow air/N2O (a hypoxic mixture).
Volatile agents are delivered by vapourisers – devices which
add a precise percentage of vapour to the gas mixture. Modern
vapourisers are agent specific and colour coded/labelled
accordingly. They have numerous mechanisms to ensure
accurate delivery, plus safety measures such as “keyed” filling
systems that match only the correct bottle; and machines that
can have more than one vapouriser fitted must have interlocks
that prevent more than one being turned on.
Pharmacology 2:
IV anaesthetic “induction” agents
Used for:

Induction of anaesthesia

Sole agent for brief procedures
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By infusion for longer procedures - in place of
inhaled agents – i.e. total intravenous anaaesthesia
“TIVA”
Classification of intravenous agents
– Thiopentone
 Benzodiazepines – Midazolam
 Dissociative agents – Ketamine
 Others- Propofol
 Barbiturates
+ Alpha-2 agonists – Dexmetomidine . . .
maybe “the next big thing”
General features of IV agents
Lipid soluble
 High volume of distribution (Vd)
 Initial distribution to VRG
 Offset of (initial) effect predominantly
by redistribution
 More complex when used as infusions

(Computerised multicompartment
pharmacokinetic modelling required)
Propofol
Most widely used agent now
 Rapid(ish) onset & offset
 Shorter elimination halftime
 Less CVS & respiratory depression
 Doesn’t predispose to laryngospasm
 ED50 for induction: ~ 2 mg/kg
 Suitable kinetics for infusion
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Other IV agents
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THIOPENTONE
First widely used agent
Rapid onset & initial offset
by redistribution
Long elimination halftime
CVS & resp depressant
Laryngospasmogenic
ED50: ~ 5mg/kg
Still used for RSI
“The correct dose of thiopentone is
enough” (and no more!!)
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MIDAZOLAM
Low CVS & resp depressant
Anxiolytic, good initial
adjuvant agent, not often used
as sole agent
KETAMINE
“Dissociative” agent
Phencyclidine derivative
Cardiorespiratory stimulant (in
vivo)
Maintains airway reflexes
Analgesic in subanaesthetic
doses
“The disaster anaesthetic”
Total intravenous anaesthesia
“TIVA”
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Not practical until introduction of propofol , with
its short elimination half life, meaning minimal
accumulation with infusion.
Usually target controlled infusion using
computerised algorithm in syringe pump software.
Operator enters patient weight, age, & desired
blood level.
Often used in combo with remifentanil &
cisatracurium infusions for long cases (these also
have good kinetics for use by infusion).
TIVA –good & bad
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Advantages
Good for cases of long
or uncertain duration
Less effects on CBF &
ICP than volatile
agents
Less likely to cause
PONV then either
volatiles or N2O.
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Disadvantages
Long setup time
More expensive
Multiple syringe
pumps required
No direct measure of
blood or effect site
concentration
Pharmacology 3: Narcotic Analgesics
& Acute Pain Management
A Definition of Pain:
“An unpleasant localised sensory experience
perceived as actual or potential tissue damage.”
May be acute or chronic
Classification of Analgesics
 Conduction
blockade
 Opiods
 Paracetamol
 NSAIDs
& COX2s
 Miscellaneous agents
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Complementary/Non pharmacological
An opiod is a drug that exhibits agonist activity at
opiate (endorphin/enkephalin) receptors. A
classification of opiods includes:
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Opiates (naturally occuring constituents of opium)
& their derivatives:
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e.g. morphine, codeine, diamorphine
(heroin)
Synthetic opiods
e.g. pethidine, fentanyl cogeners, oxycodone
Partial agonists
e.g. pentazocine “Fortral”, buprenorphine
N.B. This classification does not include the narcotic
antagonists e.g. naloxone “Narcan” & naltrexone;
however these are closely related, being n-allyl
substituted derivatives (hence their names)of opiods
Properties of opiods
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Analgesia
Spinal ( μ/κ) & supraspinal (μ)
Respiratory depression
Sedation/euphoria (addiction potential)
Emesis
Depression of GI motility
Neuraxial route
Pruritis
predominantly
Urinary retention
}
No difference in respiratory depression between
equi-analgesic doses of any narcotic agonists
So the differences between opiods are
less in their analgesic efficacy than in:
Onset
 Duration
 Potency/dose
 Histamine release
 Autonomic effects
 Chest wall rigidity
 Effective routes of administration
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Routes of administration of opiods:
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Intravenous: (a) Boluses – titrated to effect – e.g recovery pain protocol
(b) Infusions – require close monitoring due to potential for overdose as
narcotic requirements fall away.
(c) PCA – now widely used. Intrinsically safer than infusions, plus
positive psychological effect of patient knowing they are in control.
Neuraxial - Epidural or intrathecal (spinal) – usually in combination
with regional anaesthesia, but may also be stand alone technique for
postoperative analgesia. Risk of late onset respiratory depression if agent
migrates into intracranial CSF in significant amount (highest with
morphine, but this is also the longest acting)
IM/SC – decreasing importance with availability of PCA & better oral
agents, & multimodal therapy.
Oral – variable bioavailability: e.g. oxycodone high, morphine ~ 15%
due to first pass metabolism.
Sublingual(buprenorphine) /Intranasal(fentanyl) – lipid soluble agents
fairly rapidly absorbed & this route avoids first pass effect (& injection)
Transcutaneous – e.g. fentanyl patches for chronic pain
Problems with opiods
Respiratory depression/cough suppression
 Tolerance
 Abuse/addiction potential
 Accountability/access/supply difficulties
- consequent to abuse potential.
 Nausea & vomiting
 Constipation
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Multimodal analgesia options
Regional/local blockade (if possible)
 Paracetamol
 NSAID or COX2
 Basal opiod (e.g. oxycontin); or tramadol
(or both)
 prn or PCA opiod
 Other
Clonidine or ketamine
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Pharmacology 4:
Neuromuscular blockers
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Purely paralysing agents – no analgesic or hypnotic
activity.
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Two types based on modes of action:
Depolarising (Suxamethonium)
Versus
Nondepolarising
(NDNMBs, several available)
Why use paralysing drugs at all?
Permit procedures at a lighter plane of
anaesthesia – hence less CVS depression
 Intubation & ventilation
 Surgery
 Permit IPPV without interference
 Lower airway pressures by increasing chest
wall compliance.
 Lower O2 consumption in critical periods
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Properties of NMBDs
Highly polar molecules
 Low VD ( ~ ECF volume)
 Do not cross BBB/placenta
 Renally excreted (with exceptions)
 Range of actions at other ACh receptors
 Histamine releasers (most)
 Decrease VO2 /ATP & heat production
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“Sux” versus the NDNMBDs
Nondepolarisers
Suxamethonium
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Rapid onset (30s)
Fasciculations
Transient rise in ICP, IOP,
IAP/IGP, K+.
Rapid offset (usually)
by hydrolysis in plasma
Unpredictable effects in
repeat dosing
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Slower onset (3-7m)
No fasciculations
Little to no effect on
ICP, etc.
Varying durations
with different drugs
OK for prolonged use
by boluses or infusion
Nondepolarising relaxants
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First generation
Curare/tubocurarine
Alcuronium
Metocurine
Gallamine
Pancuronium
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“Modern” agents
Vecuronium
Atracurium
cisAtracurium
Rocuronium
Mivacurium
Brown = curare derivatives
Blue = aminosteroids (the “oniums”)
Green = benzisoquinolines (the “uriums”)
Side effects of suxamethonium
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Myalgia
MH trigger
Masseter spasm
Phase II block
Raises ICP
Raises IOP
Bradycardia
(Usually in infants
or with 2nd dose)
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Raises serum K+
Exaggerated action &
K+ rise in denervation,
burns, muscle injury
Prolonged action with
pseudochlinesterase
variants/deficiency.
Histamine release
Anaphylaxis (1:5000)
Problems with nondepolarisers
Slow onset – not usually a major problem
 Slow offset (situation/agent dependant)
 Awareness
 Hypothermia –reduced heat production
 Autonomic side effects
 Interactions
 Failure to reverse/recurarisation
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Paralysis obviously mandates
controlled ventilation
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Modern anaesthetic machines are all equipped
with ventilators.
Usual mode is volume controlled (delivers a set
size of breath, a set number of times a minute)
with or without PEEP.
Most can also give, or be adapted to give, pressure
controlled ventilation, which is the mode of choice
for paediatric patients (who usually have uncuffed
tubes, and hence a small leak).
The Physiology of Controlled Ventilation
“Spontaneous ventilation sucks; Controlled ventilation blows”
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Maintains constant minute volume & enables titration to
desired pCO2 – vital in neurosurgery & acidotic patients.
Uptake of volatile agents therefore usually higher than in
spontaneously breathing patient -> more CVS depression.
Recruits alveoli & prevents collapse: minimises shunt.
Raises mean intrathoracic pressure – & hence RAP, so
reduces venous return & cardiac output – especially in head up
position & with pneumoperitoneum – e.g. laparoscopic cholecystectomy.
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Risk of barotrauma – esp. w/high tidal volume or pressures.
Pharmacology 5:
Local anaesthetic agents
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Local anaesthetics are membrane stabilisers that block
depolarisation in nerves
Non specific blockers of:
 All sensory fibres (not just pain)
 Motor fibres
 Autonomic fibres (mainly sympathetics in most blocks)
Hence can produce analgesia & arreflexia in the distribution of
the nerves blocked.
Lower concentrations of LA agents effect predominantly
smaller axons: pain (Aδ & C fibres), temperature, & autonomic
(unmyelinated sympthetic post-ganglionic fibres)
“Your friendly local anaesthetic molecule”
Think of a person standing in the water
– keeping their head high & dry
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H+
N
A-
Head: benzene ring
(lipophilic)
Body: (intermediate chain)
with either ester or amide
link.
Tail: (feet) – hydrophilic due
to tertiary nitrogen capable
of accepting proton &
rendering molecule water
soluble. (This is the form it
is in in the ampoule)
“The voyage of the molecule Lignocaine”
ECF
ICF
Sodium
channel
Lignocaine
hydrochloride injected
N
H+
N
ClTissue
buffering
H+
Lower
intracellular pH
leads to reionization
HCO3-
H+
N
N
H2O + CO2
Freebase lignocaine diffuses across cell membrane
Understand this, and you will know:
Why local anaesthetics sting on injection
(because of the low pH needed to maintain ionised state)
 Why their onset of action is not immediate
(because of the buffering/diffusion/reionisation steps)
 Why local anesthesia is poorly effective in inflamed/ infected
tissue
(because of the lack of buffering capability in acidotic tissue)
 Why LAs exhibit tachyphylaxis
(exhaustion of buffering capability)
(& why cocaine users end up needing nose reconstructions –
from repeated insult to the nasal septum from an acid
substance that is also a vasoconstrictor - which inhibits
circulatory dilution of the acid load)
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Local Anaesthetic Agents
AGENT
Max dose:
Plain (+Adr)
4 (7) mg/kg
Lignocaine (“Xylocaine”)
2 mg/kg
Bupivicaine (“Marcain”)
3-4mg/kg
Ropivicaine (“Naropin”)
Levobupivicaine (“Chirocaine”) 4 mg/kg
7(9) mg/kg
Prilocaine (Citanest”)
Local Anaesthetic Problems
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Failed block - multiple causes
High block (spinals/epidurals)
CNS toxicity
 at high dose or with inadvertent IV injection
Selective cardiotoxicity (bupivicaine)
Needle/injection trauma
 Nerve damage
 Other – e.g pneumothorax
Adjuvant agents used with LAs
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Adrenaline – prolongs blockade, allows increased dose
(lignocaine/prilocaine)
Bicarbonate – Decreases acidity - speeds onset of block
 Hyaluronidase –Aids diffusion (Eye & brachial plexus
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blocks)
Glucose (spinals) – to produce hyperbaric solutions
 Narcotics (neuraxial) – synergistic analgesia
 Other analgesics – e.g clonidine in neuraxial blocks.
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Modes of Local Anaesthesia
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(a) Peripheral
Surface
 Topical (incl EMLA)
 Nebulised
 Intrapleural/peritoneal
Infitration
Intravenous regional
Nerve/plexus blocks
 Multiple types
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(b) Neuraxial
Epi(extra)dural
 Single shot vs catheter
 Bolus vs infusion
 LA only vs combinations
 Includes caudal blocks
Spinal/subarachnoid
 Usually single shot
 LA only or LA/narcotic
Combination (CSE)
Some common nerve/plexus blocks
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Eye blocks:
Peribulbar, retrobulbar,
Sub-Tenons
Superficial cervical plexus
block
Brachial plexus blocks:
Axillary, supraclavicular,
interscalene
Paravertebral blocks
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Intercostal blocks
Ilio-inguinal block
Dorsal penile nerve
block
Pudendal nerve block
Femoral (+/- LCNT)
block
Ankle blocks
Spinal Anaesthesia
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Relatively quick, defined end-point for placement
Small volume of LA
Usually single shot – “fire & forget”
Block level depends on spread – varies with:
 Volume
 Speed of injection
 Baricity
Minimal respiratory effects – unless high block
Autonomic effects: - Vasodilatation @ T12 & up
- Bradycardia @ T4 & up
Epidural Anaesthesia
Alone, or with GA, or as CSE.
 Cervical (rare), thoracic, lumbar, caudal
 Usually catheter placement (except caudal)
 High volumes LA +/- adjuvants.
 “Band” phenomenon.
 Autonomic effects similar to spinal, but
slower onset
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Considerations in regional blockade
Consent/communication
 IV access
 Adjuvant sedation/analgesia
 Time involved
 Failed block/backup plan
 Management of side effects/reactions
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Part VI:
Sub-Specialty Anaesthesia
INCLUDES:
1. Paediatrics
2. Obstetrics
3. Cardiothoracic
4. ENT/Head & neck
5. Neurosurgery
Subspecialty Anaesthetics A:
Paediatric
“They’re not just small adults”
. . . But . . .
“Nor are they all just big neonates, either”
Case Study IV
Paediatric Hypospadias Repair
History
4 year old boy (obviously!)
 Grade III hypospadias & chordee
 For EUA/repair
 Background: Mild asthma & ADHD
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Issues
Preop assessment & stabilisation
 Premedication
 Induction & IV insertion
 Prolonged surgery
 Postoperative analgesia
 Postoperative IV & IUDC
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Adult-Paediatric Differences
Psychosocial
 CNS
 Respiratory
 Airway
 Other
 Cardiovascular
 Renal/fluids

Gastrointestinal
 Hepatic/metabolic
 Endocrine
 Haematological
 Immunological
 Musculoskeletal
 Integument
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The Psychosocial Dimension
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There are (almost) always two patients – child and parent(s).
If you don’t keep the parents happy, or at least reassured, the
child won’t be either – no matter how good the anaesthetic.
Children don’t understand that you are there to help – only
that you are a stranger.
Children hate needles. Parents hate their children having
needles. Even without this, cannulation can be difficult.
Anything that ameliorates this is good: such as premedication,
EMLA to cannula sites & inhalational inductions.
Parental presence at induction can be a good idea – as long as
the parent is going to cope. If in doubt, a generous premed &
a goodbye outside may be a better option.
Anatomical Differences 1
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Body proportions
 Head larger
 Limbs smaller
Increased surface
area to volume ratio
CNS differences
Brain & spinal cord
relatively larger
Anatomical Differences 2: Airway
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Head larger
Nares (relatively) larger
Larynx higher
C3 in neonate -> C6 in
adult
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Epiglottis longer (&
softer)
Cricoid ring narrowest
part of airway
Paediatric Respiratory Physiology
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Chest wall mechanics & tracheobronchial tree
“floppier”.
Tidal volume/dead space same as adults in mls/kg
Respiratory rate & minute volume higher
FRC similar to adult in mls/kg, but vO2 higher, so
desaturate more quickly when apnoeic.
Control of respiration immature till ~ 15/12 post
conceptual age – up till then vulnerable to
apnoeas – especially post GA &/or narcotics.
Paediatric CVS Physiology Refresher

Fetal circulation/Postnatal transition
-predelivery: systemic & pulmonary circulations in parallel,
with oxygenation via placenta & high pressure/low flow on
(R) side.
-Transition at birth to systemic & pulmonary circulations in
series with fall in PVR & closure of shunts.
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Haemodynamics
Neonates & infants have fixed stroke volumes: CO dependant
on HR – i.e. bradycardia = hypotension & shock.

Autonomic control
Different in neonates & children – response to hypoxia is
bradycardia (“Diving reflex”) rather than tachycardia.
Blood & body fluids
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Blood volume 80-90 mls/kg (adult ~ 70)
Birth Hb 180-200 g/L (adult 120-160)
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Falls to ~ 110 @ 6/12 then rises.
Fetal haemoglobin (HbF)
Different chains
 Lower p50 (Hb-O2 curve shifted left)
 75% of Hb at birth  minimal @ 6/12.
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Body water 75-80% in neonate (adult 65%)
ECF compartment larger than ICF
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(crossover @ ~ 4/12)
Paediatric Thermodynamics
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Infants at higher risk of hypothermia
Higher surface area to volume ratio
Remember the four modes of heat loss:
1.
2.
3.
4.
Conduction
Convection
Radiation
Evaporation
All four occur more when the surface area to
volume ratio is higher
Heat production & regulation
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Controlled in hypothalamus
Balances heat loss & heat production
Heat production
 Shivering – poorly developed in neonate/infant
 Metabolic thermogenesis (brown fat)
Thermoneutral environment;
 Point of minimum O2 consumtion
 e.g. for unclothed term baby is ~ 33°C
Subspecialty Anaesthetics B:
Obstetrics
Remember, once again you have two
patients – but this time they are
physically connected
Case Study V
Caesarian Section
History
38 yr old lady, P0G1
 Booked LSCS
 IVF pregnancy
 Moderate PIH/pre-ecclampsia
 History of back pain
 Wants to be awake for delivery
 Needle phobic

Issues
Preop consultation
 Investigations
 Premedication
 Choice of anaesthetic technique
 Choice of IV fluids
 Backup anaesthetic plan
 Postoperative monitoring
 Analgesia plan

Principles
Pregnancy is a normal, but vulnerable
condition.
 The prregnant patient is different
 Delivery is hazardous
 Operative intervention may be required
 Labour & delivery can be agonisingly
painful
 Anaesthesia inevitably has (at least some)
foetal effects/implications.

Differences in Pregnancy
Psychosocial
 CNS
 Respiratory
 Airway
 Other
 Cardiovascular
 Renal/fluids

Gastrointestinal
 Hepatic/metabolic
 Endocrine
 Haematological
 Immunological
 Musculoskeletal
 Integument

Drugs & the Placenta
General rule: If it crosses the blood brain
barrier, it crosses the placenta!
Placental transfer:
Narcotics/Sedatives/GA agents - HIGH
Muscle relaxants -Essentially nil
Local anaesthetics – Significant (in freebase
form) . . . but peak maternal plasma levels
usually post delivery
Scenarios
Analgesia for labour
 Anaesthesia for operative delivery
 Emergency
 Semiurgent
 Planned
 Anaesthesia for post partum complications
 Neonatal resuscitation
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Analgesic options
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Inhalational – N2O as Entonox (50:50 N20/O2) or via
blender (up to 70% N2O – Caution!)
Narcotics
IM/SC prn – pethidine favoured by
midwives
 Infusions – not often used
 PCA – remifentanil drug of choice.
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Epidural – usually initial bolus then either:
(a) Infusion [&/or] (b) bolus top-ups [or] (c) PCEA
Other regional/local blocks – e.g. pudendal block for
second stage.
Anaesthetic Options for Caesarean
Regional
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Spinal vs Epidural
Spinal quicker – unless
epidural already in situ &
only needing top-up.
Most mothers want to be
awake.
Beware the failed or
patchy block.
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General
Technique of choice for
emergency LSCS
 Fastest
 Better in hypovolaemia
Riskier for mother on raw
figures, but:
 GA population includes
failed regionals & most
emergency cases.
 So are we comparing
apples to oranges?
No difference (surprisingly) in foetal outcomes between GA & RA
Subspecialty Anaesthetics C/D:
Cardiothoracic & ENT
What do these surgical disciplines
have in common?
Remember the basic rules:
1.
2.
3.
Air goes in & out
Blood goes round & round
Variations on this are a BAD
THING
. . . BUT (you knew there had to be a “but”
somewhere, didn’t you) . . .
ENT, Thoracic, & Cardiac anaesthesia all
require some flexibility of these rules!
Anaesthetic Factors in
ENT/Oral Surgery: the A to E
A.
Airway - shared with surgeon . . . And they’re not
good sharers sometimes!
B. Bleeding – even a little in the airway is a BAD
THING
C. Children – make up a large proportion of patients
D.
E.
Disruptions – see Airway!
Extubation strategies – deep versus awake:
deep prevents coughing but leaves patient without
airway protection; light ensures airway protection but
patient coughing may exacerbate likelihood of
bleeding.
(No easy answer to this – has to be case by case basis)
Airway Management Options
in ENT/Oral Surgery







None (!)
Venturi ventilation
Nasal tubes
RAE tubes
MLT tubes
Laryngeal masks (yes!)
Subglottic airway i.e tracheostomy
Anaesthetic Factors in
Thoracic Surgery





Open thorax – mandates IPPV +/- PEEP
Pre existing lung disease
Lung isolation requirements
Intraoperative hypoxia (lung isolation by
definition creates a major shunt)
Postoperative issues
 Respiratory support
 Analgesia
Lung separation techniques:
 Endobronchial
intubation
(but this time not inadvertent!)
 Double lumen ET tubes
 Bronchial blockers
 Other (generally bodgie) methods
Anaesthetic Factors in
Cardiac Surgery

Cardiopulmonary bypass
 Cardiopulmonary
bypass!
 Cardiopulmonary
bypass!!
(Scary, scary, scary stuff)
Cardiopulmonary bypass
(“CPB”) for dummies
Pump plus oxygenator
(“Heart lung machine”)
 Cardioplegia
(High K+ solution to cause
cardiac standstill)
 Hypothermia
(Enables prolonged ischaemic
times)

Problems with CPB

Non-pulsatile flow – can cause paradoxical
circulatory responses

Hypothermia/pH issues – What is the right pH in
hypothermia to maintain acid base status?

Red cell trauma – from pump rollers impellers, &
(especially “bubble” type) oxygenators


Cardiac restarting/Weaning from bypass
Post CPB syndrome – confusion & cognitive
impairment, sometimes long-term or permanent.
Other Anaesthetic Factors in
Cardiac Surgery
Pre-existing cardiac disease – well, obviously!
 Co-morbidities - high incidence CVD, PVD,

diabetes, renal impairment, etc.
 Concurrent medications – likely to be
multiple
 Monitoring – In patient on CPB: there is no
ECG, pulse (oximetry), conventional BP, or
expired CO2 there to monitor. Can monitor
MAP generated by bypass, ABGs, & BIS/entorpy
Subspecialty Anaesthetics E:
Neurosurgical
It’s not rocket science . . .
. . . but it is brain surgery
Special considerations in
neurosurgical anaesthesia:




Airway – secure, as access to it intraoperatively
may be impossible.
Breathing - may need to manipulate CO2 to
control intracranial pressure/volume.
Circulation - maintain appropriate BP for desired
cerebral perfusion pressure
Disability & Exposure - special positioning may
be required – e.g. sitting or prone, all of which
carry particular risks.
Part VII:
Emergencies,
Complications & Problems.
Anaesthetic Emergencies
Anaesthesia for
emergencies
Emergencies from (or
during) anaesthesia
A: Emergency Anaesthesia
Obstetrics
 Trauma
 Gen. Surgical
 Vascular
 Neuro-surgical/-radiological
 Cardio-thoracic
 Threatened airway

Considerations in
Emergency Anaesthesia
First: How much of an emergency is it,
really? Then:
 Airway assessment
 Cardio-respiratory status
 Full stomach/fasting status
 Pre-existing medical conditions
 Medications/allergies
Assessment may itself be difficult because
of haste, patient compromise, etc.
Anaesthetic management
Assessment
 Management plan/scheduling
 Stabilisation & preparation (as much as the

urgency of the presenting problem permits)
Pain management
 Then (& only then) commencement of
anaesthesia

Emergency Anaesthesia:
Maintenance

Includes ongoing resuscitation & Rx

Monitoring: More not less

Postanaesthetic management plan?
“LITTLE SHOP OF HORRORS”
Selected excerpts from
my trauma casebook
Trauma scenes are an everyday sight:
When racing a train to a level crossing,
coming first equal is not a good idea!
Airway Management I
“Seasonal Goodwill”
28 year old male
 3 days prior to Christmas
 Hit in face . . . with a frozen turkey (?!!)
 Le Fort III and mandibular #s

Anaesthetic Management

Topical airway anaesthesia



with nebulised lignocaine – (then)
Attempted Fibreoptic assisted awake oral
intubation – failed due blood in airway & restless
patient
Plan B: RSI
 with head up position till induction
 then Trendelenberg till airway secured
Lesson: In a crisis - do what you do best and you are
comfortable with.
Airway Management II
“Young & Silly”
 19 yr old female
 Unrestrained backseat passenger in MVA
 Hx of EtOH +++
 GCS 9, HR 120, BP 90/60, distended abdo
 . . . . . . Priorities?
Anaesthetic management


Hi-flo O2 by mask, 2x large bore IV access.
Fluid bolus, then rapid sequence intubation.



To OT for laparotomy/splenectomy.



Midazolam/ketamine/suxamethonium
In line Cx spine stabilisation
Fentanyl/N20/relaxant
Circulatory support: Fluids/blood to MAP of 90
Then CT scan – NAD.
Lesson: “Head injury + hypotension + hypoxia = Death”.
i.e. Secure the airway but oxygenate the brain too!
Airway Management III
“There are old motorcyclists and there are
bold motorcyclists . . . but are there any
old and bold motorcyclists?”
 56 yr old male motorcyclist
 Morbid obesity (approx 155kgs)
 Fractured ribs/pulmonary contusions
 Borderline hypoxia
(SaO2 90-91% on high flow O2 via NRBM)

Suspected Cx/Tx spine #s
Do you think that this just might be a
difficult intubation?
Anaesthetic management
Topicalisation of airway
 Awake fibreoptic nasal intubation

Surgical insistence on supine posture due
potential spinal #s.
 Extremely technically difficult & patient hypoxic
throughout procedure.
 Improved after intubation & IPPV/PEEP.
Lesson: Although satisfactory result, could very well
have been a failed intubation due to failure to insist
on optimal conditions for airway management.

Airway Management IV
“And Judas went and hanged himself”






18 yr old male; Hx of depressive illness
Found hanging
Cardiac output always present
GCS 3, pupils fixed & dilated,
Spontaneous respirations, trismus
Neck swollen, but no palpable subcutaneous
emphysema.
Anaesthetic Management
Inhalational anaesthesia O2/sevoflurane
 Laryngeal mask placed
 Bronchoscopy via LMA:



No evidence of laryngeal/tracheal fracture.
Then relaxant, LMA replaced with ETT.
Lesson: Beware the potential airway disruption
- the one time a correctly placed endotracheal
tube can result in fatal loss of the airway.
Respiratory Management I
“Guns don’t kill people” (. . . it’s the bullets
fired out of them that do that, sometimes).
 16 yr old male, accidental GSW to chest.
(7.62mm NATO [.308”] calibre – high velocity rifle)
Entry & exit wounds (R) chest.
 (R) haemopneumothorax.
 Haemodynamically unstable.

Anaesthetic Management
High flow O2/large-bore IV x2/chest drain.
 Rapid sequence induction



Narcotic, low dose thiopentone/suxamethonium.
(L) double lumen tube placed
Checked clinically, confirmed w/bronchoscope.
 Other options: Univent tube; bronchial blocker.
Lesson: Must have a plan for rapid placement and
checking of lung separation device; and strategies
for oxygenation with one lung ventilation: e.g.
upper lung CPAP, or intermittent inflations.

Upper lung CPAP device on a double lumen ET tube
Respiratory Management II
“Just another holiday weekend”






9 yr old girl, MVA with associated fatality
GCS 7, initial haemodynamics & SaO2 OK
Rapid sequence induction – sBP fell to 50mmHg
Abdo distension noted
Fluid challenge 20mls/kg crystalloid
– improved BP but SaO2 fell to 90%
Where to from here?
Anaesthetic Management



PEEP 5 then 10cm – improved SaO2 but BP fell
again.
Further volume expansion with colloid & blood
30° head up tilt once BP adequate, to:



Reduce ICP rise from PEEP
Improve ventilation/perfusion matching
To OT for laparotomy:

Oversewing liver lacerations & mesenteric tear.
Lesson: Beware the occult lung injury: contusion,
haemo- or pneumothorax . . . they all get worse.
Circulatory management
“Off with his head!”






23 yr old male, partial beheading with machete
Severed (R) neck muscles, carotid & subclavian
arteries, probable phrenic/vagal/accessory nerves
HR 140, peripherally shut down, BP 65 systolic
Conscious, semi-orientated, distressed.
Decreased R chest movement, SaO2 90%
Brought straight into theatre (2 mins warning).
Anaesthetic Management



Continued direct haemostatic pressure on wound.
IV access & arterial line (L) arm.
Rapid sequence induction:



(ketamine/suxamethonium)
Anaesthetic maintenance with ketamine/fentanyl
Volume support with crystalloid/blood:


to systolic BP of 65mmHg only.
Until surgical haemostasis obtained
Lesson: Resuscitation to normotension may not be
indicated – or possible
Circulatory management: Principles
Good (large) IV access vital
Peripheral: exchange/cutdown
Central: femoral/jugular
 Consider controlled
hypotension until haemostasis
 Exceptions to this:
 Neurotrauma
 Elderly/hypertensive
 Pregnancy
“Appropriate BP theorem”





Early arterial line & IABP
where indicated
Warm all fluids
Early use of blood
Monitor what you do:
 Arterial gasses
 Haematocrit
 Platelets/coagulation
(+clinical consultation)
Other problems: Hypothermia
34 year old man
 “Accidental” rectal insertion of vibrator
 Perforated sigmoid colon
 Faecal soiling & peritonitis/sepsis/MOF
 Prolonged laparotomy
 Significant hypothermia

Hypothermia in Trauma




Common problem
Increases morbidity &
mortality
Decreases coagulation
& injury response
May be therapeutic in
isolated neurotrauma



Be aware of risks
Practice passive heat
conservation
Active warming:
 Surface
 IV fluids
 Gas humidification
Other problems: Coexisting disease
“In the line of duty”





29 yr old man, bartender
Gunshot wound to stomach during armed holdup
Obese, smoker, moderate to heavy EtOH.
Conscious, distressed ++++
HR 160, BP 180/120
Anaesthetic Management



Analgesia titrated against pain, hypertension &
tachycardia.
To OT for urgent laparotomy.
Intraoperative arrhythmias & arterial desaturation.



No evidence ballistic damage to/near diaphragm
Post op diagnosed with extensive anterior AMI.
Surgical recovery but ongoing poor LV function.
Would earlier analgesia have prevented this?
Lesson: (a) Beware of occult disease even in the
young. (b) Pain does matter.
Recreational drugs
“High on cocaine – in both senses”









38 yr old woman
IVDU, formerly heroin, now IV cocaine
On naltrexone
Sex industry worker, Hep B/C +ve
3 story fall while under influence of cocaine
100% subluxation/# T12-L1
Complete neurological deficit at T10
Severe neuropathic pain
Difficult IV access
The geriatric trauma patient
“Somebody’s grandma”
 86 yr old woman, Fractured NOF
 Hypertensive on Rx (enalapril/diltiazem)
 Fall secondary to ?TIA?
 Ex smoker, mild to moderate CAL
 Exercise tolerance limited by arthritis
 For Austin Moore hemiarthroplasty
Anaesthetic Management

Potential problems:




Attempted spinal




Respiratory complications with GA
Hypertension/tachycardia with airway manipulation
Hypotension +/- cerebral ischaemia with regional
Technically difficult due calcification of spaces
Abandoned after several failures to locate space
Converted to GA: - uneventful.
CVA 2/52 post op – died 1/52 later.
Lessons: - Sometimes there is no “right” anaesthetic
- Just some may be less wrong than others
The Pregnant Patient
“Your next two patients are . . . “
 38 year old female
 P2G1 - 31/40 pregnant
 MVA with #’d femur
 For femoral nailing.
B: Anaesthetic Emergencies
& Complications
“BIG ONES”







Arrest
Anaphylaxis
Failure to intubate
Ventilator disconnect
Laryngospasm/NPPO
Aspiration
Nerve damage







“Little ones”
Agitation/delerium
Sore throat
PONV
Pain
Urinary retention
Atalectasis
Cognitive dysfunction
Post Operative Nausea & Vomiting (PONV)
“The Big Little Problem”




Still affects up to 30% of patients.
Major subjective concern – studies suggest most patients
prefer pain to N&V.
Most common cause of prolonged recovery stay, & delayed
discharge in daystay patients
Multifactorial:
Patient factors: ♀ > ♂; Non smoker > smoker.
 Surgical: High incidence in eye, ENT, &
gynaecological laparoscopic surgery.
 Anaesthetic: Narcotics, volatile & N2O all
potentially emetic. (Propofol usually not)

Treatment approach to PONV
Prevention is better than cure



General
Identify at risk patient
Anaesthetic history
Identify & ameliorate
precipitant if possible
e.g. narcotics
General supportive Rx:
IV hydration,
narcotic sparing,
multimodal analgesia
Consider TIVA

Antiemetic agents:
HT3 blockers - e.g. ondansetron.
Pre-emptive or reactively.

Dexamethasone – mode of
action unknown. Most effective
premptively.

Dopamine antagonists
- e.g. droperidol. Good for
narcotic related N&V

Others: - Anticholinergics
- Antihistamines/phenothiazines
- Prokinetics – metoclopramide
Anaesthetic Risk In Perspective
Risk of anaesthetic death (due to the
administration of the anaesthetic) < 1:50,000
No paediatric anaesthetic deaths in Australia in
the last reported quinquennium.
Typical healthy elective surgical patient probably at
more risk of death or serious injury from car trip
to/from hospital
The figures are good but may lead to:



Overconfidence amongst anaesthetists
Complacency by surgeons & under-appreciation
of risk of coexisting disease factors (which do kill
patients).
Anaesthesia & sedation services becoming a target
for cost cutting measures by politicians/managers
with consequent erosion of safety margins.
The Eternal Triangle
(In all health services, not just anaesthetics)
QUALITY
QUANTITY
Pick
any
two!
ECONOMY
(And if one of these is economy, are
you sure it’s not a false economy?!)
The Bottom Line
Safe anaesthesia may not prevent the patient
dying of the disease.
 It will however help prevent them dying of
the treatment.
 Think as a potential surgeon: Isn’t this what
you would want for your patient?
 Think as a health consumer: Isn’t this what
you would want for yourself or your family?

The End
If you have any questions about the
course material, or about
anaesthesia as a potential career
choice, feel free to contact me:
docblair@optusnet.com.au