Anaesthetics Study Guide - Emergency Medicine Education

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Transcript Anaesthetics Study Guide - Emergency Medicine Education

UNSW School of Medicine
Liverpool Clinical School
Critical Care Rotation
Anaesthetics Study Guide
Blair Munford, BMedSc, MB,ChB, FFARACS, FANZCA
Senior Specialist Anaesthetist, Liverpool Hospital
1
Aims of Anaesthetic Attachment
• 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.
2
Part I:
Scope & Development of
Anaesthetic Practice
Imagine a world without
anaesthesia . . .
3
What medicine was like prior to the
invention of anaesthesia:
• Surgical operations performed rarely & only as a last
resort. Death was the expected outcome, from shock,
haemorrhage, or infection.
• 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.
• No analgesia in labour & interventional/operative
obstetrics essentially unknown – except post mortem
(original meaning of Caesarean Section)
4
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.
5
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.
6
But what exactly 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”
7
The other triad of anaesthesia
THE MISSION IS (in order of importance):
1. 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 and science of anaesthesia
is in being able to provide all three.)
8
Anaesthesia can be:
• Cerebral
– Sedation/analgesia
– General
• Inhalational/spontaneous ventilating
• Balanced/controlled ventilation
• Neuro-interruptive
– Local
– Regional
– Neuraxial
(Or some combination of
two or more of these)
9
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
10
But wait . . . there’s more:
11
Scope of Anaesthetic Practice
•
•
•
•
•
•
•
•
•
•
•
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)
12
Part II:
Perioperative Medicine
“The way of the future”
13
What is perioperative medicine?
“Integrated multidisciplinary management
of the surgical or procedural patient’s
hospital admission & stay.”
14
Perioperative system includes:
•
•
•
•
•
•
•
•
•
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
15
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
16
The Pre-anaesthetic Consultation
• 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 basis)
• Why? To enable optimimum pre-anaesthetic
preparation, risk minimisation, informed consent,
and allaying of anxiety.
17
Pre-operative preparation may
include premedication
Use if required, not “one size fits all”
Aims:
1.
Ameliorate anxiety
Usually with a benzodiazepine such as temazepam
2.
Relieve pain – predominantly in the acute setting –
usually with narcotics.
3.
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.
4.
Treat other medical conditions
e.g. asthma prophylaxis.
18
Most regular medications are continued,
including on the day of surgery
Exceptions include:
(a) Oral hypoglycaemics
(b) Antithrombotic agents (mostly)
19
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
20
Relevance of this?
• Risk stratification
• Workload/resource utilisation planning
• Remuneration aspects
21
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
22
Preanaesthetic Clinic
• 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
23
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
24
Part III:
Safety & Monitoring
in Anaesthesia
25
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!
26
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.
27
Principles of Safety
• 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.
28
“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.
29
Monitoring in anaesthesia
Basic (all/most patients)
• Pulse oximetry
• ECG
• Noninvasive (cuff) BP
• Capnography
• Oxygen concentration
• Agent monitoring
• Airway pressures
• Temperature
•
•
•
•
•
•
•
•
•
Others as indicated
Invasive arterial BP
Precordial stethescope
Ventilator alarm(s)
Nerve stimulator
BIS/entropy
Spirometry
CVP
“Swann Ganz” (PAP)
Transoesophageal echo
30
Pulse oximetry
• 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
normal in extreme anaemia, carboxy- or methaemoglobinaemia, cyanide posoning, etc.
31
Electrocardiogram
• 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!
32
Noninvasive arterial blood
pressure (NIBP) monitoring
•
•
•
•
•
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 fistula or
lymphoedema.
33
Capnography
• “Gold standard” for verification of airway.
• 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
34
Oxygen monitoring
• Monitors machine rather than patient.
• 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.
35
Anaesthetic agent monitoring
• 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.
36
Temperature monitoring
• Anaesthesia promotes hypothermia by:
– Decreased metabolic rate -> decreased heat production
– Redistribution of blood flow -> increased heat loss
• Patients may need temperature support
– 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
37
Airway manometry
Ventilator monitor
• Usually analogue
gauge on circle circuit
• Monitors inflation
pressure
• With IPPV can help
identify:
• Mandatory when
mechanical IPPV
employed.
• Usually integrated into
ventilator w/automatic
activation.
• High (overpressure) &
low (disconnect)
functions
Airway obstruction
Bronchospasm
Circuit leaks/faults
38
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!
Direct arterial pressure
monitoring
Invasive procedure, but:
• Gold standard for real
time haemodynamic
assessment
• Accurate, reliable.
• Immediate warning of
hypo/hypertension of
any aetiology.
39
Nerve stimulator
• 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
Depth of Anaesthesia
monitoring
• 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 w/history of awareness
– Where lightest possible plane
of anesthesia is essential
40
Other monitors
• Central venous line.
- Mostly used for drug
infusions but can also
measure CVP as a (not very
accurate) guide to volume
status.
• Pulmonary artery
(Swann Ganz) catheter
- 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)
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)
• Spirometry
Measurement of pressure
volume loops & hence work
of breathing in controlled,
spont. & ass’t’d ventilation
41
Part IV:
Anaesthetic Equipment
& Airway Management
42
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 or cocktail.
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.
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.
43
A Note of Caution:
• 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.
44
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.
45
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
46
Another rule of three:
The Triad of Resuscitation
A – AIRWAY
B – BREATHING
C – CIRCULATION
Or . . . Alternatively:
(The triad of resuscitation – my own version)
1. Air goes in & out
2. Blood goes round & round
3. Variations on the first two are a BAD THING
47
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.
48
Airway Control – Why?
• Prevent obstruction
Anatomical/foreign body
• Protect against aspiration
Vomit/blood/secretions
• Permit controlled ventilation
For paralysis/deep anaesthesia
Where ventilatory support required
• Enable special manoeuvres
e.g IPPV & PEEP for thoracotomy, laryngeal
surgery with microlaryngeal tube, single lung
deflation with double lumen ET tube.
49
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)
50
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
51
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
52
Rapid Sequence Intubation:
How to do it properly
•
•
•
•
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.
53
Remember (1) : every intubation attempt is a
potential failed intubation.
• You should always have a backup plan
- i.e. a failed intubation drill.
• Backup starts 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
54
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
55
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.
56
Non endotracheal airways II
Advantages of laryngeal masks:
Disadvantages of laryngeal masks
• 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.
• 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.
57
Part V:
Practical Anaesthetic
Pharmacology &
Related Management
58
Classification of drugs used for anaesthesia
•
•
•
•
•
“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.
59
Pharmacology 1:
Inhalational Anaesthetic Agents
•
•
•
•
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.
60
Inhalational anaesthetics in modern
anaesthetic practice include:
• 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.
• Sevoflurane
• Desflurane
• Isoflurane
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.
61
Practical Pharmacology of Inhaled Agents
• 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.
62
Practical Pharmacology of Inhalational Agents (2)
• Sevoflurane has superceded isoflurane as probably the most
widely used, & 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.
63
Practical Pharmacology of Inhalational Agents (3)
• 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.
64
Pharmacology 2:
IV anaesthetic “induction” agents
Used for:
• Induction of anaesthesia
• Sole agent for brief procedures
• By infusion for prolonged procedures in
place of inhaled agents – i.e. total
intravenous anaaesthesia “TIVA”
65
Classification of intravenous agents
•
•
•
•
Barbiturates – Thiopentone
Benzodiazepines – Midazolam
Dissociative agents – Ketamine
Others- Propofol
+ Alpha-2 agonists – Dexmetomidine . . .
maybe “the next big thing”
66
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 used as infusions
(complex pharmacokinetic models)
67
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
68
Other IV agents
•
•
•
•
•
•
•
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!!)
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”
69
Total intravenous anaesthesia
“TIVA”
• 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).
70
TIVA –good & bad
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.
•
•
•
•
Disadvantages
Long setup time
More expensive
Multiple syringe
pumps required
No direct measure of
blood or effect site
concentration
71
Pharmacology 3:
Narcotic Analgesics & Acute Pain
Management
A Definition of Pain:
“An unpleasant localised sensory experience
perceived as implying tissue damage.”
May be acute or chronic
72
Classification of Analgesics
•
•
•
•
•
Conduction blockade
Opiods
Paracetamol
NSAIDs & COX2s
Miscellaneous agents
• Complementary/Non pharmacological
73
An opiod is a drug that exhibits agonist activity at
opiate (endorphin/enkephalin) receptors. A
classification of opiods includes:
• Opiates (naturally occuring constituents of opium)
& their derivatives:
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
74
Properties of opiods
• Analgesia
Spinal ( μ/κ) & supraspinal (μ)
•
•
•
•
•
•
Respiratory depression
Sedation/euphoria (addiction potential)
Emesis
Depression of GI motility
Pruritis
Neuraxial route
predominantly
Urinary retention
}
No difference in respiratory depression between
equi-analgesic doses of any narcotic agonists
75
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
76
Routes of administration of opiods:
• 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
77
Problems with opiods
•
•
•
•
•
•
Respiratory depression/cough suppression
Abuse/addiction potential
Tolerance
Accountability/access/supply
Nausea & vomiting
Constipation
78
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
79
Pharmacology 4:
Neuromuscular blockers
• Purely paralysing agents – no analgesic or
hypnotic activity.
• Two types based on modes of action:
Depolarising (Suxamethonium)
Versus
Nondepolarising
(NDNMBs, several agents)
80
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
81
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
82
“Sux” versus the NDNMBDs
Suxamethonium
Nondepolarisers
• Rapid onset (30s)
• Fasciculations
• Transient rise in ICP,
IOP, IAP/IGP, K+.
• Rapid offset (usually)
• 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
by hydrolysis in plasma
• Unpredictable effects
in repeat dosing
83
Nondepolarising relaxants
First generation
* Curare/tubocurarine
* Alcuronium
* Metocurine
Gallamine
# Pancuronium
“Modern” agents
# Vecuronium
• Atracurium
• cisAtracurium
# Rocuronium
• Mivacurium
* = curare derivatives
# = aminosteroids (the “oniums”)
• = benzisoquinolines (the “uriums”)
84
Side effects of suxamethonium
•
•
•
•
•
•
•
Myalgia
MH trigger
Masseter spasm
Phase II block
Raises ICP
Raises IOP
Bradycardia
– Usually in infants or
with 2nd dose
• Raises serum K+
• Exaggerated action &
K+ rise in denervation,
burns, muscle injury
• Prolonged action with
pseudochlinesterase
variants/deficiency.
• Histamine release
• Anaphylaxis (1:5000)
85
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
86
Paralysis obviously mandates
controlled ventilation
• 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).
87
The Physiology of Controlled Ventilation
“Spontaneous ventilation sucks; Controlled ventilation blows”
• 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.
• Risk of barotrauma – esp. w/high tidal volume or pressures.
88
Pharmacology 5:
Local anaesthetic agents
• 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)
89
“Your friendly local anaesthetic molecule”
Think of a person standing in the water
– keeping their head high & dry
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)
90
“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 91
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)
92
Local Anaesthetic Agents
AGENT
Max dose:
Plain (& +Adr)
Lignocaine (“Xylocaine”)
Bupivicaine (“Marcain”)
Ropivicaine (“Naropin”)
Levobupivicaine (“Chirocaine”)
Prilocaine (Citanest”)
4 (7) mg/kg
2 mg/kg
3-4mg/kg
2-4 mg/kg
7(9) mg/kg
93
Local Anaesthetic Problems
• Failed block
• 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
94
Adjuvant agents used with LAs
• Adrenaline – prolongs blockade, allows increased
dose (lignocaine/prilocaine)
• Bicarbonate – Enhanced buffering speeds onset of
block
• Hyaluronidase –Aids diffusion (Eye & brachial
plexus blocks)
• Glucose (spinals) – to produce hyperbaric solutions
• Narcotics (neuraxial) – synergistic analgesia
• Other analgesics – e.g clonidine in neuraxial blocks.
95
Modes of Local Anaesthesia
(a) Peripheral
• Surface
– Topical (incl EMLA)
– Nebulised
– Intrapleural/peritoneal
• Infitration
• Intravenous regional
• Nerve/plexus blocks
– Multiple types
(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)
96
Some common nerve/plexus blocks
• Eye blocks:
Peribulbar, retrobulbar,
Sub-Tenons
• Superficial cervical
plexus block
• Brachial plexus
blocks:
Axillary, supraclavicular,
interscalene
• Paravertebral blocks
• Intercostal blocks
• Ilio-inguinal block
• Dorsal penile nerve
block
• Pudendal nerve block
• Femoral (+/- LCNT)
block
• Ankle blocks
97
Spinal Anaesthesia
•
•
•
•
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
98
Epidural Anaesthesia
•
•
•
•
•
•
Alone, GA/epidural, or 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
99
Considerations in regional blockade
•
•
•
•
•
•
Consent/communication
IV access
Adjuvant sedation/analgesia
Time involved
Failed block/backup plan
Management of side effects/reactions
100
Part VI:
Sub-specialty Anaesthesia
1.
2.
3.
4.
5.
INCLUDES:
Paediatrics
Obstetrics
Cardiothoracic
ENT/Head & neck
Neurosurgery
101
Subspecialty Anaesthetics A:
Paediatric
“They’re not just small adults”
. . . But . . .
“Nor are they all just big neonates, either”
102
Adult-Paediatric Differences
• Psychosocial
• CNS
• Respiratory
– Airway
– Other
• Cardiovascular
• Renal/fluids
•
•
•
•
•
•
•
Gastrointestinal
Hepatic/metabolic
Endocrine
Haematological
Immunological
Musculoskeletal
Integument
103
The Psychosocial Dimension
• 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: premeds, EMLA,
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.
104
Anatomical Differences 1
• Body proportions
– Head larger – especially occiput
– Limbs smaller
Increased surface area to volume ratio
• CNS differences
Brain & spinal cord relatively larger
105
Anatomical Differences 2: Airway
• Nares (relatively) larger
• Larynx higher
C3 in neonate -> C6 in adult
• Epiglottis longer (&
softer)
• Cricoid ring narrowest
part of airway
106
Respiratory Physiology
• 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.
107
Cardiovascular Physiology
• Fetal circulation
• Postnatal transition
• Haemodynamics
• Autonomic control
108
Blood & body fluids
• Blood volume 80-90 mls/kg (adult ~ 70)
• Birth Hb 180-200 g/L (adult 120-160)
– 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.
• Body water 75-80% in neonate (adult 65%)
• ECF compartment larger than ICF
– (crossover @ ~ 4/12)
109
Temperature
•
•
•
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
110
Heat production & regulation
• Controlled in hypothalamus
• Balances heat loss & heat production
• Heat production
– Shivering
– Metabolic thermogenesis (brown fat)
• Thermoneutral environment;
– Point of minimum O2 consumtion
– e.g. for unclothed term baby is ~ 33°C
111
Subspecialty Anaesthetics B:
Obstetrics
Remember, once again you have two
patients – but this time they are
physically connected
112
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.
113
Differences in Pregnancy
• Psychosocial
• CNS
• Respiratory
– Airway
– Other
• Cardiovascular
• Renal/fluids
•
•
•
•
•
•
•
Gastrointestinal
Hepatic/metabolic
Endocrine
Haematological
Immunological
Musculoskeletal
Integument
114
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
115
Scenarios
• Analgesia for labour
• Anaesthesia for operative delivery
– Emergency
– Semiurgent
– Planned
• Anaesthesia for post partum complications
• Neonatal resuscitation
116
Analgesic options
• 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.
• 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.
117
Anaesthetic Options for Caesarean Section
•
•
•
•
General
Regional
• Technique of choice for
Spinal vs Epidural
emergency LSCS
Spinal quicker –
– Fastest
unless epidural already
– Better in hypovolaemia
in situ & only needing
• Riskier for mother on
top-up.
raw figures, but:
Most mothers want to
– GA population includes
be awake.
failed regionals & most
Beware the failed or
emergency cases.
patchy block.
– So are we comparing
apples to oranges?
No difference (surprisingly) in foetal outcomes between GA &118RA
Subspecialty Anaesthetics C/D:
Cardiothoracic & ENT
What do these surgical disciplines
have in common?
119
Remember the basic rules:
1. Air goes in & out
2. Blood goes round & round
3. Variations on this are a BAD THING
. . . BUT (you knew there had to be a
“but” somewhere, didn’t you) . . .
ENT, thoracic, & cardiac anaesthetics all
require some flexibility of these rules!
120
Anaesthetic A to E in
ENT/Oral Surgery
• Airway - shared with surgeon
• Bleeding – even a small amount into the
airway is a BAD THING
• Children – predominant patient population
• Disruptions – of the airway - always a risk
• Extubation strategies:
– Deep versus awake
121
Airway Management Options in
ENT/Oral Surgery
•
•
•
•
•
•
•
None (!)
Venturi ventilation
Nasal tubes
RAE tubes
MLT tubes
Laryngeal masks (yes!)
Subglottic airway i.e tracheostomy
122
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
123
Lung separation techniques:
For “one lung anaesthesia”
• Endobronchial intubation
(deliberate not inadvertent!)
• Double lumen ET tubes
• Bronchial blockers
• Other (generally bodgie) methods
124
Anaesthetic Factors in
Cardiac Surgery
• Cardiopulmonary bypass
• Cardiopulmonary bypass!
• Cardiopulmonary bypass!!
(Scary, scary, scary stuff)
125
Cardiopulmonary bypass
(“CPB”) for dummies
• Pump plus oxygenator
(“Heart lung machine”)
• Cardioplegia
(High K+ solution to cause cardiac
standstill)
• Hypothermia
(Enables prolonged ischaemic times)
126
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.
127
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
128
Subspecialty Anaesthetics E:
Neurosurgical
It’s not rocket science . . .
. . . but it is brain surgery
129
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.
130
Part VII:
Emergencies, Complications & Problems.
Anaesthetic Emergencies
Anaesthesia for
emergencies
Emergencies from (or
during) anaesthesia
131
A: Emergency Anaesthesia
•
•
•
•
•
•
•
Obstetrics
Trauma
Gen. Surgical
Vascular
Neuro-surgical/-radiological
Cardio-thoracic
Threatened airway
132
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.
133
Emergency Anaesthesia –
Management Principles
• Assessment
• Management plan/scheduling
• Stabilisation & preparation
– If time permits
• Pain management
• Then (& only then) commencement
of anaesthesia
134
Emergency Anaesthesia:
Maintenance
• Includes ongoing resuscitation & Rx
• Monitoring: More not less
• Postanaesthetic management plan?
135
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
136
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
137
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
138
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
139
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).
• Targetting for cost cutting measures by politicians
& managers with consequent shaving of safety
margins.
140
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?!)
141
The Bottom Line
• Safe anaesthesia may not directly 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 want for your patient?
• Think as a health consumer: Isn’t this what
you want for yourself or your family?
142
The End
If you have any questions about the
course material, or about
anaesthesia as a potential career
choice, feel free to contact me:
[email protected]
143