1 Anaesthetics Study Guide UNSW School of Medicine Liverpool Clinical School Critical Care Rotation Blair Munford, BMedSc, MB,ChB, FFARACS, FANZCA Senior.

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Anaesthetics Study GuideAnaesthetics Study Guide

UNSW School of Medicine

Liverpool Clinical School

Critical Care Rotation

Blair Munford, BMedSc, MB,ChB, FFARACS, FANZCA

Senior Specialist Anaesthetist, Liverpool Hospital

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Aims of Anaesthetic AttachmentAims 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.

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Part I:Scope & Development of Scope & Development of

Anaesthetic PracticeAnaesthetic Practice

Imagine a world without Imagine a world without anaesthesia . . .anaesthesia . . .

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What medicine was like prior to the What medicine was like prior to the invention of anaesthesia: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)

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Without anaesthesia . . .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.

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But what exactly But what exactly isis anaesthesia? 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”This is the “Triad of Anaesthesia”

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The other triad of anaesthesiaThe 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.)

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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)

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Classification of Anaesthetics

General Regional

Anaesthesia

Controlledventilation

Spontaneousventilation

Intubated

LMA

Mask

Intubated

Manual

Mechanical

Surface/topical

infiltration

Nerve/plexus block

Spinal blocks

SubarachnoidEpidural:

cervical, thoracic, lumbar, caudal

Single shot, intermittent, continuous

Dissociative

Auditory

Electrical

Hypnosis

Acupuncture

Local anaesthetic, narcotic/adjuvant, combination

AlternativeAlternative

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But wait . . . there’s more:

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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)

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Part II: Perioperative MedicinePerioperative Medicine“The way of the future”

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What What isis perioperative medicine? perioperative medicine?

“Integrated multidisciplinary management of the surgical or procedural patient’s hospital admission & stay.”

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Perioperative system includes: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

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But why?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 ConsultationThe 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.

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Pre-operative preparation may Pre-operative preparation may include premedicationinclude 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 conditionse.g. asthma prophylaxis.

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Most regular medications are continued, Most regular medications are continued, including on the day of surgeryincluding on the day of surgery

Exceptions include:

(a) Oral hypoglycaemics

(b) Antithrombotic agents (mostly)

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ASA Physical StatusASA 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?Relevance of this?

• Risk stratification

• Workload/resource utilisation planning

• Remuneration aspects

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Perioperative (Preanaesthetic) Clinic

Surgical clinic

Nurse Clinic

Checked up, satisfied as fit & suitable

Decides to proceed with planned time, date & procedure

Not certain;sends only case notes to

anaesthetist to review it

Satisfied with it; decides to send it back to her

for mx

Not quite satisfied; takes over review & mx

Decides to further investigate. May cancel, postpone, refer case or

decide to do it

Surgeon refers case

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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

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Based on: History

Examination, Investigation . . .

Decision:

Preanaesthetic Clinic

To do the planned

procedure

To postpone the procedure till fully

investigated optimised

To cancel the procedure

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Part III: Safety & MonitoringSafety & Monitoring

in Anaesthesiain Anaesthesia

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Safety in anaesthesia is paramountSafety 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!

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Safety Initiatives in AnaesthesiaSafety 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.

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Principles of SafetyPrinciples 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.

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“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.

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Monitoring in anaesthesiaMonitoring in anaesthesiaBasic (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

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Pulse oximetryPulse 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 met- haemoglobinaemia, cyanide posoning, etc.

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ElectrocardiogramElectrocardiogram• 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 Remember: it is entirely possible to die with a relatively normal ECG!with a relatively normal ECG!

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Noninvasive arterial blood Noninvasive arterial blood pressure (NIBP) monitoringpressure (NIBP) monitoring

• Usually automated• Convenient but not reliable:• Dependant on correct cuff size & position• Not continuous• Usually under-estimates true hyper-& over-

estimates true hypotensive values.• Interferes with IV infusions & pulse oximetry• Should not be placed on limb with fistula or

lymphoedema.

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CapnographyCapnography• “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

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Oxygen monitoringOxygen 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 N.B. Before adoption/mandating of oxygen monitoring, all reported (& thankfully very rare) monitoring, all reported (& thankfully very rare) “wrong gas” anaesthetic incidents (misconnected “wrong gas” anaesthetic incidents (misconnected pipelines or incorrectly filled cylinders) resulted pipelines or incorrectly filled cylinders) resulted in the death of the first patient exposed in every in the death of the first patient exposed in every case.case.

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Anaesthetic agent monitoringAnaesthetic 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.

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Temperature monitoringTemperature 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

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Airway manometryAirway manometry

• Usually analogue gauge on circle circuit

• Monitors inflation pressure

• With IPPV can help identify:Airway obstruction

Bronchospasm

Circuit leaks/faults

Ventilator monitorVentilator monitor

• Mandatory when mechanical IPPV employed.

• Usually integrated into ventilator w/automatic activation.

• High (overpressure) & low (disconnect) functions

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Precordial stethescopePrecordial 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 Direct arterial pressure monitoringmonitoring

Invasive procedure, but:• Gold standard for real

time haemodynamic assessment

• Accurate, reliable.• Immediate warning of

hypo/hypertension of any aetiology.

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Nerve stimulatorNerve 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 Depth of Anaesthesia monitoringmonitoring

• 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

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Other monitorsOther monitors• Central venous line.Central venous line.

- Mostly used for drug infusions but can also measure CVP as a (not very accurate) guide to volume status.

• Pulmonary artery Pulmonary artery (Swann Ganz) catheter(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 Echo-Trans-Oesphageal Echo-cardiography (TOE)cardiography (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)

• SpirometrySpirometryMeasurement of pressure

volume loops & hence work of breathing in controlled, spont. & ass’t’d ventilation

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Part IV: Anaesthetic EquipmentAnaesthetic Equipment& Airway Management& Airway Management

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Introduction to & Overview of the Introduction to & Overview of the Anaesthetic MachineAnaesthetic 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.

• “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.

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A Note of Caution: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 re-check must be carried out after any such change.

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Anaesthetic CircuitsAnaesthetic CircuitsThree principal types:

1. 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.

2. 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.

3. 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.

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Remember: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

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Another rule of three:The Triad of ResuscitationThe Triad of Resuscitation

A – AIRWAYA – AIRWAY

B – BREATHINGB – BREATHING

C – CIRCULATIONC – 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

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Note that Note that airway always comes firstairway 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.

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Airway Control – Why?Airway Control – Why?• Prevent obstruction

Anatomical/foreign body

• Protect against aspirationVomit/blood/secretions

• Permit controlled ventilationFor paralysis/deep anaesthesia

Where ventilatory support required

• Enable special manoeuvrese.g IPPV & PEEP for thoracotomy, laryngeal

surgery with microlaryngeal tube, single lung deflation with double lumen ET tube.

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Classification of airwaysClassification of airways

SUPRAGLOTTIC TRANSGLOTTIC SUBGLOTTIC

Oropharyngeal airway

Orotracheal tube Cricothyrotomy

Nasopharyngeal airway

Nasotracheal tube Transtracheal jet catheter

Laryngeal Mask Airways (various)

Intubating LMA (w/ETT placed thru it)

Tracheostomy

Combitube/PTL * (85% of placements oesophageal)

(Combitube/PTL) - if one of the 15% placed tracheally

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The winner, and still champion: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

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Emergency Airway ManagementEmergency Airway Management(in anaesthesia (in anaesthesia && resuscitation) resuscitation)

Rapid sequence Rapid sequence intubation intubation

[or unmodified (“cold”) [or unmodified (“cold”) intubation if apnoeic & intubation if apnoeic & arreflexic]arreflexic]

Other techniques:Other techniques:

Fibreoptic intubationFibreoptic intubation

Supraglottic airwaySupraglottic airway

Surgical airwaySurgical airway

>90%>90% 10%10%

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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.

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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

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Supraglottic rescue Supraglottic rescue airway e.g. LMA airway e.g. LMA

SUCCESSFUL?SUCCESSFUL?

Subglottic (surgical) Subglottic (surgical) airwayairway

1.1. Bag mask ventilationBag mask ventilation

2.2. Repeat attempt &/or Repeat attempt &/or alternate technique to alternate technique to intubateintubate

SUCCESSFUL?SUCCESSFUL?

FIRSTLY FIRSTLY MAINTAIN MAINTAIN OXYGENATION!OXYGENATION!

FAILED INTUBATION DRILLFAILED INTUBATION DRILL

CAN YOU MASK VENTILATE? [With Geudels &/or

nasopharyngeal airway if necessary]

NO

NO

YESYES

NO

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Non endotracheal airwaysNon 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:– ClassicClassic (original) & its various copies – reuseable or single use.

– ReinforcedReinforced – kink resistant & more flexible upper lumen to permit alternative positioning after insertion for oral/facial procedures.

– ProsealProseal - second lumen to communicate with oesophagus & allow drainage of gastric contents or placement of gastric tube.

– IntubatingIntubating – modified shape, more rigid, & lacking apeture bars – to enable passage of a special ET tube through it.

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Non endotracheal airways IINon endotracheal airways II

Advantages 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.

Disadvantages of laryngeal masks

• 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.

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Part V: Practical Anaesthetic Practical Anaesthetic

Pharmacology &Pharmacology &

Related ManagementRelated Management

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Classification of drugs used for anaesthesiaClassification 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.

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Pharmacology 1:Inhalational Anaesthetic AgentsInhalational 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.

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• Nitrous oxideNitrous oxide (N20N20)– 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.

• SevofluraneSevoflurane• DesfluraneDesflurane all liquids that are flourinated ethers• IsofluraneIsoflurane

Earlier volatile agents such as ether, chloroform & halothane have been superceded due to issues such as flammability, slow recovery, & toxicity.

Inhalational anaesthetics in modern Inhalational anaesthetics in modern anaesthetic practice include:anaesthetic practice include:

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Practical Pharmacology of Inhaled AgentsPractical Pharmacology of Inhaled Agents

• Used for induction sometimes (predominantly in children) & Used for induction sometimes (predominantly in children) & maintenance of anaesthesia in the majority of cases - either maintenance of anaesthesia in the majority of cases - either alone, or in combination with narcotics & muscle relaxantsalone, 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 In contrast, nitrous oxide is analgesic, but doesn’t decrease muscle tone, and is a poor hypnotic except at very high (i.e. muscle tone, and is a poor hypnotic except at very high (i.e. hypoxic) concentrations.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.

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Practical Pharmacology of Inhalational Agents (2)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 All currently used agents have relatively low solubility in blood & tissue – meaning that their partial pressures rise & blood & tissue – meaning that their partial pressures rise & fall quickly, producing more rapid induction & emergence.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.

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Practical Pharmacology of Inhalational Agents (3)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 Volatile agents are delivered by vapourisers – devices which add a precise percentage of vapour to the gas mixture. Modern add a precise percentage of vapour to the gas mixture. Modern vapourisers are agent specific and colour coded/labelled vapourisers are agent specific and colour coded/labelled accordingly. They have numerous mechanisms to ensure accordingly. They have numerous mechanisms to ensure accurate delivery, plus safety measures such as “keyed” filling accurate delivery, plus safety measures such as “keyed” filling systems that match only the correct bottle; and machines that systems that match only the correct bottle; and machines that can have more than one vapouriser fitted must have interlocks can have more than one vapouriser fitted must have interlocks that prevent more than one being turned on. that prevent more than one being turned on.

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Pharmacology 2: IV anaesthetic “induction” agentsIV 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”

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Classification of intravenous agentsClassification of intravenous agents

• Barbiturates – Thiopentone

• Benzodiazepines – Midazolam

• Dissociative agents – Ketamine

• Others- Propofol

+ Alpha-2 agonists – Dexmetomidine . . . maybe “the next big thing”

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General features of IV agentsGeneral 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)

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PropofolPropofol

• 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 agentsOther IV agentsTHIOPENTONE

• 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”

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Total intravenous anaesthesiaTotal intravenous anaesthesia“TIVA”“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).

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TIVA –good & badTIVA –good & bad

AdvantagesAdvantages• 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.

DisadvantagesDisadvantages• Long setup time• More expensive• Multiple syringe

pumps required• No direct measure of

blood or effect site concentration

72

Pharmacology 3: Pharmacology 3: Narcotic Analgesics & Acute Pain Narcotic Analgesics & Acute Pain

ManagementManagement

A Definition of Pain:

“An unpleasant localised sensory experience perceived as implying tissue damage.”

May be acute or chronic

73

Classification of AnalgesicsClassification of Analgesics

• Conduction blockade

• Opiods

• Paracetamol

• NSAIDs & COX2s

• Miscellaneous agents• Complementary/Non pharmacological

74

An An opiodopiod is a drug that exhibits agonist activity at is a drug that exhibits agonist activity at opiate (endorphin/enkephalin) receptorsopiate (endorphin/enkephalin) receptors. A . A

classification of opiods includes: classification of opiods includes:

• Opiates (naturally occuring constituents of opium) & their derivatives:e.g. morphine, codeine, diamorphine (heroin)

• Synthetic opiodse.g. pethidine, fentanyl cogeners, oxycodone

• Partial agonistse.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

75

Properties of opiodsProperties of opiods

• AnalgesiaSpinal ( μ/κ) & supraspinal (μ)

• Respiratory depression• Sedation/euphoria (addiction potential)• Emesis• Depression of GI motility• Pruritis• Urinary retention

No difference in respiratory depression between No difference in respiratory depression between equi-analgesic doses of any narcotic agonistsequi-analgesic doses of any narcotic agonists

}} Neuraxial route Neuraxial route predominantlypredominantly

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So the differences between opiods are So the differences between opiods are less in their analgesic efficacy than in:less in their analgesic efficacy than in:

• Onset

• Duration

• Potency/dose

• Histamine release

• Autonomic effects

• Chest wall rigidity

• Effective routes of administration

77

Routes of administration of opiods: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

78

Problems with opiodsProblems with opiods

• Respiratory depression/cough suppression

• Abuse/addiction potential

• Tolerance

• Accountability/access/supply

• Nausea & vomiting

• Constipation

79

Multimodal analgesia optionsMultimodal 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

80

Pharmacology 4:Neuromuscular blockersNeuromuscular blockers

• Purely paralysing agents – no analgesic or hypnotic activity.

• Two types based on modes of action:

Depolarising (Suxamethonium)

Versus

Nondepolarising

(NDNMBs, several agents)

81

Why use paralysing drugs at all?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

82

Properties of NMBDsProperties 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

83

““Sux” versus the NDNMBDsSux” versus the NDNMBDs

Suxamethonium• Rapid onset (30s)• Fasciculations• Transient rise in ICP,

IOP, IAP/IGP, K+.• Rapid offset (usually)

by hydrolysis in plasma

• Unpredictable effects in repeat dosing

Nondepolarisers• 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

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Nondepolarising relaxants

First generationFirst generation

* Curare/tubocurarine

* Alcuronium

* Metocurine

Gallamine

# Pancuronium

““Modern” agentsModern” agents

# Vecuronium• Atracurium• cisAtracurium

# Rocuronium• Mivacurium

* = curare derivatives* = curare derivatives

# = aminosteroids (the “# = aminosteroids (the “oniumsoniums”)”)

• = benzisoquinolines (the “= benzisoquinolines (the “uriumsuriums”)”)

85

Side effects of suxamethoniumSide 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)

86

Problems with nondepolarisersProblems 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

87

Paralysis obviously mandates Paralysis obviously mandates controlled ventilationcontrolled 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).

88

The Physiology of Controlled VentilationThe 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.

89

Pharmacology 5:Local anaesthetic agentsLocal 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)

90

““Your friendly local anaesthetic molecule”Your friendly local anaesthetic molecule”Think of a person standing in the water Think of a person standing in the water

– keeping their head high & dry– keeping their head high & dry

• 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)

NNH+

A-A-

91

NN NN

ECFECF

NNH+

ICFICF

““The voyage of the molecule Lignocaine”The voyage of the molecule Lignocaine”

Cl-Cl-NN

H+

Lignocaine Lignocaine hydrochloride injectedhydrochloride injected

HCO3-

H2O + CO2

Tissue Tissue bufferingbuffering

Freebase lignocaine diffuses across cell membrane

H+

Lower Lower intra-intra-cellular pH cellular pH leads to re-leads to re-ionizationionization

Sodium channel

92

Understand this, and you will know: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)

93

Local Anaesthetic AgentsLocal Anaesthetic Agents

AGENT

Lignocaine (“Xylocaine”)

Bupivicaine (“Marcain”)

Ropivicaine (“Naropin”)

Levobupivicaine (“Chirocaine”)

Prilocaine (Citanest”)

Max dose:Plain (& +Adr)

4 (7) mg/kg

2 mg/kg

3-4mg/kg

2-4 mg/kg

7(9) mg/kg

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Local Anaesthetic ProblemsLocal Anaesthetic Problems

• Failed block • High block (spinals/epidurals)• CNS toxicity

– at high dose or with inadvertent IV injection

• Selective cardiotoxicity (bupivicaine)(bupivicaine)

• Needle/injection trauma– Nerve damage– Other – e.g pneumothorax

95

Adjuvant agents used with LAsAdjuvant 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.

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Modes of Local AnaesthesiaModes of Local Anaesthesia

(a) Peripheral(a) Peripheral• Surface

– Topical (incl EMLA)

– Nebulised

– Intrapleural/peritoneal

• Infitration• Intravenous regional• Nerve/plexus blocks

– Multiple types

(b) Neuraxial(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)

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Some common nerve/plexus blocksSome 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

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Spinal AnaesthesiaSpinal 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- Vasodilatation @ T12 & up

- Bradycardia @ T4 & up- Bradycardia @ T4 & up

99

Epidural AnaesthesiaEpidural 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

100

Considerations in regional blockadeConsiderations 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 AnaesthesiaSub-specialty Anaesthesia

INCLUDES:

1. Paediatrics

2. Obstetrics

3. Cardiothoracic

4. ENT/Head & neck

5. Neurosurgery

102

Subspecialty Anaesthetics A: Subspecialty Anaesthetics A: PaediatricPaediatric

“They’re not just small adults”

. . . But . . .

“Nor are they all just big neonates, either”

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Adult-Paediatric DifferencesAdult-Paediatric Differences

• Psychosocial

• CNS

• Respiratory– Airway– Other

• Cardiovascular

• Renal/fluids

• Gastrointestinal

• Hepatic/metabolic

• Endocrine

• Haematological

• Immunological

• Musculoskeletal

• Integument

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The Psychosocial DimensionThe 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.

105

Anatomical Differences 1Anatomical Differences 1

• Body proportions– Head larger – especially occiput– Limbs smaller

Increased surface area to volume ratio

• CNS differencesBrain & spinal cord relatively larger

106

Anatomical Differences 2: AirwayAnatomical Differences 2: Airway

• Nares (relatively) larger• Larynx higher

C3 in neonate -> C6 in adult

• Epiglottis longer (& softer)

• Cricoid ring narrowest part of airway

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Respiratory PhysiologyRespiratory 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.

108

Cardiovascular PhysiologyCardiovascular Physiology

• Fetal circulation

• Postnatal transition

• Haemodynamics

• Autonomic control

109

Blood & body fluidsBlood & 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)

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TemperatureTemperature

• Infants at higher risk of hypothermia• Higher surface area to volume ratio• Remember the four modes of heat loss:

1. Conduction2. Convection3. Radiation4. Evaporation

All four occur more when the surface area to volume ratio is higher

111

Heat production & regulationHeat 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

112

Subspecialty Anaesthetics B: ObstetricsObstetrics

Remember, once again you have two patients – but this time they are

physically connected

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PrinciplesPrinciples

• 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.

114

Differences in PregnancyDifferences in Pregnancy

• Psychosocial

• CNS

• Respiratory– Airway– Other

• Cardiovascular

• Renal/fluids

• Gastrointestinal

• Hepatic/metabolic

• Endocrine

• Haematological

• Immunological

• Musculoskeletal

• Integument

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Drugs & the PlacentaDrugs & the Placenta

General rule: If it crosses the blood General rule: If it crosses the blood brain barrier, it crosses the placenta!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

116

ScenariosScenarios

• Analgesia for labour

• Anaesthesia for operative delivery– Emergency– Semiurgent– Planned

• Anaesthesia for post partum complications

• Neonatal resuscitation

117

Analgesic optionsAnalgesic options

• Inhalational – N2O as Entonox (50:50 N20/O2) or via blender (up to 70% N2O – Caution!)

• NarcoticsNarcotics– 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.

118

Anaesthetic Options for Caesarean SectionAnaesthetic Options for Caesarean Section

Regional• 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.

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 & RANo difference (surprisingly) in foetal outcomes between GA & RA

119

Subspecialty Anaesthetics C/D:Cardiothoracic & ENTCardiothoracic & ENT

What do these surgical disciplines have in common?

120

Remember the basic rules: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 ENT, thoracic, & cardiac anaesthetics all require some flexibility of these rules!require some flexibility of these rules!

121

Anaesthetic A to E in Anaesthetic A to E in ENT/Oral SurgeryENT/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

122

Airway Management Options in Airway Management Options in ENT/Oral SurgeryENT/Oral Surgery

• None (!)• Venturi ventilation• Nasal tubes• RAE tubes• MLT tubes• Laryngeal masks (yes!)• Subglottic airway i.e tracheostomy

123

Anaesthetic Factors in Anaesthetic Factors in Thoracic SurgeryThoracic 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

124

Lung separation techniques:Lung separation techniques:For “one lung anaesthesia”For “one lung anaesthesia”

• Endobronchial intubation(deliberate not inadvertent!)

• Double lumen ET tubes

• Bronchial blockers

• Other (generally bodgie) methods

125

Anaesthetic Factors in Anaesthetic Factors in Cardiac SurgeryCardiac Surgery

• Cardiopulmonary bypass

• Cardiopulmonary bypass!

• Cardiopulmonary bypass!!

(Scary, scary, scary stuff)

126

Cardiopulmonary bypass Cardiopulmonary bypass (“CPB”) for dummies(“CPB”) for dummies

• Pump plus oxygenator(“Heart lung machine”)

• Cardioplegia(High K+ solution to cause cardiac

standstill)

• Hypothermia(Enables prolonged ischaemic times)

127

Problems with CPBProblems 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.

128

Other Anaesthetic Factors in Other Anaesthetic Factors in Cardiac SurgeryCardiac 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

129

Subspecialty Anaesthetics E:NeurosurgicalNeurosurgical

It’s not rocket science . . .

. . . but it is brain surgery

130

Special considerations in Special considerations in neurosurgical anaesthesia: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.

131

Anaesthetic Emergencies

Anaesthesia Anaesthesia forfor emergenciesemergencies

Emergencies Emergencies fromfrom (or (or during) anaesthesiaduring) anaesthesia

Part VII: Emergencies, Complications & Problems.Emergencies, Complications & Problems.

132

A: Emergency AnaesthesiaA: Emergency Anaesthesia

• ObstetricsObstetrics

• TraumaTrauma

• Gen. SurgicalGen. Surgical

• VascularVascular

• Neuro-surgical/-radiologicalNeuro-surgical/-radiological

• Cardio-thoracicCardio-thoracic

• Threatened airwayThreatened airway

133

Considerations in Considerations in Emergency AnaesthesiaEmergency Anaesthesia

First: How much of an emergency is it, First: How much of an emergency is it, really? Then:really? Then:

• Airway assessment • Cardio-respiratory status• Full stomach/fasting status• Pre-existing medical conditions• Medications/allergiesAssessment may itself be difficult because

of haste, patient compromise, etc.

134

Emergency Anaesthesia – Emergency Anaesthesia – Management PrinciplesManagement Principles

• Assessment

• Management plan/scheduling

• Stabilisation & preparation– If time permits

• Pain management

• Then (& only then) commencement of anaesthesia

135

Emergency Anaesthesia: Emergency Anaesthesia: MaintenanceMaintenance

• Includes ongoing resuscitation &Includes ongoing resuscitation & RxRx

• Monitoring: More not lessMonitoring: More not less

• Postanaesthetic management plan?Postanaesthetic management plan?

136

B: Anaesthetic Emergencies B: Anaesthetic Emergencies & Complications& 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

137

Post Operative Nausea & VomitingPost Operative Nausea & Vomiting (PONV)

“The Big Little Problem”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

138

Treatment approach to PONVTreatment approach to PONVPrevention 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

139

Anaesthetic Risk In PerspectiveAnaesthetic 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

140

The figures are good but may lead to: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.

141

The Eternal TriangleThe Eternal Triangle(In all health services, not just anaesthetics)

QUALITYQUALITY

ECONOMYECONOMYQUANTITYQUANTITY

(And if one of these is economy, are (And if one of these is economy, are you sure it’s not a false economy?!)you sure it’s not a false economy?!)

Pick Pick any any two!two!

142

The Bottom LineThe 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?

143

The EndThe 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]