17-18 Chong Kar Mun's Anaesthesia Notes

Anaesthesia
Chong Kar Mun

INTRODUCTION TO ANAESTHESIA
!
introduction!
Perioperative Care Medicine

- Preoperative assessment clinic
- Anaesthesia/sedation outside OT e.g. MRI
- Pain Mx:
• Acute pain service: if predicted to have a lot of pain post-operatively
• Pain clinic: chronic pain e.g. neuropathic pain
techniques!
Local Anaesthesia
Warn patient that he will not feel sharp stimulus but will still feel pressure
Regional Anaesthesia
General Anaesthesia
RA v.s. GA: depends on patient, patient preference, doctor’s preference
Combination
E.g. TKR: spinal for operation itself, femoral nerve block for post-op analgesia
Monitored Anaesthesia Care
Chong Kar Mun Class of 2019 2

PRE-OPERATIVE ASSESSMENT & MANAGEMENT
!
introduction!
Questions to Answer
- Indication and urgency of Sx? à elective v.s. semi-urgent v.s. emergency (within 24-48h) cases
• Easier to optimise elective surgeries
• Risks v.s. benefits
- Surgical and anaesthetic risks? Is the patient in an optimal state for Sx? What can I do to optimise patient?
• Surgical: bleeding, location of Sx e.g. tonsillectomy
• Anaesthetic: airway, systemic (cardiovascular, respiratory, metabolic/endocrine, others)
• If uncontrolled HTN and elective Sx, send to polyclinic to start on anti-hypertensives and control 1st
Pre-Operative Visit
- Assess risks of anaesthesia via Hx, PE and inx
- Formulate anaesthetic plan and discuss with surgeons and patient
• Monitoring: arterial line, CVP
- Inform patient of expected risks
- Optimise patient prior to Sx
American!society!of!anaesthesiology!(asa)!grading!
Class Description Mortality Rate (%)

I Completely healthy fit patient with no medical problems 0.001
II Mild systemic illness with no functional limitation, no 0.002
end-organ damage, well-controlled
III Severe systemic illness with functional limitation, end- 0.03
organ damage, poorly controlled
IV Incapacitating systemic illness that’s a constant threat to 0.3
life
V Moribund patient not expected to live within 24h with or 6.2
w/o Sx
E Emergency Sx: don’t have time to optimize pre-existing
comorbidities, higher risk of peri-op complications
Not really to predict peri-op risks or post-op

complications, but more to communicate status of
patient to other physicians + where patient will go after
Sx (e.g. home, general ward, ICU)

history!
Basics
- Presenting complaint
- Past medical and surgical Hx, drug allergies
- Systemic illnesses: CVS, respi, endocrine, coagulation issues, OSA
- Smoking, alcohol: alcohol can induce liver enzymes so may need higher concs of drugs sometimes
Unique to Anaesthesia
- Past anaesthesia records: airway complications during previous anaesthesia (e.g. Hx of trauma during previous
airway Mx to patient’s lips, teeth, gums or mouth may indicate presence of difficult airway, Hx of multiple
attempts, Hx of being awake during previous intubations)
- Family related anaesthesia issues i.e. malignant hyperthermia
- Hx of URTI: airways are more hypersensitive so agents given can trigger bronchospasm, especially if Hx of
asthma and/or smoking
• Must be totally symptom-free for at least 2 weeks in practice, 6 weeks on paper
• Risks v.s. benefits
- Cardiovascular: determine patient’s cardiorespiratory reserves based on functional capacity and effort
tolerance (e.g. in terms of METS: metabolic equivalent activity)
- Hx of OSA: patient to go to HDU after Sx and not general ward as OSA will be worse at night because of side
effects of anaesthesia so need closer monitoring
- Other medical Hx: recent Hx of facial trauma or Sx, rheumatoid arthritis, epiglottitis, neck masses, Down’s
syndrome with facial abnormalities
- Current medications
- Last meal: avoid regurgitation and aspiration. Should fast even for regional anaesthesia cause may be
converted to GA. Usually done for at least 8 hours for elective cases (sometimes just ask patient to be fasted
after 12 midnight cause patients may be pushed up if previous cases cancelled), at least 6 hours for emergency
cases
- Smoking:
• Carbon monoxide binds to Hb, forming carboxyhaemoglobin, shifting O2-dissociation curve to left à
harder to unload O2 to tissues so poorer wound healing
• Nicotine causes vasoconstriction à SVR increases; BP will plunge if drugs given cause vasodilation
• Laryngospasm and bronchospasm
• Quitting smoking should ideally be done 4-6 weeks before Sx, if not at least 48-72h before. If stop later
than that, may cause rebound mucus production and plugging.
- Pregnancy: 1st trimester: some drugs can be teratogenic, 3rd trimester: stresses like Sx can cause pre-term
labour or intrauterine death
Physical!examination!
Basics
- Baseline vital signs
- General physical examination: alert or drowsy, comfortable or respiratory distress
- CVS: esp any murmurs, carotid bruit
- Respiratory
- Neurology:
• To check for any pre-existing nerve injures
• Post-operative delirium/cognitive issues
• Consent may be a problem
- Specific examination required depending on patient’s condition
Unique to Anaesthesia
- Airway evaluation :
• Look externally for gross features predictive of difficult mask ventilation or intubation e.g. facial
trauma, beard, large tongue, neck masses, edentulous

• Mallampati classification: check relative size of tongue
to size of oral cavity:
o Class I: complete visualization of soft palate
o Class II: complete visualization of uvula
o Class III: visualization of only base of uvula
o Class IV: soft palate not visible at all
o Corresponds with Cormack and Lehane
laryngoscopic view grade:
§ Grade 1: full view of glottis
§ Grade 2: partial view of glottis
§ Grade 3: only epiglottis seen
§ Grade 4: neither glottis or epiglottis
seen
• 3:3:2 rule:
o 3 fingers fit in interincisor distance in mouth opening
o 3 fingers fit in space from mentum to hyoid bone under chin
o 2 fingers fit in thyromental distance from chin to thyroid cartilage à floor of mouth adequate
in size to accommodate tongue
• Length and thickness of neck
• ROM of head and neck/neck mobility: whether patient can touch tip of chin to chest or extend neck
- Venous access: e.g. can’t have venous access and do nerve block if overlying skin problems like cellulitis
- Regional anaesthesia anatomy
- Loose teeth and dentition:
• Usually ask patient to move it himself to see if it’s loose
• KIV take out during airway manipulation if may aspirate teeth
• Otherwise, usually don’t take it out and refer to Dental
investigations!
General
- ASA I adults <50 yo: no inx required
- ASA I adults >50 yo: FBC, UECr, ECG
- ASA I adults >60 yo: FBC, UECr, ECG, CXR
• CXR usually not done cause pick-up rate is low, unless thoracic Sx, smoker, COPD
- All other ASA status: inx as needed:
• HBA1c, ABG, PT/PTT, LFT, trop I
• CXR, ECG: valid for 1 year if no change in status
• FBC, UECr: valid for 6 months
- Consent and GXM need to be done again if Sx postponed
Case!examples!
Diabetes
- History: any end-organ damage, glycemic control, any fainting spells
- Physical examination: vitals, peripheral vascular disease
- Inx: HbA1c
COPD
- History: effort tolerance, smoking, URTI or pneumonia episodes
- PE: use of accessory muscles of respiration, colour, auscultation (crepitations, wheezing)
- Inx: baseline saturation, ABG, spirometry, peak respiratory flow rate
- Pre-op instructions: don’t go to crowded areas to get URTI, quit smoking
IHD
- PE: signs of heart failure, auscultate carotid for bruit

- Inx: to evaluate effort tolerance, perfusion scan, 2DE
- Sartans tend to interact with anaesthetic drugs and can cause BP to plunge and stay low, so some
anaesthetists may ask for them to be stopped, but may cause rebound hypertension so risks v.s. benefits
informed!anaesthesia!consent!
- Discuss with patient types of anaesthetic options available for planned procedure
- Inform patient risks and benefits in anaesthetic plan e.g. infection and bleeding if regional technique,
peripheral nerve injury due to improper patient positioning intraoperatively (ulnar nerve most commonly
injured), post-operative N/V, dental injury, risk of hepatitis and HIV from blood transfusions, awareness under
anaesthesia, need for post-operative mechanical ventilation if patient fails to meet extubation criteria after Sx
- Signing of legal document/consent form

AIRWAY MODULE
!
Bag-valve-mask!ventilation!
Introduction
- Used as a temporising measure before definitive airway Mx
- Used to oxygenate and ventilate patients who are apnoeic from GA induction agents
- Ventilation is more important than intubation, as failure of intubation can cause airway edema and airway to
be non-ventilatable
Assembly of Equipment (Self-inflating Bag-Valve-Mask System)

- Wear gloves!
- Attach 1 way valve mouth piece to self-inflating bag
- Attach intake reservoir valve to self-inflating bag
- Check integrity of 1 way valve: right hand below 1 way valve
mouth piece, 1 hand squeezing self-inflating bag
- Attach reservoir bag to the intake reservoir valve: sometimes
when one needs to bag fast, O2 flow may not be fast enough so at
least there’s a backup where 100% O2 can be drawn from
- Attach oxygen tubing on same side as reservoir bag
- Connect other end of oxygen tubing to oxygen source
- Dial up oxygen flow and watch reservoir bag being filled up: high flow, 12-15L on wall
Bag-Valve-Mask Ventilation
- Select appropriately-sized face mask: should cover below patient’s lower lip and extend up to nosebridge,
avoid globe of eyes
- Optimise head position (ensure patient’s head at edge of bed and adjust height of bed)
- Check for cervical injury and instability
- Use head tilt-chin lift technique to open up airway
- Assess airway by looking out for loose or missing teeth and dentures. Remove FBs and secretions with care if
present.
- Place selected mask over mouth and nose, avoiding pressure on eyes
- Achieve adequate mask seal using thumb and index finger to form C shape on mask while middle and ring
fingers placed along patient’s mandible, hold angle of mandible with little finger. Avoid digging fingertips into
submandibular space as this can cause submandibular bruising, tissue swelling and displace tongue upwards
into oropharynx causing upper airway obstruction.
- Maintain airway patency by maintaining head tilt-chin lift maneuver à morning air sniffling position to align
the 3 axes (oral axis, pharyngeal axis, laryngeal axis). For obese patients, stack pillows to elevate sternal level to
where mouth position is.
- Ventilate by squeezing self-inflating bag
• Don’t hyperventilate à 8-12 breaths/min
• 6ml/kg, 1 bag ~ 1L
Sub-optimal Ventilation (Poor Chest Rise)

- Ensure seal of face mask is adequate
- Reposition fingers or adjust patient’s head position
- Use airway adjuncts to help hold upper airway open: oropharyngeal airway, nasopharyngeal airway
- 2 person bagging technique:
• 1 person to place both thumbs firmly on side of mask and apply gentle inward and downward pressure,
place other fingers along mandible to exert upward (not downwards as can flex neck and cause chin to
point downwards causing upper airway obstruction) pressure to maintain jaw thrust anteriorly,
assistant helps ventilate by squeezing bag
Oropharyngeal!airway/GUEDEL’S!AIRWAY!

- Sizing can be done from corner of mouth to angle of mandible (or tragus of ear)
- Careful of dislodging loose teeth
- Bite block is present in case patient bites on oropharyngeal airway and causes obstruction
- 2 methods of insertion:
• Insert between hard palate and tongue and advance until tip rests between base of tongue and
posterior pharyngeal wall
• Insert upside down and rotate 180° as it advances posteriorly
• Beware of pushing tongue into base of pharynx and of causing injury to patient’s lips, gums, teeth and
tongue
Nasopharyngeal!airway!
- Sizing done from nares to tragus of ear to angle of mandible (correlating with external anatomy
of face and neck)
- More comfortable for the patient, can bypass falling back of soft palate and tongue, but causes
epistaxis and can still cause gagging. Never insert in head trauma as it may enter soft cribriform
plate in basilar skull # and enter cranium instead of airway.
- Lubricate thoroughly
- Advance perpendicularly to face and parallel to floor of nose and never towards roof of nose/BOS
- Insert slowly and smoothly with firm pressure; don’t persist if resistance encountered as epistaxis is potential
complication
laryngeal!mask!airway!
Characteristics
- Described as the missing link between face mask and endotracheal tube,
reduced rates of endotracheal intubation
- Inserted blindly w/o direct vision
- Can use in latex allergy as latex-free
- Cups laryngeal inlet to provide seal
- Increased speed and ease of insertion
- Lowers incidence of cough on emergence
- Doesn’t protect lungs from aspiration of gastric contents
Steps
- Equipment needed: LMA, syringe, lubricating agent, BVM system, stethoscope, Easy Cap ETCO2 device
- Choose appropriately-sized LMA: 70-100 kg: #5, Asian males: #4, Asian females: #3
- Check integrity of cuff and pilot balloon by inflating and deflating
- Lubricate LMA on posterior surface with water-based gel
- Prepare oxygen source and suction apparatus
- Optimise head position and maintain airway patency using head tilt-chin lift technique
- Exclude FBs and secretions in airway
- Ensure pre-oxygenation with bag-valve-mask ventilation (15L of air for 3-5 min) and observe for equal chest
rise
- Hold LMA like a pen between thumb and index finger at junction of cuff and tube, cuff lumen should be facing
forward. Carefully insert in midline pressing cuff against hard palate and following curve to soft palate and back
of pharynx until resistance is encountered.
- Can use finger to push tongue away if in the way
- Teeth should be on bite block, black line (not radio-opaque) should be facing nose to tell you that you have
inserted it correctly
- Inflate LMA cuff with 30ml of air
- Connect LMA to oxygen source
- Confirm correct placement of LMA by bag-valve ventilation and looking for equal chest rise and 5-point
auscultation (start from epigastrium, L and R top anterior chest, L and R bottom mid-axillary)

- Use Easy Cap ETCO2 device to detect CO2 (litmus paper changes colour from purple to yellow) or quantitative
waveform
- Others: rhythmical fogging of ETT, improvement in saturation
- Secure LMA with tape, taping from maxilla to other
- Can check and adjust LMA cuff pressure using pressure gauge: should be <60 cm H2O
Complications
- Malposition
- Pharyngeal abrasion
- Dislodgement of loose teeth
- Sore throat
endotracheal!intubation!
Assembly of Equipment
- Equipment needed: laryngoscopy blade, ETT, stylet, syringe, lubricating agent, BVM
system, stethoscope, Easy Cap ETCO2 device
- Assemble laryngoscope by attaching blade to handle. Ensure light source is working well.
• Most commonly used laryngoscopy blades: Macintosh 3 (curved), Miller 2
(straight)
- Check ETT: check integrity of cuff and pilot balloon by inflating and deflating
• Sizing refers to internal diameter
o Asian males: size 8-8.5, Asian females: size 7-7.5, children <10yo:
size = age/4 + 4
• Murphy’s eye provides alternative escape route in case there’s distal
obstruction at end of ETT
• Radio-opaque line allows visualization on X-ray later on
- Lubricate cuff
- Stylet may be used
Steps
- Prepare oxygen source and suction apparatus
- Optimise head position and maintain airway patency using head tilt-chin lift technique
- Exclude FBs and secretions in airway
- Ensure pre-oxygenation with bag-valve-mask ventilation and observe for equal chest rise
- Remove oropharyngeal airway if present
- Keep patient’s mouth open using right hand and fingers
- Using left hand, insert laryngoscope from right side of patient’s mouth and displace patient’s tongue to left
- Advance laryngoscope to place tip of blade at valleculae. Ensure that patient’s lips are not caught between
blade and teeth.
- Lift laryngoscope upwards and away from you to visualize glottis opening via direct line of vision
- Hold distal tip of endotracheal tube using right hand like a pen and gently insert from patient’s right side
- Pass ETT through glottis opening into vocal cords, advance until black line crosses vocal cords
• Note centimeter marking of ETT at patient’s incisor or gums if endentulous; usually 21-22 mm marking
in adults à this means that ETT is ~3-4 cm above bifurcation at carina
• Some brands have 2 black markings to tell you that the 1st one should cross vocal cords but 2nd one
shouldn’t
- Remove laryngoscope and stylet
- Inflate ETT cuff with 4ml of air
- Connect ETT to oxygen source
- Confirm correct placement of ETT by bag-valve ventilation and looking for equal chest rise and 5-point
auscultation (start from epigastrium, L and R top anterior chest, L and R bottom mid-axillary)
- Use Easy Cap ETCO2 device to detect CO2 (litmus paper changes colour from purple to yellow) or quantitative
waveform
- Others: rhythmical fogging of ETT, improvement in saturation

- Secure ETT position with tape
- Can check and adjust endotracheal cuff pressure using pressure gauge: should be in green zone (20-40 mmHg,
usually shouldn’t exceed 30 mmHg)
Complications
- Endobronchial intubation à withdraw ETT
à Collapse of non-ventilated lung, hypoxia
à Hyperinflation of ventilated lung, pneumothorax
- Esophageal intubation
- Sore throat, dental damage, dislodgment of loose teeth, laceration (lip, gums, tongue, pharynx, vallecula,
esophagus), voice hoarseness
- Laryngospasm, bronchospasm
LMA!v.s.!ETT!
- ETT requires use of laryngoscope so harder to insert. Also more invasive, may damage larynx or cause local
ischemia.
- LMA is supraglottic while ETT is infraglottic
- LMA does not provide complete seal (unlike ETT which forms seal between it and tracheal wall) so can’t
completely protect airway, can cause gastric insufflation and aspiration of gastric contents into airways
- Hence, traditionally, ETT is used in patients with higher risk of aspiration e.g. pregnant
(3rd ± 2nd trimester), obesity (some anesthetists use BMI as cut-off), Hx of severe GERD,
laproscopy (pneumoperitoneum i.e. gas insufflation of abdomen needed) and
intraabdominal surgeries cause increased intraabdominal pressure. Traditionally, ETT
also used in patients having surgeries in prone position as LMA may be malpositioned.
- But depends on anesthetist’s preference
- Nowadays, challenging traditional boundaries and use of ProSeal (double lumen with
orogastric tube [Ryle’s tube] inserted in other lumen for continuous suction to prevent
gastric insufflation) has caused LMA to be used more often
oxygen!delivery!devices!
Nasal Cannula
- Hook around ears
- Formula of FiO2 (inspiratory oxygen fraction) = 21% + (4 x O2 flow rate) = 24-40% (max is 40%)
- Oxygen flow: 0.5-5 L/min, usually 1-2 L/min
- FiO2 is influenced by patient’s breathing rate, depth and pattern and tidal volume/inspiratory flow
- Patient must be awake and breathing spontaneously; unsuitable for patients who are predominantly mouth
breathers, impending cardiopulmonary collapse or severe respiratory distress
- Advantages: easy to set up, cheap, well-tolerated, doesn’t impede speech/drinking/eating
- Disadvantages: inability to control FiO2 precisely (variable performance), unable to provide FiO2 of >40%
Simple Face Mask/Hudson’s Mask

- Fit from nose bridge to chin, strap around head using elastic bands
- FiO2: 40-60% (max is <50+%)
- Oxygen flow: 5-10 L/min, at least 5 L/min
- FiO2 is influenced by patient’s breathing rate, depth and pattern and tidal
volume/inspiratory flow
- Patient must be awake and breathing spontaneously
- Advantages: easy to set up, provides higher FiO2 than nasal cannula, can use for
mouth breathers, patients with nasal irritation or epistaxis

- Disadvantages: inability to control FiO2 precisely (variable performance), obtrusive/uncomfortable/confining,
impedes speech/drinking/eating
Non-Rebreather Mask
- Simple face mask + reservoir bag filled with 100% O2
- FiO2: rarely exceeds 80% in practice
- Oxygen flow: 8-10 L/min
- Advantages: highest FiO2 among the variable performance systems (useful in emergency situations where high
FiO2 needed for short durations)
- Disadvantages: prolonged use predisposes to basal atelectasis (100% O2 in alveoli will be resorbed, no N2 left
to splint diaphragm) so only temporizing measure while you find cause, obtrusive/uncomfortable/confining,
impedes speech/drinking/eating
Venturi Mask
- Uses adjustable valves to mix O2 with ambient air, creating high-flow oxygen of precise concentration
- One way valve so that air can be breathed out but can’t come in. Bernoulli’s principle: the bigger the hole, the
more entrainment of ambient air, the more mixing with ambient air, the lower the FiO2.
- Advantages: able to control FiO2 precisely (fixed performance), useful in COPD patients who may need a
degree of hypoxemia to sustain their respiratory drive
Colour FiO2 O2 Flow Rate

Green 24 3
26 3
28 6
30 6
White 35 9
40 12
50 15
Nebuliser Mask
- High O2 flow rate passed through container of liquid medication attached to mask
- Used for patients who require delivery of nebulized medication (in aerosol form)

GENERAL ANAESTHESIA
!
Introduction!
Stages of General Anaesthesia

① Preparation/pre-induction
② Induction
③ Maintenance
④ Reversal
⑤ Recovery
Components of General Anaesthetic

① Hypnosis: patient unconscious, sleeps, not distressed and can cooperate
② Analgesia: patient doesn’t feel pain and no physiological response to pain e.g. sympathetic response
③ Amnesia: prevents memory formation
④ Reflex suppression: cough, prevents exaggerated autonomic response
⑤ Paralysis: muscle relaxation, prevents movement
à No 1 drug that can do all the above, so must use combination of multiple drugs. This may cause more side
effects (e.g. hypotension, apnoea) but means can control each component well.
à Balanced anaesthesia: give drugs from multiple classes to allow less of any one given, reducing risk of side
effects
Stages of General Anaesthesia

- Stage 1 (amnesia): patient should follow commands, respiratory pattern is regular
- Stage 2 (delirium): period of uninhibited excitation, laryngospasm if airway is manipulated, pupils divergent,
respiration irregular
- Stage 3 (surgical anaesthesia): target depth for anaesthesia during Sx, respiratory pattern is regular
- Stage 4 (overdosage): patient at risk for hypotension and cardiovascular collapse
!
PREPARATION/Pre-induction
!
Pre-operative Medications
- Antibiotics: cefazolin for most surgeries, Augmentin for diabetics, ceftriaxone + metronidazole for GI surgeries,
ceftriaxone for GU surgeries as more Gram negative organisms
- Anxiolysis: benzodiazepines e.g. midazolam
- Analgesia: opioids e.g. fentanyl
- Anti-emetics for patients at risk of PONV (e.g. past Hx of N/V or motion sickness): dexamethasone at start and
ondansetron at end 10-15 min before patient wakes up
- Antacids for patients at high risk of gastric aspiration
- Others: asthma medications and steroids, no need insulin for diabetics if fasted already

Pre-oxygenation
- Patient to inhale 100% O2 through sealed mask
- Aim to replace nitrogen of room air in Functional Residual Capacity in lungs with O2 and maximally oxygenate
all of patient’s vital organs before induction
- To ensure that patient is best able to tolerate any period of apnoea (allows 8 min of apnoea in healthy 70kg
adult before SpO2 <90%) without arterial O2 desaturation (occurs in 45s-1 min in normal person breathing RA)
from the time of anaesthetic induction to the time airway is secured
Benzodiazepines
- Examples: midazolam, diazepam, lorazepam
- Enhances GABA transmission, inhibitory neurotransmitter
- Used for sedation, anxiolysis and amnesia (esp retrograde), but no analgesic effects
- Amnestic properties esp useful in patients with poor haemodynamic status who can’t tolerate enough inhaled
anaesthetic agent to ensure complete unconsciousness
- Midazolam can cause delirium in elderly
- If patient becomes oversedated or exhibits delayed emergence from GA and suspected to be due to BZD,
reverse with flumazenil (BZD receptor antagonist, 0.1 mg every 5 min)
Opioids 46 ANESTHESIA STUDENT SURVIVAL GUIDE

●
- Examples: morphine, hydromorphone, fentanyl and its derivatives (e.g.

sufentanil, alfentanil, remifentanil), meperidine
- Used for sedation and analgesia, but no reliable amnesia
- Act on mu (μ), kappa (κ), and delta (δ) receptors
- Fentanyl: rapid onset and short-acting, 100x more potent than morphine,
given during induction to blunt sympathetic response during intubation,
can cause chest wall rigidity in high doses
- Remifentanil: rapid and ultra short-acting, shorter-acting than fentanyl,
almost always used as continuous infusion
- Context-sensitive half-time: increases markedly with long durations of administration for opioids that exhibit
Figure 4.1 Context-sensitive half time for opioid infusions (Image Courtesy J. Ehrenfeld)
accumulation (i.e. fentanyl), no effect in opioids which are enzymatically degraded as fast
include pruritus, as they
bradycardia, arterialare
and venous vasodilation, nausea and
administered (i.e. remifentanil) vomiting, urinary retention, miosis, muscle rigidity (mainly with fentanyl),
and decreased gastric motility/constipation.
- Side effect: respiratory depression (due to decrease in hypoxic drive to breathe andare increase
There in apneic
also peripheral opioid receptors located in the gastrointestinal
tract and other organs. Methylnaltrexone is an investigational peripheral opi-
threshold i.e. CO2 level above which patients are stimulated to breathe) oid receptor antagonist and a quaternary derivative of naltrexone. Unlike nal-
oxone, methylnaltrexone offers the therapeutic potential to block or reverse
- If patient is non-responsive and/or hypoventilating from overdose, reverse with naloxone
the undesired side effects(μ receptor
of opioids that are mediated by receptors located in
the periphery (e.g., in the gastrointestinal tract), without affecting analgesia or
antagonist, 0.04-0.4 mg every 2 min, may need repeated doses if half-life of opioid longer
precipitating the opioidthan naloxone)
withdrawal symptoms that are predominantly medi-
- Methylnaltrexone: blocks undesired side effects mediated by peripheral opioid receptors in GIT etc, without
ated by receptors in the central nervous system.
Blunting of the endocrine stress response is a side effect of opioids that can
affecting effects mediated by opioid receptors in CNS be beneficial, especially during surgery. Because of their ability to decrease the
stress response and minimal effects on baseline cardiovascular status, high-
- Opioids and BZD can be used for induction but due to unpredictable onset time and arelong
dose opioids favoreddurations of inactions
over other anesthetics cases where hemodynamic
instability is anticipated, or in patients where such changes would not be well
when used in doses high enough for induction, they are not commonly used alone tolerated.
!
Induction!!
Introduction
- Process of starting GA or “putting patient to sleep”
- Co-induction (inhalational + intravenous induction) or total intravenous anaesthesia (TIVA)
• Inhalational: usually in children where it’s hard to get IV access, slow, problems with stage 2, airway
irritation, environmental pollution (struggling child won’t have perfect mask fit and gases will leak)
o Sevoflurane most pleasant-smelling so used in induction in children
• Intravenous: rapid and shortened stage 2, requires IV access, loss of airway reflexes, cardiorespiratory
depression
• Advantages of TIVA: can avoid side effects of inhalational agents like N/V (e.g. past Hx of severe N/V or
motion sickness) + used for patients with risk of developing malignant hyperthermia (e.g. positive
family Hx)
- Typical intravenous induction agents: propofol, thiopental, etomidate, ketamine
Propofol

- Most commonly used induction agent (2-2.5 mg/kg), emulsion
- Highly lipophilic, distributes rapidly from plasma to peripheral tissues, will offset very quickly except in very fat
patients
- Enhances GABA transmission
- Potent cardiovascular and respiratory depressant
- Decreases BP by decreasing cardiac contractility and systemic vascular resistance (vasodilator)
- Contains egg lecithin so contraindicated in patients with egg allergy
- Pain on injection, can be reduced with concomitant administration of 1% lidocaine
- Anti-emetic, obtunds gag reflex
Thiopental
- Potent cardiovascular and respiratory depressant
Etomidate
- Minimal cardiac and respiratory depression
- Good drug to use for patients with compromised haemodynamic state (e.g. trauma patients in shock, elderly
patients, cardiac patients with heart failure)
Ketamine
- NMDA receptor antagonist, dissociate agent
- 50
OnlyANESTHESIA STUDENT SURVIVAL
induction agent GUIDE
that’s a cardiovascular stimulant , minimal effects on respiratory drive
●
- Potent analgesic and bronchodilator

- Side effects: hallucination and perceptual disturbances, emergence delirium (except in extremes of age),
Table 4.4
increased Cardiovascular
salivation effects of IV induction agents
, increased ICP
Mean Systemic Intracranial
arterial vascular Cardiac Heart pressure
Drug pressure resistance output Contractility rate
Propofol ↓↓ ↓↓ ↓↓ ↓↓ ↓↓ ↓
Thiopental ↓ ↓ ↓ ↑ ↓
Etomidate – – – – – ↓
Ketamine ↑ ↑ – – ↑ ↑
Maintenance!!
Neuromuscular Blocking Agents

Introduction
- Neuromuscular
Spontaneous respiration:
blockers (NMBs) or “paralytics” are frequently utilized dur-
• Inhalational
ing the administrationagent of
with air-oxygen
a general or nitrous They
anesthetic. oxide-oxygen mixture
are used to facilitate intu-
• Allows rapid control of depth of anaesthesia by varying concentrations of agents
bation and to improve surgical conditions by inducing relaxation of skeletal
• Pain control e.g. opioids
muscle. Theredetermines
• Patient are two major
RR andclasses of NMBs, depolarizing and nondepolar-
tidal volume
- izing. The classes
Intermittent positive are differentiated
pressure ventilation based
(IPPV): on their action at the neuromus-
• Inhalational agent with air-oxygen
cular junction. Adequacy of relaxation or nitrous
can beoxide-oxygen
determinedmixture
by use of a nerve
• Non-depolarising muscle relaxant
stimulator (see Chap. 11 on equipment). Nerve stimulator testing of a typical
• Intubation preferred
blockade with nondepolarizing NMBs demonstrates tetanic fade, posttetanic
• Pain control e.g. opioids
facilitation, train ofdetermines
• Anaesthetist four ratioRRless
and than 30 %, and the ability to be reversed
tidal volume
with anticholinesterases. In contrast, a typical depolarizing block does not dis-
Neuromuscular Blocking Agents unless a Phase II block is present (see depolarizing
play these characteristics –
- Facilitate intubation and improve surgical conditions by inducing relaxation of skeletal muscle (e.g. in
NMBs below). The appropriate NMB for a given situation is chosen based on
abdominal surgeries, need paralysis to ensure appropriate abdominal relaxation for pneumoperitoneum [gas
desired onset
insufflation time, duration,
of abdomen] elimination,
and abdominal and side effects.
manipulation)
- Depolarising v.s. nondepolarising NMBs
Depolarizing NMBs
Succinylcholine) is the only commercially available depolarizing NMB. Like
Chong Kar Mun Class
acetylcholine, of 2019
it works as an agonist on acetylcholine receptors at the neuro- 14
muscular junction. This causes depolarization, and prolonged binding of suc-
cinylcholine to the receptor prevents junctional repolarization because the
Depolarising NMBs
- Succinylcholine
- Acetylcholine receptor agonist à causes depolarisation initially (muscles will keep contracting causing
fasciculations), then prolonged binding prevents junctional repolarisation as drug is not hydrolysed by true
acetylcholinesterase (muscle then becomes relaxed)
- Quickest onset and shortest duration out of all NMBs à used almost exclusively for intubation i.e. rapid
sequence intubation, where you need to do it very quickly to protect airway
- Hydrolysed by pseudocholinesterase
- Contraindications*: elevated serum K+ levels, Hx of burn injury, Hx of denervation injury, known or suspected
myopathy, known or suspected risk of malignant hyperthermia, known pseudocholinesterase deficiency
• Can use rocuronium instead for RSI if succinylcholine contraindicated
• Side effects: hyperkalemia, bradycardia, increased ICP and IOP, increased intragastric pressure
• Post-synaptic acetylcholine receptors are upregulated in burn and denervation injuries à exaggerated
response that can cause fetal arrhythmia
- Effects can’t be reversed by acetylcholinesterase inhibitor, can make neuromuscular blockade prolonged and
more intense
Nondepolarising NMBs
- Examples: rocuronium, vecuronium, cisatracurium, pancuronium
• Atracurium is eliminated by Hoffmann degradation and ester hydrolysis at room temperature, so
should be kept in fridge when not in use
- Competitive antagonist at post-synaptic receptor (nicotinic) à prevents junctional repolarisation
- Longer onset time and duration of action à used to maintain muscle relaxation during Sx
• Onset time and duration of action: rocuronium < vecuronium < cisatracurium < pancuronium
- Neuromuscular blockade reversed by acetylcholinesterase
inhibitor (e.g. neostigmine) which prevents breakdown of
acetylcholine at NMJ à excess acetylcholine will outcompete
NMB for binding at receptor à allows muscle depolarisation à
but acetylcholine acts on both nicotinic and muscarinic receptors!
So anticholinergic (e.g. glycopyrrolate) must be added together to
prevent muscarinic overactivity side effects like severe
bradycardia, asystole and bronchospasm.
• Atropine also anticholinergic agent which crosses BBB
unlike glycopyrrolate, so can cause central
anticholinergic syndrome (delirium, excitation, fever,
flushing, tachycardia)
- Can also be reversed by sugammadex which doesn't inhibit acetylcholinesterase so no cholinergic side effects
and don’t need co-administration of anticholinergic agent
Inhalational Agents
- Examples: nitrous oxide, volatile agents (isoflurane, desflurane, sevoflurane)
- Can cause loss of consciousness, amnesia and inhibit movement
- Concept of minimal alveolar concentration:
• Definition: concentration of inhaled anaesthestic agent in alveoli in 100% oxygen at 1 atmospheric
pressure (standard conditions) which prevents reflex movement in response to 1st surgical
stimulus/surgical incision in forearm in 50% of subjects
• Application: MAC usually kept at 0.7-1. Better to watch SE on EEG monitoring: <60 means patient is
asleep.
• Why low MAC can be used: balanced anaesthesia (analgesia + sedation + muscle relaxant) à don’t
have to give so much inhalational anaesthesia
• Factors affecting MAC: age, rate of metabolism
o Give lower MAC: acute alcohol intoxication, hypothermia, elderly
o Give higher MAC: chronic alcoholism (induces enzymes so drugs metabolized faster),
hyperthyroidism

- Nitrous oxide and volatile agents can cause post-operative nausea and vomiting, volatile agents (but not
nitrous oxide) can cause malignant hyperthermia
Sympathomimetics/Vasopressors
- Many patients who need Sx are dehydrated, have significant systemic illness or underlying CVS disease
- As most anaesthetic agents are cardio-depressants, may need vasopressors temporarily to tolerate
anaesthesia (increase BP)
- Difference between ephedrine and phenylephrine:
• Ephedrine: indirectly acting, both alpha + beta receptor effects à vasoconstriction + increased HR à
increased BP and increased HR à for patients with low BP and low HR (HR <60)
• Phenylephrine: acts on alpha receptors only à vasoconstriction à increased BP. No beta agonist
effects, high BP stimulates baroreceptors à decreased HR (reflex bradycardia) à for patients with low
BP and high HR
reversal!
- Check train-of-four stimulation for residual neuromuscular blockade to assess need for reversal of muscle
relaxant with acetylcholinesterase inhibitor + anticholinergic agent
- Reversal of anaesthesia: stop inhalational gases, patient on 100% FiO2, no antagonist
- Endotracheal extubation

REGIONAL ANAESTHESIA
!
Local!anaesthetic!drugs!
Mechanism of Action
- Inhibit Na+ channels on cell membrane of nerve axon à prevents ion conduction à membrane unable to
depolarise sufficiently to reach threshold potential à prevents generation of action potential
- Weak bases that exist as equilibrium of more lipid-soluble, neutral form and less lipid-soluble charged form.
They need to exist in lipid-soluble neutral form to permeate lipid-rich neural membranes to reach their site of
action.
- Effects are terminated by absorption of drug from site of action into circulation and to lesser extent,
lymphatics
Structures
- Amides: lidocaine, mepivacaine, prilocaine, ropivacaine, bupivacaine
- Esters: procaine, tetracaine, cocaine
Factors affecting LA Action
① Fibre Size & Type:

- Differential conduction blockade
- A and B nerve fibres are myelinated, C nerve fibres are unmyelinated
- Smaller nerve fibres of same type more readily blocked than large nerve fibres
- Myelinated nerve fibres more readily blocked than unmyelinated nerve fibres
à But larger myelinated nerve fibres are more readily blocked than smaller unmyelinated nerve fibres
- E.g. large sciatic nerve takes 30 min to block
② pH:
- Low pH: slow onset of action, high pH: fast onset of action
- Add sodium bicarbonate to increase pH so that more of LA will be in neutral form à speeds up onset of action
③ Adrenaline/Epinephrine:
- Adrenaline-containing LA solutions formulated at lower pH than plain local solutions due to adrenaline’s
instability in alkaline envt à low pH slows down onset of action
- Adrenaline causes local vasoconstriction and slows down rate of absorption of LA from site of deposition à
prolonged LA action
- Effects on longer-acting LA (ropivacaine, bupivacaine) not so obvious as they are released so slowly from
neural tissue, acting for so long already and slow absorption of drugs anyway
- Avoid use of adrenaline in areas with end arteries as will cause ischemia
LA Side Effects & Toxicity

- Systemic absorption of LA during or after nerve blocks or inadvertent injection intravascularly
- Toxicity is from rate of increase in blood concentrations
à so S/S more subtle if given in staggered doses than if given in bolus
- CNS effects: early: lightheadedness/dizziness, perioral or tongue numbness; higher levels: tinnitus, slurred
speech, visual disturbances, agitation, anxiety. Late: CNS depression: unconsciousness, resp arrest, seizure
- Cardiovascular effects: cardiac arrhythmias, depressed contractility, cardiac arrest, hypotension
• Ropivacaine: cardiostable, doesn’t bind to cardiac receptors for a long time, so safer and lower risk of
cardiovascular collapse
- Prevention: use lowest effective dose, U/S guidance, incremental injection after negative aspiration of blood
(every 5 ml), maintain verbal communication with patient at all times and ask about early symptoms of LA
toxicity
- Management: infusion of lipid emulsion solution i.e. 20% Intralipid (presumed mechanism of action: lipid-
soluble fraction of LA is sequestered in lipid emulsion and removed from plasma). LA-induced seizures:
hyperventilation, BZD or small doses of propofol or thiopental.

regional!anaesthesia!
Types of Regional Anaesthetic Techniques

- Peripheral nerve blockade: e.g. axillary block for AVF repair
- Central/neuraxial blockade: spinal/subarachnoid, epidural, combined spinal-epidural (CSE), paravertebral
• CSE: combines advantages of both spinal (fast onset of anaesthesia) and epidural (placement of
catheter for continuous medication infusion) techniques
- Can be done before or after Sx (can reduce post-operative pain so can reduce amount of opioids needed)
Introduction to Central/Neuraxial Blockade

- Advantages: consciousness preserved (sometimes want patient to be awake during neurological procedures so
that can ask them questions and see if any change in mental state), good early post-operative pain relief (but
must have plan for when it goes off; late post-operative also as epidural catheter can be kept there for 72h),
simple to administer, attenuates stress response (some may still need sedation for anxiety), minimal depression
of ventilation, less intra-operative blood loss compared to GA (GA causes vasodilation), lower risk of immediate
CVS and respiratory complications (can ventilate better as pain free), lower risk of post-operative DVT (increases
vascularity and circulation, less release of inflammatory mediators in coagulation cascade)
- Disadvantages: requires technical skill/familiarity, occasional inadequate blockade, requires patient’s
acceptance and cooperation (tailor expectations, numbness will last 12-15h), requires surgeon’s acceptance
- Considerations: indications and contraindications, preoperative assessment, informed consent, IV access and
monitoring (need for sedation and may need to convert to GA), sedation if indicated (after block so that patient
can tell you if there’s pain or paresthesia à means that needle is too near or in nerve, as it’s hard to tell where
needle is even with U/S), block performed after aseptic technique, test adequacy of blockade, monitor
regression of block after Sx
- Contraindications:
• Absolute: patient refusal, infection in area of needle puncture, elevated ICP, uncontrolled bleeding,
critical aortic stenosis (fixed cardiac output so may cause uncontrolled hypotension, so send for 2DE if
ESM is heard. But if no choice, emergency Sx, then do GA and not central/neuraxial blockade)
• Relative: bacteremia, pre-existing neurological disease, cardiac disease, abnormal coagulation studies
(may cause haematoma, ask for coagulation panel)
Spinal Blockade
- Anatomy: spinal cord extends from foramen magnum to body of L1 in adults and L3 in children, so do below L3
level to avoid trauma to spinal cord. Pia mater is closely adherent to spinal cord, arachnoid mater is closely
adherent to outer dura matter. CSF is contained in subarachnoid space between arachnoid mater and pia
mater.
- Anatomical landmark: iliac crest/intercristal line (pt in lateral flexed position) à L4-L5 interspace or L4 body
• C7 is 1st prominent vertebra felt in most people
• Inferior angle of scapula à T7
- After infiltration of skin with LA, needle is advanced through skin à subcutaneous tissue à supraspinous
ligament à interspinous ligament à ligamentum flavum à epidural space à dura mater à subdural space à
arachnoid mater à subarachnoid space
- Can do paramedian approach if patient can’t flex spine e.g. elderly with hip #
- No catheter placed in subarachnoid space due to risk of infection and nerve injury
- Easier to do and faster onset than epidural (but faster onset may cause hypotension)
- LA and opioids given can only last for a few hours, not continuous
- Factors affecting distribution of LA in subarachnoid space:
• Baricity of solution: density relative to density of CSF
o Hyperbaric solutions: contain glucose/dextrose, flow in direction of gravity and settle in most
dependent areas
o Hypobaric solutions: LA mixed with sterile water or N/S, rise in relation to gravity
• Position of patient immediately after injection of solution
• Other factors: dose and volume of drug injected, level of injection, speed of injection/barbotage, size
of needle, physical status of patient, intra-abdominal pressure
- Factors affecting duration of action: drug used, dose and volume injected, use of vasoconstrictors, total spread
of blockade

Epidural Blockade
- Can be done at any level, though space for epidural needle maximal at lumbar region
- Go in through different layers. Once potential space (i.e. epidural space) is entered, N/S can be pushed in using
syringe attached to epidural needle (loss of resistance: positive pressure encountered in supraspinous ligament,
interspinous ligament and ligamentum flavum prevents plunger of syringe from depressing, but distinct loss of
positive pressure is felt as needle advances past ligamentum flavum and plunger gives way) à thread in small
catheter into epidural space à drugs can be continuously pumped into space until time of Sx
- Unlike spinal anaesthesia, level of anaesthesia in epidural is not influenced by baricity of solution or position of
patient immediately after injection
- Amount of LA needed to produce surgical anaesthesia with epidural significantly (10x more) as LA must
transverse more layers to act on nerve roots
Complications of Central/Neuraxial Blockade

- Inadequate or failed blockade
- Cardiovascular changes: hypotension (need volume replacement to restore venous return and cardiac output,
vasopressors to raise BP), bradycardia (cardioaccelerator fibres originate at T1-T4 level so sympathetic fibres
may be blocked by neuraxial anaesthesia that rises and blocks this level)
- Cauda equina syndrome: permanent neurological injury
- Transient neurological symptoms: may feel electric shock down legs during procedure if free floating nerves
are accidentally touched, self-limiting and resolves in a few days
- High/total spinal anaesthesia: excessive sensory and motor anaesthesia a/w loss of consciousness (thought to
be due to ischemia of medullary ventilator centres due to profound hypotension) as thoracic and lumbar are
blocked. Recognize, ensure ABCs, intubate and ventilate until spinal anaesthesia wears off.
- Motor blockade: pain from muscle spasm relieved but patient can’t undergo physiotherapy
- Post-dural puncture headache: CSF allowed to leak through hole faster than it is being produced if dura mater
is violated (in spinal anaesthesia and unintentionally in epidural anaesthesia) à downward displacement on
sensitive brain structures
• Headache that worsens with sitting or standing and is relieved by lying flat
• Risk factors: young, female, pregnant, big needle (16-18G needle), type of needle (cutting needle
higher risk than pencil point needle)
- Urinary retention: blockade of S2-S4 nerve roots can decrease bladder tone and inhibit voiding reflex
- Pneumothorax: brachial plexus block
- Intravascular injection causing LA toxicity: prevent by using lowest effective dose, U/S guidance, incremental
injection after negative aspiration of blood (every 5 ml)
- Spinal or epidural haematoma: mostly in patients with abnormal coagulation panels, mass effect of
haematoma causes injury via direct pressure and ischemia. Need to recognize immediately to avoid permanent
neurological deficits! MRI (F/U with patient and MRI to check for this if anaesthesia lasts longer than it’s
supposed to), neurosurgical consult, emergent surgical decompression of spine.
- Epidural abscess: back pain exacerbated by percussion over epidural insertion site à radicular pain à motor
or sensory deficit à paraplegia. Need to recognize immediately to avoid permanent neurological deficits! MRI
(F/U with patient and MRI to check for this if anaesthesia lasts longer than it’s supposed to), neurosurgical
consult, emergent surgical decompression of spine.
Peripheral Nerve Blocks

- Can be performed as sole anaesthetic for appropriate ambulatory surgeries or postoperative analgesia
- Broadly divided into UL blocks, LL blocks, truncal blocks and others
• Shoulder Sx: interscalene block
• Infraclavicular block or axillary block: anything below elbow
• Femoral nerve block: femoral #
• Intercostal block has highest risk of intravascular injection
- Ropivacaine usually used instead of lignocaine as still needed for post-operative pain relief but don’t want to
top up so use longer-acting agent instead

MONITORED ANAESTHESIA CARE
!
levels!of!sedation/analgesia
Introduction
- Depth of sedation is a continuum
- MAC for moderate sedation cases
- GA: loss of consciousness and protective airway
reflexes
- Need to differentiate between reflexes and purposeful
movements
Choice of Level of Sedation & Anesthetic Technique

- Depends on what stimulus is given/type of procedure,
patient’s comorbidities and health status, patient’s preferences (e.g. anxious patient), surgeon’s preferences
(e.g. may prefer patient to be perfectly still and not talking)
- Primary concerns when considering if patient can tolerate deep sedation and GA are airway and cardiovascular
status
introduction
Goal
- Allow patient to be cooperative and tolerate a procedure with least degree of anxiety and discomfort and
greatest degree of safety
- Monitor patient and administer medications for anxiolysis, analgesia or sedation while procedure is being done
Indication
- Reduction of fear, anxiety, stress during clinical procedures
- Provision of comfort/short-term amnesia/sleep, immobility, analgesia
- Minimally invasive surgeries, cause patients little pain or psychological discomfort
- Examples: chest tube insertion, endoscopy, cataract Sx, long MRI scans
Contraindications
- Absolute: Hx of severe allergic reaction to sedative or analgesic agent, patient not agreeable
- Relative: unstable cardiorespiratory function, aspiration risk (clear fluids: 2h, light meal: 6h, heavy meal: 8h)
guidelines
Patient Selection & Evaluation

- History: CVS/pulmonary risks, renal/liver function, ASA status, sedation/anaesthetic Hx, medications/allergy
• Note: children, elderly, pregnant, GERD (pregnant and GERD patients have higher risk of aspiration),
psychiatric illness, substance abusers, OSA (may be used to apnoea, so less sensitive so may not wake
up unlike normal people who will wake up from increased CO2 levels, so very important to monitor
them)
- PE: esp CVS, respiratory, airway, CNS
- Inx: guided by underlying conditions, trace results
- Informed consent, including benefits, limitations, risks, alternatives
- Fasting times: gastric emptying and potential for pulmonary aspiration v.s. emergency cases
- Formulate plan and back-up alternative
Personnel
- Clinicians’ responsibility to know their own institution guidelines
- Designated personnel rather than clinician performing procedure to monitor patient during and after
procedure

- Provider must be accredited for sedation and resuscitation of patient since unintended deeper level of
sedation or cardiopulmonary collapse may occur
Monitoring
- Establish baseline, vigilant monitoring, interval charting (duration of interval dependent on patients’ condition,
generally ~5 min)
- Sedation level: response to verbal command, Modified Ramsay Sedation Scale
- Ventilation: RR and patency: chest rise, stridor vs silence, misting of mask
- ETCO2/capnography: early detection of respiratory depression
- Oxygenation: continuous SpO2: late warning sign
- Hemodynamics: HR, BP, ECG: recommended esp at risk patients
Equipment
- Supplemental oxygen, suction, IV access
- Crash cart: airway, BVM, resuscitation drugs
Medications: Sedation/Analgesia & Reversal

- Start low and go slow: titrate to effect; each patient is different
- Avoid repeated oral doses
- Single agent whenever possible, combination increases risks
- Sedatives (e.g. benzodiazepines) for anxiolysis and amnesia but ineffective for analgesia and inhibiting
movement; analgesics relieve pain, when combining both reduce doses
- Choice depends on: patient reserves, duration and invasiveness of procedure
- Reversal agents available on site
- Local anaesthetic infiltration for analgesia whenever possible
- Non-pharmacological techniques: relaxation, guided imagery etc
Complications
- Be ready for the unexpected, consider calling for help
- Cardiorespiratory instability: BCLS/ACLS guidelines
- Procedure-related complications
- Adverse effects of sedatives/analgesics
Recovery
- Monitor until return to baseline consciousness and cardiorespiratory level before discharge
- Stay with your patient at all times! Patient may drift deeper w/o stimulation, fall risk
Documentation
- Assessment of patient, consent, vital signs, parameters
- Sedation/analgesia: dosages and time
- Events/incidents
- Discharge criteria, written instructions and contact numbers
special!considerations
- Don’t sedate if inability to rescue oversedation/support oxygenation/ventilation/haemodynamics, no code

blue support
- Don’t sedate if unfamiliar envt: restricted space/access, poor lighting, biohazards/noise/transport issues,
unfamiliar equipment (be self-sufficient)
- When in doubt, consult specialist/anaesthesiologist
- Call for help early if conscious sedation fails

MONITORING IN ANAESTHESIA
!
introduction!
Purpose
- Monitor depth of anaesthesia:
• Awareness during Sx is unacceptable by today’s standards, medical negligence
- Monitor patient’s physiological parameters:
• Warn us if patient is deteriorating
Minimum Monitoring Standards in Anaesthesia

Pulse oximetry, non-invasive BP, ECG, capnography, inspired oxygen analyser (make sure don’t give hypoxic
mixture to patient)
Oxygen!saturation!
Oxygen-Haemoglobin Dissociation Curve

- PaO2 of <60mmHg = <91% SpO2 = hypoxemia
- COPD: PaO2 of 40-60 is still acceptable
- Shift of curve to right (decreased affinity for O2 i.e. more difficult for Hb to bind to
O2/need higher PaO2 to achieve same SpO2 + easier for Hb to release O2 bound to
tissues): increased temperature, increased pCO2, increased 2,3-diphosphoglycerate,
decreased pH/higher H+
Pulse Oximetry
- Estimates oxygen saturation in whole blood = ratio of oxygen content over oxygen carrying capacity of Hb
- Measures transmission of light across pulsatile vascular tissue bed
- Compares absorption spectra of oxygenated Hb (HbO2) and deoxygenated Hb (Hb)!
- Limitations:
• Less accurate at SpO2 values below 70% cause they are extrapolated and not real experimental data
• Interference by ambient light
• Loss of pulsatile component: arrhythmias (AF) causes irregular blood flow, peripheral vascular disease,
hypothermia, hypoperfusion, peripheral vasoconstriction
• Movement artefact or electrical interference by diathermy
• Infrared absorption by other substances like nail varnish or nicotine staining
• Significant errors associated with absorption by abnormal haemoglobins and other compounds:
carboxyhaemoglobin, dyes in circulation (methylene blue, disulphine blue), methaemoglobin
non-invasive!BP!Monitoring!
- Clinical palpation: not acceptable except in resuscitation, can’t tell when patient is hypotensive
- Manual BP (Korotkoff sounds): still gold standard
- Automatic BP/oscillometry: not as accurate as manual BP, done at least every 5 min
• Cuff inflates well above systolic pressure and deflates slowly
• Senses oscillations as cuff pressure 1st falls below systolic pressure
• Peak at which amplitude of oscillations is the greatest is read as mean BP
• Diastolic pressure derived from systolic and mean pressures
Inaccuracies
- Inappropriate cuff size can cause falsely elevated or lowered BP measurements
- Level of cuff should be at level of heart
- Reading can be affected by motion, shivering, irregular pulse (e.g. AF)

invasive!bp!monitoring:!intra-arterial!lines!
- Sites: radial (commonest), brachial, axillary, dorsalis pedis, femoral, rarely ulnar
- Components: intra-arterial cannula, fluid-filled tubings and connectors, electromechnical pressure transducer,
electronic analyser, storage or display system
- Tubing is filled with N/S not air as fluid is non-compressible unlike air, so can transmit pressure and be read
- Arterial pulsations are transmitted via fluid column to pressure transducer, where it’s processed and output
onto electronic display, both graphically and numerically
- Can tell you heart rate also cause pulsatile waveform
- Indications/advantages: real time assessment of blood
volume and perfusion status/continuous “beat-to-beat”
monitoring (fastest non-invasive BP monitoring can do is
once every min) of systolic, diastolic and mean arterial
pressure (e.g. trauma patients, patients with AMI, very
sick, haemodynamically unstable), frequent labs/ABGs
(can draw out blood multiple times without poking
patient so many times), failure of non-invasive methods
(morbidly obese [too much subcutaneous fat surrounding
small artery]), prolonged periods of frequent BP
monitoring (may cause abrasions and petechial
haemorrhages in elderly patients with frail skin)
- Absolute contraindications: infection over insertion site
(introduce infection into arterial circulation)
- Relative contraindications: peripheral vascular disease/poor collateral circulation (may form pseudoaneurysm),
coagulopathies, vascular grafts/Sx near insertion site
Intraarterial Waveform
- Upstroke: ventricular contraction

- Dicrotic notch: closure of AV valves
Inaccuracies
- Damping/resonance
- Transducer height
Complications
- Local or systemic infection
- Bleeding/haematoma
- Thrombosis/embolism
- Vascular insufficiency
- Aneurysm
- Pseudoaneurysm not very common but higher risk in patients with atherosclerotic and calcific arteries
- Inadvertent drug injection: will cause drug concentration at target tissue à distal vascular occlusion and
gangrene
• Don’t inject drugs into arteries!

ecg!Monitoring!
Need for ECG Monitoring

- 3 lead (limb leads): displays lead II, most common monitoring lead
- 5 lead: displays lead II and V5, for patients with cardiac ischemia or cardiothoracic Sx
• Lead V5 detects about 75% of ischemic episodes
• Lead II + lead V5 raise detection rate to 80% while leads II, V4, V5 together detect 98% of ischemic
events
- ST changes 1st sign of myocardial ischemia and most sensitive
- Can also detect arrhythmias and tells you HR (identify tachycardia and bradycardia)
Points to Take Note

- Ensure that leads are placed in correct position and secured
- Ensure that lead placement doesn’t interfere with procedure being performed, ensure that it’s away from field
of Sx
• Put ECG leads on back if patient in prone position for spine Sx
- Affected by diathermy
central!venous!pressure!(CVP)!Monitoring!
- Highly inaccurate, absolute number not reflective of patient’s volume status, not as helpful as was originally
hoped in identifying which hypotensive patients will respond favourably to fluid bolus
- Gross estimation of filling pressure of RV, dependent on a lot of other factors
- Placed percutaneously into sites that lead to SVC and RA: right IJV, subclavian, antecubital, femoral (not
reflective at all cause more reflective of intra-abdominal pressure)
- Distal end of catheter must lie within large intra-thoracic vein or RA
- When inserting CVL, patient to have head down so that veins will become engorged
- Measures CVP (right-sided cardiac preload)
- Needed for central venous access: ANESTHESIA EQUIPMENT AND MONITORS 147
●
• Pressure
Central Venous Inotropic drugs: dopamine, dobutamine
(CVP) Monitoring
Central venous catheters are commonly placed percutaneously into the right
• veinSome
internal jugular chemo
as well as via a number ofdrugs
other sites that lead to the
superior vena cava and right atrium. These catheters are generally inserted for
• (1)Total
one of two reasons: parenteral
to establish nutrition
vascular access for cases (TPN)
likely to involve a to avoid burning peripheral veins
high degree of blood loss, and (2) to allow the determination of central venous
- Conduits
pressure forpreload).
(right-sided cardiac pulmonaryThese cathetersartery
can also becatheters,
useful to dialysis catheters
- Can also suction out air from heart
suction out air from the heart in a case of air embolus. In addition to provid-
ing an overall measure of central venous pressure, the pressure waveforms if air embolus
provided by a central venous catheter yield a great deal of information and are
shown in Fig. 11.8.
CVP Waveform
Figure 11.8 The central venous pressure waveform. +a wave: this wave is due to the increased
atrial pressure during right atrial contraction. It correlates with the P wave on an ECG. +c wave:
This wave is caused by a slight elevation of the tricuspid valve into the right atrium during early
- a wave: increased atrial pressure during right atrial contraction, correlates with P wave on ECG
ventricular contraction. It correlates with the end of the QRS segment on an ECG. −x descent:
this wave is probably caused by the downward movement of the ventricle during systolic con-
- c wave: slight elevation of tricuspid valve into right atrium during early ventricular contraction, correlates with
traction. It occurs before the T wave on an ECG. +v wave: this wave arises from the pressure
produced when the blood filling the right atrium comes up against a closed tricuspid valve. It
occurs as the T wave is ending on an ECG. −y descent: this wave is produced by the tricuspid
QRS complex on ECG
valve opening in diastole with blood flowing into the right ventricle. It occurs before the P wave
on an ECG (Used with permission. From Norton et al. [18])
- x descent: downward movement of ventricle during systolic contraction, occurs before T wave on ECG
- v wave: pressure produced when blood filling right atrium comes up against closed tricuspid valve, late systolic
during systolic filling of RA, occurs as T wave is ending on ECG
- y descent: tricuspid valve opening in diastole with blood flowing into right ventricle, occurs before P wave on
ECG

CVP Position
Chest X-ray: tip of CVP should end at near bifurcation of trachea
Complications
- Arterial puncture
- Pneumothorax, hydrothorax, chylothorax
- Pericardial effusion, tamponade
- Negative intrathoracic pressure in spontaneously breathing patient can suck air in so can cause air embolism.
20% of population has PFO so may travel from right to left circulation and cause cerebral embolism.
• So when taking out CVL, ask patient to have head down and Valsalva (intrathoracic pressure will
become positive)
- Nerve injury
- Infection
capnography!
- Measurement of CO2 concentrations in respiratory gas mixture

- Uses method of infrared absorption spectrophotometry
Uses
- Assesses ventilation
- Confirms ETT placement
- Disconnection monitor
- Evaluate cardiopulmonary resuscitation
- Detect venous air embolism
Capnography Waveform
- AB: exhalation of dead space

- B: start of expiration
- BC: exhalation of mixed dead space and alveolar air
- CD: plateau, exhaled CO2 from alveoli
- D: end of plateau phase, end-tidal CO2, corresponds to PaCO2 (CO2 in blood), normally around 40 mmHg
- E: start of inspiration
- Loss of trace: circuit disconnection, CVS collapse, total airway obstruction
- Low ETCO2 (more dangerous but more commonly seen due to overzealous bagging/hyperventilation):
hypotension, partial airway obstruction, low production
- High ETCO2: hypoventilation, rebreathing (soda lime and lithium hydroxide resorb CO2), high production, worry
about malignant hyperthermia but rarely seen
- Bronchospasm means decreased airway diameter so air escapes slower à
upward slope and slower rise
- Patient is moving/starting to regain muscle control when going to wake up
à spontaneous respiratory effort during mechanical ventilation à notch in
plateau (curae clefts in waveform)

temperature!monitoring!
- Core body temperature can be measured with sensors in nasopharynx, esophagus, tympanic membrane or
even rectum or bladder
- Monitored if procedure >30 min
neuromuscular!junction!monitoring!
- Peripheral nerve stimulator used to assess neuromuscular transmission when neuromuscular blocking agents
(NMBAs) are given to block MSK activity
- Used towards end of Sx to detect residual neuromuscular blockade and guide reversal of paralysis or re-dosing
of paralytic agents
- Response recorded by visual and tactile means, force transducer, electromyography, accelerometry
- Train-of-four used:
• 4 high-voltage stimulation pulses given, should see 4 contractions in response
• Each contraction should be similar in strength
• If there’s fade (i.e. 1st twitch is stronger than last twitch), means there’s blockade
• If 0, means 100% blockade so shouldn't reverse yet
Monitoring!depth!of!anaesthesia!
- Clinical (Guedel’s classification, movement, autonomic responses like lacrimation, BP and HR changes),
electrophysiological monitors (EEG, evoked potentials, lower esophageal sphincter tone)
- Prevent awareness
- Physiological parameters/movement not a good sign of awareness esp when paralysed
- Guide for dosing of medication to prevent over or underdosing
• All will cause some degree of myocardial depression and vasodilation à can drop BP
- Bispectral index (BIS): measures EMG and EEG components à gives a number
to tell you whether there’s adequate anaesthesia given:
• 100: fully awake
• Above 60: patient may wake up
• 40-60: adequate anaesthesia
• 20-40: deep anaesthesia
• 0-20: burst suppression, induce barbiturate coma
• 0: complete brain electrical silence
- EEG Entropy

POST-OPERATIVE MANAGEMENT
!
Recovery!area/post-anaesthesia!care!unit!(PACU)
Recovery Area/PACU
- Area located adjacent to or within OT which is designated and designed for management of patients
recovering from effects of anaesthesia
- Recovery trained nurses with good nurse to patient ratio
- Anaesthetist should accompany patient from OT to recovery area
Handover to PACU
- Patient biodata: age, gender, ASA grading, comorbidities, past medical Hx, regular medications, allergies
- Surgery: indications, procedure, type of anaesthesia, intraoperative issues, fluids and drugs given
- Estimated blood loss, urine output, transfusions if any
- Problems expected post-operatively
- Patient’s current status: consciousness, airway, lines/catheters/invasive monitors, vitals
- Post-operative instructions: oxygen therapy, post-operative pain Mx, blood transfusion, inx to be done,
disposition after PACU care
Management
- Observe patient for consciousness, colour, respiratory function
- Record vitals every 5 min
- Provide airway support or jaw thrust to reduce obstruction if drowsy or unconscious
- Care and assessment of pressure areas, limbs, wounds, dressings, drains
- Look for surgical problems e.g. bleeding when BP starts to increase à go back to OT
- Patient should sit up to avoid diaphragmatic splinting, can wean off oxygen supplementation better
complications!
Respiratory
- Airway obstruction: most frequent complication
• Causes: tongue falling against posterior pharynx (commonest), laryngospasm, glottis edema,
secretions/vomit/blood in airway, external pressure on trachea (e.g. neck haematoma)
o Laryngospasm: uncontrolled contraction of laryngeal cords, high-pitched crowing or silence if
glottis is totally closed. More common after airway trauma, repeated airway instrumentation
or with copious secretions/vomit/blood in airway. Mx: positive pressure mask ventilation,
oropharyngeal or nasopharyngeal airway, suctioning, small dose (1/10 of normal dose) of
succinylchloline if refractory, intubation
• Partial obstruction: noisy breathing, snoring v.s. complete obstruction: absent breath sounds,
paradoxical movement of chest with respiration (stomach and abdominal contents move in during
inspiration to try to suck air in instead of moving out usually when diaphragm moves down during
inspiration)
• Mx: supplemental O2, head tilt chin lift, jaw thrust, oropharyngeal or nasopharyngeal airway,
reintubation. If obstruction is due to extrinsic compression of trachea e.g. expanding haematoma,
reopening of wound and drainage is needed
- Hypoventilation:
• Common causes: residual depressant effects of anaesthetics (commonest), residual neuromuscular
blockade, splinting from pain, diaphragmatic dysfunction after thoracic or upper abdominal Sx,
distended abdomen, tight abdominal dressings, hypercapnia (e.g. shivering is uncoordinated, uses up a
lot of oxygen for metabolism and produces CO2)
• Slow RR, shallow breathing with tachypnoea, laboured breathing
• Mx: take control of ventilation (assist with bag-mask-valve ventilation with supplemental O2), naloxone
(opioid receptor antagonist) if opioid overdose, acetylcholinesterase inhibitor if residual paralysis,
intubation in haemodynamically unstable or severely obtunded patients

- Hypoxaemia:
• Causes:
o Anaesthetic factors: opiates, benzodiazepines, volatile anaesthetic agents, neuromuscular
blocking agents, nitrous oxide (manage relative hypoxemia by washing out with O2)
o Surgical factors: site of surgery (esp upper abdominal/thoracic), positioning during Sx
(Trendelenberg/prone), bleeding, iatrogenic FB (bite block, gauze)
§ That’s why important for analgesia and post-op PT
§ Head down for gynaecological surgeries: higher risk of basal atelectasis and
diaphragmatic splinting à increased shunting à hypoxaemia
o Patient factors: pre-existing lung dysfunction, OSA, intra-op reduction in compliance,
shivering, secretions in upper airway, bronchospasm, laryngospasm
• Restless, agitation, tachycardia (try to pump more blood), ventricular or atrial dysrhythmias
• Mx:
o Find cause: CXR
o Simple adjustments e.g. clearing secretions from upper airway, sitting position, jaw thrust,
oral/nasal airway, blankets
o Aids/adjuncts for oxygen delivery: oral and nasal airways, nasal prongs, simple face mask,
Venturi mask, non-rebreather mask, T-piece (transition between extubation, when LMA or
ETT in-situ), bag-valve-mask
o Monitor SpO2 + close and continuous clinical observation
Haemodynamic
- Can think of differentials for hypotensive + bradycardic v.s. hypotensive + tachycardic
- Hypotension:
• Decreased preload:
o Hypovolemia: important cause TRO as may need surgical intervention; blood loss, inadequate
replacement/fluid resuscitation, tachycardia may be masked
o Impaired venous return: anaesthetic agents, spinal/epidural anaesthesia, anaphylaxis,
infection, PEEP, positive pressure ventilation, pneumothorax, pericardial tamponade
o Arrhythmias
• LV dysfunction: decreased cardiac output:
o Drugs: anaesthetic agents, beta blockers, calcium channel blockers, anti-arrhythmics
o Myocardial ischemia, MI, arrhythmias or cardiac failure
o Infection and hypothyroidism
• Decreased afterload:
o Residual effects of anaesthetic drugs and techniques e.g. inhaled agents, opioids, induction
agents; sympathetic blocks (epidural/spinal)
o Vasodilation: neuraxial anaesthesia, residual effects of anaesthetic drugs, arrhythmia or pre-
existing disease, re-warming after hypothermia, transfusion or anaphylactic reaction, adrenal
insufficiency, sepsis
• 20-30% decrease in BP from baseline, disorientation, change in consciousness, nausea, decreased
urine output, angina
• Mx:
o Identify cause: check Hx, surgical/anaesthetic notes, examine patient and drains/dressings
o Treat cause
o Inform surgical team for review if required
o Fluid resuscitation
o Blood or blood products if required
o Vasopressors as necessary e.g. ephedrine, phenylephrine, noradrenaline
- Hypertension:
• Causes:
o Noxious stimuli like pain (commonest)
o Incisional pain
o Irritation from endotracheal tube
o Distended bladder: opioids can cause acute urinary retention, discomfort will cause HR to
increase causing BP to increase

o Pre-existing or poorly controlled HTN
o Fluid overload
o Metabolic derangements (hypoxemia, hypercapnia, acidosis)
o Intracranial HTN: HTN + bradycardia
o Administration of vasopressors
• Headache, bleeding, angina, ST changes on ECG
• Concerns: increased cardiac work, increased myocardial oxygen consumption (myocardial ischemia,
infarction and LVHF), cerebral haemorrhage/haemorrhagic stroke
• Mx: treat underlying cause, analgesia, sedation if patient anxious or agitated, drain bladder, correct
electrolyte disturbances, oxygen, anti-hypertensive agents (beta blockers, calcium channel blockers,
hydralazine, nitrates)
- Tachycardia:
• Causes: noxious stimuli (pain, anxiety, ETT, distended bladder), acidosis, hypoxemia, hypotension and
hypovolemia, hypoglycemia, increased ICP, myocardial ischemia, medications like bronchodilators and
ketamine
- Bradycardia:
• Causes: neostigmine, phenylephrine, opioids, beta blockers, succinylcholine, high spinal or epidural
anaesthesia (if T1-T4 are also blocked), carotid sinus massage, Valsalva maneuver, increased ocular
pressure, distended bladder (vagal response), stimulation of pharynx, severe academia, hypoxemia
Delayed Awakening
- Causes: residual anaesthetic, sedative or analgesic (commonest), hypothermia, hypotension and cerebral
hypoperfusion, hypoglycemia, hyponatremia, stroke, intracranial bleed
- Mx: treat underlying causes (e.g. apply forced air warming blanket, correct metabolic disturbances), drug
reversal with naloxone (reverse opioid) or flumazenil (reverse BZD)
Delirium
Pain, hypercarbia, hypoxia, hypotension, metabolic disturbances
Agitation
- Causes: pain, bladder distention, inadequate reversal of paralytics/muscle relaxants (patient struggling to
breathe), systemic problems (hypoxemia [do pulse oximetery!], acidosis [ABG], hypotension [vitals], electrolyte
abnormalities), surgical complications (e.g. occult intra-abdominal haemorrhage), alcohol/drug withdrawal
- Management: ensure ABCs, check neuromuscular blockade using nerve stimulator, review Hx, PE and check
medications, neurological examination (unilateral or lateralising signs), conscious level charting, rule out
biochemical abnormality (e.g. hypocount), treat cause
Shivering
- Very common, uncomfortable for patient
- Causes: hypothermia (core body temperature <35˚C), use of volatile agents, after epidural anaesthesia, sepsis,
emerging from anaesthesia (coming up from different stages, core temperature is not low)
- Effects*: increased O2 consumption and CO2 production, increases peripheral vascular resistance,
coagulopathy (impairs platelet function, decreased clotting factors), increased infection rates, cardiac
arrhythmias, myocardial ischemia (heart has to work harder), disrupts surgical wounds, prolonged
neuromuscular blockade under atracurium, delayed awakening
- Management:
• Prevention: avoid volatile agents, prevent heat loss (warmed fluids, blood, warming blanket,
humidifier)
• Warming devices: blanket, radiant heat warmer, convective warming system
• O2 therapy
• Pharmacological: low dose (sub-analgesic dose) IV pethidine can cause muscle to stop contracting so
patient will stop shivering, but doesn’t mean patient is not feeling cold
Post-operative Nausea & Vomiting (PONV)

- Leading cause of unexpected admission, patient discomfort and dissatisfaction, a/w morbidity (aspiration,
increased intraocular and intracranial pressures, may disrupt surgical sutures and cause haematoma)

- Causes:
• Patient factors: young women and children, obesity, non-smoker, past Hx of PONV, past Hx of motion
sickness, hiatal hernia
• Anaesthetic/drug factors: IV opioids, inhalational agents, gastric insufflation from facemask ventilation,
hypotension after spinal or epidural anaesthesia
• Surgical factors: laproscopic Sx, GI (increased abdominal pressure) Sx, gynae Sx, peritoneal or intestinal
irritation, ENT Sx, middle ear irritation, extraocular muscle traction (usually strabismus Sx), prolonged
Sx with longer duration of GA
• Post-op factors: IV opioids, post-op oral fluid intake
- Management:
• Identify those at risk of PONV, part of routine pre-op assessment
• RA instead of GA, or use TIVA if possible
• Use less emetic drugs (e.g. opioids), use more prophylactic anti-emetics (e.g. propofol)
• NGT to reduce gastric distention, prevent hypotension, adequate fluids for rehydration
• Anti-emetics: IV ondansetron 4-8mg 6-8h (acts centrally on vomiting centre), IV dexamethasone 4-8mg
intraop (can cause perineal pain if given to awake patients, don’t give to diabetics, how it decreases
PONV is unknown), IV droperidol 0.625-1.25mg 8h (need to be very careful cause can cause excitable
tissue conduction and QT prolongation), IV/IM metoclopramide 10mg 6h (acts peripherally, SE:
oculogyric crisis). D2 receptor antagonists like droperidol and metoclopramide physically constricts GIT
sphincter so that patient can’t vomit.
Discharge!criteria!
Introduction
- Monitored for minimum 30min in recovery ward
- According to modified Aldrete scoring system
General Condition
- Oriented to time, place, person
- Can follow commands
- No significant PONV
- Adequately controlled pain (mild): mild (≤3), moderate
(≥5), severe
Haemodynamic
- Haemodynamically stable
- BP within 20% of baseline pre-operative value
- HR and rhythm stable
Respiratory Status
- Able to protect airway and maintain ventilation and oxygenation
- Normal RR
acute!pain!
- Subjective experience: nociception + emotional

- Nociceptors à substance P is chemical mediator à modulation of pain (peripheral [allodynia, inflammatory
process around area that has been cut] and central sensitization)
Evaluation
- Type of pain: visceral, somatic?
- Location, at surgical site?
- Quality/character and intensity of pain: rating of pain score (VAS, Wong Baker faces, numerical) so that can see
if treatment is working
- Duration

- Effects on activities and function
- Effectiveness of current pain interventions, recurrence
Aims
- Provide subjective comfort
- Inhibit trauma-induced nociceptive impulses
- Reduce positive feedback loop so that acute pain won’t become chronic pain
- Blunt automatic and somatic reflex responses to pain
- Enhance restoration of function and patient can sit out of bed and reduce post-op complications like PE,
pneumonia
Post-operative Pain Characteristics

- Constant aching pain
- Acute exacerbation of pain added to basal pain due to activities e.g. coughing, getting out of bed,
physiotherapy, dressing changes
- Self-limiting usually
- Progressive improvement over relatively short period
Benefits of Post-operative Pain Relief

- Myocardial infarction or ischemia
- Risk of tachycardia and dysrhythmia
- Impaired wound healing:
• Behavioural reasons: patient moves around so more stretching and trauma, or doesn’t move around so
poorer perfusion to wound
• Molecular reasons: higher cortisol, higher adrenaline (vasoconstriction so poorer perfusion)
- Risk of atelectasis
Factors affecting Analgesic Needs

- Age of patient
- Gender
- Coexisting medical conditions e.g. hepatic or renal failure
- Cultural factors and personality
- Preoperative patient education
- Site of operation: thorax and upper abdomen worst
- Individual variation in response and pain threshold
- Attitude of ward staff
WHO Analgesia Ladder
- Multimodal
- Usually don’t give pethidine cause can cause euphoria and popular for
substance abuse
- LA infiltration also helps relieve pain, given during Sx itself
Management
- Pre-emptive, patient education
- NSAIDs, COX II (celecoxib, can’t protect against GI bleeding completely but better than NSAIDs): IV, oral,
suppository
- Paracetamol: IV, oral, suppository
- Opioids: IM, IV
• Morphine usually chosen as analgesia in PACU as it’s short-acting and can last for until after discharge,
IV (2-5 mg) as oral will be too slow and some patients just had abdominal Sx and can’t feed yet
- Tramadol

- Patient controlled analgesia
- Regional anaesthetic techniques
Patient Controlled Analgesia

- Most commonly for morphine and fentanyl
- Medication delivered via IV route most of the time, or epidural catheter (patient controlled epidural analgesia
[PCEA]) or nerve block catheter
- Continuous infusion not used commonly cause may cause sedation since it’s given even when it’s not needed;
not commonly practiced but sometimes have background infusion with continuous basal rate and bolus doses
- Few minimal side effects
- Able to change settings: e.g. infusion rate, bolus volume, maximum allowable hourly dose, lockout time
• Lockout time: patient unable to stack bolus doses of opioids with repeated presses
- Additives: anti-emetics
- If patient administers too much analgesia, will experience sedation thus inhibiting further self-administration
- Example: morphine 1mg/dose, 5min lockout, 10mg/h max

17-18 Chong Kar Mun&#39;s Anaesthesia Notes

Hochgeladen von

Dokumentinformationen

Copyright

Verfügbare Formate

Dieses Dokument teilen

Dokument teilen oder einbetten

Freigabeoptionen

Stufen Sie dieses Dokument als nützlich ein?

Sind diese Inhalte unangemessen?

Copyright:

Verfügbare Formate

17-18 Chong Kar Mun&#39;s Anaesthesia Notes

Hochgeladen von

Copyright:

Verfügbare Formate

Anaesthesia

Chong Kar Mun

Perioperative Care Medicine

Monitored Anaesthesia Care

Chong Kar Mun Class of 2019 2

Class Description Mortality Rate (%)

Not really to predict peri-op risks or post-op

Chong Kar Mun Class of 2019 3

Chong Kar Mun Class of 2019 4

Chong Kar Mun Class of 2019 5

Chong Kar Mun Class of 2019 6

Assembly of Equipment (Self-inflating Bag-Valve-Mask System)

Sub-optimal Ventilation (Poor Chest Rise)

Chong Kar Mun Class of 2019 7

Chong Kar Mun Class of 2019 8

Chong Kar Mun Class of 2019 9

Simple Face Mask/Hudson’s Mask

Chong Kar Mun Class of 2019 10

Colour FiO2 O2 Flow Rate

Chong Kar Mun Class of 2019 11

Stages of General Anaesthesia

Components of General Anaesthetic

Stages of General Anaesthesia

Chong Kar Mun Class of 2019 12

Opioids 46 ANESTHESIA STUDENT SURVIVAL GUIDE

- Examples: morphine, hydromorphone, fentanyl and its derivatives (e.g.

Chong Kar Mun Class of 2019 13

- Potent analgesic and bronchodilator

Neuromuscular Blocking Agents

Chong Kar Mun Class of 2019 15

Chong Kar Mun Class of 2019 16

Factors affecting LA Action

① Fibre Size & Type:

LA Side Effects & Toxicity

Chong Kar Mun Class of 2019 17

Types of Regional Anaesthetic Techniques

Introduction to Central/Neuraxial Blockade

Chong Kar Mun Class of 2019 18

Complications of Central/Neuraxial Blockade

Peripheral Nerve Blocks

Chong Kar Mun Class of 2019 19

Choice of Level of Sedation & Anesthetic Technique

Patient Selection & Evaluation

Chong Kar Mun Class of 2019 20

Medications: Sedation/Analgesia & Reversal

- Don’t sedate if inability to rescue oversedation/support oxygenation/ventilation/haemodynamics, no code

Chong Kar Mun Class of 2019 21

Minimum Monitoring Standards in Anaesthesia

Oxygen-Haemoglobin Dissociation Curve

Chong Kar Mun Class of 2019 22

- Upstroke: ventricular contraction

Chong Kar Mun Class of 2019 23

Need for ECG Monitoring

Points to Take Note

Chong Kar Mun Class of 2019 24

- Measurement of CO2 concentrations in respiratory gas mixture

- AB: exhalation of dead space

Chong Kar Mun Class of 2019 25

Chong Kar Mun Class of 2019 26

Chong Kar Mun Class of 2019 27

Chong Kar Mun Class of 2019 28

Post-operative Nausea & Vomiting (PONV)

Chong Kar Mun Class of 2019 29

- Subjective experience: nociception + emotional

17-18 Chong Kar Mun's Anaesthesia Notes

17-18 Chong Kar Mun's Anaesthesia Notes