Dear current/future juniors,

This belongs to a rather incomplete series of notes I compiled in the process of my preclinical and clinical studies. As
you’ll notice when you compare this set of notes and those by others, this notes is

INTENDED TO:
 Emphasize on UNDERSTANDING over EXAM PREPARATION: a lot of materials/snippets from
wiki/UpToDate/textbooks are included in this set of notes and most of them are irrelevant to exams. Therefore,
DO NOT try swallow it whole a month before summative. It’s NOT meant to be efficient for exam preparation.
 Reflect MY OWN understanding: I use this set of notes as a form of ‘memory bank’ for retention of my
understanding at the time I study them. They are probably INACCURATE in a lot of places and MANY
PARTS WILL CONTRADICT YOUR TEACHING MATERIALS. Please read my notes with a pinch of salt
and always refer to the official teaching materials for exam memorization purposes.
 Reflect MY OWN interest: again, I added a lot of information that I found interesting as well as helping in my
understanding. Just skip those parts if you found them boring (eg. cardiac embryology, MSS anatomy etc.) :P

And NOT INTENDED TO:

 Cover the ENTIRE syllabus in the medical curriculum: note-making is an arduous process and there are a lot
of teaching materials are NOT covered that I would otherwise have. As of now, my notes would cover:
□ Majority of pre-clinical materials except (1) some public health / ethics lectures (2) the entire GI block (3)
pre-clinical practicals
□ Majority of medicine and surgery except (1) ENT (2) orthopaedics (3) paediatric surgery (4) clinical
pharmacology (5) medical oncology (6) geriatrics
□ Psychiatry
□ Obstetrics and gynecology
□ Paediatric cardiology
□ Ophthalmology
 Be efficient for EXAM PREPARATION purposes: as mentioned above, if you’re looking for a quick route to
safety then this really isn’t the right notes for you...
 REPLACE your textbooks and official teaching materials: again, I’m just a student and still early in my
learning journey - there are times when I read back on my notes and I want to shred it into pieces cuz it’s just so
inaccurate. The only reason I uploaded this set of notes is that I thought by providing a systematic summary of
what I learned you guys may be able to save some time. DO NOT take this as gospel and ALWAYS read with a
pinch of salt.

The medical curriculum is a long, arduous journey necessitating extraordinary perseverance and work ethic. There
are times when you will feel like you know absolutely nothing about medicine and will absolutely be
failing/deferring or whatever regardless of your previous academic standing and the efforts you made.
Whenever you feel down or burnt out, just remember that
(1) you are NOT alone in this journey and there’s at least 210 fellow students going through similar struggle as you;
(2) as hard as it may be to believe, majority (if not all) of us are going to graduate on time;
(3) treat your colleagues well - it’s already hard in itself so please don’t make this even harder for everyone.

Lastly, I would like to offer my heartfelt gratitude to Tiffany Didik for designing the beautiful cover for this set of
notes, and for contributing to some parts of it.
I hope you find this set of notes useful and may I sincerely wish you all the success in your future studies/career.

Best wishes,
Ryan Ho, M20
July 2018
May 2020 (edited)

- Page 2 of 42 -
 Content
1 Critical Care ..................................................................................................................................... 4
1.1 Primary Survey .............................................................................................................................. 4
1.2 Acute SOB and Airway Management ............................................................................................ 6
1.2.1 Approach to Acute SOB .................................................................................................................................... 6
1.2.2 Upper Airway Obstruction and Airway Management ....................................................................................... 7
1.2.3 Management of Selected Lower Airway Emergencies .................................................................................... 13
1.3 Shock and Fluid Management ..................................................................................................... 15
1.3.1 Physiology and Approach to Shock ................................................................................................................. 15
1.3.2 Principles of Fluid Management ...................................................................................................................... 18
1.3.3 Management of Hypovolemic Shock .............................................................................................................. 21
1.3.4 Management of Cardiogenic Shock................................................................................................................. 22
1.3.5 Management of Septic Shock .......................................................................................................................... 22
1.3.6 Management of Anaphylactic Shock ............................................................................................................... 24
1.4 AKI and Renal Support ................................................................................................................ 25
1.5 Cardiac Arrest, BLS and ACLS ................................................................................................... 28
1.5.1 Approach to Cardiac Arrest ............................................................................................................................. 28
1.5.2 Basic Life Support (BLS) ................................................................................................................................ 29
1.5.2 Advanced Cardiac Life Support (ACLS)......................................................................................................... 34

- Page 3 of 42 -
 1 Critical Care
1.1 Primary Survey
Ref: Lecture Notes – Clinical Anaesthesia Ch8, Davidson Ch8, Oxford Handbook Ch19
 Ask the patient simple question → normal verbal response = ABCD intact
 Framework:
□ Airway (A): look for features of airway obstruction → Mx to ensure airway patency
□ Breathing (B): look for adequacy of breathing → Mx to support breathing
□ Circulation (C): look for features of shock or cardiac arrest → Mx to treat shock/arrest
□ Disability (D): assess conscious level → Mx to restore neurological function
□ Exposure (E): to allow complete examination of patient
Part Clinical assessment Immediate Ix/Mx
Airway Look for
 See-saw respirations: paradoxical chest and abdominal
movements w/ chest collapsing when abdomen is bulging
out
 Use of accessory muscles of respiration
 Central cyanosis (late feature) Establish patent airway
Listen for  Remove cause
 Noisy breathing for partial obstruction □ Suction
□ Stertor (snoring): low-pitched inspiratory sound □ FB removal
indicating turbulent flow above larynx, usually due to from mouth
tongue occluding the pharynx
 Airway maneouver
□ Stridor: high pitched monophonic sound heard during
breathing indicating obstruction of large airways 1  Airway adjuncts
□ Wheeze: high pitched expiratory monophonic or  Advanced airway
polyphonic sound indicating obstruction of small High flow O2 AFTER
airways airway is cleared
□ Other sounds: gurgling (fluid in mouth/upper airway),
rattling (secretions in airway), crowing (laryngospasm)
 Silence for complete obstruction or apnoea
Feel for
 Expired air at mouth/nose
Breathing Look for
 Features of respiratory distress incl. use of accessory
muscles, tracheal tug, abdominal breathing, sweating, central Pulse oximeter to target
cyanosis SpO2 at 94-98%
 Rate, depth, rhythm and symmetry of breathing High-flow O2 at
15L/min using BVM
 Impedance to normal breathing incl chest deformity and
with reservoir
abdominal distension
ABG
 Other relevant features: ↑JVP, chest drains
Mechanical ventilation
Listen for
if apnoeic
 Noisy breathing indicating airway abnormalities
 Auscultate breath sounds for any chest pathologies

1
Inspiratory = extrathoracic (more common), expiratory = intrathoracic, biphasic = fixed obstruction.

- Page 4 of 42 -
 Feel the chest for
 Tracheal deviation indicating tension pneumothorax or
massive pleural effusion
 Symmetry of chest expansion
 Surgical emphysema or crepitus
 Percussion notes
Circulation Look for
 Pale/cyanosed/mottled limbs indicating poor peripheral
perfusion
 Collapsed central/peripheral veins indicating
hypovolaemia
 Engorged central veins indicating ADHF, cardiac Measure HR/BP
tamponade, tension pneumothorax or acute severe asthma Cardiac monitor
 Signs of ↓CO incl ↓GCS, oliguria Treat shock if present
 Signs of blood/ECF loss, eg. bleeding BLS/ACLS if cardiac
Listen for arrest
 S3/4 indicating ventricular dysfunction
 Heart murmur indicating valvular heart disease
 Pericardial rub indicating pericarditis
 Very quiet HSs indicating severe emphysema or pericardial
effusion
Disability  Pupil size and symmetry
□ Pinpoint reactive → opioid, pontine lesion Check h’stix ofr
hypoglycaemia
□ Mid-sized fixed → midbrain lesion
Check drug chart for
□Dilated fixed → severe global ischaemia or hypoxia, drug-induced causes
hypoglycaemia and ↓CNS function
Consider neuroimaging
□ Unil dilated fixed → uncal herniation, CN3 palsy for 1o CNS pathologies
 GCS
Exposure  ALWAYS expose adequately for complete examination to
be carried out

- Page 5 of 42 -
1.2 Acute SOB and Airway Management
Ref: Lecture Notes – Clinical Anaesthesia Ch8, Davidson Ch8, Oxford Handbook Ch19
1.2.1 Approach to Acute SOB

Upper airway obstruction Lower airway pathologies Other pathologies

 Depressed consciousness  Lower airway obstruction  Cardiac
 Intraluminal: (wheezing): □ ADHF
□ Secretions, blood, vomitus □ Acute COPD □ Cardiac tamponade
□ FB aspiration exacerbation  Neurological
 Mural: □ Acute asthma □ Stroke
□ Infections, eg. tonsillitis,  Alveolar congestion □ MG, GBS, spinal
peritonsillar/retropharyngeal (crepitations): cord lesion
abscess, epiglottitis, croup □ Acute HF  Toxic/metabolic
□ Trauma □ Pneumonia □ Salicylate OD
□ Tumour □ ARDS □ CO poisoning
□ Oedema, eg. anaphylaxis,  Other lung pathologies: □ Metabolic acidosis
angioedema, post-op □ Pneumo- or  Diaphragmatic splinting
□ Laryngospasm haemothorax in morbidly obese pt and
 Extramural: □ Pulmonary embolism abdominal ds
□ Penetrating neck injury □ Massive pleural  Severe anaemia
□ Tumour effusion  Psychogenic
□ Oesophageal FB □ Pulmonary contusion hyperventilation
 Decompensation

 Inability to speak = life-threatening (airway, breathing or neurologically compromised)

 Quickly assess ABCDE + take Hx if possible
 In physical examination, look for
□ Signs of respiratory distress → indicates need for immediate action
→ Anxious, sitting upright or in tripod position
→ Retractions (suprasternal, intercostal, subcostal) → indicates airway obstruction
→ Use of accessory muscles → fatigue of resp muscles → impending resp failure
→ Diaphoresis → extreme symphathetic stimulation
→ Cyanosis → late and uncommon feature, suggests severe hypoxia/metHbemia
→ Altered mental status → indicates severe hypoxia/hypercarbia OR other underlying causes
□ Respiratory signs → indicates cause of pathology
→ Stridor → upper airway obstruction
→ Wheezes → lower airway obstruction
→ Crackles → alveolar congestion
→ ↓AE → non-specific
→ Mediastinal deviation + ↑resonance → tension pneumothorax
□ Cardiovascular and other systems as indicated
 Monitor: SpO2, BP/P, temperature

- Page 6 of 42 -
1.2.2 Upper Airway Obstruction and Airway Management
A. Airway Management and Equipment
 Indications for airway management:
□ Need for airway protection, eg. upper airway obstruction, risk of aspiration, ↓consciousness
□ Need for ventilation, eg. anaesthesia with NMB, IPPV indicated (for eg. resp failure)
□ Need for oxygenation, eg. significant unrelieved respiratory distress, blood gas abnormalities

 Modalities of airway management:

Basic airway management (non-invasive)
 Airway maneouvers: head tilt-chin lift, jaw thrust
 Airway adjuncts: oropharyngeal airway,
nasopharyngeal airway
 Ventilation: mouth-to-mouth, mouth-to-mask,
bag-valve-mask (BVM)
 (Removal of underlying obstruction) if possible:
□ FB removal: abdominal thrusts, back
blows/slaps, chest thrusts
□ Suction: to remove secretions
Advanced airway management (invasive)
 Endotracheal intubation (gold-standard)
 Supraglottic devices (as alternative or 2nd
line after failed intubation)
 Surgical access to airway:
□ Needle cricothyrotomy (emergency)
□ Tracheostomy (more definitive access)

1. Basic Airway Management

 Basic airway maneouvers to push tongue away from soft palate
□ Head-tilt chin-lift when C-spine injury is NOT a concern
→ ± combination w/ manual in-line stabilization to stabilize
C-spine when jaw thrust fail to open airway
□ Jaw thrust when C-spine injury IS a concern (eg. trauma)
 Simple adjuncts:
□ Oropharyngeal airway (OPA):
→ Curved plastic tube flanged at oral end
→ lie over tongue and prevent it from falling back to pharynx
→ Selection: should go from incisor to angle of mandible
- Generally, size 2 for woman and size 3 for man
→ Insertion: either insert w/ airway curving upward and turn 180o
inside posterior pharynx OR insert w/ tongue depressor
(to avoid pushing tongue into posterior pharynx)
→ Indication: ALL patients requiring prolonged BVM
(preferred over NPA alone)
→ C/I: NEVER inserted if conscious (induces gag reflex)
□ Nasopharyngea airway (NPA):
→ Round, malleable plastic tubes flanged at nasal end
→ lie along floor of nose and curve around into pharynx
→ Selection: should go from tip of nose to angle of mandible
→ Insertion: coated w/ lubricant/anaesthetic jelly beforehand
→ inserted along floor of naris into posterior pharynx behind tongue
→ rotate slightly if resistance is encountered
→ Indication: better tolerated than OPA → used when OPA is difficult or as adjunct to OPA
→ C/I: rare cases of intracranial NPA placemen t in basilar skull fractures

- Page 7 of 42 -
 Basic ventilation techniques: should be used ONLY after airway has been opened
□ Mouth-to-mouth ventilation: used in BLS only when no equipment available
→ Risk of infection and O2 enrichment impossible
□ Mouth-to-mask ventilation: used in BLS if available
→ Allows O2 supplement
→ One-way valve present → ↓↓potential risk of
infection by direct contact or airborne
□ Bag-valve-mask (BVM) ventilation with Ambu-Bag most
essential skill for ventilating patients
→ Adequate mask seal achieved by E-C grip (see RHS)
- ‘E’ on chin to achieve jaw-thrust motion
→ push chin onto mask held by ‘C’
- Two-hand technique (w/ 2 rescuers) more
preferable over single hand technique
→ Ensure patent airway by use of airway maneouvers or
airway adjuncts
→ Ventilate properly at 8-10/min if cardiac arrest and
10-12/min if respiratory arrest
→ O2 enrichment by
- W/o reservoir bag: 5-6L/min O2 can achieve FIO2 ~50%
- W/ reservoir bag: 5-10L/min O2 can achieve FIO2 ~80%

 Removal of underlying causes:

□ Foreign body aspiration:
→ Encourage to cough if only partial obstruction
→ FB removal from mouth ONLY if FB visible
- NEVER do blind finger sweep (pushes FB further in)
→ Rapid-sequence abdominal thrusts (Heimlich maneouver)
- Stand behind patient
- Make fist in one hand, thumb on belly
button and the other hand holds the fist
- Give firm, quick upward thrust
→ Chest thrust if unsuccessful or unable to
encircle abd or late pregnancy initially
→ Back blows if appropriate
→ Basic airway Mx if unresponsive
□ Secretions → suction
Recognition of FB aspiration:
 Ask whether the pt is choking
→ cannot speak = choking
 Silent cough
 Cyanosis
 Inability to speak or breathe
 Stridor suggests partial obstruction

- Page 8 of 42 -
 Difficulty in intubation:
2. Advanced Airway Management Look: obesity, receding chin,
 Endotracheal tube (ETT): dental condition, neck trauma
□ Indications: protects airway, inadequate ventilation/oxygenation, Evaluate: 3-2-1 rule
requires IPPV
Mallampati score
□ Preparations:
Obstruction: stridor, FB
→ Assess potential difficulties (LEMON)
Neck mobility
- 3-2-1 rule: thyromental distance <3 finger-breadths,
mouth opening <2 finger-breadths, anterior jaw subluxation <1 finger-breadth
- Mallampati score: pillars visible (I), fauces visible (II),
base of uvula visible (III), only hard palate visible (IV) Preparations for intubation
→ Prepare the equipments (STOP MAID) Suction
- ETT: 8mm (M), 7mm (F), age/4 + 4 (paediatrics) Tools for intubation:
- Direct laryngoscope: Macintosh 3 or 4 blade laryngoscopy blades, handle
→ visualizes upper airway Oxygen
→ can facilitate use of Yankauer catheter (for suction), Positioning
Magill’s forcep (for FB removal) or ETT insertion Monitors, incl. EtCO2,
- Bougie and syringe for ETT placement esophageal detectors, ECG,
→ Pre-oxygenate w/ 100% O2 for ~3-5min pulse oximetry, BP
□ Positioning: ‘sniffing-the-morning-air’ position Assistant, Ambu bag w/ face
→ Lower C-spine fixed, upper C-spine extended mask, Airway devices
→ Facilitates alignment of mouth, pharynx and larynx IV access
→ Requires manual fixation if C-spine injury Drugs for induction, NMB,
analgesics and other purposes
→ Neutral position if paediatric
□ Sedation: induction followed by paralysis
→ Induction: IV anaesthetic, eg. propofol
→ Paralysis: IV fast-acting NMB, eg.
suxamethonium
□ RSI vs routine induction:
2

→ RSI: NMB immediately after induction

→ apply cricoid pressure 3 but do NOT do BVM
→ ETT insertion AFTER onset of NMB (~30s)
→ Routine: IV anaesthetic induction
→ BVM to establish ability to ventilate
→ IV NMB given for paralysis
→ BVM again to establish ability to ventilate
→ ETT insertion (if failed, can do BVM)
□ Insertion:laryngoscopy blade to Rt of tongue
→ tongue pushed Lt and forward (do NOT lever on teeth)
→ epiglottis should rise to visualize larynx
→ ETT inserted through glottis into trachea

2
RSI = rapid sequence induction. Its main purpose is to reduce duration of unprotected airway. It is done when there is high
risk of regurgitation, therefore essentially ALL emergency cases (no fasting) OR planned surgery in high-risk patients (eg. in
pain/distress, hiatus hernia, high abd pressure (IO, obesity). It is contraindicated in predicted difficult airway as ability to
ventilate is NOT established by BVM attempts, therefore there is substantial danger of ‘cannot intubate, cannot ventilate’.
3
Cricoid pressure: apply pressure on cricoid (complete ring at C6 level) to occlude oesophagus and ↓risk of aspiration. This is
standard practice in HK but its evidence is controversial and may not be used in some countries eg. Europe.

- Page 9 of 42 -
□ Correct position:
→ Tip of ETT at midpoint of trachea ≥2cm above carina
→ Proximal end of cuff ≥2cm below vocal cord
→ Marking at mouth 20-22cm (F) or 22-24cm (M)
□ Malpositioned ETT can cause
→ Rt endobronchial intubation (too deep) → Lt atelectasis + Rt tension pneumothorax
→ Too shallow → accidental extubation, VC trauma, laryngeal paralysis (due to cuff pressure)
→ Oesophageal intubation → regurgitation, hypoxia
□ Confirmation of tracheal tube placement: if in doubt → take it out
→ Direct laryngoscopic visualization: ETT entering glottis
→ Auscultate both sides of chest and abdomen (occ. can hear breath sounds w/ ETT in oesophagus)
→ Look for symmetrical chest wall movement
→ Capnography (etCO2): MOST RELIABLE method
□ Complications of intubation:
→ Dental damage
→ Lacerations of lips, gums, tongue, pharynx, oesophagus
→ Laryngeal trauma
→ Oesophageal or endobronchial intubation
→ Accidental extubation
→ Insufficient cuff inflation/cuff laceration → leakage → aspiration
→ Laryngospasm or bronchospasm

- Page 10 of 42 -
 Supraglottic airway (SGA): airway sitting above glottis, used to refer to LMA and its variants
□ Indication:
→ As alternative to ETT, eg. in spontaneously
ventilating patients in GA
→ As second-line to ETT in difficult airways
→ As conduits for intubation, eg. intubating LMA,
useof flexible scope through LMA to guide ETT
□ Insertion:
→ Adequate depth of anaesthesia to avoid
coughing, gagging etc.
→ Lubricate LMA cuff
→ Hold LMA with glottis opening facing forward
→ press cuff upward against hard palate then go
backward and downward along palate until
resistance is encountered
→ Inflate cuff to ~40 cmH2O
□ Correct placement confirmed by easy PPV, appropriate
chest rise and normal capnogram trace
□ Pros: easier insertion, less traumatic
□ Cons: airway not fully protected and high pressure IPPV
cannot be used (>20cmH2O)
□ Complications:
→ Aspiration: NO full protection (~1/5000)
→ Airway complications: injury to glottis, upper
airway, irritation of oropharynx, laryngospasm

- Page 11 of 42 -
 Surgical access to airway:
□ Indication: last resort, i.e. all other measures have failed to maintain oxygenation
□ Needle cricothyrotomy:
→ Indication: failure to provide airway by any other means, severe anatomical deformity,
unrelieved upper airway obstruction, severe maxillofacial trauma
→ Equipment: large bore catheter (12-14G), 10mL syringe, 35mm tracheal tube connector,
self-inflating bag-valve or Sander’s injector (can blow high-pressure air inward)
→ Procedure: identify cricothyroid membrane
→ puncture with IV cannula connected to
syringe half-filled with saline
→ appearance of bubbles confirm
intratracheal placement
→ remove syringe and connect catheter to
bag-valve or Sander’s injector
→ inject O2 with high pressure at 1s
duration followed by 4s rest
→ expiration occurs via upper airway w/
escape of excess gas during insufflation
→ Considerations: adequate oxygenation but
limited expiration (narrow cannula)
→ ↓↓CO2 elimination
→ limited to ~30min use
→ attempt video laryngoscope intubation
or consult surgery for tracheostomy
→ Complications:
- Malposition → inability to ventilate
- Subcutaneous emphysema
- Catheter-related issues, eg. infection,
haemorrhage
- Barotrauma due to overly high RR w/ insufficient time for passive exhalation
□ Surgical tracheostomy: more definitive way of securing airway access

- Page 12 of 42 -
B. Management of Upper Airway Obstruction
 Emergent airway management:
□ Visual inspection of airway + suction of debris
□ Airway maneouvers: head tilt-chin lift or jaw thrust to open up airway
□ Ventilation: BVM w/ reservoir + 15L/min high-flow O2 ± airway adjuncts
□ ETT intubation with rapid-sequence induction (RSI) if fail any of above
□ Monitoring: pulse oximeter, non-invasive BP, ECG
 ACLS if cardiac arrest
 Considerations for ETT insertion:
□ If emergency (arrested or agonal state) OR unconscious, do direct intubation w/o giving drugs
□ If airway NOT predicted to be difficult, do intubation w/ rapid sequence induction (RSI)
□ If difficult airway predicted, choose a method that can maintain adequate oxygenation
→ Still do RSI if forced to act (eg. rapid deterioration of condition)
→ May attempt BVM or LMA if these are predicted to be likely successful
□ If failed intubation,
→ Consider alternative (eg. BVM, LMA, laryngoscopy-guided intubation) if still can oxygenate
→ One attempt at LMA and BVM ventilation if cannot oxygenate
→ NEEDLE CRICOTHYROTOMY if all else fail
 Other specific treatment:
□ UA inflammatory swelling: nebulized adrenaline in O2 (5mL 1:1000), IV dexamethasone 8mg
□ Post-op haematoma: consult surgeons → open surgical incision to allow evacuation of haematoma
□ Blocked tracheostomy: remove inner tube, deflate cuff, suction
→ remove tracheostomy tube if failed

1.2.3 Management of Selected Lower Airway Emergencies

Condition Salient features Management
 High flow O2 to keep SpO2 94-98%
 Severe dyspnoea  Repeated 5mg salbutamol nebulized with O2
 Wheeziness (d/dx COPD)  IV hydrocortisone 100mg or
 Severe attack defined as PO prednisolone 40-50mg
Acute severe □ Unable to complete  If unresponsive, then give
asthma sentences in one breath □ Slow IV MgSO4 2g
□ RR ≥25, HR ≥110 □ Add nebulized ipratropium 0.5mg
□ PEF 33-50% of best or  Repeated reassessment every 15min
predicted  ABG if SpO2 <92% or life-threatening
 Consider D/C if PEF >75% 1h after Tx
 Nebulized salbutamol 5mg/4h
and ipratropium 500mg/6h
 Controlled O2 to keep SpO2 88-92%
if SpO2 <88% or PaO2 <7kPa
Acute COPD  Increasing cough, SOB
 PO prednisolone 30-40mg QD ×5-14/7
exacerbations  Wheeziness
 PO amoxicillin if evidence of infection
 Consider NIPPV, IV aminophylline or IV
doxapram 1.5-4mg/min if no response
 Consider intubation if everything else fails

- Page 13 of 42 -
  Unequal chest expansion
 Chest wounds
Pneumothorax  ↓AE ipsilaterally
 Hyperresonance
 Surgical emphysema
Severe resp distress
Distended neck veins
Cyanosis
↓↓chest wall movement,
Tension
pneumothorax absent breath sounds,
hyperresonance
ipsilaterally
 Contralateral mediastinal
deviation
 Fever, rigors, malaise,
anorexia, ± confusion
 Septic shock
 Cough with purulent
Pneumonia sputum ± haemotysis
 Pleuritic chest pain
 ↓AE, crackles, bronchial
breathing, percussion
dullness
 Chest pain or haemoptysis
 Distended neck veins
Pulmonary  S/S of DVT
embolism  Pleural rub
 PSM at tricuspid (acute TR
murmur)
 Cough w/ pink, frothy
sputum
Acute  Distended neck veins
pulmonary
 Fine crackles, wheezes
oedema
 Gallop rhythm
 Displaced heaving apex
- Page 14 of 42 -
 High flow O2 with reservoired BVM
 CXR to assess size of pneumothorax
□ Aspiration if >2cm + 1o pneumothorax
□ Chest drain if failed drainage or 2o
 High flow O2 with reservoired BVM
 Rapid IV fluid bolus
 Emergency needle aspiration with 14/16G
needle into 2nd ICS, MCL
 Chest drain insertion at 5th ICS, MAL
 O2 supplementation to target SpO2 94-98%
 IV fluid replacement for hypotension/shock
 Empirical IV antibiotics
 CXR, ABG, microbiological workup
 Consider CPAP, NIV or IPPV if hypoxic despite
O2 to recruit lung parenchyma
 High flow (10-15L/min) O2 with reservoired
BVM
 Start SC LMWH or IV UFH until dx confirmed
 CXR, ECG, ABG, D-dimer, CTPA for dx
 IV fluid bolus 500mL if ↓BP
 Inotrope/vasopressor if persistent ↓BP
 IV tPA if circulatory collapse
 Sit patient upright
 High flow (15L/min) O2 with reservoired BVM
 If stable BP, optimize cardiac workload by
□ IV frusemide → ↓preload, ↓afterload
□ IV diamorphine → ↓preload, ↓afterload
□ IV nitrate → ↓preload, ↓afterload
 If unstable BP, treat cardiogenic shock by
□ Inotropes if high or normal filling pressure
□ IV plasma expander if low filling pressure
□ IABP or ECMO if still unstable/refractory
 If respiratory failure, initiate ventilatory support
□ CPAP (↓preload)
□ Intubation with IPPV
 ECG, CXR, coronary markers for cause
1.3 Shock and Fluid Management
1.3.1 Physiology and Approach to Shock
Ref: Lecture Notes – Clinical Anaesthesia Ch8, Davidson P.190, JC WCS11, UpToDate
 Shock: inadequate oxygen delivery (DO2) to meet cellular metabolic demands
□ Oxygen delivery (DO2) = CO × CaO2
□ Oxygen content (CaO2) = Hb × SaO2 × 1.34(4) + PaO2 × 0.027(5)
□ NOT defined as ↓BP (late manifestation, may also be orthostatic or relative instead of absolute)

 Stages of shock:
□ Pre-shock (compensated shock): compensatory changes to ↓tissue perfusion
→ Features: tachycardia, modest Δs in BP, ↓urine output, mild-moderate ↑lactate/BE
□ Shock: compensatory changes overwhelmed
→ Features: ↓BP and S/S of tissue hypoperfusion, eg. oliguria, cold and clammy skin
□ End-organ dysfunction: multiorgan failure and death
→ Features: acute renal failure, severe ↓BP, mental obtundation and coma
 Note that different tissues have different abilities to tolerate hypoxic environment
□ Fibroblasts/epidermis/skeletal muscles (hours)
□ Myocardium, hepatocytes, renal (30min-2h)
□ Neurones (3-5min) (can’t do anaerobic respiration)

 Classification of shock: classically divided into hypovolemic, cardiogenic, obstructive, distributive

Low cardiac output
Clinically characterized by features of ↓CO
 Hypotension with narrow BP
(↑DBP due to reflex vasoconstricton;
↓pulse pressure due to ↓CO)
 Compensatory tachycardia 6 and
tachypnoea
 Cold, clammy and cyanotic skin
 Weak peripheral pulses
There may also be features of ↓perfusion
 Hyperlactataemia and lactic acidosis
 Oliguria
 Mental status changes
Hypovolemic shock
 Due to ↓intravascular volume → ↓preload
 Causes: haemorrhagic (eg. trauma, GI bleed) vs
non-haemorrhagic (eg. GI, skin, 3rd space loss)
 Clinically recognized by features of ↓preload
□ ↓skin turgor, dry mucous membrane
□ Collapsible IVC on imaging
Low peripheral resistance (distributive)
Clinically characterized by features of ↑CO
 Hypotension with wide BP
(↓DBP due to peripheral vasodilatation;
↑pulse pressure due to ↓afterload)
 Compensatory tachycardia and tachypnoea
 Warm peripheries
 Bounding peripheral pulses
There may also be features of ↓perfusion
 Hyperlactataemia and lactic acidosis
 Oliguria
 Mental status changes
Septic/SIRS-related shock
 Due to systemic inflammatory response
syndrome (SIRS)→ vasodilatation
 Causes: infectious vs non-infectious
(eg. pancreatitis, burns, amniotic fluid/fat/air embolism)
 Clinically recognized by S/S of inf’n/infl’n
□ Fever or hypothermia

4
Hufner’s constant: 1.34mL O2 can be carried by every 1g Hb.
5
0.027mL O2 dissolved in plasma per each kPa pO2.
6
Tachycardia is often an early sign of shock esp if blood loss is suspected. This is important to note before anaesthesia because
anaesthesia can block sympathetic response and trigger decompensation.

- Page 15 of 42 -
 □ ↓CVP <8mmHg on PAWP monitoring
Cardiogenic shock
 Due to cardiac pump failure → ↓CO
 Causes: cardiomyopathic (eg. MI, severe DCMP,
myocarditis), arrhythmogenic, mechanical
(eg. severe VHD, ruptured LV aneurysm, atrial
myxoma)
 Clinically recognized by features of
pulmonary oedema and ↑preload
□ Diffuse lung crackles
□ Distended neck veins
□ ↑CVP >12mmHg on PAWP monitoring
Obstructive shock
 Due to impeded LV filling → ↓CO
 Causes: pulmonary vascular (eg. massive PE),
mechanical (eg. tension pneumothorax, tamponade 7)
 Clinically recognized by
□ Distended neck veins with
□ NO signs of ↑preload/↓preload
□ Localizing features (eg. pneumonia)
Neurogenic shock
 Due to interruption of neurogenic vasomotor
control → inappropriate ↓HR, ↓SVR
 Causes: TBI, SCI, neuro-axial anaesthesia
 Clinically recognized by
□ Paradoxically slow HR due to loss of SN
control
□ Compatible Hx of CNS injury
Anaphylactic shock
 Due to severe type I hypersensitivity reaction
 Causes: food, medications, insect bites/stings
 Clinically recognized by anaphylactic S/S
□ Severe bronchospasm and angioedema
□ Urticaria, widespread flushing and
pruritus

 Approach to circulatory collapse:

□ Assess and secure Airway: no airway, no oxygenation, no use having a circulation
→ Airway management measures as required
→ Rapid sequence intubation usually indicated 8 in circulatory collapse
□ Assess and secure Breathing:
→ High flow O2 (15L/min) using face-mask and reservoir for ALL pt
→ Mechanical ventilation if intractable hypoxaemia/hypercapnia, resp distress or
↓consciousness
□ Assess and secure Circulation: depends on situation Primary goals are to ensure
→ Optimize preload by volume resuscitation Adequate CO to support delivery
± vasopressors (adrenaline, noradrenaline) 9 (which in turn depends on preload,
- Secure large-bore IV access (14-18G) afterload and contractility)
- Used when there is insufficient preload Adequate Hb for delivery
(eg. ↓CVP, dry mucosa, ↓skin turgor) Adequate MABP to ensure
→ Optimize afterload by vasodilators and intra-aortic adequate perfusion of vital organs
10
balloon pump (IABP)
- Used in cardiogenic shock only
→ Optimize contractility by inotrope (dobutamine) or antiarrhythmics (if in arrhythmia)
- Used in cardiogenic shock only
→ Optimize Hb by RBC transfusion to keep Hb 7-9mg/dL (10 if IHD)
→ Optimize MABP by vasopressors esp in distributive shock

7
Cardiac tamponade refers to collection of fluid/blood in pericardial sac compressing on the heart. It can complicate any kind
of pericarditis. Other causes include malignancy, trauma, rupture of free wall of myocardium complicating MI. Features include
dyspnoea, collapse, ↑HR↓BP, grossly ↑JVP, muffled HS w/ early S3, pulsus paradoxus, Kussmaul’s sign.
8
In shock cases, etomidate/ketamine are usually used as induction as proprofol and midazolam may worsen hypotension.
9
In hypovolemic shock, vasopressors are only used in short term and are primarily directed to transiently ↑BP to allow time for
replenishing fluid.
10
IABP inflates during diastole (to restore BP) and deflates during systole (to ↓afterload).

- Page 16 of 42 -
□ Assess and manage emergencies, eg. anaphylactic shock, tension pneumothorax
□ Evaluation of underlying aetiology:
→ Clinical evaluation for type of shock and aetiology
→ Clinical monitoring: BP/P, UO, fluid balance charts, cardiac monitor
→ Early investigations:
- ECG: arrhythmia, ST changes (ischaemia, pericarditis), low-voltage (pericardial effusion,
S1Q3T3/RV strain (PE)
- CBC/D: anaemia w/ bleeding (haemorrhagic shock), ↑eosinophil (anaphylaxis), ↑/↓WBC
(sepsis or stress response), ↓PLT (bleeding tendency)
- L/RFT: ↑U/Cr (shock-induced AKI), ↑ALT/AST (shock liver), electrolyte disturbance,
dehydration (hypovolemia)
- V/ABG + lactate: lactic acidosis (poor tissue perfusion), assess need for ventilation
- Cardiac enzymes/BNP: myocardial infarction (may be cause or result to shock)
- Clotting + D-dimer: ↑PT/INR (haemorrhagic shock, septic APR), ↑D-dimer (PE, DIC)
- CXR: pneumonia, pneumothorax, pulmonary oedema, widened mediastinum (obstructive
shock), aortic dissection…
- ± bedside USG: cardiac pathologies, pneumothorax, pleural effusion, ascites, DVT…
- ± pulmonary artery catheterization: determine CVP when dx uncertain
□ Treatment of underlying pathology accordingly

- Page 17 of 42 -
1.3.2 Principles of Fluid Management
Ref: Lecture Notes – Clinical Anaesthesia P. 53, Anaesthesia at a glance Ch5, UpToDate, IBB WCS16

 Total body water (TBW) = 60% (M), 50-55% (F) of BW (~40L in 65kg male)
□ Intracellular fluid (ICF) = 60% TBW = 24L = 35% BW
□ Extracellular fluid (ECF) = 40% TBW = 16L = 25% BW
→ Intravascular fluid(plasma) = 1/4 of ECF = ~4L
→ Interstitial fluid = 3/4 of ECF = ~12L
 Daily fluid balance: (see RHS)
 Daily requirements:
□ Water = 30-40 mL/kg/day
□ Na+ = 1-1.17 mmol/kg/day
□ K+ = 0.9-1.3 mmol/kg/day
□ Ca2+ = 10-20mmol/day
□ PO43- = 18mmol/day
□ Mg2+ = 10mmo/day

 Fluid therapy should therefore meet

□ Basal requirement → maintenance fluid therapy (indicated whenever NPO)
→ ‘4-2-1 rule’: 4mL/kg/h for first 10kg + 2mL/kg/h for next 10kg
+ 1mL/kg/h for every 10kg afterwards
□ Preexisting and ongoing loss → replacement therapy to cover
→ Poor intake due to pain/cachexia
→ GI loss due to ↑output (vomiting,
diarrhoea) and ↓absorption (eg. LB
obstruction, paralytic ileus)
→ Bleeding
→ 3rd space loss, eg. in sepsis, inflammation
→ Fasting before IVF replacement

- Page 18 of 42 -
 Types of fluid therapy: crystalloid vs colloid
□ Crystalloid: solutions of crystalline solids in water
→ Isotonic solutions: contain electrolytes in a similar composition to plasma
→ equilibrated to extracellular compartment only
- Normal saline (NS, 0.9% NaCl): usual 1st line, cheap,
but risk of inducing hyperchloremic acidosis
- Balanced solution (eg. Hartmann’s solution or Ringer’s lactate): contains electrolyte
content similar to plasma
→ Glucose-containing: hypotonic but contains glucose
to replenish energy requirement
→ equilibrated to total body water
- 5% dextrose solution (D5)
□ Colloid: suspensions of high molecular weight particles
→ Equilibrated to intravascular fluid only
→ good for volume resuscitation
→ Eg. gelofusine (gelatin-derived), dextrans,
hetastarch (starch-derived, good for leaky
capillaries due to its ↑↑molecular size)

- Page 19 of 42 -
 Considerations in choice of fluid therapy:
□ Maintenance: standard regimen of 2D/1S Q6H + 10mmol KCl per pint for avg 60kg adult 11
□ Crystalloid vs colloid: replace intravascular or extravascular volume?
→ Colloid for rapid restoration of intravascular volume, eg. bleeding
- Every 1 unit of colloid given, 3-4× units of crystalloid or 13× units of D5 should be given
→ Crystalloid for correction of extravascular volume
→ For surgical patients, usually extravascular deficit > intravascular deficit
□ Buffered crystalloid vs isotonic saline: risk of hyperchloremic acidosis w/ massive NS infusion
→ Evidence equivocal, consider Ringer’s lactate if ↑↑risk of hyperchloremic acidosis
□ Rate of replacement: depends on haemodynamic status and on-going loss
→ Replace in small amounts and reassess (eg. 500mL/2h and reassess)
→ Consider risk of fluid overload in elderly, congestive HF, chronic RF or post-op patients 12

 Transfusion: usually indicated when Hb <7g/dL (<8g/dL in IHD pt)

□ Considerations:
→ Danger of anaemia > risk of transfusion
→ Symptom of anaemia severe
→ Age and co-morbidities of patient
- Low threshold if age >80y, underlying IHD, in shock w/ active bleeding
- High threshold if young, low baseline Hb, after curative cancer surgery
(transfusion causes immunosuppression → ↑risk of recurrence)
□ Types of blood products:
→ Whole blood: plasma and all elements of blood
- Effective in volume resuscitation
- However, granulocytes, platelets and F5/8 lose their functions after storage
→ Packed cells: blood with plasma (FFP), platelets (PLT concentrate) removed
- ↓risk of volume overload, only effective in correction of anaemia
□ Risks of transfusion:
→ ABO incompatibility (1/6000)
→ Allergic: febrile reaction (3%), urticaria (1%),
anaphylaxis (1/150,000)
→ ARDS (<1/10000)
→ Immunosuppression
→ Infections: hepatitis (1/150-1/5k), AIDS (1/200k),
CMV, EBV, bacterial infection
□ Massive transfusion: transfusion of >10 units
(or 1-2× blood volume)
→ Indication: severe trauma, ruptured AAA,
obstetric complications
→ Involves: empirical transfusion of packed cells:FFP:PLT = 1:1:1
(w/ repeated blood taking for Hb, clotting profile etc)
→ Risks: hypothermia, coagulopathy (haemodilution), hyperK, citrate toxicity (hypoCa, cardiac
dysfx), metabolic alkalosis

11
This refers to giving 500mL (1 pint or 1 bag) of solution composed of 2:1 mixture of 5% dextrose and normal saline with
10mmol KCl added every 6 hours .
12
After surgery, ↑↑stress hormone release (eg. ADH, aldosterone, catecholamines) favours Na and water retention.

- Page 20 of 42 -
1.3.3 Management of Hypovolemic Shock
Ref: Lecture Notes – Clinical Anaesthesia Ch8, UpToDate
 Causes:
□ Haemorrhagic: trauma, GI bleed, intra-op/post-op bleed, retroperitoneal bleed, ruptured ectopic
pregnancy, post-partum haemorrhage, uterine or vaginal haemorrhage, spontaneous haemorrhage
due to bleeding diathesis
□ Non-haemorrhagic: GI losses (eg. diarrhoea, vomiting), skin losses (eg. burns, heatstroke), renal
losses (eg. osmotic diuresis, adrenal insufficiency), 3rd space losses (eg. post-op, IO, pancreatitis)

 Clinical features: mainly characterized by ↑sympathetic outflow

□ Vasoconstriction leading to pallor, peripheral cyanosis, cold extremities, delayed capillary refill
□ Empty peripheral veins
□ Tachycardia
□ Sweating

 Management:
Vasopressors and inotropes
□ High flow O2 with BVM w/ reservoir
are generally unhelpful and are
□ Volume resuscitation: reserved as last resort to restore
→ Obtain large bore IV access tissue perfusion.
(14/16G at antecubital vein)
→ Take blood for CBC, RFT, clotting, T/S
→ Give rapid fluid challenge over 5-10min (as soon as possible)
- Give 500mL (or 1000mL) of crystalloid solution (balanced or NS)
- Colloid acceptable alternative
→ Reassess BP/P for every 5min → repeat fluid challenge if not responding
→ Consider Foley’s catheter for UO monitoring, ABG for oxygenation
→ Consider CVP monitoring if Hx of cardiac failure
→ Consider RBC transfusion depending on Hb if haemorrhagic shock
□ Treat underlying cause: may need urgent transferral to OT

- Page 21 of 42 -
1.3.4 Management of Cardiogenic Shock
Ref: Lecture Notes – Clinical Anaesthesia Ch8, UpToDate
 Causes:
□ Cardiomyopathic: MI, ADHF from DCMP, myocarditis, drug-induced
□ Arrhythmogenic: AF, AFlu, SVT, VT, VF, 3oHB
□ Mechanical: severe or acute VHD, septal or ventricular aneurysm rupture
 Clinical features:
□ Forward failure: pallor, peripheral cyanosis, cold extremities, delayed capillary refill, oliguria,
altered consciousness
□ Backward failure: dyspnoea, wheeze, cough with pink frothy sputum, cyanosis, basal crackles,
displaced apex, gallop
 Management:
□ Sit patient upright
□ High flow (15L/min) O2 with BVM with reservoir to keep SpO2 >94%
□ Optimize cardiac workload by
→ Inotropes (eg. IV dobutamine) if adequate filling pressure
→ Fluid resuscitation ± vasopressors if low filling pressure
□ Investigations and treatment for underlying cause should be done concurrently
→ RFT for any fluid/electrolytes abnormalities
→ ECG for any arrhythmias and MI
→ CXR for cardiac abnormalities and pulmonary oedema
→ ABG for acid-base abnormalities
→ Cardiac enzymes for MI
→ Echocardiogram if indicated
□ ACLS should be activated in cases of arrhythmogenic causes

1.3.5 Management of Septic Shock

Ref: Lecture Notes – Clinical Anaesthesia Ch8, JC96
 Terminology: (SEPSIS-3 guideline 2016)
□ Sepsis: life-threatening organ dysfunction caused by dysregulated host response to infection
□ Septic shock: subset of sepsis w/ circulatory and cellular/metabolic dysfunction a/w ↑risk of
mortality
□ Clinically identified by:
→ Vasopressor requirement to maintain MABP ≥65mmHg
→ Serum lactate >2mmol/L
→ No hypovolaemia
 Epidemiology:
□ Burden: 37.4% of ICU pt had sepsis, accounts for 24% of hospital mortality
□ Trend: ↑incidence, ↑organ failure, ↓mortality, poorer long-term recovery

 qSOFA score: used in out-of-ICU setting for quick recognition of sepsis with worse outcome
□ Criteria: RR>22/min, sBP <100mmHg, altered GCS
□ Significance: 0= mortality <1%; 1 = mortality 2-3%, ≥2 = mortality ≥10%

- Page 22 of 42 -
 Consequences of sepsis: manifests stereotypically as multi-organ dysfunction syndrome (MODS)
□ CVS: septic shock with high CO and vasodilatation
□ Lungs: ARDS with non-cardiogenic pulmonary oedema → T1RF and ↓lung compliance
→ Timing: acute onset ≤1 week of known clinical insult or new resp symptom
→ Chest imaging showing bilateral opacities (i.e. pulm oedema) not fully explained by effusion,
lobar or lung collapse or nodules
→ Origin: not fully explained by cardiac failure or fluid overload
→ Oxygenation: PaO2/FIO2 ratio ≤300 mmHg (i.e. inadequate oxygenation) despite PPV 13
□ Kidneys: acute renal injury
→ Clinically: acute oliguric renal failure resulting in low UO and haematuria
→ Biochemically: increased FENa (showing failure of RAAS response to conserve Na in
hypovolemia i.e. tubular damage)
→ Pathologically: ATN esp affecting PCTs
□ Blood: DIC with thrombocytopenia
□ Others: GI (GI bleeding, ileus), liver (jaundice), brain (septic encephalopathy), PNS (critical
illness polyneuropathy)
 Management of septic shock (Surviving Sepsis guidelines 2016):
□ Infection source control:
→ Identify + eradicate source asap if possible
→ Appropriate choice of IV broad-spectrum Abx asap ≤1h
- Each hour delay over first 1h → 7.6% ↓survival
- Wrong Abx → need for escalation → ↑mortality
□ Appropriate fluid resuscitation:
→ Adequate volume resuscitation:
- ≥ 30mL/kg IV crystalloids within first 3h of hypoperfusion
- Additional fluid guided by haemodynamic status
→ Crystalloid as initial fluid of choice ± albumin
- Do NOT use starch-based colloids → a/w ↑renal failure w/o survival benefit
- Balanced solutions preferred (↓risk of kidney events, eg. RF, renal-replacement therapy, death)
□ Appropriate use of vasopressors:
→ Initial target MABP at 65mmHg
- Higher BP targets (eg. 80-85mmHg) w/ similar mortality but ↑AF risk, beneficial if chronic HTN (↓RRT)
→ Norepinephrine as 1st choice ± vasopressin or epinephrine
- Inotropes does not address peripheral vasodilatation
- Dopamine w/ more beta effects → less arrhythmias
- Vasopressin more potent vasopressor effect but not superior
□ Other adjunctive therapy:
→ Appropriate ventilatory strategy: PEEP or BiPAP as
indicated
→ Appropriate renal replacement therapy: NOT to be used in sepsis-related AKI unless
otherwise indicated
→ Appropriate nutritional protocol: prefer early enteral feeding
→ Serum lactate as marker of tissue hypoperfusion for guidance of resuscitation
→ Glucose control to prevent hyperGly of >10mmol/L
- Maintaining normoGly a/w ↑mortality in large studies

13
Definition of ARDS, 2012.

- Page 23 of 42 -
1.3.6 Management of Anaphylactic Shock
Ref: Lecture Notes – Clinical Anaesthesia Ch6, Oxford Handbook of Medicine Ch19, UpToDate
 Causes:
□ Idiopathic
□ Allergens (IgE-dependent): food (peanut, shellfish, milk, egg, strawberry), insect stings, drugs
(antibiotics, biologics,), latex, food additives, semen (rare)
□ IgE-independent triggers: exercise, NSAIDs, radiocontrast agents, alcohol, cold, heat

 Clinical features:
□ Respiratory compromise: dyspnoea, wheezes, bronchospasm, stridor, hypoxaemia, angioedema,
nasal congestion, hoarseness
□ Shock: collapse, syncope, incontinence, ↓BP, tachycardia, dizziness
□ Skin/mucosal symptoms: generalized urticaria, pruritus, flushing, periorbital oedema, angioedema
□ GI symptoms: nausea, vomiting, diarrhoea, cramping abdominal pain

 Management: clinical diagnosis (no absolute C/I to epinephrine in anaphylaxis)

□ 0.5mg (0.01mg/kg) IM epinephrine 1:1000: first and most important treatment
→ Prefer in mid-outer thigh
→ Repeat every 5-15min as needed
→ Majority responds ≤3 doses, prepare IV epinephrine (0.5-1mL of 1:10000) if refractory
□ Secure Airway:
→ Immediate intubation if impending airway obstruction from angioedema
→ Cricothyrotomy if necessary
□ Ensure Breathing: 100% O2 as needed
□ Restore Circulation:
→ Place pt in recumbent position and elevate the feet to restore intravascular volume
→ Secure IV access and give rapid fluid challenge (1-2L IV NS) → repeat as needed
□ Subsequent specific therapy:
→ Antihistamines: chlorphenamine 10-20mg slowly IV or IM
→ Steroids: hydrocortisone 200mg slowly IV or IM
→ Bronchodilators: salbutamol 2.5-5.0mg nebulized or 0.25mg IV
□ Monitoring: pulse oximetry, BP/P, ABG ± UO, CVP if severe hypotension
□ Ix:
→ Plasma mast cell tryptase: elevation confirms reaction a/w mast cell degranulation
□ If refractory,
→ IV epinephrine infusion starting at 0.1mg/kg/min and titrate to BP, SpO2 and ECG
→ Vasopressors: other pressors as needed
→ IV glucagon for those on β-blocker starting at 1-5mg/5min followed by 5-15mg/min infusion

- Page 24 of 42 -
1.4 AKI and Renal Support
Ref: Lecture Notes – Clinical Anaesthesia Ch8, Davidson P.197, JC WCS80, UpToDate
 Acute kidney injury (AKI): abrupt and sustained ↓kidney function
 Defined as: an abrupt (≤48h) decline in kidney function evident as
□ An absolute increase in serum Cr of ≥26.5μmol/L
□ A percentage increase in serum Cr of ≥50%
□ A reduction in urine output with documented
oliguria of <0.5mL/kg/h for >6 consecutive hours

 Modern conception of AKI is described as a staged

model ranging from normal to death as indicated by
decreasing GFR and increasing renal damage

 Aetiology: classically separated into

□ Pre-renal disease (>1/2) due to ineffective perfusion
□ Renal disease (<1/2) due to intrinsic renal disease
□ Post-renal disease (<10%) due to obstructive uropathy (must be bilateral)
□ However, prolonged pre-renal and post-renal disease will progress to become ATN and
tubulointerstitial fibrosis respectively, i.e. intrinsic renal disease

Pre-renal disease Renal disease Post-renal disease

Hypovolemia Renovascular Prostate
14
Dehydration, eg. vomiting, diarrhoea NSAID- or contrast-related BPH
Haemorrhage Hepatorenal syndrome CA prostate
Burns Microangiopathic hemolytic anaemia Bladder
Cardiogenic shock Small vessel vasculitis Bladder neck tumour
3rd space losses Aortic dissection Urinary stones
Trauma or major surgery Glomerular UTI
Bowel obstruction Rapidly progressive glomerulonephritis Retroperitoneal fibrosis (rare)
Sepsis Tubulointerstitial
ATN: ACEI/ARB, NSAIDs,
radiocontrast, other nephrotoxins (or
pre-renal state)
AIN: antibiotic-related, CTD-related,
infections
Multiple myeloma

 Note that recognizing pre- and post-renal disease are particular important
because these are often rapidly reversible compared to renal intrinsic disease

 Clinical features: characterized by S/S resulting from diminished kidney function

□ Fluid overload: oedema, hypertension
□ Oliguria (<0.5mL/kg/h): important early sign
□ ↑creatinine, hyperK ± hypoNa esp in hospitalized pts (w/ frequent RFT monitoring)

14
These may cause acute constriction of renal afferent arteriole

- Page 25 of 42 -
 Mx of AKI:
 Immediate approach to acute kidney injury:
(1) Mx of ABC
□ Ensure and manage ABC: ‘A dead person has no renal function.’
(2) Mx of reversible causes
→ Treat hypoxaemia by O2 therapy
(3) Mx of life-threatening
→ Treat hypotension by aggressive fluid resuscitation complications
- Takes time for UO to respond → do NOT give diuretics (4) Mx of underlying cause
□ Consider and reverse pre-renal disease:
→ S/S: dry mucosa, tachycardia, ↓CVP, ↓skin turgor, hypotension…
→ Mx: treat with appropriate fluid resuscitation
□ Consider and reverse post-renal disease:
→ S/S: palpable enlarged bladder w/ ↑residual volume, blocked catheter etc
→ Mx: directed to the underlying cause
□ Consider and reverse use of any nephrotoxic drugs:
→ Examples: NSAIDs, aminoglycosides, ACEI/ARB
□ Management of life-threatening complications:
→ Fluid overload: peripheral oedema, hypertension, pulmonary oedema
- Mx: IV loop diuretics 15 (eg. furosemide), dialysis
→ Hyperkalaemia: symptoms (arrhythmia, weakness) usually only when K > 6
- Mx: IV Ca, NaHCO3- infusion, dextrose/insulin drip, PO polysulphonate 16, dialysis
→ Metabolic acidosis: Kussmaul’s breathing
- Mx: IV bicarbonate, dialysis
□ Workup and management of underlying causes (see below)
□ Consider haemodialysis

 Haemodialysis: last-resort treatment for renal support

□ Indications:
→ Acidosis: metabolic acidosis with pH <7.1 that is refractory to bicarbonate infusion 17
→ Electrolyte imbalance: hyperK >6.5 or rapidly rising K that is refractory to medical Rx
→ Intoxication: drug removal in overdose
→ Overload: fluid overload refractory to diuretics
→ Uraemia: features of uraemia, eg. pericarditis, neuropathy, ↓mental status
□ Involves: usually pumped venovenous haemofiltration via central venous catheter
→ Consider admission to ICU

15
Use of diuretics is controversial in AKI and should only be used as a temporizing agent to relieve volume overload instead
of a dialysis-sparing treatment. There is little evidence for low-dose dopamine or mannitol.
16
Polystyrene sulphonate is an ion-exchange resin that allows removal of ions eg. K+ from the gut.
17
Bicarbonate infusion may be inappropriate in the setting of volume overload.

- Page 26 of 42 -
 Workup for underlying cause:
□ Clinical evaluation: clues to cause of AKI incude
→ Timing of onset of AKI: look for any important clinical changes around day of onset
→ Review of medications: ALWAYS done in AKI
→ Assessment of volume status: volume contraction vs volume overload
→ Drug rash may suggest acute interstitial nephritis
→ Stigmata of liver disease may suggest hepatorenal syndrome (or overdialysis)
□ Urinalysis: dipstick, urine microscopy of sediments, urine protein quantification ± UPE
→ Glomerulonephritis: proteinuria, haematuria w/ dysmorphic RBC or RBC casts
→ ATN: granular or epithelial casts
→ TIN: sterile pyuria
→ Multiple myeloma: undetectable urine protein by dipstick but ↑↑UACR
→ UTI: significant bacteriuria + sterile pyuria
□ Bloods:
→ Repeat RFT w/ eGFR: U >> C may indicate a pre-renal origin
→ SPE if clinically suspicious of multiple myeloma
→ Serological tests for potential markers for glomerulonephritis
□ Imaging: for any underlying urinary tract obstruction if no obvious cause identified
→ USG kidneys/ureters as 1st line for any hydronephrosis ± stones
→ Non-contrast CT pelvis for any stones
□ Kidney biopsy if reason still unclear

- Page 27 of 42 -
1.5 Cardiac Arrest, BLS and ACLS
Ref: AHA BLS/ACLS guidelines 2015, Lecture Notes – Clinical Anaesthesia Ch8, Davidson P.557, JC
WCS11, UpToDate, SC ACLS teaching
1.5.1 Approach to Cardiac Arrest
 Cardiac arrest defined as sudden and complete loss of CO (life-threatening emergency!)
 Causes:
□ Coronary artery disease (85%): myocardial ischaemia, AMI, prior MI with myocardial scarring
□ Structural heart disease (10%): AS, HCM, DCM, ARVD, congenital HD
□ Others (5%): LQTS, Brugada syndrome, WPWS, drug-induced TdP, severe electrolyte imbalance

 Can result from four different rhythms:

□ Shockable rhythms:
→ VF: totally uncoordinated contraction of ventricles
→ Pulseless VT: LV rate too fast to pump blood effectively
→ 80% reversed by defibrillation but 10%↓survival/min delay
□ Non-shockable rhythms: more common in hospital settings
→ Asystole: flatline on ECG without any QRS complexes 18
- May be restored by precordial thump or IV adrenaline
→ Pulseless electrical activity (PEA): no pulse despite
organized electrical activity
- Often due to catastrophic mechanical events
(eg. cardiac rupture, massive PE)
- Extremely poor prognosis if not reversed
→ degenerates into asystole soon

 Diagnosis: clinical!
□ Loss of consciousness
□ Absent of major pulses ≥10s

 Management: ‘chain of survival’

□ Early access: help is called immediately
□ Early basic life support: prompt CPR administration
□ Early advanced life support: correction of underlying arrhythmia or other causes

18
If only p waves are visible, then still regarded asystole.

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1.5.2 Basic Life Support (BLS)
 Basic life support (BLS): maneouvres that you can do with your hands, mouth and AED
□ Aim: aiming to maintain low level of ventilation and blood flow to vital organs during downtime by
→ Immediate recognition with activation of emergency response system
→ High quality cardiopulmonary resuscitation (CPR)
→ Rapid defibrillation
□ Rarely can reverse the cause on itself
→ a ‘holding operation’ until advanced life support (ALS) can be used to treat underlying cause
□ Rapid deployment essential (irreversible cerebral damage in 3-4 min)

 Approach: now use CAB approach

□ Ensure safety, eg. toxic or electrical hazards
□ Diagnose cardiac arrest within 10s
→ Unresponsive
→ No breathing 19 or only gasping 20
→ No definite carotid pulse within 10s
□ Activate emergency response system
→ Call 999 if outside hospital
→ Call hospital arrest team if inside hospital
→ Should retrieve AED by 2nd rescuer (if witnessed) or by lone rescuer (if alone) 21
□ Resuscitation as indicated
→ Recovery position if normal breathing
→ Ventilation alone if no breathing but normal pulse
→ Compression followed by ventilation at 30:2 (i.e. CAB approach) if no breathing + no pulse

 Chest compressive therapy:

□ Mechanism: ↑intrathoracic pressure and directly compress heart
→ achieve adequate coronary perfusion pressure (CPP) 22 and
perfusion pressure to brain to maintain blood flow and O2 to brain and
heart
□ Process:
→ Kneel by side of victim and place one hand on top of the other
→ Apply vertical pressure with heel of hand at lower half of sternum
→ Press down for 5-6 cm at 100-120/min → allow for recoil

19
Look for chest movement, listen for breath sounds, feel for air on cheek.
20
Gasping is a pre-terminal event due to brainstem reflex attempting to increase venous return to body. It can herald cardiac
arrest and should NOT be regarded as normal breathing
21
New AHA 2015 guidelines suggest that delivering shock is more important than continuing CPR as the latter offer little chance
of restoring normal rhythm
22
CPP = aortic diasBP – RA diasBP. A minimum of 15mmHg is required for ROSC.

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 Components of high quality CPR:
□ Push fast: 100-120/min 23 for both adults and kids
□ Push hard: 5-6cm 24
□ Allow complete recoil: ↓intrathoracic pressure to allow ↑VR
□ Avoid interruption 25: only acceptable for (1) rhythm analysis (2) rescue breaths (3) defibrillation
→ In particular, do NOT interrupt CPR for setting up IV drip!
□ Switching of compressor: switching of provider every 2min to ensure chest compression quality

 Expiratory air ventilation:

□ Occlude nose, maintain chin lift
□ Breathe deeply then blow steadily (1s) into mouth until visible chest rise
□ Can be done by
→ Mouth-to-mouth ventilation
→ Mouth-to-mask ventilation
→ Self-inflating bag via bag-valve-mask or advanced airway
□ Rate: 30:2 unless advanced airway (then 10 breaths/min)
→ Hyperventilation should be avoided 26

 Use of automated external defibrillator (AED):

□ Mechanism: analyze victim heart rhythm → gives voice instructions on whether
to deliver shock or continue CPR after rhythm analysis (very easy to use)
□ Reason:
→ VF is a common and treatable initial rhythm in adult witnessed arrests
→ Rapid defibrillation is Tx of choice for VF and pulseless VT
→ Highest survival when defibrillation given within 3-5min
□ Use:
→ Connect AED as soon as it is available
(reversing the pads will still work)
→ Stop CPR to allow rhythm analysis when prompted
(no matter whether you have finished the CPR cycle or not)
→ Give shock asap when prompted
→ Continue CPR immediately after shock for 2min or 5 cycles
→ Recheck rhythm every 2min → repeat shock if indicated
□ Note: DO NOT recheck pulse every 2min! 27

23
Pushing too fast is associated with inadequate compression depths.
24
Pushing too deep will ↑risk of non-fatal injuries such as rib fractures. However, risk of pneumothorax is low.
25
It takes time for CPP to increase during CPR. Any interruption will lead to drop in CPP and thus significantly compromising
chance of ROSC. One should aim to achieve a compression fraction (proportion of total CPR time where chest compression is
being done) of ≥60% (associated with ↑survival rates).
26
Hyperventilation (1) causes hypercapnia and ↓cerebral blood flow (2) causes ↑intrathoracic pressure resulting in ↓VR (3) is
likely to insufflate large amounts of gas into the stomach and results in regurgitation and aspiration.
27
Only the rhythm should be checked. If no AED/cardiac monitor is being applied, then chance of ROSC is very low and
rechecking pulse every 2min in CPR is just a waste of time and add to interruption of CPR.

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- Page 31 of 42 -
- Page 32 of 42 -
 Keep patient in recovery position if he/she is breathing:
□ Kneel beside victim, remove spectacles
□ Place arm nearest you at right angles to his body, elbow bent and palm upwards
□ Place far arm across chest with dorsum against victim’s cheek
□ Grasp far leg at thigh and roll victim towards you
□ Keep upper leg with hip and knee bent at right angles
□ Change to opposite side after 30min

 Adjuncts to CPR:
□ Airway and breathing management during CPR:
→ Triple maneouver should be done before ventilation
→ BVM used commonly in place of mouth-to-mouth in hospital setting
→ Airway adjuncts: OPA (or NPA) can be used together with BVM ventilation
→ Advanced airways: both LMA/ETT acceptable, used when BVM inadequate
- If may interrupt chest compression, delay insertion until pt fails to respond to initial
CPR/defibrillation or demonstrate ROSC
→ IPPV: can be used to free up rescuers hands if prolonged resuscitation
→ Oxygen: give O2 at FIO2 as high as possible
□ Continuous monitoring: may include capnography, arterial BP and SvO2
□ Ultrasound: may be used to help assess myocardial contractility and identify potentially treatable
causes of cardiac arrest as long as does not interfere with resuscitation

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1.5.2 Advanced Cardiac Life Support (ACLS)
 Advanced cardiac life support (ACLS): protocol used within hospital setting
□ Still dependent on ongoing BLS!

A. Management of Cardiac Arrest

 Aim:
□ Restore normal cardiac rhythm if cause is tachyarrhythmia
□ Restore CO by correcting other underlying causes

 Initial action:
□ Call for help!
□ Give O2 at highest FIO2 as possible (to maximize O2 content in low blood flow state)
□ Attach monitors or manual defibrillator
□ Start CPR (at 2min cycles)

 While performing CPR, also initiate the following:

□ Rhythm-specific treatment, i.e. defibrillation if shockable
→ Always first thing to do no matter what you are doing
→ Continue CPR before (when the machine is being
28
prepared/charging) and 2min after delivering shock
→ Check rhythm only after 2min of CPR 29
→ Energy:
- 360J for monophasic 30
- 120-200J for biphasic depending on manufacturer
recommended (give 200J if in doubt)
- ↑energy for subsequent shocks
→ Use manual defibrillator over AED
(takes time to recognize rhythm)
□ Secure parenteral access (IV or IO)
→ Drug administration is of secondary importance!
(defibrillation and CPR more important)
→ DO NOT interrupt or delay chest compression to establish IV/IO access
□ Medical therapy, i.e. vasopressors and antiarrhythmics
→ Adrenaline 1mg Q3-5min as vasopressor For 1mg adrenaline,
Give 1 mL of 1:1000;
- Mechanism: α effect → constricts peripheral circulation
or 10mL of 1:10000.
→ ↑↑aortic diastolic pressure (>40mmHg)
Vasopressin is NOT useful as
→ ↑coronary and cerebral perfusion pressure
alternative.
(essentially, sacrifice peripheral circulation to maintain blood flow to
auto-regulated circulations, i.e. brain and heart)
- Timing: as soon as feasible if non-shockable; after 2nd shock (but usu given asap) if shockable 31
- Dose: 1mg (adults), 10μg/kg (paeds), ↑ if β-blocker or CCB overdose
- Effect: improve ROSC rate but no difference in survival to discharge

28
This optimizes nutrient and O2 supply to myocardium and ↑chance of successful defibrillation.
29
Even if the shock is successful, normal rhythm is rarely seen immediately after shock and is usually preceded by a period of
PEA or asystole.
30
A higher energy is required for monophasic shocks and thus results in more tissue damage. Majority of hospitals in HK use
biphasic shock machines nowadays because of ↓risk of tissue damage and ↑success rates.
31
Ideally, adrenaline should be given after 2nd shock so that if 1st shock is effective, the adverse effects from peripheral
vasoconstriction can be avoided. In practice, however, adrenaline is usually given asap in most clinical settings.

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 → Amiodarone 300mg as antiarrhythmic
- Mechanism: affects Na, K, Ca channels with α- + β-blocking properties
- Timing: usually after 3rd shock in VF or pulseless VT, give again after 5th shock if refractory
- Dose: 300mg or 5mgkg in 20mL dextrose IV/IO bolus followed by one dose 150mg (5th shock)
- Effect: ↑termination of arrhythmia, ↓admission but does not improve long-term survival or survival with
good neurological outcome
- Alternatives:
Lignocaine 1-1.5mg/kg IV then 0.5-0.75mg/kg IV at 5-10min interval to max 3mg/kg (if amiodarone
unavailable, less effective)
MgSO4 1-2g IV for VF/pulseless VT a/w torsades de pointes only (not for routinely)
□ Consider advanced airways:
→ Examples: supraglottic airway device, endotracheal tube
→ Indication and timing: NO agreed timing and necessity, depends on scenario
(eg. experience of clinician, whether defibrillator already ready → then do defibrillation first)
- Give 1 breath every 6 seconds (not 30:2) once secured advanced airway
(no need to stop chest compression, can be done simultaneously)
- If failed intubation once, then CALL FOR HELP (avoid multiple attempts)
→ Effect: no difference in outcomes between BVM and advanced airways
→ Advantage: free up hands of clinicians, allow IPPV and also facilitate post-arrest care
→ Disadvantage: risk of tube misplacement, requires elevation of bed → compromise CPR quality, tube
obstruction or dislodgement
→ Continuous waveform capnography:
- Most reliable method of confirming and monitoring correct ETT
placement
- Also monitor CPR quality (should achieve peak etCO2 >10mmHg)
- Helps monitor for ROSC (sudden ↑↑peak etCO2 to 35-40mmHg)
□ Identify reversible underlying cause: 5Hs + 5Ts
→ Hx + P/E: auscultation/percussion for pneumothorax/tamponade, assess volume 5Hs:
status from Hx and P/E
(1) Hypoxia
→ Send arterial blood for glucose, Hb, electrolytes, cardiac markers (2) Hypovolaemia
→ Ultrasound: bedside echocardiogram (for r/o tamponade) (3) Hypo/hyperkalemia (or
metabolic)
(4) Hypothermia
 Reassess every 2 min of CPR for
(5) Hydrogen ion (acidosis)
□ Rhythm → perfusing vs shockable vs non-shockable
5Ts:
□ If there is organized electric activity (i.e. not AF/asystole), (1) Tension pneumothorax
check for signs of circulation, eg. pulse, ↑etCO2 (2) Tamponade
□ EVEN IF a rhythm compatible w/ cardiac output appears, CPR (3) Toxins
should be continued for 1 cycle before stopping to recheck rhythm (4) Thrombosis (coronary)
and pulse (5) Thrombosis (pulmonary)

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 Shockable (VF, pulseless VT) Non-shockable (PEA, asystole)
 Deliver 1× biphasic shock at 120-200J
(or manufacturer recommendation)
as soon as can deliver defibrillation  Immediately resume CPR
Rhythm-  Immediately resume CPR for 1 cycle for 1 cycle (2min)
specific Tx  Recheck rhythm after 2min  Recheck rhythm/pulse after 2min
→ if still shockable, → restart CPR if still unshockable
deliver subsequent shocks
(escalate energy if possible, eg. 180-360J)
 Secure IV/IO access w/o interrupting
chest compression
 If failed IV access, consider  Secure IV/IO access w/o interrupting
interosseous or endotracheal routes chest compression
Drug  Give IV adrenaline 1mg every 3-5 min  If failed IV access, consider
treatment after 2nd shock interosseous or endotracheal routes
 Give IV amiodarone 300mg after 3rd  Start giving IV adrenaline 1mg every
shock, 150mg after 5th shock 3-5 min as soon as securing IV access
 Consider IV lidocaine 1-1.5mg/kg if
amiodarone unavailable
Other  Consider advanced airway  Consider advanced airway
treatment  Consider reversible causes (5H + 5T)  Consider reversible causes (5H + 5T)

 Other adjuncts: Interventions that are NOT routinely

□ Mechanical chest compression device, eg. LUCAS machine recommended:
(1) Na2CO3 – only for pre-existing
□ Capnography: failure to achieve etCO2 >10mmHg after 20min of metabolic acidosis, hyperK and
CPR can be used to guide termination of resuscitation TCA overdose
□ Extracorporeal CPR: NOT routinely used (takes ~1h to set up) (2) Ca – only for hyperK, hypoCa,
→ Indication: considered in selected patients where cause of cardiac arrest is CCB overdose
potentially reversible during limited period of mechanical support (3) IV fluid – only if definitely
hypovolemic
→ Mechanism: cannulate large veins and artery
→ venoarterial extracorporeal circulation and oxygenation (4) Precordial thump

→ Goal: support patients while reversible conditions are treated

→ Effect: ↑survival with good neurological outcome in selected patients
□ Precordial thump: striking middle of sternum with ulnar aspect of fist
→ May rarely be effective in terminating ventricular arrhythmias
→ May be considered when defibrillator not immediately ready for use
□ Steroid: methylprednisolone + vasopressin + adrenaline + post-ROSC hydrocortisone
→ Some evidence shown to be a/w better outcome than adrenaline + placebo
→ Evidence only limited to hospital arrest
→ Can be considered, more evidence needed before recommendation for routine use

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 Return of spontaneous circulation (ROSC) indicated by
□ Breathing returns
□ Pulse with BP returns (in NIBP or arterial waveform)
□ Sudden rise in etCO2 to ~40mmHg
□ Should check and support vitals including SpO2 and BP
 Post-cardiac arrest care:
□ Airway (A): consider definitive airway, eg. endotracheal tube
□ Breathing (B): ventilation ± waveform capnography to achieve
→ Oxygenation: titrate FIO2 to achieve SpO2 ≥94% 32
→ Normocarbia: titrate ventilation rate to maintain peak etCO2 35-40mmHg
→ Consider fibrinolytics if presumed or known PE
□ Circulation (C):
→ Treat hypotension to keep BP ≥90/65mmHg
- Usually achieved by IV fluid + vasopressors ± inotropes (if cardiogenic)
→ Actively look for and treat causes of cardiac arrest (5H5T)
→ 12-lead ECG asap after ROSC for acute ST elevation
→ prompt coronary angiography ± PCI if STEMI
□ Neurological care (D):
→ Targeted temperature management for all comatose pt with ROSC
- Rationale: ↓metabolic rate → ↓brain damage (allow ‘hibernation’)
- Target: 32-36oC for ≥24h (33oC similar outcome as 36oC), ↓ if seizures/cerebral oedema, ↑ if bleeding risk
- Means: cold IV fluid, ice packs with close monitoring in ICU
- Risk: coagulopathy if too cold → target higher temperature if bleeding risk
→ Manage seizures promptly using anticonvulsants
→ Sedation/analgesia may be considered if mechanical ventilation or induced hypothermia (to
suppress shivering) is required

32
Too high SpO2 may result in reperfusion injury due to ROS production.

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B. Management of Symptomatic Tachyarrhythmia
 General principle:
□ Secure ABC before evaluating rhythm by 12-lead ECG
→ Narrow complex, regular → likely SVTs
→ Narrow complex, irregular → likely AF
→ Broad complex, regular → likely monomorphic VT
→ Broad complex, irregular → likely polymorphic VT (or VF if pulseless)
□ Haemodynamically unstable patients need electrical cardioversion
□ Haemodynamically stable patients should be further worked up and given medical therapy

 Medical therapy:
□ AVN blocker for narrow complex tachycardia (for rate control)
→ Vagal maneouvers and IV adenosine for AVRT/AVNRT
- Vagal maneouvers: carotid sinus massage, Valsalva’s maneouver, cold packs, cold water
- IV adenosine: 6mg IV push followed by NS flush (1st dose), 12mg IV bolus (2nd and 3rd dose if required)
Should NOT be given if unstable or irregular/polymorphic wide-complex tachycardia
(may degenerate into VF)
→ IV non-dipine CCB or β-blockers for AF/AFlu
□ Antiarrhythmics for wide complex tachycardia (for rhythm control)
→ IV procainamide, amiodarone or sotalol for monomorphic VT
- IV procainamide: 20-50mg/min until arrhythmia suppressed (or other adverse effects)
- IV amiodarone: 150mg over 10min, repeat if recur
- IV sotalol: 100mg (1.5mg/kg) over 5min

 Cardioversion:
□ Mechanism: delivery of a current over a very short interval → depolarize heart
→ abolish all prevailing abnormal rhythm
→ hope that SAN will take the lead again as pacemaker
□ Cardioversion:
→ Synchronized shock with QRS complex → avoid R-on-T phenomenon (torsades then VF)
→ Usually requires less energy than defibrillation
→ Indications: unstable tachycarrhythmia with a pulse
- Eg. fast AF, fast AFlu, pSVT, VT with pulse
- Requires consent with sedation (midazolam) + analgesics (morphine) as it is quite painful
→ Energy: 50-100J (for narrow regular), 120-200J (for narrow irregular), 100J (for wide regular)
→ Absolute C/I: sinus tachycardia (only absolute C/I)
→ Relative C/I:
- Drug-induced arrhythmias, eg. digoxin OD
(may cause resistant VF due to unmasked ventricular ectopic focus)
- Recent arterial embolus: cardioversion may result in dislodgement of clot
- Patient with sick sinus syndrome
→ Cx:
- Inadvertent defibrillation if unsynchronized
- Skin burn
- Systemic embolism (1-3%) in AF
- Pulmonary oedema: rare, due to LV dysfunction or transient LA standstill
- Myocardial necrosis with transient ST elevation

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 Wide complex tachycardia (QRS ≥120ms) Narrow complex tachycardia (QRS <120ms)
Synchronized cardioversion should be done if haemodynamically unstable
 For SVTs and AFlu (regular narrow complex), give 50-100J biphasic shock and increase stepwise
 For AF (irregular narrow complex), give 120-150J biphasic shock and increase stepwise
 For monomorphic VT (regular wide complex), give 100J biphasic shock and increase stepwise
 For polymorphic VT (irregular wide complex), perform defibrillation as in VF
Consider precordial thump for unstable patients with ventricular tachyarrhythmia
If regular monomorphic (i.e. monomorphic VT If regular monomorphic (i.e. pSVT likely) and
likely) and haemodynamically stable, haemodynamically stable,
 Give IV procainamide, amiodarone or sotalol  Vagal maneouvers: 1st line, may terminate up
 If cannot be differentiated from SVT, IV to 25% pSVT (but other SVTs do not respond)
adenosine is relatively safe and can be used as  Push rapid IV adenosine 6mg followed by
diagnostic agent given that rhythm is regular 20mL saline flush (can repeat with two
and monomorphic (risk of degeneration into VF) attempts of 12mg bolus if failed)
 If unresponsive, should consider  Consider IV non-dipine CCB or β-blocker if
cardioversion and consult cardiologists failed
If polymorphic (i.e. polymorphic VT likely) and If AF/AFlu likely and haemodynamically stable,
haemodynamically stable,  IV β-blockers and non-dipine CCB as drug of
 Correct cause of long QT if QT is long choice for acute rate control
eg. stop associated drugs, correct hypoK/Mg,  Medical cardioversion (i.e. use of rhythm
and give IV MgSO4 2g bolus mixed with D5 control agents) usually not indicated
 Consider overdrive pacing or isoproterenol
 Otherwise should give IV amiodarone and
β-blockers for prophylaxis (likely due to MI)

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B. Management of Symptomatic Bradyarrhythmia
 Causes: 3oHB, Mobitz II 2o HB

 Approach:
□ Secure ABC: hypoxaemia is a common cause of bradycardia
□ Evaluate rhythm by 12-lead ECG
□ If haemodynamically stable, then can monitor and observe
□ If haemodynamically unstable, then should give atropine followed by pacing

 Medical therapy:
□ IV atropine 0.5mg every 3-5min: 1st line for acute symptomatic bradycardia
→ Max dose: 3mg (max 6 boluses per day)
□ Alternative drugs:
→ Dopamine infusion esp if a/w hypotension or after atropine fails
- Dose: usually 2-20μg/kg/min, titrate to patient response, taper slowly
→ Adrenaline infusion esp if a.w hypotension or after atropine fails
- Dose: 2-10μg/min, titrate to patient response

 Cardiac pacing:
□ Mechanism: regular delivery of a small direct current to stimulate contraction of the heart
□ Means:
→ Transcutaneous pacing (TCP): less reliable but easier done, 1st-line in emergency setting
→ Transvenous: more definitive with less tissue damage, to be done after TCP fails
□ Indications: bradycardia with unstable haemodynamic status
→ Should be on standby in 3o or M-II 2o HB with normal haemodynamic status
□ Use of transthoracic pacing:
→ Obtain consent! – not needed in arrest state but in symptomatic bradycardia (often awake)
→ Apply pacing pads and avoid bony surface
→ Sedate (midazolam) the patient + give analgesics (morphine) (VERY PAINFUL!)
→ Adjust current until threshold to obtain mechanical capture of heart
- Usually start at 70ppm, 30mA
- Can adjust by overshooting then slowly reducing to
get the capture or by slowly increasing current
- Electrical capture indicated by spike on ECG
- Mechanical capture indicated by palpable pulse
- Sometimes possible to get electrical w/o mechanical
→ Keep current at 5-10mA above threshold

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