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Flashcards in Airway and ventilation Deck (24)
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Rapid sequence induction.
a) Indications
b) Process: the 10 Ps
c) Induction agent is used in classic vs. modified RSI
d) What relaxant is used and why?

a) - Rapidly deteriorating situation
- Non-cooperative patient
- Oxygenation/ventilation compromise
- Full stomach (risk of reflux and aspiration); including laparoscopy - abdomen full of CO2

b) - Plan,
- prep,
- protect C-spine,
- positioning,
- pre-oxygenation,
- pre-treatment (optional: e.g. fentanyl, lignocaine and atropine),
- pressure (cricoid),
- paralysis and induction,
- placement with proof,
- post-intubation management

c) Classic RSI = Thiopentone
(modified RSI - Propofol)

d) Suxamethonium (depolarising)
- quicker onset (around 30 seconds compared with 120-180s for non-depolarising;
- however, rocuronium is quick also so may be used in a modified RSI)


a) Indications
b) Why muscle relaxant needed
c) Mallampati score
d) Cormack-Lehane classification
e) Misplaced tube - 3 locations
f) vs. tracheostomy
g) Why are ETTs and tracheostomies a 'definitive' airway

a) Anyone who can't protect their airway: reduced or fluctuating GCS, head injury (to regulate ICP), aspiration risks (laparoscopy, other major abdominal ops, bowel obstruction, other)

b) To relax tracheal opening (glottis)

c) 1 - 4: 1 (complete soft palate visualisation), 2 (tonsillar pillars not visualised), 3 (only base of uvula visible), 4 (soft palate not visualised at all)

d) 1 - 4: 1 (all glottis and cords visible), 2 (most of glottis), 3 (just epiglottis), 4 (nothing visible)

e) Endobronchial, oesophageal, herniating through cords

f) Inserted in front of neck

g) Cuffed tube below the vocal cords to create a seal and prevent aspiration


LMA (i-gel).
a) Insertion

a) Lubricate and advance into hard palate to avoid tongue. Tip of the airway should sit at oesophageal inlet


OP airway (Guedel).
a) Purpose
b) Alternative - indication, contraindication

a) Keeps tongue out of the way, aids bag mask ventilation (BMV)

b) NPA - aids BMV in conscious patient; CI - basilar skull fracture


a) Residual volume in normal lungs
b) Oxygen use per minute
c) Hence pre-optimisation to fill residual volume with lungs can provide patient with oxygen for how long?
d) How it's performed

a) 1500ml (1.5 L)

b) ~ 250ml/min

c) ~ 8 minutes ( = 1500/250)

d) 3 very large breaths or breathe normal for 2 mins

Note: pre-oxygenation has traditionally not been considered mandatory in all cases but reasonable to do so (the anaesthetist for Elaine Bromiley did NOT pre-oxygenate her)


Intra-operative oxygen.
a) How much should you give?
b) Why is 100% not recommended unless indicated?

a) Enough to maintain sats around 99-100%

b) Damages lining of the lungs, causes atelectasis when ventilation removed (nitrogen required to maintain alveolar volume - when oxygen replaces this quick diffusion causes alveolar collapse)


Airway positioning.

Neck flexed (use pillow) and occiput extended, open mouth, jaw thrust to move tongue


How to tell if airway/mask is correctly placed

- Symmetrical chest rising and falling
- etCO2 trace on machine
- Misting
- No leak


Two main techniques to manage breathing in theatre

- Spontaneous breathing - bag and mask, then insert LMA
- Controlled ventilation - induction, muscle relaxation and intubation


Invasive ventilation.
a) 2 types of control - preference in ITU vs theatres
b) Indications
c) How to oxygenate?
d) How to remove CO2?
e) Risks

a) Pres- or Vol-control:
- Pressure control (prevents barotrauma) preferred in ITU
- Either used in theatre, often volume control

b) - Pulmonary - severe pneumonia, ARDS, etc.
- Extra-pulmonary - unconscious patients, neuromuscular weakness (eg. MG, GBS)

c) - Alter FiO2 or PEEP (reduces shunt)

d) - Tidal volume or RR (to affect minute ventilation)

e) - Ventilator-associated pneumonia (VAP)
- Ventilator-associated lung injury (VALI): barotrauma, volutrauma
- Cardiac failure - reduced preload - reduced CO
- Failed extubation - need good physiological reserve pre-intubation if this is going to be likely


a) When?
b) Adjuvant treatment - why?

a) When patient can protect their own airway - they should have effective cough and be practically pulling the tube out themselves.

b) Furosemide - sudden drop from a positive pressure to negative pressure in the alveoli would cause any fluid in lungs to be sucked into the alveoli. Furosemide helps to prevent this happening.


Pre-operative assessment.
a) Clues of possible difficult intubation
b) PMHx - what should you establish about any conditions they have?
c) Reflux - how to ask?
d) Allergies - how to ask?
e) FHx - why important?

a) Mallampati 3-4, unable to protrude jaw anteriorly, neck extension difficulty, previous neck surgery, funny faces and beards, snoring/OSA

b) Does it lead to physiological decompensation (think ASA score) and does it require medicating?

c) "Any reflux, heartburn or indigestion" - get them to describe (e.g. vomiting, frequency, severity)

d) "Allergic to any medications... and anything else?" (strawberry/kiwi allergies = 50x more likely to have latex allergy)

e) Malignant hyper-pyrexia


Functional status.
b) ASA scores

a) Metabolic equivalent task - 1 = 70kg male at rest, 4 = climbing a flight of stairs (usually good enough for surgery if 4 or more)
b) ASA:
1 - no conditions.
1e - no conditions but some physiological derangement as a result of this current emergency
2 - medical condition but no physiological decompensation (e.g. well-controlled asthma)
3 - medical conditions with some decompensation (most patients in this category)
4 - severe decompensation (e.g. CCF, on HMV/LTOT)
5 - palliative, likely to die
6 - dead (organ retrieval).


Intubation: procedure

- Correct head and airway position
- Pre-oxygenate (ventilate with 100% O2)
- Laryngoscopy (hold with left hand, insert from the right and move tongue to the side)
- Lift epiglottis up to visualise vocal cords
- Go in from the right so as not to obscure view
- Vocal cords should be between the two black lines (tube is often at around 20cm at teeth)
- Inflate cuff
- Ventilate: should see symmetrical chest expansion, CO2 trace, misting of tube, maintenance of good oxygen sats, ventilator pressures at normal level (if very high, may be intrabronchial intubation - to deliver set tidal volume to one lung, pressures would need to be higher)


Difficult intubation.
a) Can't intubate - what should you do?
b) Why might poking the ETT not be desirable?
c) Can't ventilate - what should you do now?

a) Maintain SITUATIONAL awareness (don't become task-focused) - go back to BVM ventilation and ensure saturation are okay

b) Can cause trauma, bleeding and inflammation, which may lead to a catastrophic CICV scenario


End-tidal CO2.
a) If too low - could mean...?
b) If too high - could mean...?
c) When might you want to keep them particularly low intra-operatively?
d) When might you want to increase etCO2?
e) How can etCO2 tell you that a drug is working?
f) How does the etCO2 correspond to arterial CO2?
g) What physiological effects does CO2 have?

a) Low cardiac output

b) Ventilatory failure

c) Laparascopic surgery (pneumoperitoneum full of CO2 diffusing into the tissues), to lower ICP

d) To awaken patient (stimulate respiratory drive)

e) Inotropes - increase CO2 so increase etCO2

f) It is about 1.0 lower than arterial CO2 (needs to be lower to create concentration gradient and allow arterial CO2 to diffuse into alveoli and be expired)

g) Vasoconstriction, acidosis


Difficult airway society (DAS) guidelines.



Oxygen delivery: approximate FiO2 and flow rates
a) NC
b) Face masks
c) Venturi
d) NRB
e) BVM
f) Waters circuit
g) Why might some patients not achieve the stated/ intended FiO2 on a particular device?
h) Why might HFNC provide better respiratory support than 15L/min via a NRB?
i) Optimal oxygen saturations

a) - FiO2: 24 - 35%
- 1 - 4 L/min (>4 will dry out their nasal mucosa)
- variable performance devices

b) - FiO2: 35 - 60%
- 5L /min minimum to washout CO2 (range: 5 - 10)

c) - Fixed performance devices: of deliver required flow rate, it will deliver the exact FiO2 stated (24 - 60%)
- 5 options (colour-coded): 24% (2-4 L/min), 28% (4-6 L), 35% (8-10 L). 40% (10-12 L), 60% (12-15 L/min)
- Venturi principle: size of aperture determines the amount of air drawn in (so the FiO2)

d) - One-way valve with reservoir bag attached
- FiO2: 80 - 98% (if delivered with 15 L/min flow rate)
- Never 100% due to small quantities of re-breathing

e) - Crash trolley - cardiac arrests (should be used in combination with OPA/iGel* to ensure tongue out of the way so oxygen delivered to lungs and not stomach)
- Self-inflating bag and reservoir bag (wi
- Patient can either breathe spontaneously or you can give assisted breaths

*Can give continuous ventilation

f) - Gives feedback on how easy someone is to ventilate

g) - NC - if patient is mouth-breathing room air, this entrainment of air dilutes the delivered oxygen (FiO2)
- Severe cardio/respiratory failure means delivered FiO2 to the airways doesn't necessarily equate to O2 delivered to the blood/tissues

h) - Severely breathless patient may have peak inspiratory flow rates* of > 100L /min, so a measly 15 L/min will not be sufficient to meet their demand
- A higher flow rate provided by HFNC will reduce work of breathing

*Note: flow rates are NOT the same as minute ventilation

i) - 94 - 98% (not 100% - can be dangerous)
- In some chronic retainers/ at risk of T2RF: 88 - 92%


Non-invasive respiratory support.
a) Types
b) Principle of inspiratory pressure
c) Principle of expiratory pressure (PEEP)
d) Indications

a) - CPAP

b) Pressure outside lungs > pressure inside lungs so forces air in along pressure gradient (this reduces WOB). Like having hair out car window

c) - PEEP prevents alveolar collapse, splinting open the smaller bronchioles and alveoli (alveolar recruitment)
- This reduces physiological shunt, therefore reducing V/Q mismatch

d) - Worsening T1RF - requiring FiO2 60% or more
- Type 2 respiratory failure
- Evidence of respiratory distress


V/Q mismatch.
a) Shunt = ?
b) Dead space = ?
c) V/Q mismatches are the basis for what type of respiratory failure?

a) - Alveoli that are perfused, but not ventilated (so the blood must SHUNT to other alveoli for gas exchange to occur)
- As happens in severe pneumonia, collapse, pulmomary oedema, etc.

b) - Alveoli that are ventilated, but not perfused
- As happens in PE, and in some patients with chronic COPD given excess oxygen

c) Type 1 RF


a) What is it?
b) Indications
c) Advantages
d) Disadvantages
e) Mnemonic: HI FLOW

a) - Humidifies oxygen to enable delivery of high flow rates via wide-bore (special) nasal cannulae
- Can achieve flow rates of around 60 L/min

b) - Acute T1RF (hypoxaemic respiratory failure)

c) - Well tolerated
- Lower risk of infection as airways are adequately humidified
- Can provide much higher FiO2 than conventional face mask (up to 70%)
- Can provide PEEP of up to around 3 cm H2O
- Washes out expired CO2 (ie. reduces

d) - Only provides small amount of PEEP
- Doesn't work effectively if mouth-breathing

- Humidified and heated
- Inspiratory demand met - if patient is very breathless, they will have very high natural flow rates (so a high flow rate is needed to meet this, and reduce WOB)
- Functional residual capacity improved (via PEEP)
- Lighter - easier to tolerate than face mask
- Oxygen dilution risk - if mouth breathing, entrainment of room air will result in lower delivered FiO2
- Washout of CO2


a) What is it?
b) Indications
c) Advantages
d) Disadvantages

a) - Application of continuous positive airways pressure, ie. PEEP to keep distal airways open
(RESPIRATORY support, but not VENTILATORY support)

b) T1RF = impaired OXYGENATION:
- fluid in the alveoli (e.g. LHF)
- alveolar collapse (e.g. pneumonia) -

c) - Larger amounts of PEEP provided, improving oxygenation and reducing work of breathing

d) - Less tolerated than NC - claustrophobia, discomfort, communication difficulties
- Can't eat or drink


BiPAP (aka NIV).
a) What is it?
b) Indications
c) Advantages
d) Disadvantages

a) - Inspiratory and expiratory support (VENTILATORY support) by 2 different pressure levels - IPAP and EPAP

b) - T2RF (VENTILATORY failure)

c) - Ventilation support throughout respiratory cycle, improves oxygenation and CO2 removal

d) - As for CPAP


Risks of excess oxygen therapy* in certain patients
a) Only in which cohort of patients?
b) Mythical explanation for this
c) Actual explanation for this (2 mechanisms)
d) Management of these patients

*Note: even in healthy patients, excess oxygen therapy (with prolonged saturations at 100%) can be damaging. Aim for 94 - 98%

a) Patients at risk of T2RF:
- Main group are COPD (especially if known retainer, previous respiratory failure or on LTOT)
- Also... NMD/CWD, other resp disease, OHS, etc.

b) Hypoxic drive...
- Respiratory drive in normal patients comes mainly from raised CO2 and pH (and to a much lesser extent from hypoxia)
- The (mistaken) theory then suggests that COPD patients must become tolerant of raised CO2 so they rely on their hypoxia to stimulate respiratory drive
- Therefore, if you give excess oxygen, this will turn off their hypoxic drive to breathe, causing respiratory arrest (in reality, this has been proven false)

c) 1. Worsening V/Q mismatch:
- In response to low oxygen levels and poor ventilation, alveolar capillaries in these areas constrict and blood is diverted to alveoli with better ventilation - this normalises V/Q and improves CO2 excretion
- When given high flow oxygen, alveolar capillaries dliate, which leads to increased perfusion of areas with poor ventilation - this increases physiological dead space (good perfusion, poor ventilation)
- Net result = reduced CO2 excretion (hypercapnia)

2. Haldane effect
- Haemoglobin has higher affinity for oxygen than CO2
- If you increase oxygen delivery, you displace CO2 from Hb, thereby reducing its excretion (hypercapnia)

d) - Take baseline ABG - what is their O2, CO2, HCO3-
- If hypoxic, provide them with oxygen* and aim for appropriate target Sats (maybe 88 - 92%)
- Monitor their sats and clinical response very frequently initially - eg. every 5 mins
- Recheck ABG a little while later (eg. 30 mins later) - how have they responded (is CO2 rising dangerously high?)
- Titrate oxygen therapy accordingly

*Hypoxia kills before hypercapnia, so if profoundly hypoxic, stick them on 15L via NRB initially to resolve hypoxia and take ABG - then when oxygen stable, titrate O2 down if necessary