Michael Grant Anaesthetics Emergency Medicine Notes PDF

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Anaesthetics & Emergency Medicine Notes
Medicine (Queen's University Belfast)
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Downloaded by Mimansa Dixit (mimansadixit@mgims.ac.in)
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POEM
Michael Grant
Notes based on QUB online Med Portal lectures, QUB student manual, NICE Guidelines,
Oxford Clinical handbook and various external online resources

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POEM: Page 2 of 68
LEARNING OUTCOMES 2014-2015 Cricothyroid membrane -

Location of insertion of
surgical airway
Airway Management Airway
Describe the gross anatomy of the upper airway
The upper airway or the upper respiratory system consists of the nose, oral cavity,
and pharynx (itself further divided into nasopharynx, oropharynx and
laryngopharynx), while the lower respiratory system describes everything below the
vocal cords (Tracheobronchial tree)
The primary functions of the upper airway are to conduct, humidify and warm air,
prevent foreign materials from entering the lower airway, and contribute to speech,
swallowing and smell.
List the symptoms, signs and causes of upper airway

obstruction.
Airway obstruction can be partial or complete. It is important to remember to look,
listen and feel; but if a patient is able to talk to you during normal assessment there is likely a patent airway.
LOOK LISTEN FEEL

Are they conscious? Partial: Coughing, gagging, Air movements at the mouth?
stridor, dysphonia, noisy Partial: YES
See-saw movements? Complete*: drooling, gagging, Complete*: NO
Accessory muscles? aphonia, silent
Central cyanosis?
*Complete obstruction will lead to a series of rapidly progressive events including cardiac arrest and death is
inevitable if the obstruction is not relieved in 3- 5minutes.
Causes of airway obstruction include:

• CNS Depression • Haemorrhage
• Foreign body • Laryngeal oedema (allergy, hereditary
• PNS disorder (Recurrrent Laryngeal n. palsy, angioedema)
hypocalcaemia) • Trauma
• Neuromuscular disorders (laryngospasm, • Burns
myasthenia gravis) • Neoplasm (upper airway cancer, vocal polyp)
• Infection (epiglottitis, bacterial tracheitis)
If patient can talk airway is patent !!!
Explain how the airway “collapses” in the unconscious patient and list in correct
order the approach to opening the airway
In patients who are sedated, anaesthetised or unconscious, the

commonest cause is due to loss of airway muscle tone. The usual
site of obstruction is the soft palate, followed by the epiglottis and
occasionally the tongue.
Fingers on HEAD TILT AND CHIN LIFT
both sides OR
of mandible JAW THRUST
This tenses muscles in the mouth floor causing the hyoid & larynx to be lifted away from the post. pharyngeal wall.
If unconscious but breathing, consider putting patient into the recovery position.
The commonest cause of airway obstruction is loss of airway muscle tone

Michael Grant

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Adjuncts are used to secure the airway once the

airway has been opened by either a head-tilt and Always remember to put gloves on first!
chin-lift or jaw-thrust manoeuvre Airway adjuncts POEM: Page 3 of 68
Display a practical knowledge of essential airway equipment, particularly:

• Guedel/Oropharyngeal airway (OGA)
• A basic airway adjunct used to prevent the tongue from partially or completely Prevents tongue from obstructing the airway
obstructing the airway. Unconscious patients
Can simulate a powerful gag reflex
• It is indicated only in unconscious patients and as it can stimulate a powerful
gag reflex (thus vomiting leading to airway obstruction and aspiration)
• The airways come in a variety of sizes that can be estimated by placing the
flange alongside the lips and the tip to the angle of the jaw
• Sizes in adults are:
o Large 100mm Guedel 4, Red
Adjuncts o Medium 90mm Guedel 3, Orange
o Small 80mm Guedel 2, Green
• The airway is inserted upside down until contact is made with the back of the
o Beware of heavy nasal
throat, then rotated 180
bleeding - Do not use in
Bypasses airway obstruction via the nose people with anticoagulants
Intact gag reflex
• Nasopharyngeal airway (NPA)
• The nasopharyngeal airway aims to bypass upper airway obstruction at the level of the
nose, nasopharynx, or base of the tongue.
• Advantages over the oropharyngeal airway as can be with an intact gag reflex i.e. it is
tolerated better in semi-conscious patients.
• The size of NPA will vary with patient size and is measured by placing it from tip of the
nose to the tragus of the ear
• The size is described in terms of the internal diameter of the airway (in mm) with large
adults as a size 8, medium sized 7 and small adults’ 6.
• Use a small amount of water-based lubricant and with gentle but firm pressure direct backwards and downwards
o Ensure that bevel faces the septum to protect structures as NPA passes through the nasal cavity
o Typically inserted into the right nostril, hence when the bevel is facing the septum in this nostril the curve in the
NPA follows the airway – so if inserting into the left, face bevel to septum then rotate 180 degrees when tip of NPA
reaches back of nasal caviy
• Placement is contra-indicated in patients with active nose-bleeds, known or suspected nasal fractures and known or
suspected basilar skull fractures
FOR ADJUNCTS: SOFT TO SOFT (Tip of nose to tragus for NPA), HARD TO HARD (incisors to angle of
mandible for Guedel)
MUST KNOW LMA FOR OSCE !!!
Supraglottic device
• Laryngeal mask airway (LMA) Sits in patient's hypopharynx and
covers the supraglottis
• The LMA is a supraglottic device that was
developed by a British Anaesthetist called Dr
Archie Brain in the 80’s to free the hands of the
provider with the benefit of less gastric distension.
• A small elliptical mask at the patient end is
designed to sit in the patients hypopharynx and
cover the supraglottis
• The Classic LMA has a pilot balloon that allows
the operator to inflate the masks cuff.
o The volume depends on the size and is
detailed below but a good rule of thumb for adult sizes (3 - Weight Size (of Max cuff
6) is to minus 1 from the size and multiply by 10 to give (kg) LMA) volume
you volume in mls. (mls)
Cuff volume
• Contraindications to LMA placement: <5 1 4
(Size - 1) x 10 5-10 1.5 7
o Non-fasted patients
10-20 2 10
o Morbidly obese patients Pregnancy 20-30 2.5 14
o Obstructive or abnormal lesions of oropharynx 30-50 3 20 Main
o Increased airway resistance and decreased lung compliance 50-70 4 30 ones
70-100 5 40
Sizes are written on the side of the device
Michael Grant
Once inserted, you can let go, you don't have to hold airway
Know sizes of LMAs
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POEM: Page 4 of 68
MUST KNOW LMA INSERTION FOR OSCE !!!
•LMA Insertion:
1. Hold the LMA, like a pen, with index finger of the dominant hand at junction of the mask and tube
2. Slide the LMA along and pushing into the iGel - Newer generation. Doesn't need to
hard palate, to prevent the tip from folding be inflated like a LMA, can also remove
gastric secretions!
over on itself and reduce interference from
the tongue LMA
3. Advance with gentle pressure until 0) First use syringe to check it inflates fine
1) Insert it into the patient's mouth in its deflated state
resistance is met. If necessary, continue 2) After insertion, use appropriate volume of air (LMA size - 1 * 10)
pressure on the tube with the non-dominant and inflate that volume of air using the syringe
hand to fully advance the LMA to its proper
position.
4. Remove dominant hand while applying
pressure to connector with non-dominant to
prevent LMA from coming out with hand
5. Once in place, inflate the cuff (with the
appropriate volume of air – e.g. (size – 1)*10) without holding the LMA to allow it to acquire its natural
position (Approx. 8 cm of the tube protrudes from the patient’s
mouth)
• Newer generations of airway equipment have built on Dr. Brain’s design;
one such commonly used instrument is the iGel. It is also a supraglottic
device but it does not require inflation, thus can be simply inserted into
the airway with the aid of lubricant and is useful in time-sensitive
situations.
o Also features a channel through for a NG tube to be threaded
LMA vs ET through and into the esophagus.
ADVANTAGES over ET DISADVANTAGES over ET

Placement is quicker and easier Gastric insufflations more likely
Less CVS stimulation during insertion Air leak likely at air pressure >15-20cmH20
Lower incidence of cough on removal Airway less effective protected from aspiration
Lower incidence of sore throat post-op Can cause laryngospasm
Useful in situations outside of operating theatre
• Endotracheal tubes
• An advanced airway recommended to be used only by those people
with advanced airway skills (such as anaesthetists)
• Can be nasal or oral
• Sized by internal diameter (mm)
• It requires specialised equipment and generally the administration of
hypnotic drugs and muscle-relaxants
• It is considered the only secure airway because it traverses through the
airway via the oropharynx or nasopharynx and passes through the vocal INTUBATION
cords to sit a few centimetres above the bronchial carina
• Following inflation of the cuff it is presumed that the lungs are
protected from gastric contents.
• Advantages:
o Protection from aspiration
o Access to tracheo-bronchial tree for suctioning of secretions
o Does not cause gastric distension (risk of regurge)
• Complications:
o Oesophageal intubation (no capnography, can be fatal)
o Endobronchial intubation (into one of the main bronchi, only one lung ventilated, risk of barotrauma)
o Impaction (Bevel tip pressed against tracheal wall, obstructs airflow, murphey’s eye can compensate)
o Herniation (Cuff occludes opening or compression of lumen from over-inflation)
o Stretching of tracheal wall (Over-inflation causes local pressure effects leading to necrosis)
Endotracheal tube is Endotracheal tubes used in longer surgeries !! Michael Grant

the only secure airway LMAs are used in shorter procedures !!
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Connecting patient to anaesthetic machine. Anaesthetic circuit.

Blue self-inflating bag. Positive pressure ventilation POEM: Page 5 of 68
• Supplementary Oxygen Delivery
• Self-Inflating Bags:
o Positive pressure ventilation (apnoeic/hypoventilated)
o Non-return valve between bag-valve-mask
• Anaesthetic circuits (image to right)
Suctions secretions or
blood from pharynx
• Suction equipment
• Used to suction secretions or blood
from pharynx before placing endotracheal
tube. Also used to suction contents of
stomach via a nasogastric or orogastric tube

• Typically, with a Yankauer Sucker
Used to guide tracheal tubes through
vocal cord or nasogastric tubes into
• Magill's Forceps oesophagus under direct vision
• Used to guide tracheal tubes through vocal cords or nasogastric tubes into
oesophagus under direct vision. Can also be used to place throat packs for
certain ENT procedures or remove foreign bodies from pharynx.
Display a practical knowledge of how to: Cervical

• Size and apply an adjustable hard cervical collar collar
• Determine collar size:
o Using finger widths, measure vertical distance from the shoulder to
the horizontal line from the bottom of the chin (may be marked)
o Adjust so that the distance between the marker/stud to the bottom of
the collar’s plastic (not foam)
• Insert the strap end of the collar under the patient’s neck
• Secure the collar using Velcro strap as soon as it emerges on other side
• Apply the “triad” of immobilisation to the cervical spine

• After the collar, apply supportive blocks either side of their head
• Apply two tapes to secure: C-Spine Management
o Right side of bed/backboard over inferior part of the right block across chin part of cervical collar
over inferior part of the left block left side of bed/backboard
o Right side of bed/backboard over superior part of the right block across patients forehead
over superior part of the left block left side of bed/backboard
• Understand the indications for and practicalities involved in the log-roll of an immobilised
patient
• Place patient’s arms over their abdomen and position 4 people – 1 at cranial end (co-ordinates roll), other 3 on
the side that the roll will be towards
Hands firmly either side of patient’s head: “3 over, 3 under”
1. Left hand over far shoulder, right over far hip (tallest
person)
2. Left hand over far hip, right under opposite thigh
3. Left hand under far calf, right under far calf
• When everyone is ready, co-ordinatior says “Roll right 90 ̊ on 3, 1...
2... 3”, then a separate person does what is required to the patient
e.g. feels spinous processesRemoval of clothing and debris
1. Examination of back of patient; head, neck, chest, back,
buttocks, back of legs, esp. wounds
2. Palpation: spine, chest, loins for pain / swelling /
crepitus (#pelvis is huge bleeding risk > hip binders)
3. Rectal exam: Perianal sensation, anal tone
• Co-ordinatior says “Roll back to bed on 3, 1... 2... 3” Logroll method
Michael Grant
KNOW C-SPINE MANAGEMENT FOR OSCE !!!
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LEARN !!!
Tracheostomy and Laryngectomy POEM: Page 6 of 68
State and discuss the management of a tracheostomy emergency using the

national tracheostomy safety project guidelines: Tracheostomy Emergencies
The creation of a stoma into the trachea (trache-ostomy) serves several functions in the intensive care unit:
• Bypass of an airway obstruction
• Removal of airway secretions
• Patients with neuromuscular disease and to facilitate the process of
weaning off ventilator support
There are two types of Neck Breathers:
1. Post Laryngectomy patients (obligate neck breathers) RED SIGNS:

• These people cannot be intubated via the mouth
2. Post Tracheostomy patients (larynx Intact) GREEN SIGNS:
• These people may be intubated via the mouth as they may still have a
patent upper airway – but intubation may be difficult Laryngectomy =
No mouth (No patent airway)
Tracheostomy =
Can mouth (Patent airway)
The management of these patients differ.
Post laryngectomy patients have an end stoma and

cannot ventilate via the upper airway. For this reason,
the National Tracheostomy Safety Project publish a
seperate algorithm that is in red (as seen on the left)
for laryngectomy patients and green for tracheostomy
patients (seen on right)
All patients with a tracheostomy should have a sign

above their bed detailing the type of tracheostomy
they have.
Methods of Tracheostomy Insertion

1. Percutaneous Dilatation
2. Surgical
Most tracheostomies are percutaneous and are inserted

by skilled anaesthetists,
• These stomas do not maintain their patency if
the cannula is displaced and the stoma shrinks
• They must be securely taped in place and any
concerns regarding a dislodged tracheostomy
you must contact the anaesthesia team
Michael Grant

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LEARN !!! Tracheostomy POEM: Page 7 of 68
Types of Tracheostomy Tube Lumen

1. Single and Dual Cannula Cannula used as an airway
The inner cannula in these devices serve as a simple means
of maintaining a patient airway as the inner cannula is
replaced as mucus and secretions accumulate. You need to
be aware that to connect the 'tracheotwist' double cannula
tracheostomy to a bag, valve and mask the inner cannula
must remain in situ.
2. Cuffed and Uncuffed
This is important information when faced with a blocked tracheostomy. By deflating the cuff
there may now be a space for some air to move buying time until the anaesthesia team
arrive. If faced with a bleeding tracheostomy ensure the cuff is well inflated as this may
tamponade the source.
3. Speaking Valves
Remove all valves and caps when faced with an emergency situation.
• Obstruction Obstructed tracheostomy Mx

1. Apply the look, listen and feel technique we have adopted for all patients and
determine if the tracheostomy is still patent.
o Ask the patient to cough and determine if they can bypass any obstruction. If the
tracheostomy is patent and patient is ventilating apply oxygen to the
tracheostomy site until the anesthetist comes
2. If the tracheostomy is not patent, remove any speaking valves and the inner
tube if present.
3. Attempt to pass a soft suction catheter through the tracheostomy, as this will
determine if patentcy and will help to remove any secretions that may have
accumulated
4. If you cannot pass the catheter, deflate the cuff if there is one and assess the
airway at the mouth and nose
o Is there any ventilation occurring at this site now that the cuff has been
deflated? If yes, apply Oxygen here and wait for the anaesthesia team
5. If the airway is still not obtained after these measures, tracheostomy will have to be removed
o Deflate the cuff and take it out
o Immediately reassess the patient and administer Oxygen where you determine ventilation is
occurring (Mouth or tracheostomy site). This is an airway emergency and the anaesthesia team should
be en route.
o While waiting, use a bag valve mask at the mouth and cover the stoma, attempt to place a LMA and
cover the stoma or attempt to cannulate the stoma.
Obstruction can often be prevented if there is humidification of the airway for new tracheostomies. Proper
constant humidification should prevent secretion blockage
o Never prescribe Saline nebs as a substitute as they actually make the situation worse.
• Dislodgement Dislodged tracheostomy Mx

1. Apply the ABCDE approach you use for all patients while the anaesthesia team is summoned. Keep calm and
assess the dislodgement:
o How has the dislodged tracheostomy affected the patient? Is the dislodgement partial or complete? If
able to ventilate wait for the anaesthesia team to arrive, safest to reinsert under controlled conditions
2. If airway obstruction has occured and you cannot wait for the anaesthesia team can you deflate the cuff to
improve the airway
o Assess using the look, listen and feel technique and apply Oxygen where you feel ventilation is
occuring.
Michael Grant

POEM: Page 8 of 68
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• Bleeding Bleeding Tracheostomy Mx

This complication usually occurs soon after insertion so is unlikely to be encountered on the ward. Minor bleeding
can be controlled by:
• Direct pressure (without compromising the airway) with or without Adrenaline soaked swabs while help is
summoned.
• Major bleeding will require a surgeon to place an artery forcep on the vessel, the patient will then be
stabilised and transferred to theatre
In any case do not attempt to remove the tracheostomy or deflate the cuff as this is the patient's airway and the
inflated balloon may in fact help tamponade the
Downloaded by bleeding.
Mimansa Dixit (mimansadixit@mgims.ac.in)
KNOW Fi02 VALUES FOR MCQs !!!
Hudson Facemask:
- Flow Rate: 4-15 l/min
- FiO2: 0.35 - 0.6
Ideal for claustrophobic patients and for those on long-term oxygen therapy
Nasal Cannula:
- Flow rate: 2-4 l/min (6 l/min)
- FiO2: 0.24-0.36 (0.44)
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Oxygen Therapy Breathing KNOW Fi02 VALUES FOR MCQs !!!

FiO2 = Fraction of inspired oxygen
This describes the fraction of oxygen being inspired and can be explained by thinking about the composition of
room air.
Room air contains 20.9% oxygen, 78% nitrogen and 1% various other gases. When we breathe room air we can
describe the fraction of inspired oxygen (FiO2) as being 0.21. (Sometimes in practice this is described as a
percentage - 21% O2.)
Describe the indications, features and performance characteristics of the following

oxygen therapy devices:
• Hudson facemask Patients can feel
• The FiO2 delivered is variable and depends on the flow of Oxygen and the claustrophobic !!!
patient’s respiratory pattern
• Breathing through nose or mouth does not appear to influence the FiO2
greatly but it is preferential for them to expire through the mouth so as not Hudson Facemask:
to lose the nasopharynx reservoir of oxygen - FiO2: 0.35 - 0.6
• It is a clear plastic face-mask that is placed over the nose and mouth of a
patient, the FiO2 delivered is variable but at max flow rates of 15LPM with
FiO2 up to 0.6. The range of FiO2 is often described as 0.35-0.6 and again
is dependent on the patient’s respiratory mechanics and the flow rate set (4-
15LPM.)
• The disadvantages of the mask are that patient compliance can be low as
after time the mask becomes claustrophobic, prevents the patient from eating, drinking or speaking freely.
• A Tracheostomy Mask is a variation with all the features mentioned for the Hudson facemask but has been
designed to fit around a tracheostomy site.
Ideal for claustrophobic patients and for those on long-term oxygen therapy
• Nasal cannulae Nasal Cannula:
- Flow rate: 2-4 l/min (6 l/min)
• Nasal cannula ("nasal specs") are ideal for claustrophobic patients or patients on - FiO2: 0.24-0.36 (0.44)
long-term oxygen therapy.

• They work principally by utilising the dead space of the nasopharynx as a
reservoir for oxygen, when the patient inspires, the air entrained mixes with the
reservoir oxygen and the inspired gas is enriched.
• FiO2 possible with nasal cannula varies generally from 0.24 - 0.36. Some texts
describe a maximal FiO2 of 0.44 at flow rates of 6LPM (which most patients find
extremely uncomfortable)
• Higher flow rates only cause turbulence in the tubing and cannot increase the FiO2 any further
• The normal flow rates used are usually 2-4LPM, patients find this comfortable and advantages are they are
able to eat, drink and talk normally.
• The disadvantages are that the cannulae can be easily displaced by the patient, they cause nasal passage
drying and crusting and occasionally nose bleeds.
May cause nasal passage drying, nasal crusting, and nose bleeds
Michael Grant

lOMoARcPSD|4984001
ALWAYS REACH FOR THIS FIRST IN A SICK PATIENT !!!

When the patient expires the one-way valve will close preventing any expired POEM: Page 9 of 68
CO2 entering the reservoir bag thereby preventing rebreathing
Patients can feel Non-Rebreather Mask
claustrophobic !!! Flow Rate: 10-15 l/min
• Reservoir/Trauma/Non-rebreather mask FiO2: 0.6 - 0.85
• The flow rate is set at 10-15LPM and the reservoir bag must be filled with
Oxygen before administering to the patient; done by placing a finger over
the one-way valve at the neck of the reservoir bag
• When the patient expires the one-way valve will close preventing any
expired CO2 entering the reservoir bag thereby preventing rebreathing to a
certain extent.
• Some masks also have one way valves on the vents at the side of the mask
which close during inspiration to try and prevent entrainment of air. Some
entrainment will always occur however as air can leak around the sides of the
Need to fill up
mask which are often not flush or tightly opposed to the face of the patient bag with
• At 10-15LPM the range of FiO2 to be expected is 0.6 - 0.85 oxygen first!
• The disadvantages are similar to those of the Hudson mask.
The pressure drop and increased velocity of gas flow

• Nebuliser mask through a narrowing causes the nebuliser fluid to be Nebuliser Mask:
(Converts liquids to aerosols) broken into droplets that can be inhaled by the patient
• Most common nebulisers utilise a baffle within their mechanism that at
appropriately set flow rates will create droplets of a size 1-5micrometres - Gives
ideal for being inhaled to their site of action. meds as
inhaled
• Nebulisers are used to convert liquids into aerosols of a size that can be gases!
inhaled into the lower respiratory tract, by a process of atomisation.
• Nebuliser masks use the Venturi effect, the pressure drop and increased
velocity of gas flow through a narrowing is utilised to entrain the nebuliser
fluid into the jet stream causing it to be sheared and to break into
droplets. The baffle, which is placed within the jet stream further decreases
the size of the droplets and returns bigger droplets back to the reservoir
of fluid to be aerosolized once more.
• They are most commonly used in the hospital setting for inhaled bronchodilators but other drugs can be
administered through this route. (Adrenaline, Dornase alfa and some antibiotics)
• The optimal flow rate is 4-6 litres per minute, any lower and you will not aerosolize the liquid to an
appropriate size
• Nebulisers can be driven by oxygen (most common in acute or emergency settings) or medical air (more
common in home settings or on some wards)
• Self-inflating bag, valve and mask (BVM) or Ambu Bag© Know Ambu Bag !
• The bag-valve mask (BVM) is a device used most widely for ventilating patients who are not breathing, need
assisted ventilation, or are critically ill or injured.
• The system typically consists of an oxygen reservoir, a football–size self-expanding bag, a one-way valve, a
universal adaptor, and a clear flexible mask.
• The system can deliver ambient air, but in a hospital setting it should be connected to a supplemental Oxygen
supply.
• The flow rate for this device is 12–15 LPM, which deliver a FiO2 up to 0.8 depending on the quality of the seal
of the face mask. The volume delivered also can vary, depending on bag size and depth of ventilation.
• The two handed technique for BMV is the safest way to
ventilate an apnoeic patient when the operators who do
not use single-handed ventilation on a regular basis.
• Over zealous bagging leads to distension of the
stomach which can lead to increased intra-abdominal
pressure and in turn increased intra-thoracic pressure
making it more and more difficult to ventilate. There
have also been case reports of gastric perforation
following aggressive "bagging."
Aggressive bagging can lead to increased intra-abdominal
pressure which in turn increases intra-thoracic pressure Ambu Bag
- Flow rate: 12-15 l/min Michael Grant
making it more and more difficult to ventilate - FiO2 - upto 0.8
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VENTURI FACEMASK POEM: Page 10 of 68
Explain the distinction between fixed and variable performance devices in relation
to oxygen delivery and explain how Venturi masks can function as fixed
performance devices.
In simple terms, variable performance devices vary in their delivery a known FiO2 whereas fixed performance
devices reliably deliver a known FiO2; but there are additional differences.
Variable performance:
• Sometimes referred to as low flow systems referring to the fact that they cannot meet the patients inspiratory
flow demands (normal flow 25- 30L/min) and therefore additional flow is provided by surrounding room air
• The room air Fi02 alongside the Oxygen enriched gas and dilutes the mixture
• The true FiO2 depends on the patients’ respiratory demand. governed by the respiratory rate, the inspiratory
flow rate and also the length of expiratory pause, i.e. a patient in respiratory distress, their respiratory demand
will far exceed that of normal healthy individuals
• Devices in common use include nasal cannulae, the Hudson mask, and the non-rebreather facemask.
The Venturi effect is the reduction in fluid pressure that results when a fluid flows
Fixed performance oxygen delivery devices: through a constricted section of pipe. The pressure drop induced by the increase in
velocity of a fluid passing through a narrow orifice can be used to entrain air or a
• These deliver a predictable and accurate FiO2 nebuliser solution for treating patients.
• Can be divided into High Airway Flow Oxygen Enriched (HAFOE) devices also known as the Venturi Masks,
or anaesthetic breathing circuits.
• The Venturi effect is the reduction in fluid pressure that results when a fluid
L flows through a constricted section of pipe. The pressure drop induced by
E the increase in velocity of a fluid passing through a narrow orifice can be
used to entrain air or a nebuliser solution for treating patients.
A • The characteristics of Venturi masks are: Entrain air = Trap air
R • Increasing flow will not alter FiO2 (precise) Venturi masks used in CO2 patients
• The size of the entrainment port determines FiO2
N • The larger the port, the more room air entrained and the lower the FiO2
• The ranges of FiO2 available are 0.24, 0.28, 0.31, 0.4, 0.6. The coloured
apertures will often state the flow rate required for the FiO2 delivery and it
is important to abide by these flow rates to maintain accuracy.
Explain the importance of blood oxygen content and it’s relation to measured
variables such as oxygen saturation, haemoglobin concentration and oxygen
partial pressure. Oxygen tanks are white !
The theoretical maximum oxygen carrying capacity is 1.39 ml O2/g Hb, but direct measurement gives a capacity of
1.34 ml O2/g Hb. 1.34 is also known as Hüfner’s constant.
The oxygen content of blood is the volume of oxygen carried in each 100ml blood.
It is calculated by: (O2 carried by Hb) + (O2 in solution) = (1.34 x Hb x SpO2 x 0.01) + (0.023 x PaO2)
Where: How to calculate oxygen

SO2 = percentage saturation of Hb with oxygen
Hb = haemoglobin concentration in grams pre 100 ml blood
content of blood
PO2 = partial pressure of oxygen (0.0225 = ml of O2 dissolved per 100 ml plasma per kPa, or 0.003 ml per mmHg)
Oxygen delivery is the amount of oxygen delivered to the peripheral tissue, and is obtained by multiplying the
arterial oxygen content (CaO2) by the cardiac output (Q).
For CaO2 = 20.1 ml/100 ml and Q = 5 l/min:

Oxygen delivery
Oxygen delivery (DO2) = 1005 ml/min
Oxygen uptake is the amount of oxygen taken up by the tissues that can be calculated from the difference
between oxygen delivery and the oxygen returned to the lungs in the mixed venous blood. The oxygen returned
is given by the product of the mixed venous oxygen content (CvO2) and the cardiac output. For CvO2 = 15.2
Oxygen Uptake Michael Grant

lOMoARcPSD|4984001
POEM: Page 11 of 68
ml/100 ml and Q = 5.0 l/min:
Oxygen return = 760 ml/min
The primary goal of the cardio respiratory system is to deliver adequate oxygen to the tissues to meet their
metabolic requirements, a balance between VO2 and DO2.
The balance between oxygen uptake by the body tissues and oxygen delivery to them is assessed by:
• The oxygen content of mixed venous blood CvO2, which is normally about 15 ml/100 ml
• The extraction ratio, which is the ratio of VO2 to DO2 expressed as a percentage. Normally the extraction ratio
is about 25% but can double to 50% if tissue demand increases
Both of the above indices are dependant on mixed venous saturation (SvO2), and cardiac output.
Describe the haemoglobin-oxygen dissociation curve and state the factors that
cause a “shift” of the curve.
• A rightward shift indicates that the hemoglobin under study

has a decreased affinity for oxygen. This makes it more
difficult for hemoglobin to bind to oxygen (requiring a higher
partial pressure of oxygen to achieve the same oxygen
saturation), but it makes it easier for the hemoglobin to
release oxygen bound to it. The effect of this rightward shift
of the curve increases the partial pressure of oxygen in the
tissues when it is most needed, such as during exercise, or
hemorrhagic shock.
• This leftward shift indicates that the hemoglobin under
study has an increased affinity for oxygen so that
hemoglobin binds oxygen more easily, but unloads it more
reluctantly. Left shift of the curve is a sign of hemoglobin's
increased affinity for oxygen (e.g. at the lungs). Similarly, right
shift shows decreased affinity, as would appear with an increase in body temperature, hydrogen ion, 2,3-
diphosphoglycerate (also known as bisphosphoglycerate) or carbon dioxide concentration
• Bohr Effect: we blow off CO2, shifting blood pH toward the alkaline side and thus hemoglobin becomes a
stronger magnet to bind O2 as air is inhaled. Then the tissue level, CO2 (produced by metabolism) diffuses to
the blood, shifting pH to the acidic side, weakening hemoglobin’s hold on O2; releasing it to tissues.
• 2, 3 DPG interacts with deoxygenated hemoglobin beta subunits by decreasing their affinity for oxygen, so it
allosterically promotes the release of the remaining oxygen molecules bound to the hemoglobin, thus
enhancing the ability of RBCs to release oxygen near tissues that need it most. 2,3-BPG is thus an allosteric
effector.
List the limitations of oxygen saturation monitoring

Advantages Disadvantages
• Non-invasive • Is NOT a measure of ventilation
• Readily available • Does not measure pulse or CO
• Easily portable • Risk of burns to patient
• Battery operated • Time dela
Readings can be affected by:

• Poor placement (Same arm as BP cuff) • Electrical interference
• Poor peripheral perfusion • Low sats <75%
• Movement (shivering) • Excessive ambient light
• Coloured nail polish
• Abnormal haemoglobins
• eg. Carboxyhaemoglobin, Methaemoglobin
• Dyes LEARN !!!
• e.g.Methylene blue
Michael Grant

lOMoARcPSD|4984001
Review treatment of all these

Acute Respiratory DDx using OHCM & GreenBook
Respiratory Critical Illness
Pathology Presents with Signs Pathogenesis Investigation Management
Acute severe • Chest tightness • Inability to complete a Exposure to the antigen will make CD4 T cells Peak flow: severe if<50% of 100% O2 (non-rebreathing
asthma • Progressive SOB sentence in one breath differentiate into T helper cells, and they will begin best/predicted mask) with the patient sat upright
• Dry cough • RR>25 to secrete IL-4 (causes B cells to become plasma CXR: to exclude pneumothorax Give 5mg salbutamol with
• Wheezing • Tachycardia >110 cells and being secreting IgE) and IL-5 (bind to or pneumonia 0.5mg ipratropium/4-6hr via
• PEF <50% predicted eosinophils and mast cells, making them reactive Pulse oximetry nebulizer on 100% O2 (IV beta-
(or <50% patient’s own to the antigen) ABG: CO2 > 5kPa (high), O2 agonist if airway comprodmised )
best) Mast cells release histamine & prosta-glandin (as <8kPa (low), Low pH (Respiratory Give hydrocortisone 100mg IV
• Pulsus paradoxis well as leukotrienes; LTC4). U&E acidosis) or 50mg prednisolone orally
See PassMedicine for (continue daily for 5 days)
mild/moderate/severe asthma Consider MgSO4 (2g IV over 20
exacerbation criteria mins) if poor response to Rx
Exacerbation • Increased frequency • Reduced cricosternal A mix of chronic bronchitis and emphysema: FBC, renal function tests and U&E Controlled 25% O2
of COPD and severity of distance <3cm Airway narrowing due to hypertrophy and
coughing • Reduced chest hyperplasia of mucus secreting glands of the ABG: respiratory failure (Type II) Recheck the ABG after 20
• Chest discomfort expansion bronchial tree with wall inflammation and oedema. minutes
• SOB • Resonant chest Alpha 1 antitrypsin is also complicit even if not ECG: may show right ventricular – PaCO2 is steady/lower, then Checking
• Wheezing Increased sounds deficient as it is inhibited by cigarette smoke and is hypertrophy, arrhythmias, increase the O2 to 28% for
sputum productions, • Cyanosis a major protease inhibitor. ischaemia. - PaCO2 has risen >1.5kPa, respiratory
and Change in • Pursed lip breathing Emphysema is defined pathologically as the consider respiratory stimulant depression
sputum appearance • Cor pulmonale dilatation and destruction of tissue distal to the Cultures: sputum cultures. such as doxapram (1.5-4mg/min
terminal bronchioles; this leads to loss of elastic IV) or assisted ventilation.
recoil that causes a closing of airways in CXR: to identify any other cause – CO2 retention leads to
expiration. Pink puffers (mainly emphysema) and and rule out pneumothorax drowsy/confused
blue bloaters (mainly chronic bronchitis) are
described but most patients have a mix Give 5mg salbutamol with
0.5mg ipratropium via nebulizer
Exacerbations: infection, allergens, toxins, on ROOM AIR
pollution, non-compliance
IV hydrocortisone 200mg and
Anthonisen criteria: Increasing dyspnea, sputum oral prednisolone 40mg OD
volume, sputum purulence (thickness) Give a 5-7 day course of
Type I – all 3 present, Type II – 2 things present, prednisolone
Type III – one factor present If still resisting Rx, consider non-
Use antibiotics when 2 or more criteria invasive ventilation CPAP
Community- • Shortness of breath Vary with the type of Pneumonia is an inflammation of the substance of CXR (lags behind clinical course If not vomiting, and CURB65
acquired • Cough (often dry in pneumonia present: the lungs and is usually caused by bacteria and can 48hrs), score ≤2, oral antibiotics.
pneumonia infants and the elderly) S. pneu: Rapid shallow be classified anatomically (bronchopneuomnia or
• Fever breathing, Pleural rub lobar pneumonia) or on the basis of aetiology. Sputum for Gram stain plus If severe and/or vomiting, IV
• Rigors Confusion – may be the Pneumonia may also result from chemical causes C&S (preferably early morning) antibiotics required, as per
• Vomiting only sign in elderly patients (e.g. aspiration of vomit) and radiotherapy sensitivities. (Co-amoxiclav)
• Headache The CURB-65 score – It FBC w/ DWCC (lymphopenia
• Loss of appetite predicts the risk of mortality You can also classify them according to their suggests Legionella, marked red Keep Oxygen saturation >92%,
• Haemoptysis (rare) (CURB score 0 = <1% risk, aetiology; e.g. pneumococcal or atypical (e.g. cell agglutination suggests using oxygen therapy as
• Pleuritic chest pain 5= 60% risk), ≥2 requires caused by Chlamydia, legionella, coxiella burnetti). mycoplasma) required

lOMoARcPSD|4984001
POEM: Page 13 of 68
• Dyspnoea hospitalisation: Atypical are so called because they are caused by
• Tachypnoea atypical organisms, but the infection itself will tend Blood/Pleural fluid cultures IV fluids, to prevent dehydration
• Tachycardia Confusion – use the to have similar symptoms. ABG (O2 <8kPa severe disease) and shock
abbreviated mental test
(score ≤8) 75% of cases are Streptococcus pneumoniae in Urine for legionella/pneumo- All patients should receive 6
Urea - >7mmol/L cause, and 20% atypical. The remaining 5% may be coccal antigen testing week follow-up including repeat
Respiratory rate - ≥30/min caused by aspiration of vomit, radiotherapy and CXR – as persistent x-ray changes
Blood Pressure <90 allergic mechanisms: may suggest underlying
systolic, or <60 diastolic carcinoma with secondary
65 – age >65 years pneumonia
Pulmonary Small/medium PEs: Small/medium PEs: This is normally caused by a clot in the legs or Serum D-Dimer If critical/periarrest:
Thrombo- SOB, pleuritic pain and Tachypnoeic and have a pelvis that becomes dislodged, flows via the CXR: may show decreased Thrombolysis (50mg alteplase
embolism haemoptysis (only if pleural rub +/- exudative bloodstream through the right side of the heart vascular markings, raised hemi- bolus) or
infarction) pleural effusion and gets lodged in the pulmonary circulation. diaphragm, or wedge shaped 10mg bolus (1 min) then 90mg
Massive PE: opacity (infarction) IV infusion over 2 hours
Massive PE is a medical Central cyanosis, elevated It is not always a clot that causes a PE! Fat, air, ECG: T wave
Anticoagulation with LMWH e.g
emergency: JVP, right ventricular heave, amniotic fluid, bone marrow, endocarditis. For fat inversion,
enoxaparin at 1.5mg/kg/24h by
Severe central chest pain, accentuation of the second and amniotic fluid, these will normally resolve sinus
s/c inj until INR of 2then oral
shocked, pale, sweaty, heart sound and a gallop themselves with supportive care. tachycardia.
warfarin (10mg) aiming for INR
tachypnoea, tachycardia. rhythm (S3 and S4) Larger emboli can result in the
of 2-3 for 3 months after PE and
'classical' S1Q3T3 (rare)
lifelong if recurrent
VQ scan
Caval Filter if anticoag. is
PE Presentation: CT-pulmonary angiogram: more
contraindicated/recurrent PE
- Pleuritic chest pain sensitive VQ scan but emboli do
- Dyspnoea have to be large to be dectected Major embolism/peri-arrest
ABG: often low O2, low CO2 may require:
Look for source – DVT, surgery, ICU
air travel Pulmonary thrombectomy
Spontaneous In primary: In primary: Air in the pleural space, but the volume is not CXR: looking specifically to judge Standard Pneumothorax –
pneumothorax • Chest pain and mild May be none increasing. the size of the trim of air Rim of air <2cm - CXR before
breathlessness are CT Scans: can be useful in COPD treatment (unlike in tension):
usual In secondary: Spontaneous pneumothoraces are divided into: patients to ensure that consider alternate diagnosis, OR
• Patients often unaware Cyanosis Primary spontaneous pneumothorax is unknown, pneumothorax on CXR is not in small pneumothorax:
Hypercapnia (seen as but established risk factors include male sex, fact an air filled bullae Discharge w/ advice: no vigorous
In secondary: confusion) smoking, and a family history of pneumothorax exercise - and return if breathless.
• Symptoms tend to be Vocal resonance and Secondary spontaneous pneumothorax occurs in Observe every 2 weeks until air
more severe than in tactile fremitus can be the setting of a variety of lung diseases. The most is reabsorbed
PSPs, as the unaffected decreased common is chronic obstructive pulmonary disease Primary Pneumothorax: SOB +
lungs are generally (COPD), which accounts for approximately 70% of rim of air >2cm on CXR:
nd
unable to compensate cases. Can also be casued by infection, sarcoidosis, Attempt aspiration (2 ICS,
due to existing lung connective tissue disease, cancer or Catamenial midclavicular line)
disease pneumothorax (linked to ovarian cycle and due to If unsuccessful, repeat
lung endometriosis) If unsuccessful, chest drain
Secondary Pneumothorax:
SOB + rim of air >2cm on CXR:
Chest drain
- D-Dimer is a substance produced when a blood clot is broken down

Michael Grant
- CRP is a substance produced by the liver in response to inflammation
- ESR is the rate at which red blood cells sediment (sink to the bottom of the test tube) over a period of 1 hour
lOMoARcPSD|4984001
(USS Scan) POEM: Page 14 of 68

Tension Plueritic chest pain SOB If large; reduced breath Air in the pleural space, and the volume FAST Scan: especially in trauma If suspected, attempt to
pneumothorax sounds affected area and continuing to increase. Typically, due to the CXR: after attempted treatment aspirate before CXR:
hyper-resonant on formation of a one-way valve, allowing air into the Put large bore (14g) needle with
percussion, tracheal pleural space on inspiration, but not out again on syringe, part filled with 0.9%
nd
deviation (away from expiration. saline, into 2 ICS MCL and
lesion) remove plunger (air will bubble)
Can compress mediastinum Can be caused by mechanical ventilation in those followed with chest drain
decreased Cardiac with existing lung disease – especially if already
Output: increase HR & JVP, sedated If pneumothorax remains at 48
decreased BP Insert chest drain into triangle of hours or patient has reccurent
Hypoxia and altered GCS safety episodes, then do Pleurectomy
Open SOB A wound in the chest wall Pneumothorax associated with a chest wall defect CXR: after treatment Three-sided dressing acts as a
pneumothorax Trauma to chest wall is identified that appears to that, when a negative pressure is generated, air is flap-valve to allow air to escape
be 'sucking air' into the entrained into the chest cavity through the defect from the pneumothorax during
chest and may be visibly instead of trachea as it provides less resistance. If expiration, but not to enter
bubbling - this is diagnostic the hole is more than 0.75 times the size of the during inspiration.
trachea, air preferentially enters through defect.
If large; reduced breath This results in inadequate oxygenation and As soon as possible a chest drain
sounds affected area and ventilation, and a progressive build-up of air in the should be placed and the wound
hyper-resonant on pleural space. The pneumothorax may become closed
percussion tension if a flap has been created that allows air in,
but not out
Massive SOB Significant thoracic trauma Haemothorax is a collection of blood in the pleural Small-moderate haemothoraces Large bore chest drain: big
haemothorax Trauma to chest wall with external injuries or space and may be caused by blunt or penetrating are not detectable by enough to prevent intramural
palpable crepitus (#rib) trauma. Most haemothoraces are the result of rib examination and only seen on clotting
The classic signs: fractures, lung parenchymal and minor venous CXR, FAST or CT scan Thoracotomy: if loss of 200-
Decreased expansion injuries, and as such are self-limiting. Less 250mls of blood per hour from
Dullness to percussion commonly there is an arterial injury, which is more chest drain after 4-5 hours
Reduced breath sounds likely to require surgical repair.
Mediastinal/tracheal
deviation only if massive
Flail chest Bruising, grazes or seat- Paradoxical movement of A flail chest occurs when a part of thoracic cage is CXR Management includes
belt signs are visible a segment of the chest wall separated from the rest. Typically, at least two oxygenation, ventilation &
fractures per rib (producing a free segment), in at analgesia
Pain on palpation of the Palpation may reveal the least two ribs. Large flail segments may extend
chest wall or on inspiration crepitus associated with bilaterally or involve the sternum. In these cases the - O2 therapy (if severe, positive
broken ribs. disruption of normal pulmonary mechanics may be pressure or intubation)
large enough to require mechanical ventilation. - Continuous epidural infusion
The main significance of a flail chest however is that of a local anaesthetic agent (+/-
it indicates the presence of pulmonary an opioid
contusion. In most cases it is the severity and - Patient-controlled
extent of the lung injury that determines the clinical administration of opioid infusion
course and requirement for mechanical ventilation. (+/- an NSAID)
Consider surgical rib fixation
Michael Grant

lOMoARcPSD|4984001
POEM: Page 15 of 68
Pulmonary – May be obvious signs Crackles may be heard on Pulmonary contusion is an injury to lung ABG: assess oxygenation Most contusions will require no
contusion of chest wall trauma auscultation parenchyma, leading to oedema and blood CXR: Most pulmonary contusions specific therapy – supportive
such as bruising, rib collecting in alveolar spaces and loss of normal are diagnosed on plain chest X- treatment with close monitoring
fractures or flail chest Hypoxia may be present lung structure & function. This blunt lung injury ray, but CXR will often under- of fluid balance: avoid
– Tachypnea later in the pathology develops over the course of 24 hours, leading estimate the size of the contusion unnecessary fluids
– Tachycardia to poor gas exchange, increased pulmonary and lag behind the clinical
– Haemoptysis vascular resistance and decreased lung picture (24-48 hrs) Adequate analgesia to allow of
compliance. There is also a significant inflammatory CT Scan: Very sensitive for ventilation
reaction to blood components in the lung, and 50- identification of pulmonary
60% of patients with significant pulmonary contusion, and may allow O2 therapy: including
contusions will develop bilateral Acute differentiation from areas of considering tracheal intubation if
Respiratory Distress Syndrome (ARDS). Other atelectasis or aspiration ventilation and oxygenation are
complications are: respiratory failure, atelectasis insufficient
and pneumonia.
Acute heart – Dyspnea – Pallor HF causes a drop in MAP that initially stimulates ECG: 12 lead to find source of Sit up and 100% oxygen flow
failure – Anxiety – Hypotension [systolic baroreceptors that feed into medullary acute decompensation
– Tachycardia <90] cardiovascular center [MCVC]. MCVC tries to FBC Diamorphine 1.25–5mg IV
– Swollen ankles – Reduced CO increase MAP by reducing vagal tone and U/E slowly
– – Oliguria (flush catheter increase sympathetic tone leading to increase Cardiac enzymes (Troponin,
to ensure no blockage) heart contractility and rate. Sympathetic activtiy especially BNP – NICE IV furosemide 40-80mg i.v. to
– Pulmonary oedema also contracts arteries [inc. TPR] and veins [inc. guidelines: less than 100 ng/litre reduce fluid retention, hence
– venous return] and the release of adrenaline from rules out acture HF) pulmonary edema (closely
adrenal medulla, which stimulate all of the above Doppler 2D echocardiography monitor: weight, urine output)
actions. Renin-angiotensin-system [RAS] is also ABG
stimulated in heart failure due to reduced kidney CXR: Do not routinely offer the
perfusion. The end product, Angiotensin II, – Pulmonary Oedema - 'bats following unless concomitant
causes vasoconstriction, aldosterone release and wings' appearance myocardial ischaemia, severe
ADH release causing Na and water retention by the – Pleural effusions - blunting hypertension, valve disease:
kidneys. These mechanisms are beneficial initially of the costo-phrenic angles Sublingual 2 puffs nitrates or
as they increase blood volume, therefore venous – Increased vascular markings oral to myocardial perfusion
return and SV, TPR and HR, therefore maintaining a – Kerley-B lines (orizontal lines
high CO, however, these compensatory less than 2cm long, If Systolic>90 then give IV
mechanisms worsen HF: increase cardiac commonly found in the infusion isosorbide dinitrate
workload > increase 02 demands > stretching of lower zone periphery. These 2-10mg/h
ventricles > reduced contractility > peripheral lines are the thickened, If Sys<90 then treat as
and pulmonary edema edematous interlobular cardiogenic shock
Acute HF can evolve into cardiogenic shock, septa)
which is an acute circulatory failure – Increased heart size
Cardiac Dyspnoea, tachycardia, Pericardial rub (50%) Cardiac tamponade is caused by the accumulation CXR: Cardiomegaly, water- Emergency subxiphoid
tamponade and tachypnea Beck's triad: increased of blood, fluid, pus, clots, or gas in the bottle sign pericardiocentesis: performed
Clammy extremities from JVP, hypotension and pericardial space, resulting in reduced ECG: low amplitude QRS under guidance by ECHO
hypoperfusion diminished/muffled heart ventricular filling and subsequent haemodynamic complexes, alternation of QRS • Reserve sample for culture
Pericarditis-like: chest sounds compromise. Cardiac tamponade is a medical amplitude (usually in a 2:1 ratio),
pain, made worse by Pulsus paradoxus emergency. PR segment depression
inspiration HIV testing: 24% of cases
Transthoracic ECHO
(Cardiomegaly on CXR)
Michael Grant

lOMoARcPSD|4984001
POEM: Page 16 of 68
Pneumothorax Ix: Pulmonary Embolism Ix:

- CXR, CT Scan
Bloods: D-Dimer, ABG
Mx: ECG: S1Q3T3 pattern
- High-flow O2 Imaging: CXR, CTPA, V/Q Scan
(Primary Pneumothorax) Mx:

Rim of air <2cm and patient not - Oxygen if hypoxic, 10-15l/min
1 Gram (g) = 1000 Milligrams (mg) SOB: - IV Morphine 5-10mg with
- Discharge with early follow-up (if anti-emetic
1 Milligram (mg) = 1000 Micrograms (mcg) patient has underlying lung
disease, observe for 24h) Anti-coagulation: Clexane
- LMWH until PE confirmed -
Rim of air >2cm and SOB: Enoxaparin 1.5mg/kg/24h, then
Aspirate Warfarin 10mg, aim INR 2-3
Acute Asthma Mx:
- ABCDE
Always start with an ABCDE approach (2nd ICS, mid-clavicular) Thrombolysis:
- If aspiration fails, consider repeat - In massive PE, immediate
aspiration thrombolysis - Alteplase 50mg bolus
- If repeat aspiration fails, insertion Surgery:
- High-flow O2 through a Acute COPD Mx of chest drain - Embolectomy, IVC filters (prevent
non-rebreather mask at 15l/min (5th ICS, mid-axillary) recurrence)
(aim sats 94-98%) - Start on 24-28% oxygen, aim for (Secondary Pneumothorax)
- Nebulised Salbutamol 5mg sats 88-92% SOB and age > 50y, and rim of air
(back-to-back upto 3 times) - Salbutamol 5mg >2cm on CXR
- Ipratropium Bromide 500 - Ipratropium Bromide 500 Chronic Heart Failure Mx:
micrograms micrograms
1st line:
- Oral Prednisolone 50mg / IV - IV Hydrocortisone 200mg AND - ACE-inhibitor & Beta-blocker
Hydrocortisone 200mg Oral Prednisolone 30mg 2nd line:
- Magnesium Sulphate IV 2g - Antibiotics if signs of infection - Aldosterone antagonist /
Angiotensin II receptor blocker /
over 20mins - If no response to nebulisers and Hydralazine in combination with
If no response: steroids - IV Aminophylline a Nitrate Michael Grant
- IV Salbutamol - Non-invasive positive pressure - Diuretics given if patient fluid
congested
- IV Aminophylline ventilation (NIPPV) - CPAP
lOMoARcPSD|4984001
Define and differentiate between the two types of respiratory failure.

Respiratory failure is a syndrome in which the respiratory system fails in one or both of its gas exchange functions:
oxygenation and carbon dioxide elimination. In practice, it may be classified as either hypoxemic or
hypercapnic.
Type I (or hypoxemic) respiratory failure is characterised by an arterial oxygen tension (Pa O2 - the pressure
which oxygen would have if it alone occupied the volume) lower than 60mmHg with a normal or low arterial
carbon dioxide tension (Pa CO2). This is the most common form of respiratory failure, and it can be associated
with virtually all acute diseases of the lung, which generally involve fluid filling or collapse of alveolar units.
Some examples of type I respiratory failure are cardiogenic or non-cardiogenic pulmonary edema, pneumonia,
and pulmonary hemorrhage.
Type II (or hypercapnic) respiratory failure is characterized by a PaCO2 higher than 50mmHg. Hypoxemia is
common in patients with hypercapnic respiratory failure who are breathing room air. The pH depends on the
level of bicarbonate, which, in turn, is dependent on the duration of hypercapnia. Common etiologies include
drug overdose, neuromuscular disease, chest wall abnormalities, and severe airway disorders (eg, asthma and
chronic obstructive pulmonary disease [COPD]).
ABG is taken from
the radial artery !
Display a practical knowledge of how to:
• Take an arterial blood sample for blood gas analysis
1. Gather equipment:
• Alcohol wipes
• Gloves & apron
• 2 ml syringe and orange needle
• Hand cleanser
• 1% lidocaine
• ABG syringe (heparinised) and needle
• Cotton wool ball or gauze
• Tape Allen's Test - Test for
• Sharps box ulnar insuffiency
2. Check patient details and gain consent

3. Perform Allen’s test to assess palmer arterial arch (If color fails to return, the test is considered
"Negative" and the ulnar artery supply to the hand is not sufficient, meaning radial artery cannot
be safely cannulated)
4. Position patient – wrist extended (may need roll under wrist to fully extend hand) then feel for
radial artery
5. Clean skin with alcohol wipe and allow to dry for 30 sec
6. Infiltrate skin with 1% lidocaine (about 0.25-0.5mls) using 2ml syringe
7. Clean skin again, relocate artery and warn patient about coming discomfort
8. Aim toward pulse using heparinized syringe with needle at 45°, bevel
facing upward (avoiding areas that you’ve touch with your gloves) and
advance until you hit the artery
9. Allow syringe to fill with >1ml of blood, before withdrawing and disposing of needle in sharps box
ABGs have heparin
10. Place cotton wool ball over puncture site, secure with tape and apply pressure until bleeding stops inside to anti-coagulate
11. Label syringe with patient details the blood
12. Take for immediate processing or place on ice if being sent to the lab
• Take a peak expiratory flow measurement

1. Attach new disposable mouth piece to the peak flow meter.
2. Before each use, make sure pointer on the peak flow meter is reset to 'zero'
3. Ask the patient to stand if able*, then ask the patient to hold the peak flow
meter in a horizontal position keeping fingers away from the point.
4. Ask the patient take a deep breath, form a tight seal around the mouth piece
and to blow out as hard and as fast as they can. Remember a "fast blast" is
better than a "slow blow".
5. Note the value on the scale (litres per minute) then reset to zero
6. Repeat 3 times (with a 10 second interval) and record the highest of the three readings on a graph
- For PaO2, it should usually be FiO2 - 10, otherwise it is called 'relative hypoxia'
- Don't forget partial / complete compensation based on their pH
- After reading ABG, if you still can't figure out the diagnosis, look at the anion gap!!! (Only applicable in metabolic acidosis!)

lOMoARcPSD|4984001
POEM: Page 18 of 68
• Differentiate between
restrictive and obstructive
respiratory disease on
pulmonary function testing
In restrictive lung disease, both forced

expiratory volume in one second (FEV1)
and forced vital capacity (FVC) are
reduced, however, the decline in FVC is
more than that of FEV1, resulting in a
normal or higher FEV1/FVC ratio. This
change is due to pulmonary fibrosis;
caused by disease in the interstitium of
the lung –usually an increase in the
amount of tissue in the interstitium.
Causes include: asbestosis, radiation
fibrosis, drugs (e.g amiodarone, methotrexate), rheumatoid arthritis, ARDS.
In obstructive lung disease however, FEV1 is reduced while FVC remains stable, consequentially depicting a
lower FEV1/FVC ratio. Disease mechanisms affect the bronchi and bronchioles, usually in a diffuse pattern across
the whole lung. Causes include: COPD, Asthma, Bronchiectasis, CF.
Explain the concepts of:

• Minute Volume is the
volume of gas inhaled or
exhaled in 1 minute; i.e.:
Minute volume (VM) = RR x
tidal volume
• Ventilation/Perfusion
(V/Q) ratio is a
measurement used to
assess the efficiency and
adequacy of the matching
of two variables:
"V" – ventilation – the volume
of air that reaches the alveoli
"Q" – perfusion – the volume
of blood that reaches the
alveoli
In the typical adult, 1 litre of blood can hold about 200 mL of oxygen; 1 litre of dry air has about 210 mL
of oxygen. Therefore, under these conditions, the ideal ventilation perfusion ratio would be about 0.95.
If one were to consider humidified air (with less oxygen), then the ideal v/q ratio would be in the vicinity
of 1.0. However, true values depend on the location in the lung; apex ratio is higher and base lower,
with an average of 0.8. The main reason for lower V/Q ratios at the base is that both ventilation and
perfusion increase when going inferiorly to the base, but Q does it more strongly thus lowering the
V/Q ratio.
Michael Grant

lOMoARcPSD|4984001
POEM: Page 19 of 68
• Dead space refers to an area with ventilation but
no perfusion (and thus a V/Q undefined though
approaching infinity). Dead space can be:
Anatomical (i.e. air spaces with no gas
exchanges) such as the mouth, nose,
trachea, mainstem bronchi, secondary,
tertiary
Pathological such as in pulmonary
embolism and shock
• Shunt is an area with perfusion but no ventilation

(and thus a V/Q of zero). Shunt often occurs when
the alveoli fill with fluid, causing parts of the lung
to be unventilated although they are still perfused.
This can be quantified as the shunt fraction (the
percentage of blood from CO that is not fully
oxygenated. Thus, people with high shunt fractions
(such as those with pulmonary contusion or
severe pneumonia) are said to have “oxygen-resistant” hypoxia, as breathing 100% oxygen still does
not fully oxygenate the blood.
• Continuous Positive Airways Pressure (CPAP) is a form of

positive airway pressure ventilator, which applies mild air pressure
on a continuous basis to keep the airways continuously open in a
person who is able to breathe spontaneously on their own. It
stents the lungs' alveoli open and thus recruit more of the lung's
surface area for ventilation. It is used in those with sleep aponea
(mild pressure from CPAP prevents the airway from collapsing or
becoming blocked) and preterm infacts (those within sufficient
surfactant)
• Invasive Positive Pressure Ventilation (IPPV) is a method of mechanical ventilation. Positive-

pressure ventilators work by increasing the patient's airway pressure through an endotracheal or
tracheostomy tube. The positive pressure allows air to flow into the airway until the ventilator breath is
terminated. Then, the airway pressure drops to zero, and the elastic recoil of the chest wall and lungs
push the tidal volume — the breath-out through passive exhalation. Positive end-expiratory pressure
(PEEP) can be used to prevent conditions that can lead to shunting (e.g. atelectasis, alveolar collection of
material other than gas such as from pneumonia or ARDS). There are risks however:
Barotrauma including pneumothorax, subcutaneous emphysema, pneumomediastinum, and
pneumoperitoneum
Ventilator-associated lung injury clinically indistinguishable from acute lung injury or acute
respiratory distress syndrome
Diaphragmatic atrophy can develop within the first day of mechanical ventilation
Impaired motility of mucocilia in the airway leading to retention of secretions and pneumonia
• Distinguish between:
• Oxygenation is the amount of oxygen in the blood, as measured by SaO2 (although there may be up
to 5 min lag in pre-oxygenated patients before changes are seen in pulse oximetry) reflects PaO2.
• Ventilation is the rate at which we ventilate, as measured by capnography (EtCO2 measures exhaled
CO2 and reflects changes in ventilation within 10 seconds) and reflects blood PaCO2
Michael Grant

lOMoARcPSD|4984001
Central lines
Review how to read Chest X-Ray ! Pick line - Peripheral
Interpret to a basic level the following: Hickman's line - Medial
• Chest Radiograph:
DRS ABCDE
D – Details: • Check vessels, calcification.
• Patient name, age / DOB, sex
• Type of film – PA or AP, erect B – Breathing
or supine, correct L/R marker, • Lung fields
inspiratory/expiratory series • Vascularity – to ~2cm of pleural surface (~3cm in
• Date and time of study apices), vessels in bases > apices
• Pneumothorax – don’t forget apices
R – How RIPE is the image?: • Lung field outlines – abnormal opacity/lucency,
• Rotation – medial clavicle atelectasis, collapse, consolidation, bullae
ends equidistant from • Horizontal fissure on Right Lung
spinous process • Pulmonary infiltrates – interstitial (linear, reticular,
• Inspiration – 5-6 anterior ribs nodular, reticulonodular) vs alveolar pattern
in MCL or 8-10 posterior ribs (fluffly, cotton wool)
above diaphragm, poor • Coin lesions (cancer, TB, abscess)
inspiration?, hyperexpanded? • Cavitary lesions
• Picture – straight vs oblique, entire lung fields, scapulae outside lung fields, • Pleura: reflections or thickening
angulation (i.e. ’tilt’ in vertical plane)
• Exposure (Penetration) – IV disc spaces, spinous processes to ~T4, L) hemidiaphragm C – Circulation
visible through cardiac shadow. • Heart position –⅔ to left, ⅓ to right
• Heart size – measure cardiothoracic ratio on PA film (normal <0.5)
S – Structures (Soft tissues and bones)
• Heart borders – R) border is R) atrium, L) border is L) ventricle & atrium
• Ribs, sternum, spine, clavicles – symmetry, fractures, dislocations, lytic lesions, density
• Heart shape
• Soft tissues – looking for symmetry, swelling, loss of tissue planes, subcutaneous air,
• Aortic stripe
masses
• Breast shadows
D – Diaphragm
• Calcification – great vessels, carotids
• Hemidiaphragm levels – Right Lung higher than Left Lung (~2.5cm / 1 intercostal
space)
A – Airway & mediastinum
• Diaphragm shape/contour (may be flat in asthma or COPD)
• Trachea – central or slightly to right lung as crosses aortic arch
• Cardiophrenic and costophrenic angles – clear and sharp
• Paratracheal/mediastinal masses or adenopathy
• Gastric bubble / colonic air
• Carina (division of trachea) & RMB/LMB
• Subdiaphragmatic air (pneumoperitoneum)
• Mediastinal width <8cm on PA film (wider may indicate aortic dissection)
• Aortic knob E – Extras
• Hilum – T6-7 IV disc level, left hilum is usually higher (2cm) and squarer than the V- ETT, CVP line, NG tube, PA catheters, ECG electrodes, PICC line, chest tube, PPM, AIDC,
shaped right hilum, lymphadenopathy? metalwork?

lOMoARcPSD|4984001
Review ABGs !!
• Arterial Blood Gas
5 step approach:
1. Is the patient hypoxic? (>10kPa on RA)
2. Is the pH <7.35 or >7.45? High lactate =
3. What is the respiratory component? (PaCO2 – normal: 4.5-6.0kPa) Lactic Acidosis
4. What is the metabolic component? (HCO3 – 22-26mmol/L, Base excess -2 to 2)
5. Interpret data
After this intial assessment, it is important to consider the Anion Gap:

• Difference in the measured cations and anions in serum, plasma or urine; often calculated to
identify the cause of an acidosis
• If the gap is greater than normal a high anion gap acidosis is diagnosed
• Potassium can be ignored as it has little impact on the result
• Normally there are more cations (positively charged ions) than anions resulting in a positive integer
for the gap
• Given that plasma is electro-neutral, we can say that the anion gap valve represents the
unmeasured ions
([Na+] + [K+]) – ([Cl-] + [HCO3-]) = 3-11mEq/L

• Given that plasma is electro-neutral, we can say that the anion gap valve represents the
unmeasured ions
• High anion gap metabolic acidosis can be caused by KULT-R:
o Ketones Bill Maher has
o Uraemia HAGMA because he
o Lactate says “High, Anion
o Toxins (Methanol, ethylene glycol, lactic acid, aspirin, ureamia KULTeR”
phenformin, iron, isoniazid, cyanide)
o Renal failure

lOMoARcPSD|4984001
POEM: Page 22 of 68
• Normal anion gap metabolic acidosis is also known as hyperchlorarmic acidosis as Cl- is the only
other major anion that can compensate for the loss of HCO3; caused by (usually diarrhoea or renal
tubular acidosis) FUSED CARS:
o Pancreatic Fistula (loss of bicarbonate rich pancreatic fluid)
o Uretero-enterostomy (Large amounts of Cl- are exchanged for HCO3 in stool, so HCO3 is lost)
o Saline administration (NaCl provides a chloride load)
o Endocrine (Hyperparathyroidism)
o Diarrhoea (Loss of HCO3)
o Carbonic anhydrase inhibitors (Diuretic by reduces NaCl and HCO3 reabsorption in the
proximal tubule but distal segment partially compensates for the sodium loss but not HCO3)
o Ammonium chloride
o Renal tubular acidosis (failure of HCO3− resorption)
o Spirolactone
• Low anion gap metabolic acidosis is very rare and typically due to:
o Loss of albumin
• Nephrotic syndrome
• Haemorrhage
• Liver cirrhosis
• Intestinal obstruction
• Multiple Myeloma (albumin level decreases as disease progresses)
Cardiovascular Critical Illness Circulation

Define the term “Shock”:
Shock is an acute circulatory failure with inadequate tissue perfusion leading to
cellular hypoxia, dysfunction and failure of major organ systems.
State the definitions and/or relevant equations for:

• Heart Rate: Number of contractions/beats per minute (bpm)
• Stroke Volume: SV = End diastolic volume – end systolic volume = EDV - ESV
• Cardiac Output: CO = HR x SV
• Systemic Vascular Resistance: SVR = (80*(MAP – MVP))/CO
• Blood Pressure: Mean arterial pressure = MAP = (CO*SVR) + MVP
The cellular pathophysiology of all types of shock:
Michael Grant

lOMoARcPSD|4984001
Explain the pathophysiology, causes, presentation, and basic treatment of the 4 main types of shock:
Type of
Shock Pathophysiology Presentation Causes Treatment
Cardiogenic Heart failure to contract Chest pain • Myocardial ABCDE followed by:
and pump blood Nausea and vomiting infarction/cont
effectively, leading to Dyspnoea usion Echocardiology + serum BNP, troponins
decreased CO, afterload Profuse sweating • Cardiac failure
and MAP – leading to Confusion/disorientation • Arrhythmia If acute STEMI: Perform Primary PCI if it can be delivered within 120 minutes of the time when fibrinolysis could have
reduced perfusion Palpitations been given; otherwise, fibrinolysis e.g. 50mg alteplase
Faintness/syncope
Hypovolaemic Reduction in blood Tachycardia (rate >100 beats • Haemorrhage ABCDE + group & cross-match
volume leads to a per minute) • Vomiting and
decrease in MAP that Tachypnea diarrhoea Fluid replacement (If hemorrhage, try to stem and elevate legs – consider O- blood transfusion )
causing a lack of Decrease in pulse pressure, • Burns Find source of fluid loss and treat
perfusion to tissues Cool clammy skin • Pancreatitis
Delayed capillary refill (>2sec) (Third space
Anxiety loss)
Oliguria
Distributive Systemic vasodilation Sepsis: Sign of infections • Sepsis ABCDE followed by:
causes a decrease in (Cough/Sputum, cellulitis, • Neurogenic
MAP (after initial neck stiffness, rash, • Anaphylaxis Sepsis 6:
decompensation from endocarditis, line infection, 3 in: O2 therapy, IV fluids, ABx (After culture)
increased CO) leading to rapid onset joint pain), 3 out: Blood culture, ABG (for lactate), Urine (via catheter)
a lack of perfusion to abdominal Pain/Distension, Then assess procalcitonin level
tissues Vomiting/diarrhoea, Dysuria
Neurogenic: brain injury, Neurogenic: Dopamine, Vasopressin, ephedrine, atropine (increase damaged sympathetic system activity)
cervical or high thoracic spinal
cord injury Anaphylaxis: O2 therapy, IV Fluids (20 mL/kg in a child or 500-1000 mL in an adult), 0.5mg IM (1:1000) adrenaline (in
Anaphylaxis: Angiooedaema, those >12 years), repeat dose at 5-minute intervals according to response; if airway compromised called anesthetics.
dyspnea, mottled skin After initial resus: chlorphenamine 10mg IM, Hydrocortisone 200mg IM (Both in >12 years)
Obstructive Cardiac function Typically vague: • Pulmonary ABCDE followed by:
impaired by non-cardiac Plueritic chest pain embolus
factors, leading to Severe chest pain • Cardiac PE: Anticoagulation with LMWH e.g enoxaparin at 1.5mg/kg/24h by s/c inj then oral warfarin (10mg) aiming for INR of
decreased CO, afterload SOB tamponade 2-3 for 3 months after PE and lifelong if recurrent
and MAP – leading to • Tension o Caval Filter if anticoag contraindicated/recurrent PE
reduced perfusion pneumothora o Major embolism may require: ICU, Pulmonary thrombectomy, Thrombolysis (50mg alteplase)
x
Cardiac Tamponade: Emergency subxiphoid pericardiocentesis performed under guidance by ECHO (eeserve sample
for culture)
Tension pneumothorax: If suspected, attempt to aspirate before CXR, use a large bore needle with syringe,
filled with saline, to act as a water seal – followed by thoracostomy with chest drain

lOMoARcPSD|4984001
POEM: Page 24 of 68
Michael Grant

lOMoARcPSD|4984001
POEM: Page 25 of 68
Describe the presenting symptoms, signs, pathogenesis, investigation and initial management of:

Acute • >20min angina pain at • Classified based on ECG ACS is a group of conditions due to reduced - 12 lead ECG: Immediately, MONA:
Coronary rest • Radiation of pain flow the coronary arteries such that muscle • Review previous Morphine IV +metoclopramide
Syndrome • New-onset or change in • Abrupt deterioration in is unable to function properly or dies; Can • Repeat Oxygen (only to those with with
angina causing limitation stable angina with pain be due to atherosclerosis, emboli, - Troponin I & T level: SaO2: <94% or COPD: <88%)
of daily activities on minimal exertion vasculitis, cocaine use, severe anaemia, • Detectable in serum 3-6 hrs, Nitrates (Especially GTN)
• Pain may be associated • Haemodynamic hyperthyroidism (increased demand). more sensitive that CK-MB at Aspirin - 300mg (unless coag. risk or
with sweating, nausea, instability <6 hrs allergic (clopidogrel 300mg)
vomiting, fatigue, SOB and • Beware of those with DM ACSs now classified mainly on the findings of • Raised: treat for MI Further Rx:
palpitations may not complain of ECG and Troponin levels: - FBC: Severe anaemia?
Unstable angina and NSTEMI:
pain - CRP: Vasculitis? - Fondaparinux unless getting
- ST-elevation ACS: acute chest pain and - Glucose: poorer outcomes for
angiography in <24 hours; use
(>20 minutes) ST elevation. Most will develop those with hypearglycaemia; unfractionated heparin instead
STEMI regardless of DM status
- Aspirin or Clopidigrel for 12mth
- Echocardiography - Follow-up Angiography +/- PCI or
- Non-ST-elevation ACS: acute chest pain - CXR: Look for pulmonary CABG
without persistent ST-segment elevation. The oedema or other causes: STEMI:
ECG shows ST-segment depression or T- pneumothorax, aortic aneurysm - Primary PCI + Clopidogrel if
wave inversion, flat T waves, pseudo- - Cardiac angiogram possible in <120 mins of when
normalisation of T waves, or no changes.
fibrinolysis could have been given;
NSTE-ACS is further divided into:
otherwise, fibrinolysis +
Unstable angina: normal troponin levels.
fondaparinux e.g. 50mg alteplase
NSTEMI: a rise in troponin levels.
Anaphylaxis • Exposure to known • Skin and/or mucosal Occurs in an individual after reexposure to Mast cell tryptase: useful in the ABCDE followed by:
allergen changes (flushing, an antigen to which they have produced IgE follow-up of suspected reactions, 1. Lie flat and raise legs
• Itching of the palate or urticaria, angioedema) IgE antibodies that recognize epitopes of the lags by 30mins and peaks at 2hr. 2. 0.5mg IM (1:1000) adrenaline
external auditory meatus • Dyspnoea +/- laryngeal allergen. These then bind to the high-affinity (in those >12 years), repeat dose
• Palpitations oedema (stridor) and IgE receptor (FcεRI) on the surface of mast at 5-minute intervals according to
• Nausea, vomiting wheezing cells and basophils. Upon reexposure, the response
• Syncope (bronchospasm) allergen may cross-link bound IgE resulting in 3. If available: O2 therapy, IV Fluids
• Sense of impending doom • Cap refill >2sec degranulation as well as de novo synthesis of (20 mL/kg in a child or 500-1000
mediators. Histamine is thought to be the mL in an adult), Airway adjunct
primary mediator (pruritis, rhinorrhea, 4. After initial resus: (Anti-histamine)
Chlorphenamine 10mg IM,
tachycardia, and bronchospasm) but PGD2
Hydrocortisone 200mg IM (Both
and LTC4 contribute to bronchospasm and
in >12 years)
vasodilation as well.
Diabetic Keto- • Drowsiness, vomiting and Triggers: Infection; surgery; There is excessive glucose, but lack of insulin
acidosis (DKA) dehydration in type 1 MI; pancreatitis; wrong cell uptake. The body enters a starvation-like
- IV Fluids
diabetic insulin non-compliance state where ketoacidosis is the only - IV Insulin (0.1 units/kg/hr)
• Kussmaul breathing (blow mechanism of energy production - KCl if low K
off CO2 to help acidosis)
Meningococal SEE BIA PATHWAY OVERLEAF
septicaemia
Michael Grant

lOMoARcPSD|4984001
POEM: Page 26 of 68
Upper Gastro- Haematemesis Look for signs associated Bleeding from the upper gastrointestinal Glasgow-
Intestinal Tract • Vomiting blood with: tract (GIT) is about four times as common as Blatchford
Haemorrhage • Fresh • Peptic ulcer bleeding from the lower GIT. It is important score: If 0,
• ‘Coffee-grounds’ (acid • Gastritis/erosions to identify patients with a low probability of consider
conversion of • Oesophagitis re-bleeding from patients with a high discharge
haemoglobin to • Mallory-Weiss tear probability of re-bleeding. The size of the Rockall Score:
methaemoglobin) Varices bleeding vessel is important in prognosis. identify patients
Melaena • Portal hypertensive Visible vessels are usually between 0.3 mm at risk of
• Passage of black tarry gastropathy and 1.8 mm. Large bleeding vessels cause rebleeding
malodorous stools • Malignancy faster blood loss. Generally, larger vessels outcome following AUGIB - <3 good prognosis, >8 high risk of mortality
• Oxidisation of haem by are found deeper in the submucosa and ABCDE followed by:
intestinal and bacterial serosa and more specifically high in the Immediate (if unstable) or <24hr endoscopy; Rx based on findings:
enzymes lesser curve of the stomach and postero- - Non-variceal bleeding: Clips, thermal coag. w/ adrenaline, Fibrin or
inferiorly in the duodenal bulb. Throbin (w/ adrenaline); followed by PPI treatment post-op
- Variceal bleeding: Offer terlipressin & prophylactic ABx at
presentation, then depending on endoscopy findings:
Gastric varices: endoscopic injection of N-butyl-2-
cyanoacrylate
Osophageal varices: endoscopic band ligation or, especially in
cases of alchoholics, stent insertion
For severe, acute variceal bleeding: Balloon Tamponade (Sengstaken –
Blakemore tube for)
Ectopic • Abdominal pain. • Pelvic or abdominal 97% of ectopics occur in Fallopian tubes. The - Pregnancy test If ectopic pregnancy detected, offer
Pregnancy • Pelvic pain. tenderness. majority occur in the ampulla (80-90%) or - Refer immediate to Obs & Rx based on the hCG level:
• Amenorrhoea or missed • Adnexal tenderness isthmus (5-10%). 2-3% occur as interstitial Gynae if there: • <1500 IU/L: Methotrexate
History of 6-8 weeks period. • Abdominal distension. ectopic pregnancies (arising the part of the • Positive preg. test + any of: • 1500-5000 IU/L: Either
amenorrhoea followed by • Vaginal bleeding (+/- • Enlarged uterus tube passing through the uterine wall), and pelvic, cervical motion, or • >5000 IU/L: surgical removal by
light vaginal bleeding and clots) • Rebound tenderness are a dangerous types. The rare remaining abdominal tenderness laparoscopic salpingectomy (if
constant lower abdominal • Shoulder tip pain NB: Possible risk of rupture of locations include cervical, fimbrial, ovarian, Once referred: fertility issues: ?salpingotomy)
pain • Cervical motion an ectopic pregnancy on peritoneal, and c-section scars. As a general - USS (Preferably transvaginal) For those undergoing surgical Rx:
tenderness (Chandelier's) palpation, so internal exam rule, only an intrauterine pregnancy is viable. Anti-D (50mcg) is required
• Dizziness, fainting or would not be performed if TVUSS Repeat hCG once per week until a
syncope. ectopic is suspected negative result is obtained
• Breast tenderness.
Abdominal Asymptomatic: Asymptomatic: An aneurysm is an abnormal vessel dilation Surveillance w/ USS abdomen: Endovascular Repair (EVAR):
Aortic • None • Non-tender epigastric with increase of >50% the expected diameter • 3 – 4.4 cm: every 12 months Stent is introduced through femoral
Aneurysm Symptomatic: mass (+/- bruit) • Aorta > 3cm considered Aneurysm • 4.5- 5.4 cm: every 3 months arteries and
• Abdominal Pain radiating • Pulsatile & expansile o < 5.5 cm Small Aneurysm • >5.5cm: Consider treatment channels blood
to Back / Groin Symptomatic (above plus): o > 5.5 cm Large Aneurysm ESR/CRP: Rule out inflam. cause to allow
• Intermittent Claudication • Tender epigastric mass • 50% of aortic aneurysms are in abdo ECG aneurysm to clot. Requires a 1.2 cm
Rupture: • Limb ischaemia Typically begin as atherosclerotic plaque that CXR 'neck' below the renal arteries
• Abdominal Pain radiating • Retroperitoneal Fibrosis is weakens wall with inflammatory infiltrate CT: can show, mural thrombus, Open Surgical Repair:
to Back / Groin Rupture (above plus): and the action of MMPs the 'crescent sign' (blood within Exposure of aorta, aortic &
• Collapse • Acute abdomen Genetic Factors: Hereditary Risk: 10-fold, the thrombus, ?imminent rupture) iliac clamping and
• Lumbar haematoma Gender Male: 6-fold MRI angiography insertion of prosthetic
• Shock/LOC Environmental: age, smoking, CV disease graft. Higher mortality.
Michael Grant

lOMoARcPSD|4984001
DKA Dx - Always ask these 3 !!!

DKA and Meningitis / Meningococcal Septicaemia Management
- pH - Blood Glucose - Ketones
DKA Mx:
- IV Fluids
- IV Insulin
- KCl if necessary
Undertake a risk a
Fever, stiff neck,

headache
LP; Blood cultures
Meningitis - 2g IV
Cefotaxime /
Ceftriaxone
Fever
Stiff neck
Headache

lOMoARcPSD|4984001
VTE Prophylaxis POEM: Page 28 of 68

Assessment of a surgical patient for venous thromboembolism including decisions on use of
mechanical and chemical prophylaxis.
Patients who are at risk of VTE
Medical patients:
• If mobility significantly reduced for ≥ 3 days
• If expected to have ongoing reduced mobility relative to normal state plus any VTE risk factor (see below).
Surgical patients and patients with trauma:

• If total anaesthetic + surgical time > 90 minutes
• If surgery involves pelvis or lower limb and total anaesthetic + surgical time > 60 minutes
• If acute surgical admission with inflammatory or intra-abdominal condition
• If expected to have significant reduction in mobility or
• If any VTE risk factor present (see below).
LEARN VTE RISK FACTORS FOR OSCE !!
VTE risk factors:
• Active cancer or cancer treatment endocrine or respiratory pathologies; acute
• Age > 60 years infectious diseases; inflammatory conditions)
• Critical care admission • Personal history or first-degree relative with a
• Dehydration history of VTE
• Known thrombophilias • Use of HRT
• Obesity (BMI > 30 kg/m2) • Use of oestrogen-containing contraceptive
• One or more significant medical comorbidities • Varicose veins with phlebitis
(for example: heart disease; metabolic,
Exam: swollen leg, calf tenderness/redness, +ve Homan's Sign, Fever
Investigation: Doppler U/S, D-dimer Memorise !!
VTE prophylaxis:
Mechanical:
• Anti-embolism stockings that produce a pressure of 14–15mmHg at calf (thigh or knee length); unless
contraindicated by: peripheral arterial disease, peripheral neuropathy, local skin conditions, CCF +/- oedema,
• Foot impulse devices
• Intermittent pneumatic compression devices (thigh or knee length)
Chemical prophylaxis:
• If the risk of VTE outweighs the risk of bleeding and the bleeding risk is low, offer LMWH, e.g. enoxaparin
(a.k.a. clexane), Fondaparinux, Dabigatran or UF Heparin (for patients with severe renal impairment)
• Continue until mobility is no longer significantly reduced, typically 5-7 days
o (with the exception of orthopedic surgeries such as hip replacement, requiring 28–35 days)
Michael Grant

lOMoARcPSD|4984001
Cardiac Arrest Mx
Resuscitation
Apply a standardised approach to the Critically Ill:
• Use the ABCDE format:
• Treat acute pathology as it presents: Remember to treat as

you meet.
Diagnose and manage in hospital cardiac arrest in an adult:

lOMoARcPSD|4984001
Know treatments for all these!!

• Exclude the reversible causes of cardiac arrest:
Reversible cause
of Cardiac Arrest:
- 4 H's
- 4 T's
Know all reversible causes

of Cardiac Arrest by heart !!
• Identify the following arrhythmias:

Shockable:
• Ventricular Fibrillation:
o Bizarre irregular waveform
o No recognisable QRS complexes
o Exclude movement/interference as cause
• Ventricular Tachycardia (Pulseless)
o Monomorphic: regular and with a similar
QRS morphology of all the beats
o Polymorphic: a form of ventricular

tachycardia in which there are multiple
ventricular foci with the resultant QRS
complexes varying in amplitude, axis and
VT can be with pulse /
duration.
pulseless, so always
remember to check pulse!
§ Torsades des pointes: a specific form
of polymorphic ventricular tachycardia
occurring in the context of QT
prolongation; it has a characteristic
morpholog y in which the QRS
complexes “twist” around the isoelectric line e.g. hypokalaemia

lOMoARcPSD|4984001
POEM: Page 31 of 68
Non-shockable (1mg IV Adrenaline 1:10,000, 3-5min):
• Pulseless Electrical Activity refers to a clinical diagnosis of
cardiac arrest in which a heart rhythm is observed on the ECG
that should be producing a pulse, but is pulseless.
• Asystole refers to a ECG with an absent of ventricular (QRS)

activity, although p-waves may still persist – so there is rarely a
true “flat-line”.
• Have a working knowledge of commonly used antidotes Overdose Rx

Common overdose agents:
Naloxone has a short half-life Opiate Overdose Triad:
• Opiates: - Reduced GCS
- Pinpoint pupils
o Naloxone 2mg/IV every 2min until sufficient respiratory drive opioid naïve patients - Reduced depression
Naloxone o Duration of action is 30 to 90 minutes, so patients monitored for 4hr in case of relapse with airway support
2mg/IV
o May cause opioid withdrawal, give 2 Lomotil tablets/6hr; in severe dependence, may need methadone
• Benzodiazepines:
o Pure BZD overdose is rarely life-threatening so Rx is therefore largely supportive until the effects wear off but
patients may need occasional respiratory support.
Supportive
o In Resp. Arrest: Flumazenil (200mcg/IV) then additional 100mcg every min up to 600mcg in 6min users
Flumazenil
200mcg/IV o There are no known issues:
§ BZD-dependence & tricyclic antidepressants due to risk of seizures
§ Prodysrhythmic drug (e.g., tricyclic antidepressants or carbamazepine) due to risk of arrhythmia –
use with ECG monitoring
§ Flumazenil has a shorter half-life than most BZDs, with 30% of Px becoming re-sedated
• Carbon Monoxide:
o Remove the person (and others) from the source and advise to stay away from the area until it has been
ventilated; may have headache, vomiting, tachypnea, fits, arrest
100% o 100% oxygen (despite not LOOKING hypoxic) with ECG monitoring and ABG (O2 will correct acidosis)
Oxygen o Measure HbCO; O2 until >10% levels but if >20% or cardiovascular/neurologic impairment/pregnant
transfer to hyperbaric oxygen facility
o Serial neurologic examinations, including funduscopy, CT scans, and, possibly, MRI, to assess cerebral
edema – if found: Head elevation, mannitol, and moderate hyperventilation to 28-30 mm Hg PCO2
• Paracetamol:
o May present with no symptoms or vomiting and RUQ pain (liver); if presenting late, Jaundice
o Liver damage from centrozoidal necrosis is maximal 3–4 days after paracetamol overdose and may lead to
Activated charcoal 1g/kg
N-Acetylcysteine 150mg/kg
encephalopathy, haemorrhage, hypoglycaemia, cerebral oedema, and death
in 5% dextrose o If less <4hr since overdose (esp. if large >7.5g), give activated charcoal 1g/kg (up to 50kg)
o Test blood paracetamol level: Acetylcysteine (150mg/kg in 5% dextrose over 1 hr) protects the liver if
infused up to, and possibly beyond, 24hrs of ingesting paracetamol. It is most effective if given within 8
hours of ingestion For Paracetamol overdose, activated charcoal oral 50g
• Cyanide: given if patient has presented within ~1 hour of overdose
o Can present: mild (dizzy, tachycardia, nausea), moderate (vomiting, reduced GCS, cyanosis), severe (coma)
o Mild: Administration of 100% oxygen
Dicobalt edetate o Moderate/Severe: Dicobalt edetate 300mg/IV/1min (a cobalt and EDTA compound) can be used to bind
300mg/IV/min cyanide due to cobalt similarity to iron but is toxic, and potentially fatal, if administered in the absence of
cyanide poisoning; hence reserve for severe cases
o Alternatively, a regimen of sodium nitrite followed by sodium thiosulfate can prove effective
• Calcium channel antagonists:
o Glucagon promotes calcium entry into cells via stimulation of a receptor separate from adrenergic receptors
Glucagon 5-10mg o Administer glucagon (5-10 mg IV bolus up to 15 mg, followed by an infusion) after fluid resuscitation
IV bolus
o Since glucagon dilates the lower esophageal sphincter, vomiting and aspiration may occur
• Beta Blockers:
o An intravenous injection of atropine for bradycardia (3 mg for an adult, 40 micrograms/kg for child)
Atropine 3mg o If cardiogenic shock unresponsive to atropine is probably best treated with an bolus glucagon 2–10mg/IV
(CHILD 50–150mcg/kg, max.10 mg) in glucose 5% followed by an intravenous infusion of 50
micrograms/kg/hour
Salicylate levels (Aspirin) Work out anion gap
Resp alkalosis + Metabolic acidosis Causes: MUDPILES mnemonic Tricyclics - Wide QRS complex
Mx - Intralipid Michael Grant
100ml bolus
lOMoARcPSD|4984001
REVIEW BRADYCARDIA AND

NARROW-COMPLEX / POEM: Page 32 of 68
Identify and describe the management of: BROAD-COMPLEX TACHYCARDIA Rx
• Bradycardia (2010 Resuscitation Council guidelines)
Bradycardia
Mx
• Tachycardia (2010 Resuscitation Council guidelines)
Tachycardia
Mx
Michael Grant

lOMoARcPSD|4984001
Cardiac Arrest in specific situations

POEM: Page 33 of 68
• Cardiac arrest in pregnancy

• Aortocaval Compression: compression of the abdominal aorta and inferior vena cava by the gravid uterus
when a pregnant woman lies on her back causing supine hypotension
o >20 weeks: Place a towel or wedge under the right hip, so that the central weight has a left
lateral tilt at least 15 degrees and elevate legs to increase venous return
o Increased risk of aspiration due to increased abdominal pressure
• Delivery of Fetus: If there is no response to correctly performed CPR within 4 minutes of collapse or if
resuscitation is continued beyond this in women beyond 20 weeks of gestation, caesarean section should
be undertaken to assist maternal resuscitation.
o Perimortem caesarean section can be performed anywhere, scalpel being the only essential
equipment, time should not be wasting moving to theatre. With no circulation, blood loss is
minimal and no anaesthetic is required.
o After delivery, continue materal resuscitation and move to a operating theatre
• Secure airway: Bag valve mask until possible to get intubation with a cuffed endotracheal tube
• Consider disease of Pregnancy:
o Thromboembolic Disease
o Pre-Eclampsia
o Amniotic Fluid Embolism - Amniotic fluid, fetal cells, hair, or other debris enters the mother's
blood stream via the placental bed of the uterus and triggers an allergic-like reaction; rare but
th
severe, 5 most common cause of materal mortality.
• Cardiac arrest in a hypothermic patient

o
• Defined as a Core Body Temperature <35 C
o You are not dead until you’re warm AND dead
o J waves on ECG
• Rewarming
o Removal of wet clothing, warm saline, bair hugger,
thoracic/peritoneal lavage, cardiopulmonary bypass
o
• Temperature <30 C:
o Withhold all Drugs
o 3 attempts at defibrillation
o
• Temperature 30-35 C:
o Double time intervals of all drugs i.e. 6-10minutes
o Defibrillation as normal
• Cardiac arrest in a hypovolaemic patient

• ABCDE
• Modern ideas include avoiding excessive crystalloid fluid resuscitation
by allowing permissive hypotension and early use of blood and massive
transfusion protocols with damage control surgery to combat the lethal
triad of hypothermia, coagulopathy and acidosis.
o O negative / Type specific / Cross matcheds
o Emergency cell salvage with auto-transfusion
o Massive transfusion protocol: 1(unit):1:1 Blood : FFP :
Platelets required to prevent coagulopathy by dilution
o Minimise crystalloid administration
§ Reduce effects of coagulopathy, hypothermia, acidosis
• Haemorrhage control - Where is the blood?:
o Consider reversal of anticoagulants
o Tranexamic acid
o Chest – chest drain
o Abdomen/pelvis – see on FAST scan, theatre, pelvic splint
o Long bones – reduction, immobisation, Thomas splint (provides
traction to #), tourniquet
o Floor – gauze and pressure initially
Michael Grant
Hypovolaemic Cardiac Arrest:
=> ALWAYS remember to check if they are losing blood from somewhere
lOMoARcPSD|4984001
POEM: Page 34 of 68
Central venous access:
• Cardiac arrest in a suspected drug overdose - Internal Jugular Vein, Subclavian Vein, Femoral Vein
- Used when peripheral access cannot be gained
In the case of a suspected poisoning: - Correct level of insertion is - Junction of SVC and right atrium (at level of carina)
• Take a detailed history and ensure the protection of team - Central line - Stays max 7 days
- Peripheral line - Stays max 3 days
• Aim to reduce absorption:
o Gastric Lavage: consider if fatal amount of poison ingested and if can be performed within 60 minutes of
ingestion
o Activated Charcoal: indicated where it is likely that toxin remains in the gastrointestinal tract (i.e. within one hour of
ingestion for most agents) and where the potential benefits outweigh the potential risk
• Seek advice specific to the agent: BNF or Toxbase

Venepuncture Attempt distal vein first!
• Take venous blood samples and manage the blood samples correctly (including use of the
correct containers, appropriate labelling and completion of laboratory forms)
Bottle colours
Anaerobic blood culture bottle
• Select, insert and secure an intravenous cannula using an aseptic technique.

Pick lines used for patients
with chronic illness
- Stays in for max 1 year
Cannula
Cannula Sizes
SMALL GAUGE = BIG CANNULA + FAST FLOW RATE

BIG GAUGE = SMALL CANNULA + SLOW FLOW RATE
Michael Grant
As the gauge number increases, the cannula size decreases
(14 is largest and 24 is smallest)
The larger the gauge number, the smaller the cannula diameter is
lOMoARcPSD|4984001
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Hazards of periperhal cannulation:
• Haemorrhage, haematoma
• Needle trauma
• EXTRAVASATION
o KCl/NaHCO3/Thiopentone
• Thrombophlebitis
o Inflammation e.g.
KCl/Antibiotics/Amiodarone –
Infective
• Air embolism
• Drug interactions within cannula Air embolism via returning
vein to vena cava can
cause pulmonary
obstruction
Things to consider:
• Do you need to take blood at the same time?
(Axillary node
• Size of cannula? Reason for insertion clearance i.e. in
• Position - Avoid arm with AV fistulae or post ANC breast cancer
patients)
• Consider manual BP cuff
• Perform and interpret an Electrocardiograph

o Consent, remove upper body clothing and lie down
o Remove excess hair where necessary
o Stickers over bone
o Ask the patient to relax and lie still
3 Lead ECG:
3-lead system approximates to I, II, III
Apply sensors:
o Colour coded (Red: right arm, Lemon: left arm, Green: left leg)
12 Lead ECG:
More sophisticated, 3D interpretation of the electrical activity of the heart
10 electrodes (Red, Lemon, Green, Black, V1-V6) produce the 12 leads:
• Bipolar Leads (I, II, III)
o Reference point on one limb, ‘sensing’ electrode on another
o Lead I ‘looks’ left. (LA-RA)
o Lead II towards left foot from the right (LL- RA)
o Lead III towards left foot from the left (LL- LA)
• Augmented limb leads (aVR, aVL, aVF)
o Use same electrodes positions as I,II,III
o Formula used to allow different views of the heart to be
combining vectors from those leads (Wilson’s central
terminal)
o aVF points directly down.
o
o aVL points 30 north of lead I
o aVR ‘looks’ at the heart from up and right, deflections are
therefore negative
• Chest leads (V1-V6)
o Looks at the heart cross-sectional axis
th
o Septal leads: V1, V2 (either side of sternum in 4 ICS)
o Anterior leads: V3 (inbetween V2 & V4), V4 (5th ICS MCL)
o Lateral leads: V5 (inbetween V4 & V6), V6 (5th ICS mid
axillary line)
o R waves progress from being less dominant, mixed and onto
dominant as you go from lead V1 to V6
Michael Grant

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ECG Waveforms:
• P wave = Atrial depolarization
• PR interval = 0.12-0.20 secs (3-5 small squares)
• QRS complex = ventricular depolarisation (0.08 - 0.12 secs)
o Q wave: representing depolarization of bundle of His, which it does
from left to right in the opposite direction to the main conduction (right
to left) causing a small, downward deflection (from the perspective of
Lead II)
o R wave: Ventricular depolarization toward the direction of lead II. More
muscle, more cells, more electricity leads to a bigger wave. Small square = 0.04sec, Large square = 0.2sec
o S wave: Depolarisation of the Purkinje fibres causes negative deflection (in lead II) as it represents the last, more
superior, compents of the ventricles contracting (given that ventricles contract from apex upward)
• If the R-wave > S-wave: depolarisation is moving towards that lead
• If the R-wave < S-wave: depolarisation is moving away from that lead
• If the R-wave = S-wave: depolarisation is travelling at exactly 90° to that lead
• QT interval = <0.44sec but will vary with heart rate
• ST segment: end of the S wave to the start of the T wave and should be flat or slightly upsloping
o Elevation: if elevated in a few leads (>2mm chest, >1mm limb) indicates the possibility of MI
• If in most leads, question possibility of pericarditis, especially if PR depression
• Concave elevation in all 12 leads is diagnostic of pericarditis
o Depression is diagnostic of ischaemia
• However, beware aware of digoxin’s “reverse tick” ST depression
• T wave = Ventricular repolarization
o Inversion implies ischaemia/infarction
o Hyperkalaemia (“Tall tented T waves”)
Cardiac axis:
• The cardiac axis gives us an idea of the overall direction of
electrical activity when the ventricles are contracting
• Normal axis: In healthy individuals you would expect the axis to
lie between -30° and +90º
o Thus overall direction of electrical activity is towards
leads I,II & III (green segment) giving them all positive
deflection – thus is is useful to use these three leads
when trying to make decisions about the axis
o And the most negative in aVR (as it looks at the heart
from the opposite direction)
• Right axis deviation (RAD): is usually caused by
right ventricular hypertrophy, causing the overall
direction of electrical activity is distorted to the
right (between +90º and +180º)
o Thus deflection in Lead I becomes more
negative & the deflection in Lead III more
positive
o Usually when right side has to work harder (RVH, chronic lung
disease, pulmonary hypertension, pulmonary embolism, ASD, VSD) or when left side works less (Left
posterior fasicular block, lateral MI); although it can be normal in children and very tall, thin people
• Left axis deviation (LAD): direction of overall electrical activity becomes distorted to the left (between -30°
and -90°)
o This causes the deflection in Lead I and aVL to become more positive & the deflection in Lead III to be
more negative
o Usually when left side has to work harder (LVH, Pregnancy) or when right side works less (RBBB, inferior
MI);
o Common causes of LAD include left ventricular hypertrophy (LVH), left anterior fascicular block (or
hemiblock) and, rarely, Wolff-Parkinson White syndrome
Michael Grant

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POEM: Page 37 of 68
Bundle Branch Block:
• Seen as a wide QRS complex despite sinus rhythm (QRS width
>0.12sec (>3 small squares))
• Look at QRS complexes in the V1 & V6 (LBBB, RBBB “WilliaM MorroW”)
• Left bundle-branch block:
o Complete LBBB block is seen with a QRS of >0.12sec
o The depolarisation wavefront travels in more or less the normal
direction in LBBB, the deflections seen are generally normal.
o However, because of the abnormal sites of initiation (from the
right ventricle rather than the conduction system) the electric
heart vector makes a slower and larger loop to the left and is
seen as a broad and tall R-wave, usually in the lateral leads:
leads I, aVL, V5, or V6.
o Causes include: Cardiomyopathy, Acute MI, Hypertension,
Aortic valve disease
• Right bundle-branch block:
o Occurs when the RBB is defective so that the electrical impulse
cannot travel through it to the right ventricle; thus,
depolarisation reaches the right ventricle through the left
ventricle, after it depolarises, via the septum.
o This is slower than the conduction system and leads long QRS-
complex (>0.12sec)
o activation of the right ventricle is so much delayed, that it can be
seen following the normal activation of the left ventricle
o RBBB causes an abnormal terminal QRS-vector that is directed
to the right ventricle (i.e., rightward and anterior). This is seen in
the ECG as a broad terminal S-wave in lead I and a double R-wave in lead V1
o Causes include: Normal variant, COPD, PE, ASD, VSD, tricuspid/pulmonary valvular disease.
Heart Block:
• In Mobitz type 2; it is important to clarify the

frequency of lost beats, i.e. number of P waves for
every missed QRS; 2:1, 3:1, 4:1, etc.
Michael Grant

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POEM: Page 38 of 68
ECG interpretation:
ECGs are RAWW data
• Rate: Number of large squares between R waves, divided by 300
• Rhythm: Look at the R-R intervals again – if they are equally spaced from
each other the rhythm is regular? Use sticky note to check quickly.
• Axis: Look at leads I, II and III – are they all positively deflected?
• Waveform, ride from start to finish:
o P waves present? All followed by a QRS?
o PR interval 0.12-0.20secs? PR depression?
o QRS width 0.08-0.12? Large amplitude – LVH? Check
V1 & V6 for WilliaM MarroW?
o ST elevation? Depression?
o T wave inversion? Tall, tented?
Beware of Hyperkalaemia ECG changes:
• Interpret a MEWS Chart and Score
• NEWS >5 is coded red which means that immediate review of the patient by a senior doctor is
required and patient assessed for transfer to ICU
o This also applies to any patients with scoring 3 in one parameter
• Patients with NEWS 5-6 are coded amber, require urgent medical review and may require transfer
to an enhanced care medical bed (level 1).
• All doctors should be aware of red flag scenarios - symptoms and signs of acute illness, which may
not be detected by NEWS, for example cardiac chest pain.
Hyperkalaemia Mx:
- Stop any potassium-sparing medications
- 10% Calcium Gluconate
Michael Grant
- 10mg nebulised Salbutamol
- 10 units short-acting insulin in 50ml of glucose
lOMoARcPSD|4984001
Disability (Neurological)
POEM: Page 39 of 68
Assessment of Level of Consciousness

List the differential diagnosis for the unconscious patient:
Prolonged loss of consciousness (coma, defined as a Glasgow Coma Score of 8 or less) is seen commonly:
• following head injury,
• after an overdose of sedating drugs,
• In the situation of ‘nontraumatic coma’, where there are many possible diagnoses, but the most common are
postanoxic, postischaemic, systemic infection, and metabolic derangement, e.g. hypoglycaemia.
The key components of the neurological examination of the comatose patient are:
•
•
Glasgow Coma Score — list the components; e.g. E4V5M6 = GCS 15
The pattern of breathing
Unconscious and
• Size and reactivity of the pupils comatose patients
• Eye movements and oculovestibular responses
• Motor responses and limb movements (tone, reflexes and posturing)
• Meningism (Neck stiffness, headache, photophobia, Kernig’s sign) and signs of the underlying cause
CAUSES OF COMA
Causes with focal signs:
• No meningism — stroke, space occupying lesions (e.g. tumor,
hemorrhage, abscess), injury, inflammation
• Meningism (Neck stiffness, headache, photophobia, Kernig’s sign) —
meningoencephalitis, subarachnoid haemorrhage (SAH)
Systemic causes without focal signs (TOMES):

• Toxins
• Organ failures
• Metabolic — check COATPEGS (CO2, O2, ammonia, temperature, pH, electrolytes, glucose)
• Endocrine
• Seizures
Remember that systemic causes
can sometimes have focal signs!
(e.g. Todd’s paresis – post-seizure
paralysis, hemiparesis due to
hypoglycemia)
Display a practical
knowledge of how to: PROPERLY
LEARN
• Record the Glasgow GCS
Coma Score (GCS)
A Coma Score of:
• >13: mild brain injury
• 9-12: moderate injury
• <8: severe brain injury (call anaesthetist
for airway)
• Test and interpret pupil reflexes Both pupils dilated

and non-reactive =
In trauma patients with head injuries, Brainstem injury
think SSR:
• Size
• Symmetry
• Reaction
Michael Grant

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POEM: Page 40 of 68
LOC – LEVEL of conciousness
• Move the unconscious patient safely
• Measure blood glucose at the patient’s bedside
D=
ALWAYS
MEASURE
BLOOD
GLUCOSE
Michael Grant

lOMoARcPSD|4984001
Mannitol used to reduce

Describe the presenting symptoms, signs, pathogenesis, investigation and management of: cerebral oedema and ICP

Head Injury • Pain #BOS? The pathological processes involved include: FBC + U&E ABCDE
• Reduced GCS <13 • Panda/raccoon eyes Direct trauma Glucose C-spine immobilization
• Amnesia of event or • bruising behind the ear Cerebral contusion: rupture of capillaries Blood alcohol GCS <8: Intubate
leading up to injury (Battle's sign) may occur at site of trauma, or ‘contra-coup’ Toxicology screen Refer to neurosurgery:
• Confusion and • Blood/CSF from the ear from recoil ABG • Persisting coma (GCS ≤8) after
disorientation canal or nose Diffuse axonal injury: shearing force causes Clotting (Brain bleeds) initial resuscitation
• Headache Anterograde amnesia: petechial haemorrhages in white matter, and Head/Trauma series CT Scan • Unexplained confusion for >4hrs
• Dizziness • Extent of loss correlates stretching/tearing of axons & myelin sheaths immediately if: • Deterioration in GCS score after
• Blurry vision to severity of injury Cerebral swelling (oedema): focally around • GCS <13 admission (esp. motor)
• Nausea and vomiting Assess risk of C-Spine w/ an intracerebral haematoma or diffusely • Focal deficits/seizure • Progressive focal neurological
(esp. if more than once) CT: throughout the brain, due to disturbance of • Suspected #BOS signs
• Seizure • Plain X-rays are vasomotor tone causing vasodilatation • Vomitting >once • A seizure without full recovery.
• Changes in behaviour suspicious Intracranial haemorrhage: may be • LOC of >5min +/- >65yo, • Depressed skull fracture.
• GCS <13 intracerebral, subdural or extradural; can coagulopathy, RTC, antero. • Definite or suspected
• LOC +/- >65yo, focal lead to herniation Amnesia >30min penetrating injury.
deficit, RTC Hydrocephalus: early after a head injury and • Child: any above or suspect • A CSF leak.
• If no risk factors and has may be due to obstruction of the fourth of non-accidental injury
been ambulatory since ventricle by blood/swelling in posterior fossa, • Pre-op to assess C-Spine High-dose mannitol is beneficial in
w/ no pain: rotate head or result of subarachnoid haemorrhage; CT scan within 8hrs: none of the pre-operative management of
45 degrees each way blocking arachnoidal granulations above + warfarin, >65yo, RTC acute intracranial haematomas
Status • Seizure lasting >30mins • If no Hx of epilepsy, Seizures are sustained by excess excitation FBC ABCDE
Epilepticus or multiple without then >50% brain lesion (usually glutamate acting on NMDA receptor) U&E
intervening and reduced inhibition (Usually GABA). LFT Lorazepam (4mg) slow bolus
consciousness Failure of inhibitory processes is thought to Glucose Repeat if no response in 10 minutes
• Tonic-clonic, absent or be the major mechanism behind SE. Serum calcium +
localised? Significant physiologic changes accompany Toxiciology screen Glucose (50 ml of 50% solution)
generalized SE (eg, tachycardia, cardiac and/or intravenous thiamine (250
arrhythmias, hyperglycemia), thought to EEG can be useful mg) as high potency intravenous
result from the catecholamine surge. SE Pabrinex if any suggestion of
affects mechanical aspects of breathing and alcohol/malnutrition (Wernickes
causes pulmonary edema. Many of the encephalopy may be cause of SE)
medications used to treat SE (specifically,
benzodiazepines and barbiturates) also If seizure continues:
inhibit respiratory drive. The duration of SE Rectal Diazepam CALL ANESTHETIST if >20min
correlates with outcome and likelihood that IV Lorazepam Phenytoin 20mg/kg IVI at
neurons will be damaged by excitatory Buccal Midazolam 50mg/min
neurotransmitters; leading to cell death from
If no improvement at 60 minutes:
high intracellular calcium caused by long
Expert referral w/ continuous EEG
exposure to excitatory neurotransmitters
General anesthesia
Sub-arachnoid • Sudden explosive • Intraocular haemorrhage SAH is usually the result of bleeding from a CT Scan ASAP Endovascular Aneurysm Coiling (if
Haemorrhage headache (Thunderclap) • <GCS or Coma berry aneurysm in the Circle of Willis. Angiography: CT or Catheter not possible, open clipping)
• Rare: vomiting, • Focal signs: esp. palsy Thought to be mostly congenital but may (latter offers option to coil) If hydrocephalus: LP or ventricular
meningism, seizures of the oculomotor nerve involve susceptibility of elastic lamina LP: >12hrs may show RBCs drain
hypertension and atherosclerosis. ECG: long QT, ST elevation noted Secondary preventions

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Hypoglycaemia • Odd behaviour • Tachycardia Brain metabolism depends primarily on Blood glucose ABCDE
• Sweating glucose for fuel in most circumstances. A Blood alcohol
• Seizure limited amount of glucose can be derived U&E 20-30g glucose IV:
• LOC from glycogen stored in astrocytes, but it is Calcium • 10% Dextrose 200-300ml
• Coma consumed within minutes. In most people, ABG • Glucagon 1mg IV/IM is as
subtle reduction of mental efficiency can be HbA1C effective as dextrose but will not
observed when the glucose falls below 65 work if drunk
mg/dl (3.6 mM). Impairment of action and • Above are preferred to 50%
judgment usually becomes obvious below 40 Gluscose as it harms veins
mg/dl (2.2 mM). Seizures may occur as the
glucose falls further. Nervous, hormonal and Monitor closely and upon recovery:
metabolic responses raise the blood sugar Sugary drink and meal
via glycogenolysis and gluconeogenesis or
provide alternative fuels until depletion.
Sepsis • Cough/Sputum • Line Infection Sepsis is technically classified as: FBC ABCDE
• Chest Pain • Cellulitis/Septic Arthritis Systemic inflammatory response CRP
• Abdominal • Dysuria syndrome (SIRS) – i.e. 4<WCC>12, Urine dipstick & sample: Sepsis 6:
Pain/Distension • Headache with neck 36<temp>38, HR >90, RR >20 microscopy, C&S 3 in: O2 therapy, IV fluids, ABx (After
• Vomiting/Diarrhoea stiffness + Renal function culture)
• *RASH* • Endocarditis Suspected or Present Source of Infection LFTs - hypoalbuminaemia likely 3 out: Blood culture, ABG (for
Glucose - hyperglycaemia can be lactate), Urine (via catheter)
Severe Sepsis: above + Lactic acidosis or
present
SBP <90
Clotting screen including D- Then assess procalcitonin level
Septic shock: Severe Sepsis w/ hypotension,
dimer, looking for *DIC*
despite adequate fluid resuscitation
Blood cultures - at least two are ICU Referral if:
Multiple Organ Dysfunction Syndrome
3 things to give: required • Sepsis: early if it looks like they will
(MODS): Septic shock + >1 organs failing
Radiology - including CXR, quickly deteriorate
- High-flow O2
abdominal ultrasound looking for • Severe Sepsis: Progressing to
- IV Fluids Aetiology: Gram- 45% (e.g E. Coli,
a collection, and CT scan looking organ failure
- IV Antibiotics Pseudomonas), Gram+ 43 (Strep, staph),
for source • Septic Shock
fungi 17% (candida)
Measures of lactate and oxygen
3 things to measure: saturation of venous blood Surgery may also be required - eg,
- Urine output Arterial blood gases - metabolic wound debridement, abscess
- Serum lactate acidosis is common drainage
- Blood cultures
INSERT PAGE ON SEPSIS HERE !!! Michael Grant

lOMoARcPSD|4984001
POEM: Page 43 of 68
Michael Grant

lOMoARcPSD|4984001
Anaesthesia
Pain Management
List the complications of inadequate pain
management
Pain is detected by nociceptors and transmitted to the dorsal horn of
the spinal cord. They respond to one or several of:
mechanical, chemical, thermal or inflammatory insults.
They have different axons:
• A fiber axons – myelinated, fast (20m/s)
• C fiber axons – unmyelinated, slow (2 m/s)
In the spinal cord they use either glutamate or substance
P as neurotransmitter to the second order pain neurons
that pass the signal onto the thalamus via the
spinothalmic tract. From the thalamus, pain sensations
are sent on to the cerebral cortex via fibers from the
internal capsule. In return, the brain can release hormones with
analgesic effects via the hypothalamus. There is descending inhibition of pain is achieved by signals from
periaqueductal grey matter to raphe nucleus, in turn projecting to the substantia gelatinosa region of the
dorsal horn in order to mediate the sensation of spinothalamic inputs.
Aside from not wanting to leave patients in pain unnecessarily, not effectively treating pain can cause:
• Patients being unable to move/mobilise adequately, e.g. post hip-replacement
o This may lead to an increased risk of postoperative of DVT
• Abdominal/thoracic surgery patients to reduce their tidal volumes e.g. flail chest
o This may lead to basal airway closure and secretion retention, in turn lead into a spiral of
hypoxia, lung collapse and bacterial infection
• Severe pain suffers often mount a marked sympathetic response inducing Tachycardia/hypertension
o Undesirable especially in patients with significant heart disease or STEMI
Explain the ‘Analgesic Ladder’

Starting with simple (non opioid) analgesics (NSAIDs and Paracetamol)
it moves to moderate opioids (Codeine or Tramadol) and finally
receives if necessary strong opioids such as Morphine. The concept has
really been superseded with the application of multimodal analgesia.
Explain the concept of multimodal analgesia

The use of drugs with different mechanisms of action, often with synergistic effects, results in sufficient
pain control that there can be a reduction in dose and therefore adverse effects of sole administration.
Drugs co-prescribed with opioids allow a dose reduction and are said to have an opioid sparing effect,
reducing the likelihood of respiratory depression, post operative V&D and/or constipation. From a practical
perspective, although there are many types of analgesics available, the major drugs that are used in acute
pain are:
• Opioids (Morphine, codeine, tramadol, fentanyl, sufentanil, etc.)
• NSAIDs (Diclofenac, ibuprofen, naproxen, etc.)
• Paracetamol
• Local Anaesthetics (Lidocaine, Bupivacaine, novocaine, benzocaine, prilocaine etc.)
Describe a ‘Patient-Controlled Analgesia System’ (PCAS) for Morphine.

Device containing an opioid is operable by patient via a handet. Patient is able to
deliver a IV bolus of painkiller on demand, with settings to prevent overdose (with additional
limit of a patients’ drowsiness preventing further doses). This system can be used with other
routes (e.g. epidural) and can be controlled by nurses (usually in the case of children)
• Patients on PCAS shouldn’t be prescribed other opioids
• Require additional observations and will have a blue MEWS chart

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Describe the presenting symptoms, signs and initial management of:
Opioid overdose:
• Symptoms/Signs: "Opioid Overdose Triad":
o Reduced GCS Opioid overdose triad
o Pinpoint pupils
o Respiratory depression
• Management: Give naloxone, eg 0.4–2mg IV; repeat every 2min until breathing is adequate (it has a short
1⁄2
t , so it may need to be given often or IM; max ~10mg). Naloxone may precipitate features of opiate
withdrawal— diarrhoea and cramps, which will normally respond to diphenoxylate and atropine (Lomotil®—eg 2
tablets/6h PO).
Local anaesthetic toxicity: Local Anaesthetics

• Symptoms/Signs:
o Local: Urticaria, rash, anaphylaxis (rare)
o Systemic:
§ Hematologic: Metheamoglobinemia (increased level of methaemoglobin, form of Hb
containing [Fe3+] iron and has a decreased ability to bind oxygen) can be seen with hypoxia
and cyanosis – esp. with benzocaine
§ CNS: tinnitus, a metallic taste, perioral paresthesia, tonic-clonic seizrues, coma (high levels)
§ CVS: bradycardia, hypotension, arrhythmia (high levels)
• Management: Intravenous lipid emulsion (such as Intralipid) may be a useful antidote for refractory
cardiovascular collapse; thought to act as a lipid sink for lipophilic compounds.
Have a working knowledge of Lidocaine and Bupivacaine including maximum

permitted dosage, preparations and routes of injection:
Drug Max Dose Preparations Routes
Lidocaine 200mg (or 500mg if in • 5 mg/mL (0.5%) • SC for field block
preparation with adrenaline) • 10 mg/mL (1%) • Topical
Generally: 3mg/kg (7mg/kg • 20 mg/mL (2%)
with added adrenaline)
Bupivacaine* 150mg (can be repeated • 2.5mg/ml (0.25%) • SC for field block
every 3 hrs) in single dose • 5mg/ml (0.5%) – not to be • Epidural
Generally: 2mg/kg used for SC field block • Intra-articular
LA can be used with adrenaline to: prolong effect, reduce bleeding, reduce systemic effects
Remember – when thinking about medicines like these with percentage concentrations: 1ml:1%:10mg
– Children’s weight in kg: 2*Age + 8
*Chiracaine/Levobupivacaine is a version of the drug made up exclusively of the S enantiomer; other prepartions
include hyper- or hypobaric preparations that can float or sink in the CSF, for targeted pain relief
Have a working knowledge of Non Steroidal Anti Inflammatory Drugs (NSAIDs) including
Paracetamol
All NSAIDs have the same mechanism of action inhibiting the enzyme cyclooxygenase
(COX) and consequently prostaglandin synthesis, which in turn reduces tissue inflammation
and pain:
• NSAIDs mainly act peripherally
• Most NSAIDs are relatively non-selective, inhibiting COX-1 and COX-2 enzymes
o Ratio of inhibition varies from drug to drug
• Selective COX inhibitors are more potent at the COX-2 enzyme
• Caution is required when using NSAIDs because of certain common side effects:
o GI irritation and risk of GI bleeding, renal toxicity, potential drug-drug interactions
o Some selective COX-2 drugs have serious CVS side effects like MI, stroke and
hypertension
o Must be used cautiously older patients with impaired renal function and heart failure
Michael Grant

lOMoARcPSD|4984001
POEM: Page 46 of 68
Paracetamol must be set apart from NSAIDs
because, unlike them, it predominantly inhibits on
central prostaglandin synthesis. It shares this class
with metamizole, and neither of their mechanisms of
action have been fully explained.
Paracetamol is an aniline derivative and is used

widely as an analgesic and antipyretic, but it has
no significant anti-inflammatory effects.
Paracetamol is associated with risk of liver damage

(centrizoidal necrosis) at high doses.
Measure level of sensory block in a patient with an epidural

Epidural analgesia consists typically of a mixture of both local anaesthetic (usually
Bupivicane) and opioid (usually Fentanyl) which have a synergistic action. The epidural is a
plastic tube that is inserted into the epidural space in theatre, in the thoracic or lumbar spine.
These patients require additional observations and are given a yellow MEWS
chart.
The local anaesthetics work first on the smallest diameter fibres, which are more
sensitive to the drugs: autonomic fibres will be blocked first then sensory fibres
then motor fibres. producing:
• Sympathetic block – hypotension
• Sensory block – pain relief, urinary retention
• Motor block – paralysis, urinary retention
Since pain and temperature nerve fibres (spinothalmic tract) are similarly
affected by local anaesthetic drugs, changes in temperature perception
indicate the area where the epidural is working. This can be running an
ice cube down both sides of the patient to ensure:
• Epidural is covering the site of patient's pain/surgery
• That block is not too extensive, which may increase the risk of
complications
o Heart is innervation from T1-T4, so sensory block above the level of
the nipples cause trigger a PROFOUND HYPOTENSION
§ Hit red stop button and call anaesthetist
Touch the cube to the patient's face as a control then run laterally along the
patient with their eyes closed. Ask them to tell you when it feels as cold as it did
when it was on their face.
• Assess left AND right sides
• Document the upper and lower limits of the block: e.g. T7-L1 L = R; or R:
T7-L1 L: T10-L2
Assessment of motor block is difficult due to reduced power those with epidurals and the because they are
to remain in bed. However, in ward-based epidurals, patients should still be able to raise heel off bed.
• Onset of severe weakness and back pain may indicate an epidural haematoma/abscess:
o Contact on call anaesthetist
o Requires urgent MRI
Assessment of sympathetic block is achieved with the enhanced observations these patients receive
(yellow MEWS). For any epidural patient who is hypotensive, press the red stop button on the pump,
apply the ABCDE approach, determine the mechanism of shock and contact the on call anaesthetist.
Measuring level of sensory block after an epidural

Michael Grant

lOMoARcPSD|4984001
POEM: Page 47 of 68
Explain the side effects of epidural analgesia and, in a patient with an epidural, their
initial management
Benefits of Epidural Analgesia Risks associated with Epidural Analgesia
Superlative pain relief Hypotension and its associated risks (MI, renal failure, stroke and
excess fluid administration)
Opioid sparing Reduced mobility, need for urinary catheter
Reduced incidence pulmonary Poor, patchy, unilateral or failed analgesia
thromboembolism
Reduced blood loss and transfusion
rates Post dural puncture headache
Reduction in some respiratory Transient neurological damage
complications
Quicker return of GI function Permanent neurological damage
Stress response reduction
Accidental dural puncture with headache (common, about 1

in 100 insertions). The epidural space in the adult lumbar spine
is only 3-5mm thick, which means it is comparatively easy to
cross it and accidentally puncture the dura (and arachnoid) Anaesthetic Toxicity Mx
with the needle, allowing CSF to leak out. This produces a post
dural puncture headache (PDPH)
• Caused by a reduction in CSF pressure
• Characterised by postural exacerbation when the subject
raises his/her head above the lying position
• If severe, treated with epidural blood patch (a small
amount of the subject's own blood given into the epidural
space which clots and seals the leak)
High block is the loss of sympathetic nerve input to the heart

(T1-T4), which may cause a significant decrease in heart rate
and blood pressure. For any epidural patient who is
hypotensive, press the red stop button on the pump, apply
the ABCDE approach, determine the mechanism of shock and
contact the on call anaesthetist.
Principles of management for LA adverse reaction:

1. Stop LA; Call for help; Give 100% O2
2. Manage presenting features appropriately (eg.
benzodiazepine for seizures)
3. If in cardiac arrest Intralipid bolus followed by infusion (usually found in theatres)
Describe the anaesthetic, surgical and patient

factors that are associated with post-operative
nausea & vomiting (PONV). General Anaesthesia
Postoperative nausea and vomiting (PONV) is an unpleasant
complication affecting about a third of the 10% of the
population undergoing general anaesthesia each year.
Emetogenic drugs commonly used in anaesthesia include

nitrous oxide, physostigmine and opioids. The
Anaesthesia that causes nausea and vomiting Michael Grant

lOMoARcPSD|4984001
POEM: Page 48 of 68
intravenous anaesthetic propofol is currently the least emetogenic general anaesthetic.
A major problem particularly with opioid analgesia. Patients should be prescribed antiemetics and the use of a
multimodal treatment to reduce total opioid dose is useful.
A combination of antiemetics is also useful e.g. 5-HT3 receptor antagonists (Ondansetron) and low dose
steroids (Dexamethasone – antiemetic mechanism unknown).
A Cochrane review found droperidol, metoclopramide, ondansetron, tropisetron, dolasetron, dexamethasone, SBAR
cyclizine, and granisetron effective for preventing PONV.
Patient
Non Cognitive Skills Handover
Students should be able to apply the SBAR
model to handing over clinical information
concerning a patient
Trauma Management (PDF downloaded)

Demonstrate an understanding of the basic
principles of:
Trauma Management
• The primary survey and the rationale of the
secondary survey in the management of trauma
The sequence of trauma management:
1. Preparation/Prehospital phase (Paramedics –
only link between scene and hospital, very
important information)
2. Triage <C> ABCDE
3. Primary survey
• <C> Catastrophic bleeding: pressure, tourniquets,
haemostatics
• Airway + C-spine control
• Breathing + Ventilation
• Circulation + Haemorrhage control
o Control haemorrhage: direct pressure,
tourniquet, splintage, surgery / interventional
radiology
o Where is the blood?
§ Chest – chest drain
§ Abdomen/pelvis – see on FAST scan,
theatre, pelvic splint
§ Long bones – reduction, immobisation,
Thomas splint (provides traction to #),
tourniquet
§ Floor – gauze and pressure initially
§ Tranexamic acid
o Consider reversal of anticoagulants
o O negative / Type specific / Cross matcheds
o Emergency auto-transfusion
o Massive transfusion protocol: 1:1:1 Blood : FFP :
Platelets
o Minimise crystalloid administration
Michael Grant
<C> ABCDE
lOMoARcPSD|4984001
POEM: Page 49 of 68
§ Reduce effects of coagulopathy, hypothermia, acidosis
• Disability
• Exposure + Environmental Control
o Logroll to examine back: Removal of clothing, inspect wounds, loins for pain /
swelling / crepitus (#pelvis?), palpate spine, perianal sensation, anal tone
o Prevent hypothermia: take temperature, blankets/warm saline/bair huggers/bypass
4. Resuscitation
5. Adjuncts to primary survey & resuscitation: monitoring/radiology/bloods/ABG Traumas
6. Transfer to relevant department
7. Secondary survey: Head to toe
evaluation including history, examination
and investigation. The secondary survey is a
more detailed and complete examination,
aimed at identifying all injuries and
planning further investigation and
treatment. Chest injuries identified on
secondary survey and its adjuncts are:
• History: AMPLE; Allergies,
Medications, Past medical, Last
meal, Events leading up
• Head/Face: Cranial nerve Neuro’
exam? Palpate the bony margins of
skull; scalp, face, eyes orbits? Test
eye movements, pupillary reflexes,
vision and hearing.
• Neck: Neck pain? Crepitus?
Anterior neck swelling? Hoarse
voice/stridor? Penetrating neck
injury causing progressive
vascular/tracheal injury?
• Chest: Rule out medical causes of
trauma (e.g. MI causing LOC)?
Inspect, palpate (including for
clavicular and rib tenderness),
percuss, auscultate? Order imaging;
FAST, CXR, CT?
• Abdomen/Pelvis: abdo exam;
Inspect, palpate, percuss,
auscultate? Further CT eg with IV /
PO contrast? Sphincter
tone/prostate position? Beware -
Pregnancy
• Upper/Lower limbs:
o 7 P’s; Pallor, Pain, Pulse, Panaesthesia, Paralysis, Perishing cold, Perspiration?
o X-ray > #; Realign, splint and reassess?
o Inspect all the limbs and joints, palpate for bony and soft tissue tenderness and check
joint movements, stability and muscular power
• Examine sensory and motor function of any nerve roots or peripheral nerves that may have been
injured. Beware – compartment syndrome
• Back / buttocks: full full PNS exam including rectal exam, Thoracic and lumbar spine x-ray / CT
8. Adjuncts to secondary survey: monitoring/radiology/bloods/ABG
9. Post resus care
10. Definitive care
Michael Grant

lOMoARcPSD|4984001
Exposure POEM: Page 50 of 68

• Cervical spine management in trauma
C-Spine
Management
• Management of soft tissue Injuries

A Soft tissue injury (STI) is the damage of muscles, ligaments and tendons throughout the body. Common
soft tissue injuries usually occur from a sprain, strain, a one off blow resulting in a contusion or overuse of a
particular part of the body. Soft tissue injuries can result in pain, swelling, bruising and loss of function.
Healing involves:
• Inflammatory Response Phase: Starting from time of injury to 4 days post-injury
• Fibroblastic Repair Phase: Overlapping the inflammatory response phase, typically starts at 4 days post-
injury and continues for up to 6 weeks
• Maturation-Remodeling Phase: Starts around the 6th week post-injury and can last for 2-3 years
Management is PRICE: "P"rotection "R"est "I"ce "C"ompression "E"levation

• ’PROTECTION’ from further injury and keep further hazards away from the individual
• ‘REST’ from any activity that causes pain; if this including simple movements (bending, straightening or
walking) then ‘’rest’’ means immobilizing the injury by splinting or preventing weight bearing with
crutches is essential
• ’ICE’ during first 72 hour, ice for 15 minutes every 4 hours to help control the swelling and pain
• ‘COMPRESSION’ to control the initial bleeding of joint or limb tissues, or to reduce residual swelling;
must be applied within the first few minutes following the injury to see the benefits
• ‘ELEVATION’ of the injured part above the level of the heart, in combination with ice and compression, as
much as possible for the first 72hours, to reduce swelling Muscle Injury Mx
Michael Grant

lOMoARcPSD|4984001
Burn Management POEM: Page 51 of 68

• Burns managment
There are different types of burns:
• Thermal (hot and cold)
• Electrical
• Chemical
• Radiation (esp. sun burns)
• Friction
1% 1%
Rule of thumb:
Age + % burn = Predicted mortality
The prognosis of burns is dependent on your BAI:

o Burn area >40%
BAI o Age >60yrs
4 x 18%
o Inhalational injury
Burns typically effect the skin:

• Largest Organ of body
• Primary function BURN MORTALITY w/ BAI:
o Thermal regulation and prevention of fluid loss Absence risk 0.3%
o Barrier against infection Single risks 3%
o Sensory receptors Two risks 33%
o
• Temps >44 C compromises all functions Three risks 90%
Given this burns can be classified by:

• Depth of Burn
o Superficial or Deep
o First to Fourth degree
• Extent of Burn Burn DDx
o % of Total Body Surface Area (TBSA) involved (Rule of 9 or hand as 1%)
§ Lund Browder charts for paediatrics
[3] Layers
Type Appearance Sensation Healing Time Prognosis Example
involved
Heals well;[3] Repeated

Superficial Red without sunburns increase the
Epidermis[4] Painful[3] 5–10 days[3][16]
(1st-degree) blisters[3] risk of skin cancer later
in life[17]
Superficial Extends into Redness with

Local
partial superficial clear blister. less than 2–3
Very painful[3] infection/cellulitis but
thickness (papillary) Blanches with weeks[3][11]
no scarring typically
(2nd-degree) dermis[3] pressure.[3]
Yellow or white.
Deep partial Extends into Scarring, contractures
Less blanching. Pressure and
thickness deep (reticular) 3–8 weeks[3] (may require excision
May be discomfort[11]
(2nd-degree) dermis[3] and skin grafting)
blistering.[3]
Scarring, contractures,
Stiff and Prolonged
Full thickness Extends through amputation (early
white/brown[3] No Painless [3]
(months) and
(3rd-degree) entire dermis[3] excision
blanching[11] incomplete[3]
recommended)[11]
Extends through
Amputation, significant
entire skin, and
Black; charred Requires functional impairment,
4th-degree into underlying Painless
with eschar excision[3] and, in some cases,
fat, muscle and
death.[3]
bone[3]
Michael Grant

lOMoARcPSD|4984001
Referral indications POEM: Page 52 of 68

Indications for Referral:
• Ignore First degree burns
• Third Degree: >5% TBSA (Total burn surface area)
• Burn >20%TBSA in patients 10-50 yrs
• Burn >10% TBSA in patients <10 or >50 yrs
• Burn to face, hands, feet, genitalia or major joints
• Significant chemical, inhalational or electrical burn
Management of burns:
1. Remove from source of burn Burn Mx
2. Remove charred clothing
3. Apply cold water/icepacks within 15 mins
o Beware Hypothermia
4. ABCDE
Burn fluid resus o Breathing: assume CO poisoning if enclosed fire
- Use Hartmanns o Circulation: IV access x2
Give first half over o Circulation: Parkland Formula for fluid Resus:
first 8 hours
%TBSA x weight (Kg) x 4 = Total fluid
Give second half
over next 16 hours requirements in mls for first 24 hours - given as
Hartmanns
o Disability: Analgesia (iv opiates)
5. Inhalational injury?:
o History: Enclosed space?
Alcohol/Drugs?
Damage to airways o Facial Burns? 60% will also have
due to smoke or
chemical exposure
inhalation burns
o Singed Nasal Hair?
o Hoarseness/Wheeze?
o Carbenaceous sputum?
o Bronchoscopic Diagnosis
Systemic Effects
• SIRS Burn Cx
• ARDS
• Infection (burns disrupt neutrophil function so
Normal Burn Victim
look out for opportunist infections)
• Renal Failure (Aim to keep output >0.5ml/kg/hr)
• Hypercatabolism - early nutrition
• Curlings Ulcers (ulcer of the duodenum from Other types of burns
severe burns due to cell necrosis (sloughing) of Chemical • Protect Yourself
the gastric mucosa) • Wash off chemical
o Acids usually 30-60mins of lavage
Definitive therapy o Alkalis >hours of lavage
• Neutralising agents may generate heat
• Escharotomy (Full thickness burn incised into
Electrical • Effect depend upon voltage, type of current,
subcutaneous fat and underlying soft
pathway and duration
• tissue; no anaesthetic is required)
• Internal tissues suffer greater injury
• Debridement • Less cutaneous damage
• Grafting • Higher incidence of renal failure
• Reconstruction Burn Rx • May develop compartment syndrome
• Rehabilitation • May have associated spinal compression
• Physiotherapy fractures
• Psychiatry
Michael Grant

lOMoARcPSD|4984001
Fracture Management POEM: Page 53 of 68

• Fracture management
BEFORE AND AFTER MANAGEMENT*: NEUROVASCULAR
ASSESSMENT DISTAL TO FRACTURE:
• Sensory (Fine touch, proprioception, pain,
temperature)
• Motor (Power, specific movements to check nerves,
tone, reflexes)
• Vascular (7 P’s, CAPILLARY REFILL, assess pulses)
Three things with a fracture: put the bone back together

(reduction); hold the bone in place so it heals properly
(immobilisation); and then getting the bone and related body
parts back to their best possible level of function
(rehabilitation). REDUCE
STABILISE
Reduction: REHABILITATE
• Under appropriate anaesthesia (local, regional, general) the
fracture fragments should be manipulated and reduced into
normal alignment.
• To reduce: combinations of distraction, increasing and then
reducing the deformity of the fracture; followed by holding
the reduction with 3 point fixation. This technique of
reduction is also used with open fractures.
• Most fractures are associated with fractures that are
displaced, impacted and shortened.
(A) It is common that the periosteum on one side
of the fracture is intact, while that of the other
side is torn.
(B) The first step in reducing a fracture is
disimpaction where traction is applied along
the axis of the bone to draw the fracture ends
apart. In young patients, this may be difficult
because of the very thick a and resilient
periosteum
(C) The next is to increase the deformity so that
the opposing ends of the fracture may be
approximated.
(D) The final step of reduction once the fracture
ends are opposed is to correct the deformity and to apply three point fixation to hold the fracture
reduction (arrows). The arrows point to areas where pressure must be applied while shaping the plaster-
of-Paris cast
Fracture immobilization:
• Splintage Minor fractures (e.g. phalanges) may be treated using small metal or plastic splints.
• Plaster of paris cast is a conventional method of immobilising the fracture following closed reduction. This
may be either a completely encircling moulded cast or an incomplete encircling cast (plaster slab).
• Traction is required in some fractures, particularly those involving the lower limb, and can be treated
temporarily or definitively by the application of traction along the line the limb. Traction encourages normal
alignment of the fracture and the increased tension of the surrounding soft tissue helps to provide internal
splintage of the fracture.
• External fixation is the application of transfixing pins and bars to create a construct that lies external to the
limb and acts to hold the fracture following either open or closed reduction.
• Internal fixation is indicated when closed reduction has failed, when closed non-operative immobilisation
constitutes a risk to the patient, or when internal fixation allows earlier mobilisation, rehabilitation and earlier
Michael Grant

lOMoARcPSD|4984001
POEM: Page 54 of 68
return to normal function. Internal fixation includes the use of transfixing wires, inter fragmentary screws, metal
plates, and intra-medullary rods.
Outcome
• Fracture union:
o Closed reduction are said to have united when no mobility occurs at the fracture site. Complete union
has occurred when there is no tenderness of the fracture site upon stressing. Radiographic assessment
of union is made by observing the development of fracture callous and the gradual disappearance of
the fracture line
o Rigid and internal fixation make clinical assessment of union difficult,so is assessed using radiographs
to demonstrate the disappearance of the fracture line.
• Delayed union: occurs when a fracture has not united in a period of time that is at least 25% longer than the
expected
• Non-union is said to have occurred when no evidence of union is seen on sequential X-rays over a six-month
period of time
• Mal-union occurs when the fracture unites with a loss of anatomical alignmen
Rehabilitation
On removal of a plaster cast, the joints adjacent to a fractured limb require rehabilitation to prevent or treat
stiffness. This involves passive and active range of motion exercises and proprioception exercises to improve the
sense of balance in the recovering joint. In addition, it is important to return the strength and endurance of the
muscles in the injured limb by a regime of exercises.
• Limbs treated with internal fixation may undergo earlier mobilisation because the fracture is usually more
stable than those treated by plaster immobilisation.
Basic Principles of Open Fracture Management in the Emergency Room

Fracture management begins after initial trauma survey and resuscitation is complete:
• Antibiotics: initiate early IV antibiotics and update tetanus prophylaxis as indicated
• Control bleeding:
o Direct pressure will control active bleeding
o Do not blindly clamp or place tourniquets on damaged extremities
• Assessment
o soft-tissue damage
o Neurovascular exam
• Dressing
o Remove gross debris from wound
o Place sterile saline-soaked dressing on the wound
• Stabilize: splint fracture for temporary stabilization
o decreases pain, further injury from bone ends, and disruption of clots
Display a practical knowledge of:

• Obtaining intraosseous access
The procedure for IO insertion in the proximal tibia is as follows:
1. Identify the consistent flat area of bone 2 cm distal and slightly medial to the
tibial tuberosity (avoids hitting the growth plate.)
2. Support the flexed knee by placing a towel under the calf.
3. If time permits, cleanse the area with an iodine solution, drape it and use
sterile gloves
4. Inject local anesthetic (1% lidocaine) into the skin, into the subcutaneous
tissue, and over the periosteum, especially if the patient is awake.
5. Use intraosseous gun per instructions at this location; Or, if gun unavailable,
Insert the IO needle through the skin and, upon reaching the bone, hold the
needle with the index finger and thumb as close to the entry point as possible and,
with apply pressure with the palm of same hand, use a twisting motion
6. Advance the needle from the cortex into the marrow space, at which point a popping sensation or lack of
Michael Grant

lOMoARcPSD|4984001
POEM: Page 55 of 68
resistance is felt. Do not advance the needle any farther.
7. With proper placement, the needle stands up on its own. At this point, remove the inner trocar, attach a
syringe to the needle, and aspirate bone marrow. Obtaining marrow confirms placement.
a. If marrow is not aspirated, push a 5-mL to 10-mL bolus of isotonic saline through the syringe. Resistance to
flow should be minimal, and extravasation should not be evident
• Measuring body temperature using an appropriate recording device

A pulmonary artery catheter (PA) is considered to be the best site for measurement of core body temperature
because the observed temperature at this site results from the convective
mixture of blood from the entire body. However, this is inaccessible in a
normal resuscitation setting. Thus, the clinician is often left with various
methods of oral, axillary, nasopharyngeal, rectal, bladder, distal oesophageal,
epitympanic membrane and temporal artery measurements, all of which are
considered to have varying degrees of success in accurately detecting
temperature.
Tympanic temperature is most often assessed in hospital settings, using an
electronic thermometer. This is achieved by place a new safety cover on the
tip, inserting it into a patients auditory meatus and pressing a button.
• Understand practicalities involved in warming a hypothermic patient

The patient should ideally be managed in a critical care
setting. Attempts to re-warm the patient actively should
not delay transfer to a critical care setting:
• Assess for and treat any associated disorders - eg,
diabetes, sepsis, drug or alcohol ingestion, or occult
injuries.
• Blood investigations: FBC, electrolytes, blood
glucose, alcohol, toxin screen, creatinine, amylase and
blood cultures.
• Cardiac monitoring: dysrhythmias, changes of
hyperkalaemia; J waves are pathognomonic of
hypothermia:
o Cardiac output falls proportionately to the degree of hypothermia and cardiac irritability begins
at about 33°C. Ventricular fibrillation occurs <28°C, and at <25°C asystole can occur.
o Cardiac drugs and defibrillation are not usually effective in the presence of acidosis, hypoxia
and hypothermia; reserve until the patient is warmed until at least 28°C
• Oxygen: Administer 100% oxygen (ideally warmed and humidified) while the patient is being re-warmed
• ABG are probably best interpreted uncorrected, ie the blood warmed to 37°C, and those values used as
guides to administering sodium bicarbonate
• Rewarming technique depends on the patient's temperature, response to simple measures and the presence
of any injuries.
o Mild and moderate exposure: passive external rewarming in a warm room, using warm blankets,
clothing, warmed intravenous fluids, bair huggers
o Severe hypothermia: may include invasive surgical re-warming techniques - eg, peritoneal
lavage, A-V re-warming or cardiopulmonary bypass (patients presenting in cardiac arrest from
thoracic lavage)
• Determination of death can be very difficult in the hypothermic patient and should not be pronounced
dead until they are re-warmed (eg, to 35°C; don't have to reach 37°C).
Michael Grant

lOMoARcPSD|4984001
Wound Management POEM: Page 56 of 68

• Basic first aid (including wound care and basic wound dressing for
surgical or traumatic wounds)
Types of open wound injury:
• Abrasions - Partial thickness skin loss Types of wounds
• Lacerations - Break in skin of varying depth
• Avulsion - Full thickness skin loss, degloving or flap injuries are avulsions
• Amputations - A part of the body is partially or completely severed or torn from the body
• Punctures/ penetrations - Caused by a foreign object that enters the body, underlying damage can be
extensive
• Bite - Breakage of the skin caused by animal or human teeth, all bites are considered contaminated
Assessment
Elicit a careful history of injury i.e.:
• Mechanism of injury; associated blood loss; risk of contamination; deeper structure damage;
o How did the wound occur?
o Color (Pink - usually indicates healthy tissue, Black - indicates poor tissue perfusion, necrosis, Red -
indicates infection(
o Wound size and boundaries - edges of wound smooth or irregular
• Tetanus status;
• Consider Non accidental Iinjury;
• Underlying chronic illness or disability.
Fully examine the injured part in particular checking for:

• Underlying nerve, vessel and tendon damage. This requires assessment of movement while exploring the wound
(especially in palmar or hand wounds)
• Assess tissue damage or loss
Request special investigations where appropriate:
• Xray for foreign body or underlying fracture
• Ultrasound is useful for puncture wounds with a radiolucent foreign body (e.g. thorn or splinter)
Neurovascular status of the affected extremity MUST be assessed prior to wound treatment:
• Pulse quality, location, rate
Always assess
• Capillary refill, unreliable indicator in adults neurovascular status first
• Skin color/temperature
• Sensory-motor function
Cleaning wounds
Cleaning Wounds
• Superficial Wounds: Can be cleansed with saline or aqueous chlorhexidine.
• Deep Wounds: Those which require exploration should be anaesthetised first to allow more thorough cleaning.
Foreign bodies must be removed.
o Thorough irrigation with saline under pressure (with a 19 Ga needle on a 10-20 ml syringe) and
removal of foreign bodies
• Ragged Wounds: Trim edges where the viability is in doubt, aiming for an elipical shape along langers lines
• Glass Injuries: should be x-rayed if there is the possibility of retained glass. All haematomas should be evacuated as
glass is usually found within
Types of dressing: Wound Dressings

• Film dressings
o These dressings can be used as primary or secondary dressings.
o Film dressings can also be used as a barrier to protect an area of the body that might
be experiencing friction or shear forces, e.g. small superficial wound, producing little
exudate or a superficial heel ulcer
• Simple island dressings
o Simple island dressings are only to be used over wounds closed by primary intention,
in other words over a suture line.
o The dressings have a central pad of cellulose material to absorb any oozing from the
suture line during the first 24 hours post-surgery.
• Non-adherent dressings
o Many dressings are termed ‘non-adherent’, meaning they are designed not to stick to the drying secretions
of the wound, thereby resulting in less pain and trauma on removal.
Michael Grant

lOMoARcPSD|4984001
POEM: Page 57 of 68
• Moist dressings
o Moist dressings function by either preventing the skin surrounding the wound from losing moisture, or
actively donating moisture to the area.
o Work by a process known as autolytic debridement, whereby the dressing accentuates the body’s process
of ridding itself of dead tissue
o Moist dressings can be divided into two groups:
§ Hydrocolloid dressings – do not contain moisture but form a ‘seal’ at the wound surface. This
prevents the normal daily evaporation of moisture from the skin
§ Hydrogel dressings - generally contain between 60–70% water, which, with other constituents, is
held in a viscous form known as the hydrogel. applied to wounds containing necrotic or dead tissue
as it become shard and desiccated due to the loss of a blood supply; hydrogel dressing donates
water to the dead tissue, softening it and aiding the body’s process of autolytic debridement
• Absorbent dressings
o There are a vast number of different absorbent dressings, mainly because one of the most dif cult tasks in
wound management is the containment of exudate.
§ Alginate dressings absorb exudate and form a gel-like covering over the wound and can be used
to lightly fill a cavity but should always be covered by a secondary dressing.
§ Hydrofiber dressings are fibrous dressings that are applied dry and, on absorbing exudate, are
transformed into a gel-like sheet; used on moderate to heavily exuding wounds and must be
changed when fully saturated with exudate.
§ Foam dressings absorb exudate — some lock fluid within the core of the dressing, others transform
into a gelling foam
• Safe administration of local anaesthesia (either applied directly to the skin or

injected into skin or body tissues)
A neurone has Na channels in its membrane, which normally are closed. The NaKATPase pump maintains the resting potential,
keeping Na+ and K+ concentrated outside and inside the cell respectively. Stimulation of the neurone causes a slow rise of Na+
until the threshold potential is reached, where the Na+ channels open, creating a voltage (about 70mV) or action potential.
Local anaesthetics are known as sodium channel blockers and work in various ways to inhibit the influx of sodium that
propagates the action potential.
They can be used:
• Local infiltration: subcutaneous injection (or topical application to skin, mucosa or eye)
• Peripheral Nerve Block: injection around nerve in limb or trunk; guided by ultrasound (ideally), landmarks, or nerve
stimulator
• Central Neuraxial Block: usually a spinal or epidural injection into the back; a spinal or intrathecal injection is into CSF
and requires a very small amount of drug for profound effect and associated hypotension, while an epidural or extradural
injection may be followed by a catheter to maintain analgesia for hours or days
While there are quite a number of LA drugs, the most What does a foundation doctor need to know about local anaesthetics:
commonly used are Lidocaine (previously Lignocaine) and
1. Ensure that there are no contraindications to local anaesthesia,
Bupivacaine, as these are suited well to local infiltration and e.g. infection.
regional anaesthesia – both are amides. Lidocaine is quick to 2. Obtain the patient’s consent: explain the risks vs benefits
act but quick to wear off, Bupivacaine takes longer to work but 3. Perform the procedure in an appropriate environment with
longer to wear off. assistance and resuscitation equipment available (in case of
complications, including local anaesthetic toxicity).
4. Secure intravenous access.
Other LA drugs have more specific (often topical) uses: 5. Attach monitoring as appropriate, e.g. pulse oximeter, blood
• Lidocaine and Prilocaine create a mix known as EMLA pressure.
used for topical anaesthesia for skin; Eutectic Mixture of 6. Know the anatomy of the area and confirm the correct side/site.
Local Anesthetics, refers to the fact that is has a lower 7. Know the correct technique, the correct dose and the
management of potential complications. Never exceed the
melting point than it components do separately
maximum dose
• Oxybuprocaine are in common use for eye drops (topical 8. Use an aseptic technique.
anaesthesia) 9. Aspirate before you inject to avoid intravenous injection.
• Cocaine used in ENT procedures is one of the only LA 10. Fractionate doses greater than 5mls and aspirate between
esters (it has notable vasoconstriction preventing bleeding fractionations.
11. Record technique in the notes and document any complications,
– but can cause nasal septum ischaemia and coronary
e.g. bleeding.
artery vasospasm)
• Ropivicaine is sometimes favoured as an alternative to bupivacaine for regional anaesthesia injections
Michael Grant

lOMoARcPSD|4984001
Closing wounds
POEM: Page 58 of 68
• Wound closure techniques

Wound Examination:
• Location • Neurovascular function
• Size • Tendon function
• Shape • Underlying structures
• Margins • Wound contamination
• Depth • Foreign bodies
• Alignment with skin lines
Minimize the Pain of Injection:

• Use sodium bicarbonate mixed with the lidocaine (1 ml/10 ml solution)
• Using the smallest needle possible: Wound
o Insert needle through open wound edge and skin that has already been anesthetized
o Inject slowly closures
Wound Preparation:
• Foreign Body Removal
o Visual inspection
o Imaging: Glass, metal, gravel fragments >1mm should be visible on plain radiographs but organic substances
and plastics are usually radiolucent
• Irrigation
o Local anesthesia prior to irrigation
o Do not soak the wound
o Use normal saline in a large syringe (with a 19 Ga needle on a 10-20 ml syringe)
• Debridement
o Removes foreign matter & devitalized tissue
o Creates sharp wound edge
o Excision with elliptical shape respecting Langer lines
• Tetanus Prophylaxis
o A wounds or burns where a significant amount of tissue has been removed, or puncture-type injuries such as
animal bites, particularly if they have had contact with soil or manure
o wounds containing any substance that shouldn't be there, such as dust or dirt (foreign bodies)
Wound Closure:
Intention:
• Primary intention
o Wound edges are brought together by suture, staple, adhesive, or tape
o Performed on recently sustained lacerations: <12 hours generally and <24 hours on face
• Secondary intention
o The wound is allowed to granulate, resulting in broader scar
o Examples: gingivectomy, gingivoplasty, tooth extraction sockets
• Tertiary intention (Delayed primary closure or secondary suture)
o The wound is initially cleaned, debrided and observed, typically 4 or 5
days before closure
o Examples: healing of wounds by use of tissue grafts
Techniques:
• Staples - Quick, poor aesthetic result
• Adhesives (e.g. Dermabond) – painless, petroleum dissolves
• Tape - Steri-strips
• Sutures – Absorbable (e.g. Vicryl), Non-Absorbable (e.g.
Silk), Monofilament vs. braided
o Before placement of the sutures, wound closure
may require sharp undermining of the tissues to
minimize tension on the wound:
Skin Closure by sutures:

• Key – wound edge eversion
• “Approximate, don’t strangulate”
Michael Grant

lOMoARcPSD|4984001
POEM: Page 59 of 68
• Choose appropriate size of suture for location of laceration
• Use the rule of halves when placing initial sutures
• Aim to keep distance at 0.5cm between sutures
• Simple Interrupted stitches:
Dressing:
• Maintain dry for 24-48 hours
• Use antibiotic to maintain moist environment
• If overlying a joint, splint in a position of function
• Sun protection to prevent scar hyperpigmentation
• Suture removal instructions!
o Compartment
(% of body Volume Biochemistry
IV Fluids weight)
Intravenous Fluid Management Na 10mmol/l Ca
Classify the different types of intravenous Intracellular 28 <0.01mmol/l K
40% litres 150mmol/l Mg
fluids. 25mmol/l
Fluid Compartments 14
The body contains approximately 60% water. Approximately 2/3 of this litres Na 140mmol/l K
Extracellular
is intracellular, and 1/3 extracellular, the extracellular fluid further 10.5 4mmol/l
20% Interstitial
subdivides into interstitial and intravascular fluid. There are 2 litres Ca 2.5mmol/l Mg
Intravascular
compartmental divisions: 3.5 1.5mmol/l
litres
• Cell wall – permeable to water. Impermeable to most ions except
via channels eg Na/K pump 42
Total 60%
litres
• Capillary basement membrane – impermeable to most proteins,
but permeable to ions.
Types of Intravenous Fluids
Crystalloids: Crystal Solutions (e.g. 0.9% NaCl/Hartmann’s /5% Glucose) that can pass through semipermeable membrane.
• Hartmann's Solution is most similar to ECF (although contains lactate rather than bicarbonate). Hartmann’s is the
traditional crystalloid used in theatres. Note that there are 5mmol/l of Potassium in this fluid
o Never add additional electrolytes to Hartmann’s solution.
o Lactate is metabolised to Bicarbonate in hours, but still not advised in severe sepsis, hypoxia, diabetic
ketoacidosis or kidney failure
• 0.9% Saline sometimes called 'Normal Saline', buit has a calculated osmolality (measure of the dissolved solute content of
the solution) of 308mosm/l making it slightly hyperosmolar compared to plasma.
o The Sodium content allows a greater proportion of fluid administered will remain intravascular for
longer
§ Thus crystalloid of choice for volume resuscitation.
o Excessive 0.9% saline can cause a hyperchloraemic acidosis.
• 5% Glucose fluids have the glucose is metabolised leaving water. This will distribute freely within the total body water.
Therefore for every 1litre of 5% glucose administered IV only a little over 100mls will remain in the vascular
compartment.
o Large infusions reduce the osmolality of the entire system as water moves across membranes along its
concentration gradient
Michael Grant

lOMoARcPSD|4984001
POEM: Page 60 of 68
o There is a risk of causing dilutional hyponatraemia
o Never prescribe 5% Glucose in isolation or more than 1 litres in any 24hours
Colloids: Colloids are suspensions of osmotically active large particles that are largely confined initially to the vascular
compartment although some have only a relatively short half-life prior to excretion and have side effects
• Gelatin is the most commonly used colloid.
o Poor evidence that performance is better than crystalloid.
o Gelatin might be associated with acute kidney injury
o Colloids may cause approximately 4% of all perioperative anaphylactic reactions and the vast
majority of these are caused by Gelatin.
• Albumin is a colloid but carries many of the risks of allogenic blood transfusion
o It is used in the management of severe sepsis in the intensive care unit
o Not recommended for the resuscitation of patients with head injury.
• Hydroxyethyl Starch was in vogue but the research underpinning its use has been discredited and observational
studies have indicated it was associated with an increased risk of mortality and renal injury in critically ill adult
patients. It was suspended from UK clinical practise in June 2013.
Blood and blood products: Blood from a donor is split into several components, called blood products
• Packed Red Cells: Erythrocytes (with contained haemoglobin) by removing plasma and white cells
• Fresh Frozen Plasma (FFP): Frozen to store, thawed to transfuse. Contains clotting factors.
• Platelets: Platelets concentrated within plasma. Short shelf life.
• Cryoprecipitate: Related to FFP but rich in fibrinogen and factor VIII. Pooled from several donors.
• Albumin: Plasma protein. Heat-treated. Available as 4.5% or 20% solution.
• Immunoglobulin: Polyclonal immunoglobulins (i.e. Antibodies) pooled from many donors
• Coagulation factors: Some specific clotting factors are available, and genetic engineering, therefore no risk from donor
blood can produce some.
• Prescribe intravenous fluids safely

It is imperative for prescribers to review the patient with recent observations and investigations before writing any fluid
prescription. It is also recommended that fluids should not be prescribed for more than twelve hours at a time to
encourage regular review and re-review. Start with assessment then follow the 5 R’s:
Assessment:
A careful history may give you a time frame for fasting or key symptoms of dehydration. Look around the bed space,
is there a urinary catheter, what does the fluid balance chart tell you regarding cumulative balance. Beware that
patients may also be in a state of fluid excess and no longer need IV fluids.
To identify a fluid deficit look out for the following:

• History
o Fasting, vomiting, diarrhoea, diuresis, sweating, blood-loss.
o Symptoms such as thirst, dry mouth, headache, faintness on standing
o Preceding losses from fluid balance chart.
• Examination signs
o Peripheral perfusion, reduced capillary refill time, oliguria, tachycardia, postural changes in heart rate
and BP.
o Mouth and mucus membranes
o Daily Weight
o Input and Output Charts
• Laboratory investigations
o Full blood count: increased haematocrit (Hct), (long-term dehydration) increased MCHC
o Urea (increased), creatinine (increased) and electrolytes (Hyponatraemia)
If you feel there is a deficit administer a fluid challenge of no more than 500mls attempting to match the constitution
of the fluid lost. You must then return and reassess your patient to determine the effect of that challenge. If you feel
there is still clinical evidence of a deficit after reassessing 3 times call for senior advice.
1. Resuscitation
Michael Grant

lOMoARcPSD|4984001
POEM: Page 61 of 68
• Attempt to identify the mechanism of shock (hypovolaemic, distributive, obstructive or cardiogenic) and treat accordingly.
• Not all mechanisms of shock require IV fluids (cardiogenic or obstructive shock).
• Failure to restore blood pressure after a bolus of 20mls/kg or maximum of 2,000mls should prompt senior review and
consideration for vasopressors.
2. Routine Maintenance
Where possible oral fluids should be promoted as the safe mechanism to prevent the formation of a deficit. This of course is
not always possible and the fasting patient will require maintenance prescription for both water and electrolytes to account for
both insensible (skin, stool and respiratory) and urinary losses. Patients presenting for elective surgery only need to fast for
2 hours from clear fluids.
• Why do we give maintenance fluids?
o Only if unable to drink oral fluids
o To account for daily fluid volume turnover and loss –
• Daily fluid output in healthy male:
– Urine 1500ml
– Faeces 100ml
– Insensible loss 900ml
– Sweat Negligible
– TOTAL ~2500ml
• A safe prescription for maintenance employs a variety of intravenous fluids, namely 0.9% Saline, Hartmann's solution
and 5% Glucose.
o Excess 0.9% Saline may cause a hyperchloraemic acidosis
o Too much 5% Glucose may cause a potentially fatal hypo-natraemic and hypo-osmolar state; for this reason
patients should be prescribed no more than one litre of 5% Glucose per day.
• Adult maintenance requirements are: 1 – 1.5 ml/kg/hour.
o Examine the fluid balance charts to avoid a cumulative balance of greater than 2,000mls.
o The prescription of maintenance fluids must be guided on the cumulative fluid balance of that patient; it may be
appropriate not to prescribe a maintenance rate
3. Replacement
There are many indicators that can assist in determining if there is a
deficit:
• Weight is a simple and underused measurement useful in
observing measurements over several days.
• In theory fluid balance charts e.g. input/output charts should be
useful but in practice may be inaccurate or incomplete.
• Skin turgor (<0.5s normal, <2s moderate dehydration, >2 severe
dehydration) and capillary refill may be useful when dehydration
is marked but may be affected by other causes such as cachexia
and old age
• Urine output is another useful indicator of fluid balance and will
require a urinary catheter and hourly measurements for this to be
undertaken accurately. However there are other factors here:
o Diuretics will increase urine output
o Major surgery will reduce urine output.
o Usually 0.5mls/kg/hour (or 30mls/hour in total) is taken as
the minimum amount
• On going losses must also be considered and replaced to prevent
the formation of a deficit.
o Serous losses should be replaced with a salt-rich fluid, such
as Hartmann's Solution.
o E.g. increased losses from diarrhoea, vomiting, stomas, drains, polyuric states and losses from pyrexia.
o In the perioperative setting most of the clues relating to on going losses will come from fluid balance and
observation charts.
4. Redistribution
• Seek expert help if patients have a complex fluid and/or electrolyte redistribution issue or imbalance, or significant
comorbidity, for example:
o gross oedema
o severe sepsis
o hyponatraemia or hypernatraemia
o Renal, liver and/or cardiac impairment.
Michael Grant

lOMoARcPSD|4984001
POEM: Page 62 of 68
5. Reassessment
• Administer intravenous fluids safely
• Prescribe potassium chloride safely

In terms of electrolyte requirements, if the normal prescribing rule for saline use are followed then it is likely that
the daily requirements for Sodium will be met quite comfortably. The daily requirements for Potassium are
unlikely to be met, however, so supplementation will be required according to the formula:
1 – 1.5 mmol/kg/day of Potassium Chloride (KCl: atomic mass 74.551)
In the prescription of Potassium the following rules apply:

• The concentration of Potassium in peripheral fluids must not exceed 40mmol/litre
• The infusion rate for Potassium must not exceed 10mmol per hour
• Hartmann's Solution already contains Potassium at a concentration of 5mmol/l
Potentially dangerous
• Hyperkalaemic complications if infusion too fast (must be ≤10mmol/hr)
• Phlebitis/pain in high concentration (must be ≤40mmol/l)
• Comes in ready prepared bags (20mmol/l, 40 mmol/l) for peripheral IV infusions
• Maximum concentration = 40mmol/l
• Maximum infusion rate = 10mmol/hr
• For example, what is the fastest prescription for treating hypokalaemia using 1000ml of 0.9% Saline?
o 40mmol KCl addedà250ml/hr.
• Interpret fluid balance charts:

Most fluid balance charts do not account for several losses such as insensible losses and sweating; therefore,
euvolaemia is more likely to be at least + 500ml.
Daily weights, if available will provide an accurate measure of dynamic change in total body fluid with 1kg=1litre.
Progressive increases in total body weight should alert the prescriber to hypervolaemia.
Michael Grant

lOMoARcPSD|4984001
POEM: Page 63 of 68
10 Golden Rules to IV Fluid Prescription:

1. Assess/Resuscitate/Routine Maintenance/Replacement and Redistribution/Reassessment
2. Preoperative patients only need to fast from clear fluids for 2 hours.
3. The cause of shock must be determined before IV fluid is prescribed.
4. Cases of shock that do not respond after a bolus of 20ml/kg or 2,000mls should be considered for
vasopressors
5. Oral fluids are the safest approach to avoiding a fluid deficit.
6. Maximum concentration of potassium is 40mmol/l.
7. Maximum rate of potassium infusion ≤10mmol/hour.
8. Reassess patient to determine the effect of the current prescription.
9. Do not prescribe > 24hours in advance.
10. Some cases may not need maintenance fluids if they are in a cumulative positive balance.
List the different types of blood products.
Blood and blood products: Blood from a donor is split into several components, called blood products
• Packed Red Cells: Erythrocytes (with contained haemoglobin) by removing plasma and white cells
• Fresh Frozen Plasma (FFP): Frozen to store, thawed to transfuse. Contains clotting factors.
• Platelets: Platelets concentrated within plasma. Short shelf life.
• Cryoprecipitate: Related to FFP but rich in fibrinogen and factor VIII. Pooled from several donors.
• Albumin: Plasma protein. Heat-treated. Available as 4.5% or 20% solution.
• Immunoglobulin: Polyclonal immunoglobulins (i.e. Antibodies) pooled from many donors
• Coagulation factors: Some specific clotting factors are available, and genetic engineering, therefore no risk from donor
blood can produce some.
Special requirements (e.g.. for immunocompromised patients) may be appropriate, such as CMV negative, Methylene blue
treated or irradiated blood products
Michael Grant

lOMoARcPSD|4984001
POEM: Page 64 of 68
The most common type of transfusion is replacing Packed Red Cells. The threshold for replacement varies depending on the
patient and situation, and varies by hospital policy. A local example of “transfusion triggers” would be:
o <65 years; No cardiovascular/cerebrovascular history: <70 g/L
o >65 years; No cardiovascular/cerebrovascular history: <80 g/L
o Cardiovascular/cerebrovascular history: <90 g/L
o Acute active haemorrhage: <100g/L
To transfuse a person with a Hb already above a transfusion trigger, or to transfuse too much, is inappropriate due to lack of
benefit but the significant risks that transfusion carries.
Cross-Matching is the process of matching a patient with suitable donor blood that is compatible with their anti-body profile.
There are many proteins on the surface of blood cells that can act as antigen and trigger agglutination when put into new hosts
that have anti-bodies against them.
• The most important set of surface antigens for transfusion are the “ABO” group and Rhesus groups (+ or -)
• There are many other proteins making other blood groups, but these are rarer. However, you need be aware of these, as a
person can develop antibodies due to repeated transfusions, and this can make cross-matching of blood very slow
(potentially days to attain appropriate blood).
Agglutinogens are not present in all blood products, only Packed Red Cells, Fresh Frozen Plasma and Platelets need cross-
matched (or at least matched to blood group).
Cross-matching takes time; to fully cross-match blood (i.e. test donor blood with recipient blood in laboratory for
compatibility) takes 40 minutes or more. While this is the safest blood to transfuse, this can be too long in some situations, so
the options to consider are:
• Full cross-match: (as above) 40 minutes
• Group-specific, where the patient’s blood group is tested for, and blood of that group then dispatched without testing for
compatibility in laboratory. This should take 15 minutes.
• O–ve, which should always be compatible can immediately be taken “off the shelf”
If a patient’s blood sample is in the laboratory and/or has been tested for blood group already, the time can be shortened
significantly. For example, group-specific can be released immediately. This is why “Group and Hold” samples before major
surgery are important.
Blood Transfusion Cx
List the complications of blood product transfusion
It is vital to be aware that complications and reactions can be caused by blood product transfusion, despite all the above
precautions. Therefore, if presented with a patient becoming unwell while receiving a blood product, stop the transfusion!
Complications of transfusion may be classified as:
• Acute Transfusion Reactions
• Delayed Transfusion Reactions
• Massive Transfusion Complications
Acute Transfusion Reactions:

• Acute haemolytic reactions
• Febrile non-haemolytic reactions
• Bacterial infection
• Allergic/urticarial
• Anaphylaxis
• Transfusion associated lung injury (TRALI)
o Acute onset of non-cardiogenic pulmonary edema following
transfusion
• Graft v's host disease (GVHD)
o associated with transfusion of un-irradiated (thus active WBCs) blood to
immunocompromised recipients
• Fluid Overload
Delayed Transfusion Reactions

• Delayed Haemolytic Reactions: antibodies developed from previous transfusion/ pregnancy
• Transfusion transmitted infections (cJD, HIV, Hepatitis have been transmitted in the past – any known transmissible
infections are tested for)
• Iron overload
• Increased mortality (remains controversial, but some evidence in trauma and elective surgery)
Michael Grant

lOMoARcPSD|4984001
POEM: Page 65 of 68
Complications of Massive Transfusion An acute haemolytic reaction is the most common complication of blood
product transfusion. The presentation is not typical, but may include:
• Hypothermia (Packed Red Cells are cold)
• Pyrexia
• Coagulopathy • Anxiety
• Rash
• Thrombocytopenia • Pain at infusion site
• Respiratory distress
• Unexpected bleeding, eg. at infusion site
• Hypocalcaemia (citrate toxicity, used as anti- • Severe tachycardia
• Renal failure
coagulant) • Hypotension
• DIC
• Hyperkalamia • Loin/back pain
• Death
• Acidosis
Emergency Drugs
Pharmacology of Emergency Drugs
Volume of Distribution:
• Theoretical volume = concentration found in plasma
• Indicates distribution in tissue phase
• Affected by
o Lipid Solubility
o Ionisation
o Plasma protein binding
Bioavailability: Fraction of administered dose that reaches the systemic

circulation unchanged
Routes:
• PO - Oral • TD – Transdermal
• IV – Intravenous • PR – Rectal
• SC – Subcutaneous • NG - Nasogastric
• IM – Intramuscular • INH - Inhaled
• IT – Intrathecal (CSF) • PEG - percutaneous enteral gastrostomy
• EPI – Epidural • PV - Vaginal
• SL – Siblingual
Dosing Regimes:
• QID/QDS – 4 times a day • OD – once daily
• TID/TDS – 3 times a day • PRN – when required
• BD/BID – 2 times a day • STAT – immediately
• Mane – in the morning • Tarde – in the evening
• Nocte – at night
Drug Mechanism Dose/Route Indication Side effects Contraindications

Adenosine Adenosine causes - 6 mg bolus by rapid IV – Paroxysmal SVT – Nausea – Asthma and COPD
transient heart block in injection – Up to 2 doses of – Aid diagnosis of – AV Block – Second or Third degree
the atrioventricular 12mg if needed regular broad and – Angina heart block
(AV) node. This is narrow complex – Sick Sinus Syndrome
mediated via the A1 tachycardia of – Prolonged QT Syndrome
receptor, inhibiting uncertain nature – Decompensated heart
adenylyl cyclase, – Wolff Parkinson failure
reducing cAMP and so White
causing cell
hyperpolarization by
increasing inward K+
flux via inward rectifier
K+ channels,
subsequently inhibiting
Ca2+ current.
Adrenaline – Beta adrenoreceptor CPR dose = 1mg = 10mls – CPR BP - Arrhythmias
agonist 1:10,000 IV – Anaphylaxis HR – Cardiovascular disease
– Anaphylaxis dose = 0.5ml 1 in – Positive inotrope – Arrhythmias – Elderly
1,000 IM – Bronchodilator - Hyperglycaemia,
– Vasoconstrictor with raises lactate
local anaesthetics – Anxiety
Amiodarone Amiodarone shows Bolus at cardiac arrest – Broad-complex and – Irritant to veins – Heart block
beta blocker-like and – 300 mg over 20-60 min IV – narrow-complex Cardiac effects: pro- - Prolonged QT syndrome
arrhythmic, HR,
calcium channel 900 mg infusion over 23 h tachycardia - Thyroid dysfunction
BP Respiratory
blocker-like actions on effects: pneumonitis,
the SA and AV nodes, fibrosis, Thyroid
increases the refractory dysfunction
Michael Grant

lOMoARcPSD|4984001
POEM: Page 66 of 68
period via sodium- and – Corneal deposits,
potassium-channel peripheral neuropathy
– Drug
effects
interactions:Warfarin,
– Lengthens duration of Phenytoin,ABx
action potential
– Prolongs QT interval
Aspirin - COX inhibition – 300mg in ACS (SL or chewed) – Acute Coronary – GI Irritation – Children<16 years (Reyes
– Reduction of Syndrome – Bronchospasm Syndrome) – Peptic
Thromboxane A2 and – Analgesia – Increased Ulceration
thus platelet – Pyrexia bleeding time – – Haemophilia
aggregation Renal Effects – Aspirin interacts with a lot
of drugs
Atropine – Muscarinic – Bradycardia rate < 40 = 200- – Bradycardia HR – Caution with CVS disease
acetylcholine 0.6mg IV – Antisialogue (reduce – Dilated
antagonist. – Maximum dose 3mg in saliva) pupils/blurred
– Blocks vagus input to treatment of symptomatic – Antispasmodic vision
AV and SA node. bradycardia – Organophosphorous secretions - dry
– Tertiary amine Poisoning (insectisides mouth,
therefore crosses or nerve agents) – Relaxes bronchial
blood brain barrier and GI smooth
muscle –
Confusion
– Urinary retention
• Calcium • Stabilise the • 10mls 10% Calcium Chloride • Hypocalcaemia • Arrhythmia • Hypercalcaemia
myocardium against / Gluconate (2.25mmol Ca2+) • Hyperkalaemia • Can you now calculate a
Chloride/Gluconate arrhythmia • Chloride more irritant corrected Calcium?
• Replace Calcium • Bolus/Infusion depending on • Corrected calcium
deficit urgency with ECG monitoring (mmol/L) = measured total
Ca (mmol/L) + 0.02 (40 -
serum albumin [g/L])
• Clopidogrel • ADP receptor Initially 300mg then 75mg PO • ACS • Dyspepsia • Active Bleeding
inhibition causing anti OD • Ischaemic Stroke • Bleeding • Breast Feeding
platlet effects Disorders Clopidogrel
• Neuroaxial Techniques
(epidural/spinal blocks)
• Diamorphine • Opioid receptor • 5mg initially IV/IM/PO • ACS • Respiratory • Delayed gastric
agonist • Analgesia Depression emptying •
• Pulmonary Oedema • Syncope Phaeochromocytoma
• Raised ICP
• Enoxaparin Binds to antithrombin • VTE risk according to BMI, • VTE prophylaxis • Bleeding • Delayed gastric
(a circulating standard dose 40mg SC • Treatment of DVT •Thrombocytopenia emptying •
anticoagulant) to form • Treatment dose DVT/PE and PE • Osteoporosis Phaeochromocytoma
a complex that 1.5mg/kg SC • Treatment of MI and
irreversibly inactivates Unstable angina
clotting factor Xa
• Flumazenil • Benzodiazepine • 200mcg to max 1mg IV • Benzodiazepine • Nausea • Raised ICP
Antagoinist Overdose • Flushing • Status Epilepticus
• • Anxiety
• Convulsions
(rare)
Glucose 50% • Substrate for aerobic • 50mls IV • Symptomatic • Hyperglycaemia • Hyperglycaemia
metabolism hypoglycaemia • Hypokalaemia
• Promotes intracellular • Hyperkalaemia • Phlebitis
reabsorption of
potassium via
endogenous Insulin
surge
• Glucagon Mobilisation of hepatic • 1mg hypoglycaemia IV/IM • Insulin induced • Hyperglycaemia • Phaeochromocytoma
glycogen • High dose beta blocker hypoglycaemia • Hypokalaemia
overdose • Beta blocker • Hypotension
overdose
• Glyceryl Trinitrate • Coronary • 0.3-1mg SL • Prophylaxis and • Postural • Aortic stenosis

vasodilation • 10-200mcg/min IV infusion treatment of angina hypotension • Hypotension
• Reduction left SL/IV/TD • Left ventricular failure • Headache • Check patient has not
ventricular work • Anal Fissure already taken at home
(reduced venous • Sildenafil interaction
return)
• Hydrocortisone Corticosteroid 200mg IV Asthma and • Adrenocortical • • Abrupt withdrawal – risk
Anaphylaxis management insufficiency Mineralocorticoid of adrenal crisis from
• Anaphylaxis effects suppression of HPA axis
• Asthma • Glucocorticoid • Immune Suppressed
effects • Live vaccine
• Pregnancy
• Insulin Regulation of • Local protocol for DKA IV/SC • IDDM • Hypoglycaemia • Hypoglycaemia
carbohydrate and fat • 5 international units • DKA Hypokalaemia
metabolism hyperkalaemia protocol • Hyperkalaemia
• Intralipid A Lipid sink absorbing AAGBI Protocol by IV Cardiac Arrest Hyperlipidaemia Currently only licenced for
lipid soluble drug secondary to local use during cardiac arrest
anaesthetic overdose secondary to local
anaesthetic toxicity
Michael Grant

lOMoARcPSD|4984001
POEM: Page 67 of 68
• Ipratropium Antimuscarinic 500mcg INH repeated as • Acute severe asthma • Dry mouth • Acute closure glaucoma
bronchodilator necessary • Rhinitis • Nausea
• Headache
• Lorazepam • Benzodiazepines 4mg IV repeated once after • Status Epilepticus • Apnoea • Unstable myasthenia
enhance the effect of 10min if necessary • Hypotension gravis
the neurotransmitter
gamma-aminobutyric
acid
• Always check for an
alcohol history in
seizing patient,
administer B vitamins
• Magnesium • Essential for many • Pre-eclampsia 4g IV followed • Pre-eclampsia • Nausea Hypermagnesaemia
enzyme systems by 1g/hr for 24hours • Arrhythmia • Arrhythmia
• Exact mode of action • Arrhythmia 2g IV (8mmol) • Hypomagnesaemia • Confusion
unsure • Loss of tendon
reflexes
• Morphine • Opioid receptor 1mg increments to achieve • ACS • Respiratory • Chronic constipation
agonist effect • Analgesia Depression
Sulphate IV/IM/Oral • Pulmonary Oedema • Reduced GI
• Cough in terminal motility
care • Syncope
• Hypotension
• N-Acetyl Cysteine Paracetamol normally See protocol max 4g/24hours Paracetamol overdose Hypersensitivity Caution only in astmatics
metabolized in liver. In IV infusion like reaction 7.5g can cause severe
overdose normal hepatocellular (and renal)
metabolic pathway necrosis
saturated drugs acts as
an alternative substrate
for conjugation with
toxic Paracetamol
metabolite.
• Naloxone Opioid receptor 400mcg IV , up to 2mg to Opioid overdose • Pain Caution with long acting
antagonist achieve effect • Withdrawal opioids, repeat bolus or
symptoms consider an infusion
• Shorter duration
of action than
most opioids
• Oxygen Essential component of • Non rebreather mask up to • Any patient you Retinopathy of Oxygen supports
aerobic metabolism 75% consider to be critically Prematurity combustion (beware home
• Reduces work of • Call for anaesthesia to secure ill • Blunt hypoxic oxygen and cigarette
breathing airway 100% • Carbon Monoxide drive (rare) smokers and high flow
poisoning oxygen during
defibrillation at cardiac
arrest)
• Phenytoin Binds and stabilises 15mg/kg (<50mg/min) IV/PO Management of Status • CVS Caution narrow
sodium channels loading Epilepticus (hypotension, therapeutic index
• Roughly~1g for adult arrhythmias, heart
• Then ~100mg tid PO or IV as block, CVS
per BNF collapse)
• CNS (ataxia,
paraesthesia,
confusion)
• Potassium Serum electrolyte • Maximum 40mmol/l IV Hypokalaemia Arrhythmia • Hyperkalaemia
• Maximum infusion rate • Caution with renal
Chloride 10mmol/hr impairment
• Prothrombin Factors II, VII, IX, X and IV dose depends on INR: Rapid reversal of a Thrombotic events • Recent MI
protein C and S raised INR • History of Heparin
Complex induced
Concentrate (PCC) thrombocytopenia
• Salbutamol Short-acting β2- • 2.5 – 5mg nebulised repeat as • Management of • Bronchodilation • Caution with
adrenergic receptor required Asthma • Tachycardia/ hypokalaemia
agonist • IV see BNF • Hyperkalaemia palpitations /dry • Caution with arrhythmia
• Tocolytic mouth
• Lactate rise /
muscle cramps
• Tremor
• Hypokalaemia
• Nervousness/
sleep disturbance
• Arrrhythmias /
ischaemia
• Sodium Buffer for H+ ions According to extent and Management of life • Alkalosis • Intracellular acidosis
• Shifts acidosis to severity of acidosis (Central IV threatening acidosis • Intracellular • Precipitation with Ca
Bicarbonate intracellular space infusion) Acidosis containing solutions
• Hypernatraemia • Extravasation and
• Hyperkalaemia necrosis
• Tranexamic Acid Binds to the lysine site • 10mg/kg Management of major • CVS • In elective surgery history
on plasminogen and • Roughly~1g for adult haemorrhage hypotension, of DVT/PE, severe
plasmin preventing • In trauma use 1g over 10 min prothrombotic ischaemic heart disease,
thrombolysis then 1g over 8 hours. Look up • CNS seizures stroke and epilepsy.
Michael Grant

lOMoARcPSD|4984001
POEM: Page 68 of 68
the CRASH 2 study online
IV/PO/Topical
• Vitamin K Necessary for the 5-10mg IV/IM/PO • Reversal of a Interactions with • Caution only in
production of clotting prolonged other vitamins see pregnancy
factors prothrombin time BNF • Give IV injection slowly
• Neonates at birth
Michael Grant

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lOMoARcPSD|4984001

Anaesthetics & Emergency Medicine Notes

Medicine (Queen's University Belfast)

StuDocu is not sponsored or endorsed by any college or university

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LEARNING OUTCOMES 2014-2015 Cricothyroid membrane -

List the symptoms, signs and causes of upper airway

LOOK LISTEN FEEL

Causes of airway obstruction include:

In patients who are sedated, anaesthetised or unconscious, the

The commonest cause of airway obstruction is loss of airway muscle tone

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Adjuncts are used to secure the airway once the

Display a practical knowledge of essential airway equipment, particularly:

ADVANTAGES over ET DISADVANTAGES over ET

Endotracheal tube is Endotracheal tubes used in longer surgeries !! Michael Grant

Connecting patient to anaesthetic machine. Anaesthetic circuit.

stomach via a nasogastric or orogastric tube

Display a practical knowledge of how to: Cervical

• Apply the “triad” of immobilisation to the cervical spine

State and discuss the management of a tracheostomy emergency using the

There are two types of Neck Breathers:

1. Post Laryngectomy patients (obligate neck breathers) RED SIGNS:

Post laryngectomy patients have an end stoma and

All patients with a tracheostomy should have a sign

Methods of Tracheostomy Insertion

Most tracheostomies are percutaneous and are inserted

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LEARN !!! Tracheostomy POEM: Page 7 of 68

Types of Tracheostomy Tube Lumen

• Obstruction Obstructed tracheostomy Mx

• Dislodgement Dislodged tracheostomy Mx

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• Bleeding Bleeding Tracheostomy Mx

KNOW Fi02 VALUES FOR MCQs !!!

Oxygen Therapy Breathing KNOW Fi02 VALUES FOR MCQs !!!

Describe the indications, features and performance characteristics of the following

long-term oxygen therapy.

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ALWAYS REACH FOR THIS FIRST IN A SICK PATIENT !!!

• The disadvantages are similar to those of the Hudson mask.

The pressure drop and increased velocity of gas flow

VENTURI FACEMASK POEM: Page 10 of 68

Where: How to calculate oxygen

For CaO2 = 20.1 ml/100 ml and Q = 5 l/min:

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• A rightward shift indicates that the hemoglobin under study

List the limitations of oxygen saturation monitoring

Readings can be affected by:

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Review treatment of all these

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- D-Dimer is a substance produced when a blood clot is broken down

(USS Scan) POEM: Page 14 of 68

Consider surgical rib fixation

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Pneumothorax Ix: Pulmonary Embolism Ix:

(Primary Pneumothorax) Mx:

Define and differentiate between the two types of respiratory failure.

2. Check patient details and gain consent

• Take a peak expiratory flow measurement

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