Week : 1

Overview
Poor compliance = Amount of pressure generated to expand lungs with a given volume

- The more pressure that has to be exerted to inflate the lungs → Less compliance

Lung Volume + Capacity

Tidal volume = Amount of air inhaled in a normal breath at rest

Inspiratory Reserve = Amount of air inhaled over + above tidal volume

Expiratory Reserve = Amount of air actively exhaled over + above tidal volume

Residual Volume = Amount of air remaining in lungs after exhaling

Functional Residual Capacity = Amount of air present in lungs throughout the respiratory cycle
during normal tidal breathing

Inspiratory Capacity = Maximum volume of air inspired after reaching the end of expiration

Vital Capacity = Total volume of air that can be displaced from the lungs by maximal expiratory
effect

Total Lung Capacity = Maximal volume of air in the lungs

Minute Ventilation = Volume of fresh air entering alveoli per minute. MV = RR x TV

Ventilation = Exchange of gas between alveoli and external environment

1
Perfusion = Flow of blood through tissues or supply of blood to an area in the lungs

V/Q Ratio

- V/Q ratio is the matching of ventilation to perfusion. It is the amount of air that reaches the
lungs divided by the amount of blood flow in the capillaries (V/Q = 1 - Normal ventilation +
perfusion)

V/Q Mismatch

- Causes tissue hypoxia, which won’t respond well to increasing inspired oxygen.
Intrapulmonary shunts (R-to-L shunt) creates V/Q mismatch which can cause tissue
hypoxia. It occurs in any illness that permits blood flow through the lungs without picking
up enough action to fully saturate the haemoglobin, which decreases arterial oxygen
concentration leading to hypoxia.
- In circumstances of intrapulmonary shunting, large volumes of poorly oxygenated blood is
mixed with maximally oxygenated blood, which results in reduced oxygen for tissue
metabolism. Reduced amount of air entering reduces the FiO2 (flow of O2), which
produces minimal increase in arterial O2 concentration.
- An area with no ventilation but normal perfusion is termed shunt. Alveoli with no
ventilation have PCO2 values that are the same as those of mixed venous blood because
the trapped air in the unventilated alveoli equilibrates with mixed venous blood.

Dead Space

- An area of the lung that receives ventilation but no perfusion is called dead space (e.g.
PE)
- 3 types:
1. Alveolar - alveoli are ventilated but not perfused. It can change from minute to
minute with alterations in cardiac output + pulmonary blood flow
2. Anatomical - parts of resp. Tract are ventilated but not perfused. Called anatomical
because its fixed by anatomy and doesn't change
3. Physiological - combination of alveolar + anatomical dead space

Acid-Base Disorders

- The bicarbonate/carbonic buffer system - major buffer system for fixed acids in blood
- Respiratory Acidosis = Acid-base disturbance associated with increased carbonic acid
(H2CO3) concentration (CO2 retention). Show high ETCO2/PACO2 levels
- Respiratory Alkalosis = Acid-base disturbances associated with decreased H2CO3
concentration (CO2 lost). Low levels ETCO3/PACO2

2
- Type I respiratory failure - Hypoxaemia with PaO2<60mmHg
- Type II respiratory failure - Hypoxaemia with PaO2<60 mmHg,& hypercarbia with
PaCO2>45mmHg

3
Basics of ABG (arterial blood gas)

Oxygen Delivery to Tissues

Partial pressure of gas = The partial pressure of any gas is the pressure which it would exert if it
were alone and unaffected by changes in other gases in a contained space.
Dalton Law: The total pressure of a gas mixture is equal to the sum of the partial pressures of the
component gases.
Henry’s law: helps to explain the relationship of partial pressures above and within a solution.
The quantity of a gas that dissolves in a volume of liquid is directly proportional to the partial
pressure of that gas, the pressure remaining constant.

Bohr Effect: decreased O2 affinity of Hb in response to decreased blood pH resulting from

increased CO2 in blood

Oxygen Dissociation

4
 - The curve illustrates the % of Hb saturated within O2 at different PaO2

→ Shift to left = Hb hold tighter + doesn’t release easily to tissues

→ Shift to right = Hb holds less tightly on to O2 and releases it easily to tissue

Auscultation

5
Week : 2
Asthma

Definition
Asthma is a heterogeneous disease, characterised by chronic airway inflammation. It is defined
by the history of respiratory symptoms such as wheeze, SOB, chest tightness and cough that vary
over time and intensity, together with variable expiratory airflow limitation.

Pathophysiology
Extrinsic (Atopic / allergen) and Intrinsic (Idiosyncratic / non-allergen)) Induced

Allergen

Pathogens (pollen, dust mites, mould) binds to mast cells through Immunoglobulin E (IgE), which
activates the release of inflammatory chemical mediators (histamine, eosinophils, neutrophils,
cytokines, etc.). Histamines bind to H1 & H2 receptors, which invoke responses. H1 receptors
induce bronchoconstriction and increase vascular permeability (airway inflammation), whereas H2
receptors cause goblet cells to secrete excessive mucus, lining up the airway. Thus, this creates a
decreased airway lumen, which increases airflow resistance and wheeze, resulting in airway
collapse, which can lead to hypoxia, hypercapnia and cardiac arrest.

Non-Allergen

Non-allergen pathogens (exercise, cold air, smoke, infection, etc.) stimulates the sympathetic
nervous system, activating mast cells. This releases inflammatory chemical mediators and
induces bronchoconstriction, airway inflammation and mucus production in the same pathway as
allergen-induced asthma. Further, it also stimulates the parasympathetic nervous system, which
increases vagal tone preventing bronchodilation and inducing bronchospasm. Thus, the neural
pathways decrease airway lumen which increases airflow resistance and wheeze, resulting in
airway collapse, which can lead to hypoxia, hypercapnia and cardiac arrest.

Clinical features
- Wheeze

6
 - Dyspnoea
- Chest tightness or cough
- Tachypnoea
- Tachycardia
- Accessory muscle usage
- Diaphoresis
- Cyanosis (late sign)
- Classified into: Mild/Moderate, Severe, Life-threatening

Management
1. Bronchospasm:
1. Patients would respond well to aerosolized (Neb/MDI puffer) B2-stimulants, e.g.
Salbutamol.
2. Anticholinergics, such as Ipratropium Bromide (antimuscarinics), will stop any
parasympathetic innervation, and enhance the effects of the B2-agonists.
3. Magnesium sulphate produces smooth muscle relaxation, via an unknown
mechanism.
2. Bronchial oedema:
1. Treatment of choice is corticosteroids (hydrocortisone), which will suppress the
inflammatory response.
3. Excessive mucus secretion:
1. Primary approach is to improve hydration.
2. Mucolytics are sometimes used, but most often in the hospital setting.
Ventilation strategies:
- Slow rate
- Larger tidal volume
- Prolonged expiratory phase
- Alveolar plateau (EtCO2) reached before next breath

Other key features

Status

1. Current Exacerbation
- Mild
- Moderate
- Severe
- Life-threatening

7
8
2. Chronic Status
- Intermittent: only use SABA prn
- Persistent: Gets an ICS, with or without additional therapy, e.g. LAMA, LABA, LKT
receptor antagonist.
3. Current Control
- Poor
- Partial
- Good

9
Week : 3
COPD

Definition
Chronic obstructive pulmonary disease (COPD) is a common preventable disease, characterised
by persistent respiratory symptoms and airflow limitation that is due to airway and/or alveolar
abnormalities usually caused by significant exposure to noxious particles or gases.

Pathophysiology
Constant exposure to noxious gases/irritants causes inflammation of the airway epithelium.
Simultaneous disease processes occur in the airway including emphysema and bronchitis.

Emphysema

Inflammatory cells infiltrate the alveolar wall, releasing cytokines (neutrophils, macrophage,
lymphocytes, leukotrienes, etc.). This inhibits normal endogenous antiprotease, as well as
increases protease activity with the breakdown of elastin in connective lung tissue. This results in
breakdown of walls between the alveoli, which forms large air sacs (decreased surface area for
gas exchange) and loss of elastic recoil of the alveoli.

Chronic Bronchitis

Constant exposure to noxious gases/irritants, result in the infiltration of inflammatory cells and
releases cytokines in the airways. This leads to systemic effects (muscle weakness, weight loss),
as well as continuous bronchial irritation and inflammation. This causes bronchial oedema,
hypersecretion of mucus and bacterial colonisation of the airway.

Both emphysema and bronchitis cause airway obstruction, air trapping, loss of SA for gas
exchange and frequent exacerbations. This can lead to hypoxia (poor gas exchange) and
hypercapnia (airway outflow obstruction).

10
Clinical features
- Dyspnoea
- Cough
- Hypoxaemia
- Hypercapnia
- Cor pulmonale
- breathlessness on exertion
- Cough and sputum production
- Chest tightness
- Wheeze
- Malnutrition and obesity common
- Polypharmacy, limited effect
- Older age group
- Signs of advanced Dx:
➔ Chest hyperinflation
➔ Soft breath sounds, prolonged expiratory phase
➔ Hypoxia + Hypercapnia
➔ Inactivity, poor appetite and weight loss
➔ History of long term O2 therapy

Management
CPG Management
- Minimise patient exertion
- Patient reassurance
● Mild/Moderate resp.distress
- Oxygen (maintain spo2 at 88%-92%)
- Salbutamol (6L/min)
- IB
- Hydrocortisone
● Severe resp. Distress
- Oxygen (maintain spo2 at 88%-92%)
- Salbutamol
- IB
- Hydrocortisone
- Adrenaline → LAST RESORT
- IPPV

JP Management:

11
 1. Airway and breathing:
1. Position the patient in an upright and/or comfortable position, to assist with
mechanics of breathing.
2. Oxygen therapy (controlled or low dose):
■ Should be T.T.E, achieving a SaO2 88 to 92%.
■ If SaO2 ≥ 88%, monitor closely and add O2 if < 88%.
■ If SaO2 < 88%, administer via nasal cannula at 2 – 6 lpm,
■ If SaO2 < 88% following O2 administration, administer via SFM @ 5 – 10
lpm, to achieve a SaO2 > 88%.
■ If SaO2 remains < 85%, use NRBM, or consider escalating to CPAP
therapy if associated with signs of respiratory failure.
2. IV therapy: early IV access for drug/resuscitation therapy. Conservative fluid boluses to
maintain perfusion for any hypotension. Hypotension may also be due to gas trapping.
3. Drug therapy:
1. B2 stimulant (Salbutamol 5mg) and anticholinergic (Ipratropium Br 0.5mg)
2. Consider inotropic support for cardiovascular instability.
1. Anticipate for rapid deterioration:
1. Prepare for BVM ventilations, advanced airway equipment, etc.
1. Ventilations administered at 4 to 6 breaths minute (1 breath every 10 to
15 seconds).
2. Monitor EtCO2 closely ensuring, ensuring patient has exhaled before
delivering next breath, to avoid gas trapping.
2. Consider attaching defib pads.
3. Notify back up early.

Other key features

Ventilation = movement of oxygen to the alveoli

Perfusion = flow of oxygenated blood (gas exchange)

(1) Hypoxic Pulmonary Vasoconstriction (HPV)

Damaged alveoli receive decreased O2 (decreased ventilation), which causes the body to
compensate by pulmonary vasoconstriction (constricting the blood vessels to the affected area)
to match the perfusion with poor ventilation.

When oxygenating a COPD pt the partial pressure of oxygen at the alveoli increases, which
abolishes the HPV compensatory mechanism. This increases perfusion to poorly ventilated
alveolus, but CO2 cannot be offloaded from the blood into the alveolus, decreasing ventilation.
This creates a V/Q mismatch and increases arterial CO2 levels.

12
 (2) Hypoxic Drive

At rest, CO2 is the main stimulus for respiration. However for COPD pts they experience a
chronic expiratory airflow limitation (retainer of CO2), making them insensitive to increased CO2
as a stimulus for breathing. The backup mechanism is O2. Decreased O2 takes over as a primary
trigger for respiration, developing the hypoxic drive.

When Oxygenated, the increased O2 decreases hypoxia, however, the increased O2 decreases
the stimulus to breathe resulting in apnoea.

(3) Haldane Effect

Oxygenation results in O2 to competitively bind to haemoglobin, which kicks C02 off the
haemoglobin. This leads to CO2 dissolving in the blood.

E.g. Taxi (haemoglobin) picks up O2, which kicks CO2 off the taxi into the blood.

Status

1. Current Exacerbation (refer to asthma)

- Mild
- Moderate
- Severe
- Life-threatening
2. Chronic Status
3. Risk for Exacerbation

13
14
Week 4:
N-C APO

Definition
Pulmonary oedema is the presence of serous fluid in the interstitial spaces between the alveoli
and the pulmonary capillaries and within the alveoli, bronchioles and bronchi. APO is a sudden
accumulation of serous transudate.

Difference Between C-APO and N-CAPO

1. Cardiogenic (Increased Hydrostatic pressure)
1. Backward pressure from the left atrium causes pulmonary venous congestion.
2. Often called CHF
3. Can result from left ventricle dysfunction, or cardiac disease (e.g. mitral stenosis).
2. Non-cardiogenic (high permeability)
1. Increased capillary permeability in certain disease states allows fluid to pass from
the bloodstream into the interstitium of the lung, and if severe crosses into the
alveoli

Pathophysiology
Summary:

15
Detailed Explanation

An injury to the capillary endothelium leads to an increase in capillary permeability and disruption
of surfactant production by alveoli. This leads to movement of fluid and plasma from capillary to
interstitial space and alveoli.

- Neurogenic and drug APO pathophysiology

16
 -
- Chemical burns and toxic inhalation

-
- Drowning

17
- Negative pressure

- High altitude pulmonary oedema

- Occurs in non-acclimatized people, in altitudes greater than 3000m (10000Ft)
above sea level
- High altitudes → partial pressure of oxygen and air much lower

- ARDS (Acute resp distress syndrome)

18
 - Fulminant (severe and sudden in onset) form of respiratory failure. It is characterised by
acute lung inflammation and diffuse alveolar-capillary injury. All disorders that result in
ARDS cause severe non-cardiogenic pulmonary oedema.
- Causes:
- Direct: insult to lungs e.g. Pneumonia, chest trauma, smoke
- Indirect: pathology elsewhere in body causing same effects in lungs e.g. Sepsis, burns,
drugs, pancreatitis

Clinical features
- Dyspnoea
- Distress
- Pallor
- Sweating
- Tachycardia
- Poor perfusion
- Crackles

Management
- treat the underlying cause
- Position semi-fowlers (30 degrees)
- O2 therapy
- If ventilations required use peep

19
 - CPAP therapy early if indicated
- Cautious fluid therapy - do not overload pt (unless hypovolemic or septic shock or
SBP<90 or inadequate perfusion)

Other key feature

CPAP therapy:
- Recruits and rexpands collapsed alveoli
- Increases SA to improve gaseous exchange
- Splints/keeps alveoli open
- Decreases WOB

CPAP provides pressure during inspiration and exhalation. A PEEP valve only provides pressure
during expiration. CPAP improves lung mechanics, gas exchange and oxygenation by recruiting
alveoli (forcing alveoli open, thereby increasing surface area and preventing alveolar collapse),
improves pulmonary compliance (by splinting airways open to increase gas exchange), increasing
functional residual volume (FRV), and reducing the work of breathing.

20
Week 5:
ACOS
Definition
Overlap exists among different types of COPD, many have bronchial inflammation with features
of both asthma and COPD.

Asthma-COPD Overlap Syndrome is characterised by persistent airflow limitation with several

features usually associated with asthma and several features usually associated with COPD.

21
Management

- Treat pathology
- Is pt more COPD or Asthma side of spectrum
- Administer O2 pathology
- Rest of management prehospitally

Week 6:
LRTI

Definition
Lower respiratory tract infection is an overarching terminology that includes acutre bronchitis,
pneumonia, acute exacerbations of COPD/ Chronci bronchitis, and acute exacerbation of
bronchiestasis.

Pneumonia:

An infection in the lungs caused by microbes. It causes water to enter the lungs and create
breathing difficulties. Three categories of pneumonia:

- Bronchopneumonia (throughout lungs, bronchioles & alveoli)

- Atypical or interstitial (around alveoli in interstitium)
- Lobar pneumonia (consolidation of whole lobe)

Acute bronchitis:

Bronchitis can be referred to as a chest cold, it occurs when the airways of the lungs swell and
produce mucus in the lungs resulting in a cough

A self-limited inflammation of the large airways characterized by cough without evidence of

pneumonia, without an alternative medical disorder to explain the symptoms, or without a history
of chronic lung disease.

Pathophysiology
Pneumonia (Hospital Acquired, Community Acquired, Aspirated, Ventilator):

22
Microbes invade lung tissue and colonise the bronchioles or alveoli, this triggers an inflammatory
response. The effected tissue gets flooded with exudate and white blood cells (consolidation).
Bacterial pneumonia causes an intense inflammatory response in the alveoli and causes a
productive cough. Atypical organisms are not as intense and result in a milder or non-productive
cough.

Pneumonia causing microbes:

Viral

- Influenza

Bacteria

- Streptococcus Pneumoniae
- Haemophilus Infleunzae
- Staphylococcus Aureus
- Mycoplasma Pneumoniae (atypical or walking pneumonia)
- Chlamydophila Pneumoniae (atypical or walking pneumonia)
- Legionella Pneumoohila (atypical or walking pneumonia)
- Mycobacterium tuberculosis (Mycobacteria)

Acute Bronchitis:

Acute inflammation of the bronchi most commonly triggered by viral infection, allergens,
pollutants, etc. The inflammation of the bronchial walls leads to mucosal thickening, epithelial-cell
desquamation, and denudation of basement membrane.
● Viral: Influenza (A & B).
● Bacterial: Streptococcus pneumoniae.

Clinical features
Pneumonia (Alveolar):

- Fever
- Cough
- Dyspnoea
- Increased RR
- Crackles (scattered, late inspiration) and/or wheezes + bronchial breath sounds
- Pleuritic chest pain
- Bronchial breathing

23
 - Fatigue
- Coloured sputum
- Dullness to percussion (lobar pneumonia)

Acute bronchitis:

- Swelling of the bronchus

- Acute and persistant cough (productive or dry)
- Fever
- Fatigue
- SOB
- Slight fever
- Chest discomfort

Constitutional symptoms and upper respiratory symptoms

- Fever, muscle aches, and malaise (general feeling of discomfort).
- Rhinorrhoea, sore throat and cough (upper respiratory).
Hypersensitivity of tracheobronchial epithelium
- Productive cough, lasting 1 – 3 weeks.
- Bronchospasm, inflammation of the bronchi, and mucus production.

The diagnosis of acute bronchitis is made using clinical findings and historical information: when
acute cough (dry or productive) is present for more than 5 days and when evidence of
pneumonia, acute asthma, or an alternative explanation for the symptoms is absent.

Chronic bronchitis (COPD):

- Cough and daily mucus production

- For at least three months
- For two or more consecutive years

Management
Pneumonia:

- Airway support
- Oxygen
- Ventilation as needed
- IV fluids
- Cardiac monitoring

24
Bronchitis:

- Oxygen
- Neb if wheezes
- Temp. control
- Potential fluids
- Often secondary to URTI

Other key features

Lower Respiratory Tract:

- Trachea
- Primary bronchi
- Bronchioles
- Lungs

25
Week 6:
URTI

Definition
Infection of the upper respiratory tract including any section of the respiratory tract from the
larynx upwards. Can results in irritation and inflammation of the respiratory tract.

URTI generally harmless, however, can trigger pre-existing conditions, this is usually severe.

Viral URTIs can lead to secondary bacterial infections URTIs and LRTIs.

Pathophysiology
Infection caused by virus or bacteria that triggers an immune response, resulting in red, hot ,
painful and swollen upper resp tract.

Clinical features
- Sore throat
- Mild fever
- Headache
- Facial pain (sinusitis)
- Purulent nasal drainage
- Halitosis (bad breath)
- Cervical adenopathy (enlarged cervical lymph nodes)
- Red pharnyx (pharyngeal inflammation/irritation)
- Dry cough

Bacteria:

- Gradual onset
- Localised symptoms
- Pus (exudate)
- Swollen/tender glands

26
Virus:

- Rapid onset
- Systemic symptoms
- Watery discharge
- Less likely (glands)

Management
- Cooling
- Pain relief
- Oxygen is required
- IF causes exacerbation of COPD/asthma NEB w/ salbutamol 5mg and iprtropium bromide
500mcg
- IV fluids (septic)

Other key features

Upper Respiratory Tract:

- Larynx marks the end of upper tract

- Nose
- Nasal cavity
- Mouth
- Throat (pharynx)
- Larynx

Common URTI:

- Common cold
- Pharyngitis (Sore throat)
- Rhinitis (Runny nose)
- Tonsilitis (Painful to swallow)
- Sinusitis (Change in voice)
- Strep throat (Pus)
- Laryngitis
- Otitis media
- Epiglottitis (unable to swallow)

27
 - Pertussis
- Influenza

Vaccine-preventable RTI:

- Influenza
- Pertussis
- Pneuococcus (Strep pneumoniae)
- Varicella
- Measles

28
Week 7:
Croup

Definition
Croup refers to an infection of the upper airway, which obstructs breathing and causes a
characteristic barking cough. The cough and other symptoms of croup are the result of the
swelling around the vocal cords (larynx), windpipe (trachea) and bronchial tubes (bronchi)

Pathophysiology
The viral infection that causes croup leads to swelling of the larynx, trachea, and large bronchi
due to infiltration of white blood cells (especially histiocytes, lymphocytes, plasma cells, and
neutrophils). Swelling produces airway obstruction which, when significant, leads to dramatically
increased work of breathing and the characteristic turbulent, noisy airflow known as stridor.

Causative agents

- Viral
- parainfluenza virus
- influenza virus A
- influenza virus B
- Rhinovirus
- Respiratory syncytial virus (RSV)

Clinical features
- Barking cough
- inspiratory stridor
- Hoarseness
- difficulty breathing
- fever
- coryza
- retractions

29
 - drooling may be present

Management
- Do the westley croup score

30
-
- Adrenaline - Reduces bronchial and tracheal epithelial vascular permeability thereby
decreasing airway oedema, increasing the airway radius and improving airflow
- Dexamethosone - A long acting synthetic corticosteroid that produces anti-inflammatory
and immunosuppressive effects. The effect corticosteroids have on croup are thought to

31
 be on vasocontrictive actions in the upper airway, followed by the systemic
anti-inflammatory effect
- Oxygen - utilised to prevent hypoxia and resp distress
- Rest and reassurance to reduce anxiety as this can make the situation worse

Other key features

Also referred to as laryngotracheobronchitis

32
Week 7:
Epiglottitis

Definition
Rapidly developing inflammation of the epiglottis and adjacent tissues, due to bactertial infection,
may cause life-threatening airway obstruction

Pathophysiology
- epiglottitis is an inflammation of the lining of the cartilaginous tissue that protects the
airway during swallowing
- infection of this structure is predominantly caused by the bacteria haemophilus
influenzae. It can also be caused by other bacteria or viruses causing respiratory illnesses
and non-infection aetiologies

An infant epiglottis is comprised of cartilage that is far more pliant when compared to that of an
adult, whose epiglottis is more rigid (this is the natural progression of cartilage maturation). It is
not surprising, then, that an infectious process that leads to edema and increase in weight and
mass of the epiglottis is more likely to cause symptoms in a child - the pliancy of the cartilage
allows a ball-valve effect, where each inspiration pulls an edematous epiglottis over the laryngeal
airway, causing symptoms. In adults, whose cartilages are stiffer, an isolated epiglottic infection
and the resultant increase in epiglottic mass may be resisted by the more rigid
laryngeal/epiglottic cartilage; but an infection that encompasses more of the tissues of the
supraglottis, leading to edema, can lead to symptoms and an unstable airway.

Causative agents

- Heamouphilus influenza type b (Hib), streptococcus pyogenes, streptococcus

pneumoniae, staphylococcus aureus i.e. bacterial cause

Clinical features
- airway inflammation/ obstruction
- tachycardia

33
 - restlessness
- retractions
- anxiety
- inspiratory stridor
- drooling

Management

Other key features

- DO NOT EXAMINE THROAT - THIS CREATES RISK OF FULL OBSTRUCTION
- Also known as supraglottitis

34
Week 7:
Bronchiolitis

Definition
An inflammatory bronchial reaction in young children and infants.

Bronchiolitis is almost always caused by a virus. The condition most commonly occurs during the
winter months.

Pathophysiology
The underlying pathophysiology is inflammation of the small airways (bronchioles). Infection of
the bronchiolar and ciliated epithelial cells produces increased mucous secretion, cell death and
sloughing, followed by a peribronchiolar lymphocytic infiltrate and submucousal oedema. This
combination of debris and oedema results in distal airway obstruction. During expiration, the
additional dynamic narrowing produces disproportionate airflow decrease and air trapping. The
effort of breathing is increased due to increased end expiratory lung volume and decreased lung
compliance.3 Recovery of pulmonary epithelial cells occurs after 3–4 days, but cilia do not
regenerate for approximately two weeks.3 The debris is cleared by macrophages.

Respiratory Syncytial virus (RSV) is the most common cause of bronchiolitis and pneumonia. RSV
causes infection of the lungs and breathing passages, is a major cause of respiratory illness in
young children. In adults, it may only produce symptoms of a common cold, but in premature
babies and kids with diseases that affect the lungs, heart, or immune system, RSV infections can
lead to other more serious illnesses.

Clinical features
- SOB
- Increased resp rate
- wheezing
- difficulty breathing
- inadequate tidal volume

35
 - dehydration
- fever
- loss of appetite
- malaise
- coughing
- nasal congestion
- Brief period of apnoea

Management
- If over 1 nebulised salbutamol and ipratropium bromide
- if not oxygen and supportive measures to lower anxiety
- stimulate child
- prepare for brief period of apnoea

Other key features

36
Week 7:
Pertussis

Definition
A highly contagious respiratory tract infection that is easily preventable by vaccine.

Whooping cough is particularly dangerous for infants.

Pathophysiology
Bordetella is a gram-negative coccobacillus that adheres to ciliated respiratory epithelial cells.
Local inflammatory changes occur in the mucosal lining of the respiratory tract. Released toxins
(pertussis toxin, dermonecrotic toxin, adenylate cyclase toxin, and tracheal cytotoxin) act locally
and systemically, although the organism itself does not fully penetrate the respiratory tract, and
almost never is found in blood cultures.

Clinical features
- ‘whoop’ sounding cough
- coryza
- low-grade fever
- Apnea in infants
- long inspiratory effort
- Cyanosis
- vomiting exhaustion

Management
- Rest and reassurance
- oxygen
- supportive measures

37
PAED Airway Conditions

38
Week 8:
Pulmonary Embolism

Definition
PE is venous thromboembolism generally from a DVT that travels to the lungs and occludes a
vessel, resulting in difficulty breathing, infarction, pain and potential arrest.

Pathophysiology
PE occurs when a DVT (blood clot) or part of it breaks off from the vein. The clot travels through
the blood stream, to the heart and migrates towards the lung. The clot blocks a vessel in the lung,
interrupting blood supply.

Sudden obstruction of blood flow to the lungs, pulmonary hypertension and severe strain on
heart. Lung tissue becomes infarcted and patient feels sharp pleuritic pain. Pleuritic pain is
caused by the infarcted lung dying, the pt becomes hypoxic and RR increases to compensate for
non-functioning lung tissue. Patient my begin to have massive haemoptysis. The heart speeds up
as it tries to compensate for impaired blood flow, but, if clot is massive, it can’t keep forward flow
and obstructive shock occurs.

Infarction causes inflammation in the lung and pleura

Increased dead space causes increased V/Q mismatch, causing abnormal gas exchange.

Shunting attempts to compensate for increased dead space by sending CO to remaining lung
tissue. If clot too large, then capillaries become engorged, and diffusion distance for O2 and CO2
is far. Hypoxia and eventually hypercapnia (late sign) follow.

Virchow’s Triad

39
Clinical features
- Dyspnoea
- Pleuritic chest pain
- Syncope
- Haemoptysis
- Cough (potentially)
- Calf or thigh pain + swelling
- Tachypnoea
- Tachycardia
- Hypotension
- JVD
- Crackles/rales (potential)
- Most common ECG sinus tachycardia, non-specific ST and T wave changes
- ECG S1Q3T3/ RV strain/ RBBB

Management
- Oxygen
- IV large bore bilateral
- Fluids prepped or given if haemodynamically stable
- 12-lead ECG
- Analgesia

40
Wells score

41
Other key features
Risk Factors:

- Recent surgery/immobility
- Pregnancy
- OC pill
- Extended travel (>12 hrs)
- Acute or chronic illness
- Malignancy

ETCO2

Increased dead space means lung ventilation is normal, however, not all is perfused. This results
in reduced EtCO2 as some air moves in and out of the lungs without contac with blood.
Furthermore, the compensatory pulmonary shunting that follows causes the perfusion distance
within the capillaries to increases and prevent optimal gas exchange. Thus, less CO2 can be
exhaled in the parts of the lung that are still being perfused.

A reduction in CO also affects EtCO2

EtCO2 is not reflective of PaCO2 - known as A-a gradient

Differential diagnosis:

- AMI
- Pneumonia
- Pericarditis
- CHF
- Pleurisy
- Pneumothorax
- Pericardial tamponade

42
Week 9:
Cystic Fibrosis

Definition
CF is a genetic disease where they have a genetic defect that affects their Chloride (Cl-) channel
in the exocrine gland, consequently affecting the balance needed to maintain normal thin mucous
layers that is easily removed by the cilia. As a consequence of the Cl- channel defect, the
patient’s mucous has less water, is extremely thick and is poorly removed by cilia, and thus, the
excess mucous accumulates in the respiratory tree.

Pathophysiology
In normal people, the cystic fibrosis transmembrane regulator (CFTR) channel is responsible for
moving Cl- ion outside the cell. Consequently, Na+ follows Cl-, and water follows Na+, and thus
mucous can be cleared.

In CF patients, they have a genetic defect on the CFTR, meaning that Cl- ion cannot move, thus
causing sticky mucous to build up on the outside of cell.

Clinical features
Clinical feature

- Sputum → increased volume, more purulent/green indicating infection

- Dyspnoea → during exacerbation, pt will experience increase SOB
- Wheeze / bronchospasm present during exacerbation

Respiratory symptom

- Persistent productive cough

- Frequent respiratory tract infection
- Wheeze
- Headache and pain over sinus (from chronic sinusitis)

Clinical findings

43
 - Clubbing of digits
- Pallor of conjunctiva (due to anaemia from chronic disease & iron deficiency)
- Mild hyper-resonance to percussion (obstructive)
- Coarse crepitation which may change/clear on coughing, may hear audible crackles at
mouth
- wheeze

Management
- Airway → suction to remove mucous
- Breathing:
- O2 in controlled/low dose → aim SaO2 of 88-92%
- NEB salbutamol + ipratropium bromide for bronchospasm → consider NEB
hypertonic saline
- Escalate O2 therapy to reverse persistent hypoxia (after unresponsive to
conventional O2 therapy)
- Circulation
- IV access & fluids → pt may be dehydrated

Other key features

44
Week 9:
Coal workers Pneumoconiosis

Definition
Interstitial lung disease caused by inhalation of certain dusts. Prolonged activation of the immune
system in the interstitium → detrimental negative effects

Usually caused by certain occupations:

- Coal workers pneumoconiosis - inhalation of coal dust

- Silicosis - inhalation of crystalline silica
- Asbestosis - inhalation of asbestos

Pathophysiology
Interstitial Lung Disease
All forms of interstitial lung disease cause thickening of the interstitium. The thickening can be
due to inflammation, scarring, or extra fluid (oedema). Some forms of interstitial lung disease are
short-lived; others are chronic and irreversible. In most cases, the thickening is due to fibrotic
tissue which leads to an increased diffusion distance, and poor gaseous exchange. Loss of
elasticity in the lungs causes lung volumes to shrink, and as a result patients have smaller tidal
volumes, with minute volumes sustained through an increased respiratory rate. Thus, ILD is
classed as a Restrictive Lung Disease.

Pulmonary Fibrosis:
1. Poor lung compliance - small TV as lung cannot expand well
2. RR needs to increase to compensate in order to maintain MV
3. Diffusion impairment (O2 battles to cross thickened fibrotic alveolar membrane)
4. In severe forms, the capillaries tend to compensate for damaged areas of the lungs by
shunting blood away from poorly ventilated areas and sending them to less diseased
areas. The compensatory systems lead to increased pulmonary hypertension, hypoxia,
cor pulmonale and resp. Failure

Coal Workers Pneumoconiosis

45
Inhalation of coal mine dust particles are engulfed by macrophages in the lung as part of the
immune system's response to a foreign particle. The macrophages containing the coal dust
accumulate to form “coal macules”. Should these macules combine, they will form masses of
fibrous tissue. Fibrosis produces impairment of gaseous exchange due to interstitial thickening.
This causes dyspnoea.

Clinical features
Asymptomatic round opacities on chest X-ray. This is important to be aware of, as most patients
live with this condition for many years and remain symptom free.
- Impairment of lung function
- Breathlessness
- Resp. distress

Management
1. Airway and breathing:
1. Position the patient in an upright and/or comfortable position, to assist with
mechanics of breathing.
2. Oxygen therapy (MODERATE):
■ Should be T.T.E, achieving a SaO2 > 93%.
■ If SaO2 < 94%, administer via nasal cannula at 2 – 6 lpm, or SFM @ 5 – 10
lpm, to achieve a SaO2 > 93%.
■ If SaO2 < 85%, use NRBM to achieve SaO2 > 93%.
■ If patient is a diagnosed COPD patient as well, treat as for conditions
requiring CONTROLLED or LOW-DOSE therapy.
■ If above fails to reverse hypoxia, with signs of respiratory failure, call for
back up and consult for CPAP therapy.
2. IV therapy: early IV access for drug/resuscitation therapy. Conservative fluid boluses to
maintain perfusion for any hypotension.
3. Drug therapy:
1. If wheezes present, consider Neb therapy.
4. Anticipate for rapid deterioration:
1. Prepare for BVM ventilations, advanced airway equipment, etc.
■ BVM ventilations should be delivered using the following:
■ Smaller tidal volumes (4 to 8 ml/kg, start lower at 4). So, rule of
thumb of delivering sufficient TV to produce visible chest rise still
applies. Smaller volumes are best.

46
 ■Faster rates (20 to 35/min) to maintain minute volume, with each
breath delivered over ½ a second (instead of over 1 second under
normal conditions).
■ Mild to moderate PEEP is allowed.
2. Consider attaching defib pads.
3. Notify back up early

Other key features

Interstitial Lung Disease

47
Week 9:
Asbestosis

Definition
Fibrosing conditioning of lungs caused by inhalation of substantial asbestos dust. Most common
manifestation is from pleural plaques

Pathophysiology
Diffuse pleural thickening is extensive and progressive pleural fibrosis occurs, which involves
both the visceral and parietal pleura.
In contrast to pleural plaques, diffuse pleural thickening may markedly reduce lung volumes,
resulting in exertional dyspnoea.

Clinical features
- Exertional breathlessness + dry cough
- Usually signs HF → Myocardial workload = increased hypertrophy
- Late inspiratory crackles + finger clubbing
-

Management
1. Airway and breathing:
1. Position the patient in an upright and/or comfortable position, to assist with
mechanics of breathing.
2. Oxygen therapy (MODERATE):
■ Should be T.T.E, achieving a SaO2 > 93%.
■ If SaO2 < 94%, administer via nasal cannula at 2 – 6 lpm, or SFM @ 5 – 10
lpm, to achieve a SaO2 > 93%.
■ If SaO2 < 85%, use NRBM to achieve SaO2 > 93%.
■ If patient is a diagnosed COPD patient as well, treat as for conditions
requiring CONTROLLED or LOW-DOSE therapy.

48
 ■ If above fails to reverse hypoxia, with signs of respiratory failure, call for
back up and consult for CPAP therapy.
2. IV therapy: early IV access for drug/resuscitation therapy. Conservative fluid boluses to
maintain perfusion for any hypotension.
3. Drug therapy:
1. If wheezes present, consider Neb therapy.
4. Anticipate for rapid deterioration:
1. Prepare for BVM ventilations, advanced airway equipment, etc.
■ BVM ventilations should be delivered using the following:
■ Smaller tidal volumes (4 to 8 ml/kg, start lower at 4). So, rule of
thumb of delivering sufficient TV to produce visible chest rise still
applies. Smaller volumes are best.
■ Faster rates (20 to 35/min) to maintain minute volume, with each
breath delivered over ½ a second (instead of over 1 second under
normal conditions).
■ Mild to moderate PEEP is allowed.
2. Consider attaching defib pads.
3. Notify back up early.

Other key features

1. Mesothelioma is a malignancy that can arise in the pleura from Asbestos exposure. This
can manifest as chest wall pain in association with pleural thickening. This should raise
the suspicion of pleural malignancy.
2. Pulmonary hypertension with Cor pulmonale.

49
Week 9:
Silicosis

Definition
Workplace activities such as grinding, cutting and polishing

Silicosis is an interstitial lung disease that occurs with the inhalation of crystaliline silica, triggering
an immune response. The immune response attacks the silica particles and causes fibrosis
(scarring) of the lung which creates a stiffness and thicker tissue, making diffusion difficult and
difficulty in taking normal breathes due to stiffness and decreased volume capacity. Damage is
irreversible and may continue to progress when exposure is removed.

● Classic Silicosis:
○ Most common - pts usually remain asymptomatic until after an interval of 10-20
years of continuous silica exposure.
● Accelerated
○ Associated with a much shorter duration of dust exposure (typically 5-10 yrs)
clinical presentation may be as early as 1 yr after exposure. Otherwise, similar to
classic.
● Silicoproteinosis
○ Acute and rapidly progressive following very high levels of exposure. Presentation
within 1 year of exposure and death within 5 years

Pathophysiology
Macrophages ingest the silica particles & triggers a massive inflammatory response. This causes
fibroblasts to multiply and produce collagen, causing fibrosis of the interstitium. Silica particles
also trigger the formation of oxygen free radicles which further damage the lung. Macrophages
are outlived by the silica deposits in the lung, and so are engulfed by new macrophages, adn the
cycle continues as the deposits cannot be removed.

50
Clinical features
- SOB
- Shallow TV
- Potential ECG changes

With occupational asthma exacerbation:

- Wheeze
- SOB
- Low SpO2
- Fast RR
- Tachycardia
- Potential ALOC

Management
- Remove from trigger
- Oxygen
- IV
- If ventilation required faster RR (>10bpm), smaller tidal volume (sufficient TV to produce
visible rise)

With occupational asthma exacerbation:

- NEB 8L/min salbutamol 5mg and Ipratropium 500mcg (repeat Salbutamol when finished,
ipratropium repeated at 20 min)
- Hydrocortisone 100mg IV
- Life-threatening - Adrenaline IM 500mcg (repeat 5 mins)

Other drugs considered, not administered (CCP only): i. Magnesium sulphate – 10mmol over
10mins • Syringe preparation – Mix 10 mmol (5ml) of MgSO4 with 15 ml NaCl 0.9% in a 30ml
SPRINGFUSOR syringe to achieve a final concentration of 10 mmol/20ml. Ensure syringe is
appropriately labelled. Administer via SPRINGFUSOR at a rate of 60ml/hour (over 20 min).

1. Airway and breathing:

1. Position the patient in an upright and/or comfortable position, to assist with
mechanics of breathing.

51
 2. Oxygen therapy (MODERATE):
■ Should be T.T.E, achieving a SaO2 > 93%.
■ If SaO2 < 94%, administer via nasal cannula at 2 – 6 lpm, or SFM @ 5 – 10
lpm, to achieve a SaO2 > 93%.
■ If SaO2 < 85%, use NRBM to achieve SaO2 > 93%.
■ If patient is a diagnosed COPD patient as well, treat as for conditions
requiring CONTROLLED or LOW-DOSE therapy.
■ If above fails to reverse hypoxia, with signs of respiratory failure, call for
back up and consult for CPAP therapy.
2. IV therapy: early IV access for drug/resuscitation therapy. Conservative fluid boluses to
maintain perfusion for any hypotension.
3. Drug therapy:
1. If wheezes present, consider Neb therapy.
4. Anticipate for rapid deterioration:
1. Prepare for BVM ventilations, advanced airway equipment, etc.
■ BVM ventilations should be delivered using the following:
■ Smaller tidal volumes (4 to 8 ml/kg, start lower at 4). So, rule of
thumb of delivering sufficient TV to produce visible chest rise still
applies. Smaller volumes are best.
■ Faster rates (20 to 35/min) to maintain minute volume, with each
breath delivered over ½ a second (instead of over 1 second under
normal conditions).
■ Mild to moderate PEEP is allowed.
2. Consider attaching defib pads.
3. Notify back up early.

Other key features

Diffusion issue

Reduction in lung volume

Difficulty inhaling due to stiffness inside lung tissue or chest wall

52
Week 10:
Haemoptysis

Definition
Haemoptysis is the expectoration of blood from lung.

Massive/severe hemoptysis is life-threatening expectoration of blood between 100-600mL of

blood over 24 hours. (note → 1 cup of blood is 250mL, thus minimum of 4 cups)

Pathophysiology
Haemoptysis is a result from the disruption of blood vessels within the walls of the airway (i.e.
trachea, bronchi, bronchioles and lung parenchyma). Bronchial circulation attributes to 90% of
haemoptysis cases due to the high-pressure system (unlike pulmonary arteries due to it’s
low-pressure system, despite accounting to 99% of arterial blood flow).

Inflammatory and infectious process can lead to haemoptysis → e.g. coughing in setting of
transient airway inflammation (e.g. acute bronchitis) can lead to minor bleeding, even in healthy
lungs.

Chronic inflammation (e.g. tuberculosis, cystic fibrosis, COPD) causing haemoptysis → bronchial
arteries are proliferated and enlarged to enhance delivery of oxygenated blood to alveoli.
Consequently, the vessels are thin & fragile, brone to rupture. Additionally, chronic disease can
lead to bronchiectasis (i.e. chronic bronchial wall inflammation), leading to dilation and
destruction of the cartilaginous support, predisposing blood vessels to rupture.

Distal pulmonary embolism can lead to infarction of lung tissue, leading to oedema and
haemorrhage.

Clinical features
History taking / risk factors

53
 - Smoking → predispose chronic lung inflammation and vascular disruption; increase risk of
bronchogenic carcinoma
- TB (leading cause) → ask about travelling
- Previous venous thrombotic disease → PE may cause the haemoptysis
- Tapeworm (Echinococcosis spp.) can lead to hydatid cyst within lung
- Cocaine / heroine inhalation can trigger diffuse alveolar haemorrhage
- Nitrogen dioxide exposure may cause haemoptysis
- Anticoagulant usel procedure like swan-ganz catheter insertion, bronchoscopy

Physical examination

- Sputum → check blood streaks; clots of blood

- Tachypnoea
- Tachycardia
- Hypotension
- Laboured respiration
- Hypoxemia

Management
Mild:

- Supportive care
- Urgent transfer to definitive care

Massive:

- More time-sensitive → require rapid transport to definitive care

- Stabilize pt with sufficient O2 therapy to maintain SpO2 >94%
- IV Access → hypovolaemic shock, so consider administering fluid to maintain SBP
90mmHg or radial pulse?
- Place pt on lateral position on side of bleed → side with reduce breath sound (indicate
side of bleed)

Other key features

54
Week 10:
Pleural effusion

Definition
Pleural effusion is the pathological accumulation of fluid between visceral pleura and parietal
pleura.

Pathophysiology
2 MAIN CAUSES:

- Too much fluid enters

- Too little fluid exit pleural space

(either way → both causes the pleural space to have too much fluid, causing the lung to collapse)

Mechanism 1 → increase hydrostatic pressure in parietal capillaries

- Consequence → more fluid is forced across capillary membrane

- Cause: pulmonary hypertension → from condition like right heart failure, pulmonary
fibrosis, liver disease

Mechanism 2 → Decrease oncotic pressure (i.e. pressure exerted by protein) within capillaries

- Occurs when there’s a reduction in plasma protein, which then causes fluid to escape
from parietal capillaries into pleural space more easily. Additionally, the lung cannot
remove the excess fluid as fast as the amount is coming in.
- Disease that causes a reduction in plasma protein → severe malnutrition, liver failure (from
cirrhosis), nephritic syndrome (excessive exertion of protein in proteinuria), pt with pleural
effusion secondary to hypoalbuminemia

Mechanism 3 → Damage to capillary wall

- Injury and inflammation damages the capillary wall, which consequently increases
permeability of capillary wall. This means protein can escape the extravascular space and

55
 accumulate in the pleural fluid, increases the oncotic pressure, attracting more fluid into
the pleural space via osmosis
- Seen in pt with pneumonia

Clinical features
- Chest pain (pleuritic), worsens on inspiration
- Dry non-productive cough
- Dyspnea
- Orthopnoea (i.e. SOB when supine)
- Tachypnoea → compensation for impaired minute ventilation from reduced tidal volume
caused by diminishing lung size from pleural effusion
- Asymmetrical rise and fall of chest → collapsed lung as volume increase
- Dullness / stony on percussion
- Decreased breath sounds, crackles (fluid in alveoli just above effusion), pleural rub
- Tracheal deviation TOWARDS unaffected side

Management
- AIRWAY → nil
- BREATHING:
- Oxygen therapy aim to maintain SpO2 92-96%
- If pt doesnt respond to O2 therapy & exhibit signs of hypoxia → consider CPAP
- CIRCULATION:
- Fluid therapy may be beneficial if pt suddenly deteriorates due to poor perfusion
- If pt’s mediastinum shifts, bolus of fluid unlikely to help
- OTHER:
- Place pt in comfortable position
- Pain relief → fentanyl?

Other key features

2 main types of pleural effusion

1. Exudates
- Fluid in pleural with high conc. of protein

56
 - Cause → breakdown of normal vascular mechanism that retain protein in capillaries. Pt will
have high conc. of WBC as a result of inflammatory processes involving the pleura/lungs
- E.g. pneumonia, malignancies, TB, asbestosis, ARDS, hypothyroidism, pre-existing
pulmonary embolism
2. Transudate
- Fluid in pleural with low conc. of protein
- E.g. congestive heart failure, nephrotic syndrome, liver cirrhosis, nephrotic syndrome, liver
cirrhosis, low serum albumin

Other cause of fluid accumulation in pleural space

- Mesothelioma → rare type of tumour cased by asbestos exposure

- Found near surface of lung, affecting pleural and cause pleural effusion
- Empyema → presence of pus
- Haemothorax → presence of blood
- Chylothorax → presence of chyle

57
Week 10:
Pneumothorax

Definition
​The presence of air or gas in the cavity between the lungs and the chest wall, causing collapse of
the lung.

Pathophysiology
Primary spontaneous pneumothorax

- This type of pneumothorax is described as primary because it occurs in the absence of lung
disease such as emphysema. Spontaneous means the pneumothorax was not caused by an
injury such as a rib fracture. Primary spontaneous pneumothorax is likely due to the
formation of small sacs of air (blebs) in lung tissue that rupture, causing air to leak into the
pleural space. Air in the pleural space creates pressure on the lung and can lead to its
collapse

Secondary spontaneous pneumothorax

- Secondary spontaneous pneumothorax occurs in patients with underlying pulmonary

disease. It most often results from rupture of a bleb or bulla in patients with severe
chronic obstructive pulmonary disease, HIV-related Pneumocystis jirovecii infection, cystic
fibrosis, or any underlying pulmonary parenchymal disease. Secondary spontaneous
pneumothorax is more serious than primary spontaneous pneumothorax because it
occurs in patients whose underlying lung disease decreases their pulmonary reserve.

Iatrogenic pneumothorax

- Iatrogenic pneumothorax is a traumatic pneumothorax that results from injury to the

pleura, with air introduced into the pleural cavity secondary to diagnostic or therapeutic
medical intervention

Traumatic pneumothorax

58
 - Traumatic pneumothoracies are caused by penetrating or blunt trauma; many patients
also have a hemothorax (hemopneumothorax). In patients with penetrating wounds that
traverse the mediastinum (eg, wounds medial to the nipples or to the scapulae), or with
severe blunt trauma, pneumothorax may be caused by disruption of the tracheobronchial
tree. Air from the pneumothorax may enter the soft tissues of the chest and/or neck
(subcutaneous emphysema), or mediastinum (pneumomediastinum).

Tension pneumothorax

Tension pneumothorax occurs when the air enters into the pleural space but is not able to fully
exit, similar to a one-way valve mechanism through the disrupted pleura or tracheobronchial tree.
During inspiration, a sizeable high-pressure air collection accumulates in the intrapleural space
and is not able to completely exit during expiration. This will cause the lung to collapse on the
ipsilateral side. As the pressure increases, it will cause the mediastinum to shift towards the
contralateral side, contributing further to hypoxemia. In severe cases, the increased pressure can
also compress the heart, the contralateral lung, and the vasculature leading to hemodynamic
instability. This is due to impaired cardiac filling and reduced venous return. Hypoxemia also
triggers pulmonary vasoconstriction and increases pulmonary vascular resistance. As a result,
hypoxemia, acidosis, and decreased cardiac output can lead to cardiac arrest and, ultimately,
death if the tension pneumothorax is not managed in a timely fashion

Hemopneumothorax

Hemopneumothorax or less commonly haematopneumothorax or pneumohemothorax, is a term

given when there is concurrent presence of a hemothorax (presence of blood in the pleural
space) and pneumothorax (presence of air in the pleural space)

Hemopneumothorax is typically seen in the setting of trauma (traumatic hemopneumothorax) and

thoracic intervention (e.g., insertion of pacemakers, or in cases of pneumonectomy).

Clinical features
Pneumothorax

- Sharp, stabbing chest pain that worsens when trying to breath in.
- Shortness of breath.
- Bluish skin caused by a lack of oxygen.
- Fatigue.
- Rapid breathing and heartbeat.
- A dry, hacking cough.

59
Tension Pneumothorax

- SOB
- Acute chest pain
- Decreased BP
- Decreased SPO2
- Increased HR

Management
Pneumothorax without tension

- Supportive cares
- Treat symptomatically
- Prepare for deterioration

Tension pneumothorax

- Decompress chest on side of tension

Other key features

Blebs and bullae

- Blister-like air pockets that form on the surface of the lung.

- Bulla (or Bullae for plural): air-filled cavities within the lung tissue.
- Caused by underlying disease process such as emphysema / chronic obstructive
pulmonary disease.
- But also (blebs in particular) may also be found in young, healthy people with no other
medical issues (smoking, and smoking cannabis have been implicated in the
development of spontaneous pneumothorax in young (otherwise healthy) patients.) •
- Bullae, or are more commonly associated with chronic disease processes such as chronic
obstructive pulmonary disease (emphysema).
- Blebs may be present on an individual's lung (or lungs) for a long time before they rupture.
Many things can cause a bleb to rupture, such as changes in air pressure or a very
sudden deep breath

60
Week 6:
Sepsis

Definition
Sepsis (organ dysfunction + infection):

Life threatening organ dysfunction caused by dysregulated host response to infection

Septic shock (shock + infection):

A subset of sepsis with profound circulatory, cellular and metabolic abnormalities

Pathophysiology
No single pathophysiology. However, sepsis results when an infectious insult triggers a localised
inflammatory response then spills over to cause systemic symptoms of fever or hypothermia,
tachycardia, tachypnoea and either leukocytosis or leukpenia

Clinical features
Adult:

High risk:

- RR >25
- SBP <90mmHg (or a drop > 40 mmHg from normal)
- HR =/> 130bpm
- Need O2 to maintain SpO2 >92%
- Non-blanching rash/mottled/ashen/cyanotic
- ALOC
- Recent chemotherapy
- Anuria in lst 18 hrs OR significantly reduced urine output

Moderate risk:

61
 - RR 21-24
- SBP 90 - 99 mmHg
- HR 90 - 129 bpm or new dysrhythmia
- Temp < 35.5 or >38.4
- Anuria in last 12 - 18 hrs OR significantly reduced urine output
- Acute deterioration in functional ability

Paed:

High risk:

- Severe tachycardia or bradycardia

- Severe resp. distress/tachypnoea/apnea
- Needs O2 to maintain SpO2 >92%
- Hypothermia
- Non-blanching rash/mottled/ashen/cyanotic
- ALOC

Moderate risk:

- Moderate tachycardia
- Moderate Resp. distress/tachypnoea
- Cap refill >/= 3 sec
- Hypoglycaemia
- Unexplained pain or restlessness
- Pale or flushed/mottled/cold extremities
- Reduced urine output

Management
- Oxygen
- Antipyretic
- IV/IO access
- IV/IO fluids

62
63
Other key features

64
Week 11:
FBAO

Definition
FBAO → when the individual has inhaled a foreign object, causing either:

- Complete obstruction → can lead to hypoxia, and cardiac arrest

- Pt inable to talk, cough, breath; apnoea present; paradoxical respiration noted
- Partial obstruction → present with cough, wheeze, stridor and dyspnoea; or may be
asymptoamtic
- Breathing maintained

2 categories of FBAO

- Long-standing FB (>24 hours)

- Foreign body in bronchus or in more distal airway
- Pt often mismanaged as asthma/pneumonia
- Often develop secondary consequence, such as chronic cough, wheeze,
consolidation, infection distal to obstruction
- Acute presentation (<24 hours)
- Undistressed child → suspected when cough develops after a witnessed choke.
Pt saturate well, but may have wheeszse and/or hyperinflation / suspected
collapse in area
- Risk of FB dislodgement → pt may become distressed
- Acutely distressed → present with respiratory distress, wheezing, stridor,
tachypnoea, subcosta/intercostal recession, tracheal tugging,
consolidation/hyperinflation
- Complete obstruction / emergency → acutely choking

Pathophysiology
Type of FB obstruction

65
 1. By-pass valve
- FB partially obstruct inspiration and expiration
- Initially result in expiratory wheeze, then inspiratory & expiratory wheeze
- Local oedema may also occur, due to damage to lining of the airway from obstruction
2. Check-valve
- FB allows air to be inhaled distally, but cannot pass during exhalation
- This causes hyperinflation of distal lob, emphysema, tension pneumothorax
3. Stop valve
- Complete obstruction in distal airway
- Consequence → resultant collapse and consolidation of distal lobe
4. Ball Valve
- Air can be exhaled but not inhaled
- Consequence → collapse of broncho-pulmonary segment beyond the foreign body

Laryngospasm → sustained closure of vocal cords resulting in partial/complete loss of pt airway

- High-pitched inspiratory stridor

- Suspected when airway obstruction occurs
- In prehospital setting → pt with decreased ALOC, increased sputum production, vomiting,
sedating (esp. ketamin), children
- Complications → hypoxia, bradycardia, negative pressure pulmonary oedema, ischemic
end organ injury, death

66
Clinical features
- Note → only ⅓ of pt with aspirated foreign body have classic triad of cough, wheeze &
decreased breath sounds

Complete

- No chest wall movement with no breath sound on auscultation

- No stridor / airway sound
- Sudden loss of CO2 waveform
- Inability to manually ventilate
- Inability to talk, cough, breath
- Apnoea and cyanosis present
- Pt present as acute choking
- Asphyxia → leading to reduced level of consciousness

Incomplete

- Ability to breath is maintained

- Hallmark features → Inspiratory stridor and increased WOB
- Respiratory distress
- Wheezing
- Stridor
- Tachypnoea
- Subcostal / intercostal recession
- Tracheal tugging
- Consolidation / hyperinflation / air trapping

67
Management

Other key features

68
Adrenaline
Indications
- Cardiac arres
- Anaphylaxis OR severe allergic reaction
- Severe life-threatening bronchospasm OR silent chest (pt must only be able to speak in
single words AND/OR have haemodynamic compromise AND/OR ALOC
- Shock unresponsive to adequate fluid resuscitation
- Bradycardia with poor perfusion (unresponsive to atropine AND/OR transcutaneous
pacing)
- Croup (moderate to severe)

Contraindications
- Nil

Precautions
- Hypertension
- Hypovolaemic shock
- Concurrent MAOI therapy
- Quetiapine toxicity

Side effects
- Anxiety
- Hypertension
- Palpitations/tachyarrythmias
- Pupil dilation
- Tremor

Dose

Route Adult Paed

Anaphylaxis

IM 500mcg (repeated 5 min) 6 years or older - 300mxg

69
 1 year - < 6yrs - 150mcg
6 month - < 1yr - 100mcg
<6 months - 50mcg
(repeated at 5 min)

NEB 5mg (single dose, after 3x IM 5mg (single dose, after 3x IM adrenaline)
adrenaline)

Severe life-threatening bronchospasms

IM 500mg (repeated 5 min) 6 years or older - 300mxg

1 year - < 6yrs - 150mcg
6 month - < 1yr - 100mcg
<6 months - 50mcg
(repeated at 5 min)

Croup

NEB 5mg (single dose)

70
Dexamethasone
Indications
- Croup

Contraindications
- Allergy AND/OR ADR
- Children < 6 months or > 6 years (consultation required)
- Steroid administration within 4 hours

Precautions
- Nil

Side effects
- Nil

Dose

Route Paed

PO 6 months - 6 years - 0.3 mg/kg (rounded to nearest 0.5mL)

Weight `Volume (8mg/2mL presentation)

> 5 - 10 kg 0.5 mL

> 10 - 15 kg 1.0 mL

> 15 kg 1.5 mL

May be repeated once to ensure desired dose for resistant children (e.g. spat out)
Total MAX 0.6mg/kg (or 12 mg)

71
Hydrocortisone
Indications
- Asthma (excluding mild)
- Acute exacerbation of COPD (with resp. distress)
- Refractory anaphylaxis with persistant wheeze (unresponsive to 3x IM adrenaline)
- Suspected, or at risk of, acute adrenal insufficiency (adrenal crisis)

Contraindications
- Allergy AND/OR ADR

Precautions
- Hypertension

Side effects
- Nil

Dose

Route Adult Paed

- Asthma
- Acute exacerbation of COPD

IM 100mg (singe dose) 4mg/kg (single dose, not to exceed 100mg)

IV 100mg (single dose, over 1 min) 4mg/kg (single dose, over 1 min, not to
exceed 100mg)

Refractory anaphylaxis with persistent wheeze (after 3x IM adrenaline)

IM 200 mg (single dose) 4mg/kg (single dose, not to exceed 100mg)

IV 200 mg (single dose, over 1 min) 4mg/kg (single dose, over 1 min, not to
exceed 100mg)

Adrenal Crisis

IM 100mg (single dose) 0-4 years - 25mg

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 5-10 yrs - 50mg
>10 yrs - 100mg
(single dose)

IV 100mg (single dose) 0-4 years - 25mg

5-10 yrs - 50mg
>10 yrs - 100mg
(single dose, over 1 min)

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Ipratropium Bromide
Indications
- Moderate bronchospasm (unresponsive to initial QAS salbutamol NEB)
- Severe bronchospasm

Contraindications
- Allergy AND/OR ADR
- Patient < 1 year

Precautions
- Glaucoma

Side effects
- Dilated pupils
- Dry mouth
- Palpitations

Dose

Route Adult Paed

- Moderate bronchospasm
- Severe bronchospasm

NEB 500mcg (repeated at 20 min >/= 6 yrs - 500mcg (repeated 20 min intervals)
intervals) Total MAX 1.5mg
Total max dose - 1.5mg
1 - 5 yrs - 250mcg (repeated 20 min)
Total MAX 750mcg

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Salbutamol
Indications
- Bronchospasm
- Suspected hyperkalaemia (with QRS widening AND/OR AV dissociation)

Contraindications
- Allergy AND/OR ADR
- Patients < 1 year

Precautions
- APO
- Ischaemic heart disease

Side effects
- Anxiety
- Tachyarrhythmias
- Tremors
- Hypokalaemia

Dose

Route Adult Paed

Bronchospasm

MDI 12 (1.2mg) MDI inhalations (repeat at 1 - 5 yrs - 6 (600mcg) MDI inhalations

10 min) >/= 6 yrs - 12 (1.2mg) MDI inhalations
(repeated at 10 min)

NEB 5mg (PRN) 1 - 5 yrs - 2.5mg

>/= 6 yrs - 5mg
(PRN)

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