Respiration Flashcards
(133 cards)
1
Q
effect of removal on breathing
A
cortex and pons: slow gasping breaths
medulla: breathing stops
2
Q
expiratory neurons
A
inhibit inspiratory neurones.
inspiratory neurones activate expiratory neurones
3
Q
lung receptors
A
c fibre endings, afferent nerve fibres carried in vagus
4
Q
chemoreceptors
A
central = fast response to arterial pO2 on surface of medulla , arterial pCO2, arterial {H+} and peripheral pCO2
5
Q
Slowly Adapting Receptors (SARs)
A
aka stretch receptors, mechanoreceptors situated close to airway smooth muscle, stimulated by stretching of airway walls during inspiration, help inititate expiration and prevent overinflation. afferent fibres= myelinated
6
Q
rapidly adapting receptors (RARs)
A
aka irritant receptors, located airway epitheloim, respond to rapid inflation, smoke, dust , RARs in trachea initiate cough, mucus, bronchocontricition
myelinated
7
Q
C-fibre endings
A
unmyelinated nerve endings, stimulated by increased interstitial fluid (oedema) and inflammatory mediators
8
Q
hypoxia and co2 buildup
A
common in copd patients, leads to chronic hypercapnia, loss of sensitivity of central chemoreceptors. ig given o2 abolishes drive to breathe as has become controlled by hypoxia
9
Q
drug respiratory depressants
A
anaesthetics, opiod analgesics, sedatives
10
Q
drug respiratoy stumlants
A
doxapram, b2 agonsits aka bronchodilators
11
Q
regulation of breathinh
A
Midbrain neural activity stimulates breathing during
wakefulness (“wakefulness drive to breathe”)
During sleep:
• Respiratory drive decreases (loss of wakefulness drive)
– reduction in metabolic rate
– reduced input from higher centres such as pons and cortex
12
Q
upper airway muscle activity
A
phasic: contraction of upper airway muscles, opening of upper airway, facilitates inward flow
tonic: continous background activity, maintains airway
during sleep loss of tonic activity
apnoea= cessation of breathing
13
Q
obstructive sleep apnoea
A
important cause of rtcs
rfs: obesity, alcohol, nasal obstruction `
14
Q
respiratory rhythm originates in medulla
A
hypoxia and hypercapnia feedback via chemoreceptors
15
Q
elastic recoil
A
lung= inward
chest wall= outward
16
Q
inspiration
A
alveolar pressure
17
Q
expiration
A
Alveolar pressure > atmospheric
18
Q
what causes SOBOE in COPD
A
decreased lung elastic recoil
obstruction, inability to increase tidal volume effectively
19
Q
inspiration is active
A
expiration is passive ( recoil)
20
Q
breathing disrupted by
A
airflow obstruction - copd and asthma
weakness of expiratory muscles (MND. advanced respiratory disease, diaphragm failure)
lung tissue damage (emphysema)
thoracis cage disorders ( ankylosing spondylitis, kyphoscoliosis)
21
Q
dalton’s LAW
A
gases in a mixture exert pressures that are independant of each other
22
Q
henry’s law
A
the concentration o a fissolved gas is dirctly proportional to its partial pressure
23
Q
nitrogen in blood
A
high atmospheric content, low water solublility, under high pressure has an anasthetic effect, nitrogen narcosis, on reduction of pressure N2 emboli cause local ischaemia - bends
24
Q
2,3 -bisphosphoglcerate
A
binds to deoxy-Hb and lowers Hb affinity for o2 imroving o2 delivery to tu=issues
foetal Hb has a lower affinity for 2,3 BPG so has a higher oxygen affinity than Hba
25
Haemoglobin
A tetramer: 2 alpha and 2 beta subunits
Each subunit has a Haem group
• A porphyrin with a central Ferrous atom: binds O2
• Combines loosely with Oxygen
• Combination alters its shape and charge
26
Oxygen/Hb Dissociation
The affinity of binding O2 increases with each successively bound O2
molecule: Allosteric Effect
• Once bound a number of factors can change the ability of Hb to take
up and liberate oxygens
• Ultimately we want Hb to take up O2 in the lung and liberate O2 at
the tissues (muscles)
27
in practice
nearly all the oxygen carried in the blood is bound to haemoglobin
28
Partial pressure of oxygen PO2
| kPa
```
Gas exchange is driven
by partial pressure
• Partial pressure of
oxygen in the alveolus
equals the partial
pressure in the blood
draining the alveolu
The partial pressure of
oxygen in mixed
alveolar gas is higher
than that of arterial
blood
• This is due to shunting
```
29
shunting
```
To move something from
one place to another,
usually because that thing is
not wanted, without
considering any unpleasant
effects
Anatomical shunts
• A small amount of arterial blood doesn’t
come from the lung (Thebesian veins)
• A small amount of blood goes through
without seeing gas (bronchial circulation)
• Physiological shunts (V) and alveolar
dead space (Q)
• Not all lung units have the same ratio of
ventilation (V) to blood flow (Q)
• V/Q mismatch
```
30
Summary
Gas exchange allows oxygen into blood and CO2 out
• The passage of oxygen to the blood is by diffusion
• The carriage of oxygen is mainly performed by Hb
• The level of oxygen in the blood is roughly the same as that in the
alveolus in health
31
What causes a low level of oxygen in the blood?
Hypoventilation
• Hypoventilation allows less air (and oxygen) to enter the alveoli so
less oxygen available to the blood
• Decreased environmental oxygen e.g. altitude
• A problem with the alveolar/capillary membrane
• Miss-match of ventilation and perfusion (next lecture)
32
What can increase the partial pressure of oxygen?
Hyperventilation
| • Administration of oxygen
33
Increase in available PO2
| in healthy state
• At a normal PO2
, blood carries nearly as much oxygen as it
possibly can
• Therefore increasing the PO2 has very little effect on the
oxygen content
• However in disease oxygen therapy is a key intervention
34
CO2 changes dynamically with hyper and
| hypoventilation
whilst o2 stays fairly constant
35
Normal” V/Q mismatch
```
• Less airflow and blood flow at
the top of the lung but V>Q =
high V/Q
• Middle of lung V/Q normal
• Bottom of lung more ventilation
and more blood flow but V
```
36
Increased V/Q Ratio
```
Lots of ventilation to
alveoli, not much blood
• Alveoli and blood reach
an equilibrium which is
closer to air
• PO2
is therefore higher
• (and PCO2
is lower)`
```
37
Low V/Q ratio
```
Less ventilation to alveoli,
lots of blood
• Alveoli and blood reach an
equilibrium which is closer
to venous blood
• PO2
is therefore lower (and
PCO2
is higher)
```
38
Physiological Dead Space
Physiological Dead Space
39
V/Q mismatch
```
Calculate the expected alveolar
PO2 (PAO2
) using the alveolar gas
equation
• Compare with the measured
arterial PO2 (PaO2
)
• If PAO2 = PaO2 then no mismatch
```
40
A-a Gradient
```
Tells us the difference between
alveolar and arterial oxygen
level
• Can help to diagnose the cause
of hypoxaemia
• High A-a gradient
• Problem with gas diffusion
• V/Q mismatch
• Right to left shunt
```
41
CO2 is mostly dissolved in blood
o2 bound to hb
42
Won’t breathe: control failure
Brain failure to command e.g. drug overdose
43
Can’t breathe: broken peripheral mechanism
* Nerves not working e.g. phrenic nerve palsy
* Muscles not working e.g. muscular dystrophy
* Chest can’t move e.g. severe scoliosis
* Gas can’t get in and out e.g. asthma/COPD
44
Type 2 respiratory failure
```
Decrease in PO2
• Increase in PCO2
• Common causes in hospital:
• Severe COPD (can be acute or chronic)
• Acute Severe Asthma
• Pulmonary Oedema in acute Left Ventricular failure
• Due to hypoventilation as main feature
```
Give oxygen
• Controlled in COPD patients with chronic respiratory failure
• Treat the underlying cause to reverse hypoventilation e.g.
bronchodilators for acute asthma or opiate antagonists for overdoses
• Support ventilation
• Non-invasive ventilation
• Invasive ventilation
45
What causes V/Q mismatch?
```
Most lung diseases effecting
the airways and parenchyma
• Lung infection such as
pneumonia
• Bronchial narrowing such as
asthma and COPD (although
they can also progress to
type 2 resp failure)
• Interstitial lung disease
• Acute lung injury (COVID)
Pneumonia causes mismatch
```
46
What happens to arterial CO2 in V/Q mismatch?
• Blood leaving areas of low V/Q ratio has
• Low PaO2
• High PaCO2
• High PaCO2 stimulates ventilation
• ‘Extra’ ventilation goes to areas of normal
lung and areas with high V/Q ratio so get
blood with low CO2
• Blood from both areas mixes so overall
CO2
is normal
47
What happens to arterial O2 In V/Q mismatch
```
• Blood leaving areas of low V/Q ratio has
• Low PaO2
• High PaCO2
• High PaCO2 stimulates ventilation
• ‘Extra’ ventilation goes to areas of normal
lung and areas with high V/Q ratio
• But extra ventilation can’t push O2
content much higher than normal
• Blood from both areas mixes but cannot
overcome the low oxygen level
```
48
How do we treat respiratory failure
Give Oxygen
| • Treat the underlying cause
49
V/Q mismatch due to perfusion
| problems
Pulmonary embolism
• Can range form small PTE causing no problem with gas exchange
ranging to massive PE with hypoxia
• Emboli effectively cause areas of dead space where there is
ventilation but no perfusion causing hypoxia
• Massive emboli can cause circulatory failure and death
50
Treatment of Pulmonary Emboli
Oxygen in acute episode
• Anticoagulation to stop further clot propagation
• Thrombolysis in some cases where circulatory compromise
51
Asthma and Respiratory Failure
```
Hypoxaemia suggests significant
asthma attack
• Bronchospasm and mucous plugging
causes ventilation defects and V/Q
miss match
• Type 2 resp failure develops when
severe bronchospasm causes
hypoventilation of alveoli or
exhaustion
• The patient needs oxygen to survive
• Invasive ventilation may be required
```
52
COPD and Respiratory Failure
```
• COPD is a mixture of chronic airways
inflammation and narrowing and
emphysema
• Problems with V/Q mismatch and
hypoventilation
• May present acutely with respiratory
failure type 1 or type 2
• May have chronic type 2 respiratory
failure in advanced disease
• Treat respiratory failure with oxygen
but with caution in chronic type 2
respiratory failure
```
53
Masks
```
Variable performance
• Cheap and cheerful
• Exact inspired O2
concentration not known
• Fixed function
• Constant, known inspired concentration
• Reservoir mask
• High inspired concentration of O2
Controlled oxygen therapy: Venturi Mask`
```
54
How do we quantify oxygen carriage?
```
Haemoglobin saturation
• Because it’s very easy to do!
• Assuming Hb is normal, it’s an accurate reflection of oxygen content
2. Arterial blood gases
• More complicated and invasive
• PaO2
reflects haemoglobin saturation but is a measure of the partial
pressure of O2
in the blood
```
55
Carbon monoxide poisoning
Carbon monoxide binds to haemoglobin in the place of oxygen to
form carboxyhaemoglobin
• (also interfers with mitochondrial respiration)
• Death by asphyxia
• Treatment is high concentration oxygen (to displace the CO from the
haemoglobin)
56
Type 1 Respiratory Failure
```
Low PaO2
• Normal (or low) CO2
• Caused by V/Q mismatch
decreasing adequate gas
exchange
• e.g. Pneumonia
Lung diseases effecting the parenchyma
• Interstitial lung disease
• Bronchiectasis
• Obstructive airways disease e.g. asthma and COPD (but these can also
cause type 2 RF)
• Pulmonary embolism
• Treat with oxygen whilst treating underlying cause
```
57
Type 2 Respiratory Failure
```
• Low PaO2
• High PaCO2
• Caused by hypoventilation
• May be acute or chronic
• If acute will have respiratory
acidosis
Low oxygen level due to
hypoventilation of (diseased)
lungs
• High CO2 due to increased levels
in alveolar space and less
removed from blood
• Acute rise in blood CO2 leads to
respiratory acidosis
Hypoventilation due to any cause
• Opiate toxicity
• Neuromuscular disease
• COPD
• Acute severe asthma
• Important to differentiate acute from chronic type 2 resp failure
```
58
Acute hypoventilation e.g. due to opiate toxicity leads to hypoxia,
hypercapnia and acidosis
• Chronic hypoventilation e.g. neuromuscular disease or severe COPD
leads to hypoxia and hypercapnia but may not have acidosis due to
compensation
59
Respiratory Alkalosis
Not usually associated with
respiratory failure
• Caused by hyperventilation
• Have low PCO2 and low H
60
Metabolic acidosis
usually a sign of a sick patient
• Excess acid production by the body e.g. lactic acidosis or
diabetic ketoacidosis
• Kussmal breathing is a classical clinical sign of acidosis as a
compensatory mechanism to increase CO2 removal from the
blood
• Full compensation is difficult: need to treat the underlying
cause of increased acid load e.g. treatment of DKA
61
Interpreting bicarbonate
```
Actual bicarbonate:
• Calculated with actual H+ and pCO2
values
• Standard bicarbonate:
• Calculated with actual H+ and a pCO2 of 5.3kPa (normal pCO2
)
• Standard bicarbonate is therefore only influenced by metabolic
effects
```
62
Base excess
The amount of base needed to be removed from a litre of blood
at a normal pCO2
in order to bring the H+ back to normal
• Sounds complicated but it’s not:
• It is calculated with a normal CO2
, so it only looks at the
metabolic component
• Normal value is zero (-2 to 2 mmol/l)
• A big negative value indicates a metabolic acidosis
• A positive value seen in compensated respiratory acidosis
63
high fever,
myalgia, sore throat and dry cough x24h
• On exam she has Temperature (T)= 39.1°C,
Pulse rate (PR)=88 beats per minute (bpm)
and respiratory rate (RR) 18/min.
flushed.
• Pharynx mild erythema.
• Chest occasional crackles on auscultation
```
Viral illnesses;
Rhinoviruses (45-50%)
² Influenza A virus (25-30%)
Usually transient
• Complications sinusitis, pharyngitis, otitis
media, bronchitis, rarely pneumonia
• May lead to bacterial super-infection
• Influenza A virus in particular causes systemic
symptoms
```
64
```
A 74 year old man
previously well apart from
obesity and hypertension.
• Developed fever, cough
and loss of smell 10 days
ago.
• In last 2 days has become
increasingly short of
breath.
• O2 saturations 86%,
requiring 60% oxygen to
maintain staturations at
93%
```
Emerging respiratory virus infections
SARS-CoV-2
(MERS-nCV)
65
```
A 19 year old presents
with sore throat x 24
• He has noted tender
glands in the neck
• T 38.5°C, VS stable
• Large tonsils with
exudate
• Tender anterior
cervical LN
```
```
Pharyngitis
Viral
Streptococcus pyogenes,
Glandular fever Epstein Barr virus
Acute HIV infection
```
66
A 48 year old housewife presents with fever,
facial pain and purulent nasal discharge
• She has no fever but complains of pain in the left
ear and into the teeth
• She has seen her dentist who has found no dental
problems
• She has has cold 10 days ago and has had the
facial pain for a week
• She has a past history of allergic rhinitis and uses
a steroid nasal spray
```
Sinusitis
Usually viral (as per causes URI)
• Bacterial sinusitis (distinguish these from the
viral cases to avoid inappropriate
antimicrobial use)
Streptococcus pneumoniae (40%),
• Haemophilus influenzae (30-35%)
• Other Moraxella catarrhalis
Complications brain abscess, sinus vein
thrombosis, orbital cellulitis
```
67
A 45 year old African woman presents with
sore throat and pain on swallowing
(‘odynophagia’)
• She is febrile, sitting in an erect position and
makes a high pitched wheezing noise when
she breathes in (‘inspiratory stridor’)
• She has been unwell for the last 6 months and
complains of fatigue, weight loss and
diarrhoea with oral thrush
```
Acute epiglottitis
• Formerly an illness of children 2-4
year old who presented with fever,
dysphagia, drooling and stridor
• Caused by Haemophilus infuenzae
type B (Hib) but now rare due to
use of Hib vaccine
• Adults can also have disease.
²Most severe due to Haemophilus
influenzae
²also from causes of pharyngitis, other
bacterial infections of airway
²Additional pathogens in
immunocompromised e.g. AIDS
```
68
```
A 23 year old mother with a 4
month old child presents with a
chronic cough
• She has had a cough for four
weeks and gets bouts of
coughing during which she
occasionally vomits
• Denies fever or weight loss • On exam afebrile and vitals
stable. Sub
-conjunctival
haemorrhage but lungs clear to
auscultation
```
Bordatella pertussis
Adults chronic cough, paroxysms of coughing and 50% post
ptussive vomitting but fairly specific for pertussis
• Complications; pneumonia, encephalopathy,
subconjunctival haemorrhage
69
A 3 year old presents to casualty with his
mother
• He has a prominent barking cough and is
crying
• O/E febrile, RR40, cyanosed with prominent
intercostal recessions
• Has inspiratory stridor (a high pitched
wheezing noise due to turbulent airflow in
upper airway
Croup
• Acute laryngo-treacheobronchitis
• A disease of children , 6 yo , most 3mo-3
years)
• Mainly due to Parainfluenza viruses, ( also
RSV, IAV and other respiratory viruses)
70
```
A 3 month old child is admitted from casualty
with severe respiratory distress
• O/E O2 saturations 88%
• RR 40, respiratory retractions
• Widespread crackles and wheeze
• The baby has a history of being born
premature at 28 weeks gestation.
```
```
Bronchiolitis
infections due to
Respiratory syncytial
virus (RSV) (80%)
(rarely other viruses)
• Inflammation of
bronchioles and mucus
production cause
airway obstruction
```
71
Bronchitis
Aetiology:
Ø Frequently viral
Ø May be bacterial including Haemophilus influenzae or Streptococcus pneumoniae,
Moraxella catarrhalis, Mycoplasma pneumoniae
• Clinical Features:
Ø Cough may be productive or non-productive
Ø SOB and often wheeze
Ø May be fever but not systemic features of infection
Ø Wheeze but no signs of focal consolidation
• May cause acute exacerbations of COPD or asthma with increased wheeze
• Investigations:
Ø Arterial blood gas/oximetry for those with chronic lung disease-helps determine if need
hospitalisation
Ø CXR shows no features of pneumonia, usually normal
• Treatment:
Ø Usually none especially if viral, sometimes antimicrobials
Ø Manage exacerbation of COPD/asthma with steroids and increased inhalers
72
Bronchiectasis
Abnormal dilatation of airways and
suppurative infection
• Chronic scarring of lung with excessive sputum
production (‘bronchorrhoea’)
• Aetiology
üCongenital; Cystic fibrosis, ciliary dysfunction,
hypogammaglobulinemia
üPost-infectious; TB, suppurative pneumonia, measles ,
whooping cough
Other; Foreign body
```
Symptoms
üChronic cough
üCopius sputum
üRecurrent pneumonia
ü Weight loss
• O/E
üClubbing
üCoarse ‘wet’ crackles
• Can be complicated by
haemoptysis
```
73
```
A 33 year old soldier
presents with a 3 day
history of dry cough and
shortness of breath
• O/E T 38.6°, PR 84, BP
114/76mm/Hg, RR=28
• O2 sat 95%
• Dull Right mid lung,
coarse crackles
• WBC 7K
```
Pneumonia
• Streptococcus pneumoniae (40%)
• Mycoplasma pneumoniae (~10% peaks in epidemic
seasons)
• Chlamydophila pneumoniae (~10%)
• Legionella pneumophila and other spp.(<5%)
• Haemophilus influenzae (<5%)
• Klebsiella pneumoniae (rare; homeless and in hospital)
• Staphylococcus aureus (low % in community but
increased after influenza and in hospital especially)
• Viruses (≥10%)
74
Community Acquired Pneumonia
| CAP
```
Incidence 5-11 per 1,000
• 20-50% Hospitalised, 5-10% require ITU
• Mortality 1% community, 10% in hospital, 30%
ITU
• Hospitalisation 6-8 days
• Costs > £400 millions/ year to the UK
• Significant short and long term mortality from
other causes after pneumonia
```
75
S. pneumoniae
any age but increases at extremes of age
| ücan be severely ill with respiratory failure or sepsis
76
Mycoplasma pneumoniae
usually younger adult, milder illness
ümay have extrapulmonary features; haemolytic anaemia
(cold agglutinins),Raynauds (cold agglutinins) erythema
multiforme, bullous myringitis (blisters on tympanic
membrane), encephalitis
77
Chlamydophila pneumoniae
like M. pneumoniae, maybe older age group more
| prolonged wheezing
78
Pneumonia
Extra-pulmonary features;
Ødiarrhoea,
Øabnormal liver function tests,
Øhyponatremia,
Ømyalgia, raised creatinine kinase,
Øinterstitial nephritis,
Øencephailitis, confusion
eatment
• Prompt but appropriate initiation of antimicrobials;
ideally establish diagnosis and start treatment ≤4h
• Use narrowest spectrum to stop spread of resistance,
MRSA acquisition and Clostridium difficile inf
79
A 52 year old man is admitted with a three
month history of cough, weight loss and night
sweats
• T 37.8°C, PR 80, BP 112/60, RR18
• Cachectic
• Coarse crackles and reduced air entry right
upper lobe
Tuberculosis
• Chronic respiratory tract infection (can also be extrapulmonary), usually due to reactivation of
latent infection.
• Specific epidemiological groups e.g.
ü exposed to a case
ü born in country of high incidence,
ü homeless,
ü alcoholic HIV infection, anti-TNF treatment
• Clinical features;
ü Cough, hemoptysis, short of breath
ü weight loss, fever, night sweats,
ü swollen lymph nodes or other extrapulmonary features
• Multiple radiological appearances but
ü upper lobe disease with cavities,
ü pleural disease,
ü multiple tiny nodules (‘miliary’),
ü lymphadenopathy in chest
• and failure to resolve with routine antibiotics all suggestive
Patients require isolation if admitted as may be highly infectious to others
80
Obstructive Lung Diseases
```
Asthma
• Chronic Obstructive Pulmonary Disease (COPD)
• Causing obstructive picture
• Bronchiectasis
• Cystic Fibrosis
```
81
Factors Affecting Airway Internal Diameter
Increased mucus production
• Anatomical features
• Autonomic and Non-Adrenergic/Non-Cholinergic (NANC) systems
• Inflammation
82
How do we measure obstruction
Peak flow
• Spirometry
• Lung Volumes and flow
83
Peak Flow
```
Peak expiratory flow rate (PEFR)
• Measures maximum speed of
expiration
• Crude measurement of
conducting airway flow
• Can aid in Asthma
diagnosis/management
• Excellent bedside and patient
based tool
```
84
FEV1
How much can the patient exhale in a given time, e.g. 1
| second:
85
FVC
How much they can exhale altogether:
86
Ratio of FEV1
| to FVC
Useful to differentiate between obstruction and restriction
• If less that 0.7 then suggests obstructive airways pathology
• In mild obstruction biggest impact on FEV1
• In severe obstruction also lose FVC
87
Reversibility of spirometry
Used as a diagnostic test in Asthma e.g. following bronchodilator
• Asthma reversible vs. COPD fixed airways obstruction
• Can also use bronchial challenge agents (histamine) to induce
bronchospasm and obstructive spirometry
88
Localised Airway Obstruction
Airway obstruction
• Lesion outside the wall e.g. large lymph node
• Lesion in the wall e.g. tumour
• Lesion in the lumen e.g. foreign body
• Causes distal collapse or over-inflation
• May be distal lipid or infective pneumonia
• Normal pulmonary function tests
89
Diffuse Obstructive Airways Disease
```
Reversible and intermittent OR Irreversible and
persistent
• Centred on bronchi and bronchioles
• Diffuse disease as many airways involved
• Pulmonary function tests ‘obstructive’
• Reduced vital capacity (VC)
• Reduced FEV1 / FVC ratio
• Reduced peak expiratory flow rate
Several clinico-pathological entities
• Chronic bronchitis
• Emphysema
• Asthma
• (Bronchiectasis)
• Chronic obstructive pulmonary disease (COPD)
• Spectrum of co-existence of chronic bronchitis and
emphysema
```
90
Host Defences
```
Defences
• Cough reflex
• Cilia
• Mucus
• Antibody deficiency e.g. IgA
• Immunosuppression - disease, drugs
• Macrophage dysfunction
• Pulmonary oedema
```
91
Chronic Bronchitis
```
Clinical definition
• Cough and sputum for 3 months in 2 consecutive
years
• Aetiology - pollution, smoking
• Clinical
• Middle-aged heavy smokers
• Recurrent low-grade bronchial infections (exacerbations)
• H. influenzae, S. pneumoniae, viruses
• Airway obstruction may be partially reversible
Progression of disease
• Hypercapnia
• Hypoxia
• Pulmonary hypertension
•
‘Cor pulmonale’ - right ventricular failure
• ‘Blue bloater’
```
92
Emphysema
• Irreversible dilatation of acinar spaces with
destruction of walls
• Traditional definition confined to alveoli but often
extended to include respiratory bronchioles
• Associated with loss of surface area for gas
exchange
Strongly associated with smoking
• Seen in some with pneumoconiosis, particularly
coal-workers
• Most commonly in upper lobes
• Respiratory bronchiolitis often present
Paraseptal
• Distension adjacent to pleural surfaces
• May be associated with scarring
• Irregular
• Associated with scarring
• Overlap with paraseptal emphysema
• Others
• Bullous: distended areas >10mm
• Interstitial
Clinical features
• Hyperventilation
• Normal pO2, pCO2
• ‘Pink puffer’
• Weight loss
• Right ventricular failure
• Often co-existing chronic bronchitis, in which case
clinical features are mixed
93
Chronic Obstructive Pulmonary Disease
• A combination of the features of chronic bronchitis
and emphysema
• Most patients exhibit a mixture of features
• Typically assessed using pulmonary function tests
e.g. FEV1/FVC < 0.7 for diagnosis and percent
predicted FEV1 to assess severity
FEV1 – forced expiratory volume in 1 second
FVC – forced vital capacity
94
Asthma
```
Reversible wheezy dyspnoea’
• Increased irritability of the bronchial tree with
paroxysmal airway narrowing
• Five aetiological categories
• Atopic
• Non-atopic
• Aspirin-induced
• Occupational
• Allergic bronchopulmonary aspergillosis (ABPA)
```
Asthma can lead to
sudden death due to
mucus plugging
95
Atopic Asthma
Associated with allergy
• Triggered by a variety of factors
• Dust, pollen, house dust mite etc etc
• Often associated with eczema and hay fever
• Bronchoconstriction mediated by a type I
hypersensitivity reaction
Hypersensitivity reaction leads to:
• Bronchial obstruction with distal overinflation or
collapse
• Mucus plugging of bronchi
• Bronchial inflammation
• Mucous gland hypertrophy
• Bronchial wall smooth muscle hypertrophy
• Thickening of bronchial basement membranes
96
Non-Atopic Asthma
* Associated with recurrent infections
* Not immunologically mediated
* Skin testing negative
97
Aspirin-induced Asthma
• Associated with recurrent rhinitis, nasal polyps
| and urticaria
98
Occupational Asthma
Hypersensitivity to an inhaled antigen
• May be non-specific in those with hyper-reactive
airways
• May be a specific allergic response
99
Hypersensitivity to an inhaled antigen
• May be non-specific in those with hyper-reactive
airways
• May be a specific allergic response
Specific allergic response to the spores of Aspergillus
fumigatus
• Mixed type I and type III hypersensitivity reaction
• Mucus plugs common
• Associated with bronchiectasis
• Not to be confused with an aspergilloma, which is a
fungal ball, usually colonising a pre-existing cavity in
the lung (often tuberculous)
100
Bronchiectasis
• Permanent dilatation of bronchi and bronchioles
• Due to a combination of obstruction and inflammation
(usually infection)
• May be localised or diffuse, depending on cause
• Historically seen in patients with pulmonary
tuberculosis involving hilar lymph nodes
• Classically associated with childhood infections,
particularly measles and whooping cough
• Diffuse bronchiectasis seen in patients with cystic
fibrosis
Clinical features
• Chronic cough productive of copious
sputum
• Finger clubbing
• Complications
• Spread of infection
• Pneumonia, Empyema, Septicaemia, Meningitis,
Metastatic abscesses e.g. brain
• Amyloidosis
• Respiratory failure
101
Defence mechanisms
Immunological
• IgA & antimicrobials in mucus
• Resident alveolar macrophages & dendritic cells
• Innate / adaptive immune responses
102
73 year old woman. Smoker. History of colorectal cancer (right hemicolectomy
2018) and currently undergoing post-op chemotherapy and radiotherapy.
Presents with three day history of shortness of breath, cough and haemoptysis,
pyrexia
Examination: Right basal crepitations
Bloods: WBC 16.2 (neutrophils 14)
Chest x-ray: Right basal consolidation
```
Diagnosis: Pneumonia
Cough
• Sputum
• Pyrexia
• Pleuritic chest pain
• Haemoptysis
• Dyspnoea
• Hypoxia
```
103
Acute respiratory distress syndrome
```
ncidence 10-14/100,000/yr
• Mortality rate ~40%
• Clinical diagnosis
• Hypoxia (PaO2/FiO2 ≤ 300mmHg )
• Non-cardiogenic pulmonary oedema
• Causes
• Direct – pneumonia, aspiration, hyperoxia, ventilation
• Indirect – sepsis, trauma, pancreatitis, acute hepatic failure
```
104
Tuberculosis
```
• Predisposing factors
• Alcoholism
• Diabetes mellitus
• HIV / AIDS
• Some ethnic groups
Treatment
• Socio-economic conditions
• Drugs – triple antibiotic therapy
• Prevention e.g. BCG vaccination
```
105
Tuberculous bronchopneumonia
Infection spreads via bronchi
• Results in diffuse bronchopneumonia
• Well developed granulomas do not form
106
• Miliary Tuberculosis
* Infection spreads via blood-stream
* Organisms scanty
* Multiple organs
* lungs, liver, spleen, kidneys, meninges, brain
107
Complications of Bronchiectasis
```
Local
• Distal airway damage / loss and
lung fibrosis
• Pneumonia
• Pulmonary abscess formation
• Haemoptysis
• Physiological complications
• Respiratory failure
• Cor pulmonale
• Systemic complications
• Metastatic abscess
• Amyloid deposition
```
108
15 year old boy. Long history of productive cough and thick purulent
sputum.
Diagnosis of bronchiectasis on CT scan.
109
• 69 year old retired coal miner. Presents with slowly worsening
shortness of breath, cough and ankle oedema
• CT scan – honeycomb and ground glass changes in both lower lobes
• Restrictive defect on pulmonary function tests
Idiopathic pulmonary fibrosis
110
Acute inflammation
* Pneumonia
| * Neutrophils & macrophages
111
Granulomatous inflammation
Tuberculosis
| • Host pathogen interactions
112
Fibrosing lung diseases
Defective repair mechanisms
| • Failure of clearance
113
OBSTRUCTIVE DISORDER
A disorder in which the radius of an airw
114
RESTRICTIVE DISORDER
A disorder in which prevents normal expansion of the lungs
115
Lung restriction can occur due to:
```
Extra-pulmonary
disease
i.e. visceral pleura,
pleural space, chest
wall including parietal
pleura, bones,
muscles, nerves
scoliosis
asbestos
exposure
myasthenia
gravis
```
```
Intra-pulmonary
disease
i.e. alveoli and surrounding lung tissue
(=parenchyma)
Rheumatoid-lung
Asbestosis
Silicosis in a
pneumoconiosis
stonemason
```
116
COMPLIANCE
This is the measure of distensibility (stretchability) of a tissue
A lung with low compliance means a greater inflation pressure is
required to inflate the lung.
A lung with low compliance generates more elastic recoil i.e. it
deflation is easy
A lung with high compliance means a smaller inflation pressure is
required to inflate the lung
A lung with high compliance generate less elastic recoil i.e.
deflation is hard
117
Surfactant
produced by alveolar Type II cells
• composed of lipids (90%, mainly phospholipids) and proteins (10%)
• reduces surface tension
118
Respiratory Distress Syndrome of the
| Newborn
CAUSE = lack of SURFACTANT
119
Surfactant in adults
```
Adult respiratory distress syndrome (ARDS)
• Pneumonia
• Idiopathic pulmonary fibrosis
• Lung transplant
……
```
120
RISK
HAZARD X EXPOSURE
121
bronchodilators relax smooth muscle dilating airways
most common:
| beta 2 agonists (salbutamol), anticholinergics (ipatropium), methylxanthines (theophyline)
122
corticosteroids
anti-inflammatory drugs normally administered by inhalation (beclometasone) sometimes given by mouth (predinsolone) during disease exacerbations
123
leukotreine receptor antagonists
motelukast inhibit the activity of leukotrienes and have both anti-inflammatory and bronchodilator effects
124
adverse respiratoey function
bronchoconstriction, inflammation, fibrosis, suppress of respiration
125
common bronchoconstrictors
beta blockers, NSAIDs (aspirin, ibuprofen)
| paradoxical bronchospasm caused by inhaled beta 2 agonists occasionally
126
commonest drugs associtaed with interstitial lung disease
antibiotics (nitrofuratonin, anti-rheumatic drugs (bleomycin), anti arrhythmic (amiodarone)
127
respiratory depression
opiod analgesics (morphine, oscydocone) benzodiazepines (diazepam), barbiturates (ethanol and oxygen)
128
beta 2 agonists
activate beta 2 adrenocreptors in bronchial smooth muscle leading to generation of secondary messenger cAMP by adenylate cyclase the commonly used drugs ate short acting salbutamol and long acting salmeterol
129
adverese effects of beta 2 activation
tremor, palpitations, arrhythmias, hyperglycaemia
130
antimuscarinics
antagonise muscarinic M3 receptors and reduce generation of ionsitol triphosphate and availability of calcium ions, commonly given by inhalation and either short acting (ipratropium bromide) or long acting (tiotropium)
131
antimuscarinics
cause drymouth, blurred vision, tachycardia, constipation, urinary retention, glaucoma
132
methylxanthines
theophlline are phosphodiesterase inhibiotrs that reduce breakdown of cAMP and potentiate the activity of beta 2 adrenorecptors they are given by mouth or intravenously n emergenciees
133
theophlines
narrow therapeutic range and significant inter individual variation in pharmaco kinetics drug interactions
