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Other conditions: UK
https://t.me/med1917
DVLA
states it must be informed if a driver suers
from medical conditions including
• Epilepsy (the patient must have had at least two seizures in the last 5yrs). An
epileptic patient who has suered an epileptic attack while awake must not
1
yr from the date of the attack. Patients who have seizures that do not
drive for
aect their consciousness (eg simple partial seizures) or seizures only during
sleep may be allowed to drive. Being allowed to drive is conditional on the patient following medical advice and there not being reason to believe they are at
high risk of further seizures.
•
TIA
or s troke . Thes e patien ts sh ould n ot dr ive fo r at le ast 1 month. There is no need
to inform the
visual field defect. If
of attacks may be required.
• Sudden attacks or disabling giddiness, fainting, or blackouts.
• Chronic neurological conditions including multiple sclerosis, Parkinson’s (any
‘freezing’ or on– o eects), and motor neuron diseases.
• Severe mental disorders; including serious memory problems and severe psy-
chiatric illness. Those with dementia should only drive if the condition is mild
(do not rely on armchair judgements: on- the- road trials are better). Encourage
relatives to contact
desire to breach confidentiality (the
or psychotic patients (tel.
accidents are found to have Alzheimer’s.
• A pacemaker, defibrillator, or antiventricular tachycardia device fitted.
• Diabetes controlled by insulin or tablets. The main issues which may result in
driving bans are impaired awareness of hypoglycaemia and impaired vision.
• Angina while driving.
• Any type of brain surgery, brain tumour. Severe head injury involving inpatient
treatment at hospital.
• Continuing/ permanent diculty in the use of arms or legs which aects ability
to control a vehicle.
• Dependence on or misuse of alcohol, illicit drugs, or chemical substances in the
past
• Any visual disability which aects both eyes (do not declare short/ long sight or
colour blindness).
• Vision (new drivers) should be 6/ 9 on Snellen’s scale in the better eye and
6/ 12
needed, and
The above- listed rules apply to standard licences only, for group
HGV
drivers) see: www.dvla.gov.uk/ medi cal/ atagla nce.aspx
DVLA
unless there is residual neurological defect after 1 month, eg
TIA
S have b een recurrent and freq uent, a
DVLA
if a dementing relative should not be driving.
3
yrs (do not include drink/ driving oences).
GMC
01792 783686
approves) and inform
). Many elderly drivers (~1 in 3) who die in
3
- month period free
GP
DVLA
S may
of demented
on the Snellen scale in the other eye, wearing glasses or contact lenses if
3/ 60
in each eye without glasses or contact lenses.
2
entitlement (eg
151
3 Cardiovascular medicine
Flying after a stroke or
Patients with a recent MI may travel after 7– 10 days if there are no complications.
As there is the potential risk for barotrauma after
acic surgery, these patients should wait
PCI
such as angioplasty with stent placement may be fit to travel after 3 days,
but individual assessment is essential. Following a stroke, patients are advised to
wait
10
days following an event, although if stable may be carried within 3 days
of the event. Cardiovascular contraindications to commercial airline flight include
MI
uncomplicated
signs/ symptoms of heart failure) within
CHF
sated
within 7 days, complicated MI (eg recurrent event, EF <40% or
, uncontrolled hypertension,
uncontrolled cardiac arrhythmia, and severe symptomatic valvular heart disease.
MI
CABG
and other chest or thor-
10– days. Patients with uncomplicated
4– 6
weeks, unstable angina, decompen-
CABG
within 10 days, stroke within 3 days,
ARDS
4
https://t.me/med1917
Chest medicine
Contents
Respiratory health 153
Investigations
Bedside and lung function tests in
chest medicine
Further investigations in chest
medicine
Pulmonary conditions
Respiratory failure
Asthma
Management of chronic
asthma
Chronic obstructive pulmonary
disease (
Pneumonia
Specific pneumonias
COVID- 19
Fungi and the lung
Complications of pneumonia
Pleural eusion
Acute respiratory distress
syndrome (
Bronchiectasis
Cystic fibrosis (CF)
Lung tumours
Lung tumours: staging and
treatment
Pulmonary embolism (PE)
Pneumothorax
Obstructive sleep apnoea
syndrome
Pulmonary hypertension
Cor pulmonale
Sarcoidosis
Interstitial lung disease (
Hypersensitivity pneumonitis
(
HP
)
193
Idiopathic pulmonary fibrosis
(
IPF
)
Occupational lung diseases
154
156
158
160
164
COPD
)
166
168
172
170
174
176
)
178
180
181
182
184
186
188
189
190
194
ILD
186
188
175
Fig 4.
1
In December
identified as the cause of a cluster of pneumonia
cases in Wuhan, a city in the Hubei Province of China.
This outbreak spread rapidly through China and then
the rest of the world, becoming the first global pandemic since Spanish 'flu. Novel coronavirus disease
COVID- 19
) (p
(
the World Health Organization, is caused by severe
acute respiratory syndrome (
2
virus, primarily manifesting as an acute respiratory
illness with interstitial and alveolar pneumonia, but it
)
192
can aect multiple organs such as the kidney, heart,
digestive tract, blood, and nervous system. To date,
it has infected over
and has caused nearly
to the pandemic, most countries around the world
instituted strict lockdown measures including the
195
closure of all non- essential businesses, schools, and
shops, and restriction of all non- essential travel and
movement. At- risk or vulnerable individuals were encouraged to 'cocoon' or 'shield' themselves safely at
home. Though there was much sorrow and sacrifice,
there was also an outpouring of generosity and solidarity. We were reminded of the words of Dr Bernard
Rieux from Albert Camus' The Plague, 'the whole
thing is not about heroism... It may seem a ridiculous
idea, but the only way to fight the plague is with decency.' Pandemics aside, the art and practice of medicine should always be about decency.
2019
172
), as it was subsequently termed by
700
million people worldwide
7
million deaths. In response
, a novel coronavirus was
SARS
) coronavirus (CoV)
Artwork by Gillian Turner.
We thank Nicola Ronan, our Specialist Reader and Gemma Smith, our Junior Reader for this chapter.
4 Chest medicine
Respiratory health
Right main
br
Right uppe
lobe
Right
upper lobe
br
Right lower
lobe
y
Tr
Larynx
https://t.me/med1917
The lungs provide a vital physiological function in allowing gas exchange, but are
also at the vanguard of a constant battle between host, pathogens, and pollutants. Respiratory medicine exemplifies how careful epidemiology, science, and
randomized controlled trials have revolutionized our understanding of common
diseases, leading to preventative measures and eective treatments. However,
the importance of poverty and general improvements in public health cannot be
underestimated. Rates of
vaccination and streptomycin, largely due to improvements in sanitation and less
TB
in the UK declined well before the introduction of
BCG
dense living conditions. Public health campaigns and taxation have helped lower
smoking rates, although reductions in lung cancer will lag behind for many years.
Increasing air pollution levels, diminished air quality, and climate change pose
new challenges for lung function and respiratory disease.
153
achea
r
onchus
onchus
Middle lobe
Smaller
bronchi
Fig 4.
2
Segmental anatomy of the lungs and main bronchi. The left lung has two lobes and the
right has three.
Primary bronchi
Secondary bronchi
Tertiary bronchi
Smaller bronchi
Left upper
lobe
Left primar
bronchus
Left
lower lobe
bronchus
Left lower
lobe
Smaller
bronchi
4 Chest medicine
Bedside and lung function tests in chest medicine
https://t.me/med1917
154
There is no substitute for careful history taking and examination in making the
‘correct’ diagnosis. Tests should help clarify and assess severity. When examining
the chest think about the anatomy, and the location of pathology (
Sputum examination Collect a good sample; if necessary ask a physiotherapist to
help. Note the appearance: clear and colourless (chronic bronchitis), yellow- green or
brown (pulmonary infection), red (haemoptysis), black (smoke, coal dust), or frothy
white- pink (pulmonary oedema). Send the sample to the laboratory for microscopy,
culture/ sensitivity. If indicated, ask for
Peak expiratory flow (
peak flow meter. It correlates well with the forced expiratory volume in
FEV
) & is used as an estimate of airway calibre in asthma, but is eort dependent.
(
1
Pulse oximetry Allows non- invasive assessment of peripheral O2 saturation (SpO2).
Useful for monitoring those who are acutely ill or at risk of deterioration. Target
oxygen saturations are usually
certain pre- existing lung pathology (eg
failure). Oxygen saturation of <
arterial blood gases (
perfusion, movement, skin pigmentation, nail varnish, dyshaemoglobinaemias, and
carbon monoxide poisoning. As with any bedside test, be sceptical, and check
whenever indicated (
Arterial blood gas (
radial or femoral artery (
nerve proximity and it is an end artery. pH, P
automated analyser. For
Lung function tests
1
Spirometry (See table
tory volume in
1
full forced expiration into a spirometer (Vitalograph®); exhalation continues
until no more breath can be exhaled.
gives a good estimate of the severity of airflow obstruction; and helps classify
COPD
severity. Bronchodilator testing may be performed if reversible airflow
obstruction (eg asthma) suspected— a
is defined as a response. Obstructive defect: (
COPD,
cystic fibrosis. Restrictive defect: fibrosis, sarcoidosis, pneumoconiosis,
interstitial pneumonias, connective tissue diseases, pleural eusion, obesity,
kyphoscoliosis, neuromuscular problems.
2
Lung volume measurement Total lung capacity (
are useful in distinguishing obstructive and restrictive diseases (
RV
are increased in obstructive airways disease and reduced in restrictive
and
lung diseases and musculoskeletal abnormalities. Combined obstructive and
restrictive defects can be seen in certain conditions such as sarcoidosis.
volume loop
(fig 4.5) measures flow at various lung volumes. Characteristic
patterns are seen with intrathoracic airways obstruction (asthma, emphysema) and extrathoracic airways obstruction (tracheal stenosis).
3
Gas exchange The gas transfer coecient (
oxide diusing capacity
by measuring carbon monoxide uptake from a single inspiration in a standard
time (usually
ment of parenchymal lung disease, pulmonary vascular disease, and/ or anaemia. Low in emphysema, interstitial lung disease, and pulmonary vascular
disease; high in alveolar haemorrhage and left- to- right shunt.
Of note, obesity can aect
10
s) and lung volume by helium dilution. It is an indirect assess-
Lung clearance index (
the multiple- breath washout test. The test involves following the washout of an
inert tracer gas from the lungs during relaxed tidal breathing. The
marker of lung disease severity in cystic fibrosis.
fig 4.2).
ZN
PEF
stain, and
) Measured by a maximal forced expiration through a
94– 98
% in a well patient or 88– 92% in those with
COPD
92
ABG
p
158
ABG
s (
% in a normally well person is a serious sign and
S) should be checked. Causes of erroneous readings: poor
).
) analysis Heparinized blood is usually taken from the
p
755
). The brachial artery is used less because of median
ABG
interpretation, see p
4.1
.) Measures functional lung volumes. Forced expira-
FEV
) and forced vital capacity (
1
FEV
PCR
.
with a history of type 2 respiratory
, PaCO2, HCO3 are measured using an
aO2
159
.
FVC
) are measured from a
is less eort dependent than
1
12
% and
200
mL change in
fig 4.3) asthma, bronchiectasis,
TLC
) and residual volume (RV)
fig 4.4).
KCO
(DLCO
) corrected for alveolar volume. It is calculated
PFT
S, decreasing lung volumes and increasing
LCI
) A measure of ventilation distribution obtained from
) represents the carbon mon-
1
LCI
is a sensitive
1
FEV
DLCO.
second
ABG
PEF. FEV
or
FVC
1
TLC
Flow–
S
1
4 Chest medicine
Table 4.
https://t.me/med1917
1
Spirometry results (data source
Normal
Restrictive
Obstructive
*
FEV
can also be normal in restrictive lung disease.
1
FEV
1
>
80
% predicted >80% predicted
<
80
% predicted* <80% predicted >70% normal
80
% predicted
<
NICE COPD
2010
guidelines)
FVC FEV
Normal or low
/
FVC
ratio
1
75– 80
%
<70% predicted
155
Fig 4.
3
Examples of spirograms.
Fig 4.
4
Lung volumes: physiological and pathological.
Fig 4.
FEF
flow at
5
Flow– volume loops.
= forced expiratory flow at 25%
25
50
%
TLC
.
PEF
= peak expiratory flow;
TLC; PIF
= peak inspiratory flow;
FEF
= forced expiratory flow at 50%
50
FIF
= forced inspiratory
50
TLC
;
4 Chest medicine
Further investigations in chest medicine
https://t.me/med1917
156
Radiology Chest x- ray See p
drainage of pleural eusions (particularly loculated eusions) and empyema.
Radionuclide scans Ventilation/ perfusion (
diagnose pulmonary embolism (
are seen). Bone scans are used to diagnose bone metastases.
cancer and inflammation.
and staging lung cancer, imaging the hila, mediastinum, and pleura, and guiding
biopsies. Thin (
interstitial lung disease, emphysema, and bronchiectasis.
CTPA
(
1– 1.5
mm) section high- resolution CT (
) is used in the diagnosis of PE (fig 4.6). Pulmonary angiography Now rarely
706
. Ultrasound Used in diagnosing and guiding
V/ Q
, p
722
PE
), eg in pregnancy (unmatched perfusion defects
Computed tomography (CT, p
) scans are occasionally used to
PET
714
) Used for diagnosing
HRCT
) is used in the diagnosis of
CT
pulmonary angiography
used for diagnosing pulmonary hypertension.
Fibreoptic bronchoscopy (See fig
aesthetic via the nose or mouth.
4.7
.) Performed under sedation with local an-
Diagnostic indications Suspected lung carcinoma,
slowly resolving pneumonia, pneumonia in the immunosuppressed, interstitial lung
disease. Bronchoalveolar lavage fluid may be sent to the lab for microscopy, culture, and cytology. Mucosal abnormalities may be brushed (cytology) and biopsied (histopathology).
lobar collapse, removal of foreign bodies, stenting or treating tumours, eg laser.
Pre- procedure investigations
ABG
(if indicated). Complications Hypoxia, bleeding, infection, pneumothorax
and
fig
16.44
, p
(
733
cation; gene profiling of cell sample may improve this.
Therapeutic indications Aspiration of mucus plugs causing
FBC
, coagulation,
CXR, CT
, spirometry, pulse oximetry,
). Diagnostic sensitivity for cancer 50– 90%, depends on tumour lo-
2
May also be used to de-
liver an ultrasound probe (endobronchial ultrasound), and treatments— eg stents,
or cryotherapy.
Bronchoalveolar lavage (
stilling and aspirating a known volume of warmed, buered
BAL
) Performed at the time of bronchoscopy by in-
0.9
% saline into the
distal airway. The scope is wedged in a segmental airway. It diers from simple
bronchial washings as it samples cells from alveolar airspaces as opposed to
just cells from the proximal airway. It can also provide a cell count and dierential that can be useful to distinguish the dierent types of
indications for washings or
munosuppressed (especially
tive), interstitial lung diseases (eg sarcoidosis, hypersensitivity pneumonitis,
histiocytosis
transient
X
). Complications Hypoxia (give supplemental O2), transient fever,
CXR
shadow, infection (rare).
Endobronchial ultrasound (
BAL
Suspected malignancy, pneumonia, in the im-
HIV
), bronchiectasis, suspected TB (if sputum nega-
EBUS
) A bronchoscopic technique that uses ultrasound to visualize structures within the airway wall, lung, and mediastinum. Most
commonly used in combination with transbronchial needle aspiration (
to sample hilar and mediastinal lymphadenopathy, endobronchial or peribronchial
lesions in order to diagnose lung cancer, lymphoma, sarcoidosis, etc.
Lung biopsy May be performed in several ways. Percutaneous needle biopsy is
performed under radiological guidance and is useful for peripheral lung and pleural
Transbronchial biopsy performed at bronchoscopy may help in diagnosing
lesions.
interstitial lung diseases such as sarcoidosis or lung transplant complications.
Cryoprobe transbronchial biopsy, a newer diagnostic procedure, provides larger
biopsies that are usually crush artefact free and therefore of higher diagnostic
Alternatives If unsuccessful, consider open lung biopsy or video- assisted
yield.
thoracoscopy.
Surgical procedures These are performed under general anaesthetic. Rigid
bronchoscopy
bleeding, and removal of foreign bodies.
able examination and biopsy of the mediastinal lymph nodes/ lesions.
allows examination and biopsy of pleural lesions, drainage of pleural eusions, and
provides a wide lumen, enables larger mucosal biopsies, control of
Mediastinoscopy and mediastinotomy en-
talc pleurodesis and pleurectomy.
scans to assess
ILD
. Diagnostic
EBUS- TBNS
Thoracoscopy
)
4 Chest medicine
Echocardiography and right heart catheterization
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Echocardiography This is the best screening test for significant pulmonary hyper-
p
102
tension (
right ventricular systolic pressure, which in the absence of pulmonary valve sten-
). The tricuspid regurgitant jet velocity can be used to estimate the
osis, is equal to the pulmonary artery systolic pressure (
ventricle can be assessed to determine whether there is a contribution from left
ventricular systolic or diastolic dysfunction to elevated pulmonary arterial pressure. Atrial and ventricular dimensions and wall thickness can be measured, and
paradoxical bowing of the intraventricular septum into the left ventricular cavity
may be seen during systole as a consequence of greatly elevated right- sided pres-
Right heart catheterization This can confirm the diagnosis of pulmonary
sures.
hypertension and provide important prognostic information. An elevated mean
pulmonary arterial pressure >
vated pulmonary capillary wedge pressure (
left heart disease. Indicators of right heart failure, and hence poorer prognosis, in-
1
an e levated r ight a trial press ure (>10mmHg); 2 an elevated right ventricular
clude:
end- diastolic pressure (>
<63%); and 4 reduced cardiac output (<2.5L/ min). Vas orea ctiv ity te stin g
(SvO
2
This may be undertaken at the time of right heart c atheterization, us ing inhaled nitric oxide or an
patients with pulmonary arterial hypertension who are likely to respond favourably
to long- term treatment with vasodilator therapy, eg nifedipine.
IV
infusion of epoprostenol or adenosine, to identify the subgroup of
Fig 4.
6
Image from a CT pulmonary angiogram at the level
of the right main pulmonary
artery demonstrating dilatation
of the main pulmonary artery
with laminated thrombus in
the distal right pulmonary artery
(arrow) in keeping with proximal
chronic thromboembolic pulmonary hypertension.
Reproduced from Stirrup J et al.
Cardiovascular Tomography (
with permission from Oxford
University Press.
Fig 4.
7
The videobronchoscopic
appearance of (a) the trachea
and main bronchi; (b) segmental
bronchi in the right lower lobe;
(c) polypoid tumour arising from
a bronchial segment; and (d) submucosal disease.
Reproduced from Firth et al.,
Oxford Textbook of Medicine
(
2020
), with permission from
Oxford University Press.
PAS P
). In addition, the left
20
mmHg at rest is the accepted definition. An ele-
10
mmHg); 3 a reduced mixed venous oxygen saturation
PCWP
) (>15mmHg) generally indicates
2019
),
157
4 Chest medicine
Respiratory failure
https://t.me/med1917
158
Respiratory failure occurs when gas exchange is inadequate, resulting in hypoxia. It
is defined as a P
<8kPa and subdivided into two types according to PaCO2 level.
aO2
Type I respiratory failure Defined as hypoxia (PaO2 <8kPa) with a normal or low
. It is caused primarily by ventilation/ perfusion (
P
aCO2
fusion, right- to- left cardiac shunts. Examples of
monary oedema, asthma, emphysema,
ARDS
(p
178
V/ Q
).
V/ Q
) mismatch, abnormal dif-
mismatch:
PE,
Type II respiratory failure Defined as hypoxia (PaO2 <8kPa) with hypercapnia
>6.0kPa). This is caused by alveolar hypoventilation, with or without
(P
aCO2
match. Causes include:
• Pulmonary disease
sleep apnoea (
• Reduced respiratory drive Sedative drugs,
• Neuromuscular disease Cervical cord lesion, diaphragmatic paralysis, poliomyel-
itis, myasthenia gravis, Guillain– Barré syndrome.
• Thoracic wall disease Flail chest, kyphoscoliosis.
COPD
OSA
, pneumonia, end- stage pulmonary fibrosis, obstructive
, p
188
), obesity hypoventilation syndrome (prevalence).
CNS
tumour or trauma.
Clinical features Features of the underlying cause together with symptoms and
signs of hypoxia, with or without hypercapnia.
Hypoxia Dyspnoea; restlessness; agitation; confusion; central cyanosis. If long-
standing hypoxia: polycythaemia; pulmonary hypertension; cor pulmonale.
Hypercapnia Headache; peripheral vasodilation; tachycardia; bounding pulse;
tremor/ flap; papilloedema; confusion; drowsiness; coma.
Investigations Aimed at determining the underlying cause:
• Blood tests:
• Radiology:
• Microbiology:
cultures (if febrile).
• Spirometry (
FBC, U&E, CRP, ABG.
CXR
± CT thorax
COVID
COPD
, neuromuscular disease, Guillain– Barré syndrome).
See table
4.2
/ CTPA
.
.
/flu swabs, respiratory BioFire®
PCR
panel, sputum and blood
Management Depends on the cause. Senior support essential. At an early stage,
consider the appropriateness of the management setting and the ceilings of care.
Typ e I respiratory failure
• Treat underlying cause.
• Give oxygen (24– 60%)— see
• Get
ICU
support and consider high flow nasal cannula (p
tive airway pressure) if requiring >
BOX
‘Administering oxygen’.
40
% O2. The latter is a mask covering the nose and
159
) or
CPAP
mouth that provides fixed positive pressure to the airways throughout the breathing
cycle, to splint open the respiratory tract and improve gas exchange. The standard
CPAP
sta rting pres sure is usual ly 5cmH2O. Most useful in
Type II respiratory failure The respiratory centre may be relatively insensitive to
and respiration could be driven by hypoxia.
CO
2
• Treat underlying cause.
• Controlled oxygen therapy: target SpO2 of 88– 92% if
tention; start at
don’t leave the hypoxia untreated.
• Recheck
28
%. If PaCO2 has risen >1.5kPa and the patient is still hypoxic, consider assisted
ventilation (eg
24
% O2. Oxygen therapy should be given with care. Nevertheless,
ABG
after 20min. If PaCO2 is steady or lower, increase O2 concentration to
NIPPV
, p
797
, ie non- invasive positive pressure ventilation).
CHF, COPD
, or
COPD
and history of CO2 re-
• If this fails, consider intubation and ventilation, if appropriate.
pneumonia, pul-
V/ Q
mis-
(continuous posi-
OSA
.
When to consider
• Any unexpected deterioration in an ill patient. (Technique: see p
• Anyone with an acute exacerbation of a chronic chest condition.
• Anyone with impaired consciousness or impaired respiratory eort.
• Signs of CO2 rete ntion , eg bo undin g puls e, drow sy, tremo r (flap ping) , head ache.
• Cyanosis, confusion, visual hallucinations (signs of PaO2; SaO2 is a n alte rnativ e).
• To va l i d a t e m e a s u re m e n t s f r o m t r a n s c u t a n e o u s p u l s e o x i m e t r y ( p
ABG
(arterial blood gas) measurement
755
.)
154
).
4 Chest medicine
ABG
https://t.me/med1917
interpretation
Normal pH is 7.35– 7.45. pH <7.35 indicates acidosis and >7.45 indicates alkalosis.
Table 4.
2
Interpreting blood gas analysis
Metabolic acidosis
Respiratory acidosis
Metabolic alkalosis
Respiratory alkalosis
Steps to ABG in terp reta tion
1 PO2: is this normal given the FiO2 (fraction of inspired oxygen)?
2
pH: acidosis or alkalosis?
3
Is the primary disturbance respiratory or metabolic? See table
4
Is there any compensation (ie changes in pCO2/ HCO
derlying imbalance)? Is this partial (pH abnormal) or complete (pH normalized)?
5
If metabolic acidosis present, calculate the anion gap: (Na
p
662
for cau ses of ra ised a nion g ap (normal 10– 18
See
6
In a non- anion gap acidosis, determine the urinary anion gap: urinary Na
−
(s ho ul d b e <−40 in ac id ae mi a; us ed to id en ti fy re na l t ub ul ar ac id os is ; s ee p
Cl
7
In an anion gap acidosis, determine if there is a pre- existing metabolic disorder
with the delta gap (ratio of rise in anion gap to fall in bicarbonate; see
Administering oxygen
Oxygen should be prescribed. Titrate the amount guided by the patient’s SaO2 an d cli nical condition. Use the lowest flow delivery system necessary to maintain SpO
target range. Humidification is only required for longer- term delivery of O
flow rates and tracheostomies, but may exp ect orati on i n bro nchi ecta sis .
Nasal cannulae For mild– moderate hypoxaemia. Preferred by patients, but O2 de-
livery is relatively imprecise and may cause nasal soreness. The flow rate (
min) roughly defines the concentration of O
when nebulizers need to be run using air, eg
S
aO2
Simple face mask Delivers a variable amount of O2 depending on the rate of in-
flow. Less precise than venturi masks— so don’t use if hypercapnia or type
spiratory failure. Risk of CO
gas) if flow rate <
5
L/ min. Be careful in those with
Venturi mask For controlled oxygen therapy. Provides a precise percentage or
fraction of O
•
BLUE
•
WHITE
•
YELLOW
•
RED
•
GREEN
(FiO2) at high flow rates. Start at 24– 28% in
2
= 24% at 2L/ min
.
= 28% at 4L/ min.
= 35% at 8L/ min.
= 40% at 10L/ min.
= 60% at 15L/ min.
Non- rebreathing mask These have a reservoir bag and deliver high concentra-
(60– 90%), determined by the inflow (10– 15L/ min) and the presence of
tions of O
2
flap valves on the side. They are commonly used in emergencies, but are imprecise and should be avoided in those requiring controlled O
High- flow nasal oxygen (aka Optiflow™/
is humidified, warmed oxygen delivered at up to
vantages it has over standard oxygen are that it provides some positive endexpiratory pressure, which improves oxygenation by 'recruitment' of alveoli, that
it can deliver an FiO
~
100
2
Promoting oxygenation Other ways to oxygenation to reach the target SaO2
(this should be given as a number on the drug chart):
• Tre at a na em ia ( tr an sf us e i f es se nt ia l ).
• Improve cardiac output (treat heart failure).
• Chest physio to improve ventilation/ perfusion mismatch.
• Consider patient positioning (eg sitting upright in pulmonary oedema etc.).
pH
P
aCO2
Low Normal/ low
Low High
High Normal/ high
High Low
−
to try and correct an un-
3
HCO
Low
Normal/ high
High
Normal/ low
+
+
+ K
) − (Cl− + H CO
4.2
–
3
.
mmol/ L).
(24– 40%). May be used to maintain
2
COPD
.
accumulation (within the mask and so in inspired
2
COPD
(p
796
).
COPD
. Colours of masks:
therapy.
2
™
AIRVO
, high- flow nasal cannula) This
60
L per minute. The major ad-
%, and that it is well tolerated.
+
+ K
662
p
662
).
within
2
at high
2
1– 4
II
3
+
re-
−
−
L/
).
).
159
4 Chest medicine
Asthma
https://t.me/med1917
160
Asthma aects 8% of the population. It is characterized by recurrent episodes of
dyspnoea, cough, and wheeze caused by reversible airways obstruction. Three factors contribute to airway narrowing: bronchoconstriction, triggered by a variety of
stimuli; mucosal swelling/ inflammation, caused by mast cell and basophil release
of inflammatory mediators; and increased mucus production.
Occupational asthma, aspirin- sensitive asthma, and eosinophilic asthma are dis-
tinct syndromes that typically have their onset in adulthood.
Symptoms Episodic: ≥1 of wheeze, breathlessness, chest tightness, and cough
occurring in episodes with periods of no (or minimal) symptoms between episodes.
Precipitants Respiratory irritants (smoke, perfume, pollution, etc.), allergens (house
dust mite, pollen, fur), infection (particularly viral), drugs (
- blockers via bronchospasm), cold air, exercise (typically after
Diurnal variation Symptoms or peak flow may vary over the day but tend to be
worse at night or in the early morning. Marked morning dipping of peak flow is
common and can tip the balance into a serious attack, despite having normal peak
figs
4.9, 4.10
, p
flow (
163
Exercise Quantify the exercise tolerance.
Disturbed sleep Quantify as nights per week (a sign of severe asthma).
Acid reflux 40– 60% of those with asthma have reflux; treating it improves spiro-
metry, but not necessarily symptoms.
Other atopic disease Eczema, hay fever, allergy, or family history?
The home (especially the bedroom) Pets? Carpet? Feather pillows or duvet?
Floor cushions and other ‘soft furnishings’?
Job If symptoms remit at weekends or holidays, work may provide the trigger (15%
of cases are work- related— more for paint sprayers, food processors, welders, and
animal handlers).
and at home (at the same time of day) to confirm this.
4
Ask the patient to measure their peak flow at intervals at work
Exacerbations Fr equ enc y, sev eri ty, du rati on, a nd re qui red tr eat men t (ne ed fo r ste r-
A&E
visits, hospitalizations, and intubations), days per week o work or school.
oids,
Adherence to treatment. Observe inhaler technique.
Signs Tachypnoea; audible wheeze; hyperinflated chest; hyperresonant percussion
note; air entry; widespread, polyphonic wheeze with prolonged expiratory phase.
Presence of nasal polyps, rhinitis, rash (allergic component).
a severe or life- threatening attack on p
Te st s The diag nosis is ult imate ly cli nical suppo rted b y obje ctive tests that s eek to dem-
onstrate variable airflow obstruction or the presence of airway inflammation. Compare
results when asymptomatic vs symptomatic to avoid false negative results and to detect variation over time.
tial structured clinical assessment (
fig
4.8
). The diagnostic indications for referral for specialist advice/ investigations are
(
table
4.4
shown in
blood cultures.
ventilation). If P
repeat the
unit or
eort.
2– 4
wks (p
structive defect (
. Acute attack See p
ABG
analysis usually shows a normal or slightly PaO2 but PaCO2 (hyper-
is normal but the patient is hyperventilating, watch carefully and
aO2
ABG
a little later. If PaCO2 is normal or raised, transfer to high- dependency
ITU
for c lose mo nitori ng ± ventilatory support, as this signifies failing respiratory
CXR
(to exclude infection or pneumothorax). Chronic asthma
164
): a diurnal variation of >15% on ≥3d a wk for 2wks. Spirometry: ob-
FEV
agonists or steroid trial with increase in volume ≥
Histamine or methacholine bronchial challenge tests. Fractional exhaled nitric oxide
(FeNO) to detect eosinophilic airway inflammation or atopy.
Per for m to con firm sens iti vit y to sus pec ted alle rgi c tr igg ers — suggested by raised
tests
allergen- specific
philia. Consider
Aspergillus, mucus plugging, or central bronchiectasis on
IgE
levels, positive skin- prick tests to aeroallergens, or blood eosino-
ABPA
an d che ck Aspergillus serology if eosinophilia, a positive skin test to
NSAID
S via leukotrienes,
5– 15
minutes).
) at other times.
3
Recognize signs of
794
.
Initial diagnosis Assess probability of asthma based on ini-
table
4.3
) and then follow the diagnostic algorithm
794
.
PEF
(or
FEV
,), sputum culture,
1
/
FVC
,
RV,
p
164
1
); usually ≥12% improvement in
200
mL (= significant reversibility).
CXR
CXR
.
FBC, U&E, CRP
PEF
monitoring for
FEV
following 2
1
: hyperinflation. Allergy
,
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