Airway disease Flashcards
Obstructive airway diseases
a disease that causes obstruction affects all of the airways in both lungs - global airway obstruction.
not including lung cancer, tumour, inhaled foreign bodies and chronic scarring diseases like bronchiectasis and secondary fibrocaseous or tuberculosis as these are not primarily obstructive diseases.
In relation to obstructive diseases how can we measure function?
testing with FEV1 and FVC
take a deep breath in and try blowing out as much air as possible and as fast as possible.
fev1 - forced expiratory volume of air in first second
fev1 is usually about 70%-80% of fvc
normal fev 1 is about 2.5-4L
normal fvc is about 5L
normal ratio fev1:fvc is 0.7 -0.8
what % is normal fev1 of fvc
fev1 is usually about 70%-80% of fvc
what is normal fev1 volume
normal fev 1 is about 2.5-4L
what is normal fvc volume
normal fvc is about 5L
what is normal ratio fev1:fvc
normal ratio fev1:fvc is 0.7 -0.8
what is another way to measure airflow limitation other than fev1/fvc
peak flow
what is normal peak expiratory flow rate?
400-600litres per min
what is a normal peak expiratory flow rate range %
80-100%
what is the % of a moderate fail of a peak expiratory flow rate?
50-80%
what is a maked fail of a peak expiratory flor rate %?
<50%
explain asthma what is it?
type 1 hypersensitivity in the airways because of bronchial constriction
reduction in the luminal cross-sectional area. granulation of mast cells in airways releasing chemical factors from mast cells reduce diameter.
In asthma what do the chemical factors do in the airway
chemical factors induce inflammation by attracting inflammatory cells = swelling and oedema within the bronchial mucosa.
chemicals have a direct effect on bronchial smooth muscle leading to constriction of airways.
= airflow narrowing and limitation
is bronchial asthma reversible?
yes generally reversible obstruction spontaneously or with medical intervention
the bronchial smooth muscle contraction and inflammation can be modified with drugs.
aetiology of chronic bronchitis and emphysema
SMOKING
- atmospheric pollution
occupation: dust
alpha1 antiprotease (antitrypsin) deficiency extremely rare cause of emphysema
- age and susceptibility
prevalence - men more than women
increasing in developing countries
Chronic bronchitis is defined clinically as:
cough productive of sputum most days in at least 3 consecutive months for 2 or more consecutive years
(excludes tb, bronchiectasis)
clinically may be confused with chronic bronchial asthma
complicated chronic bronchitis when sputum turns mucopurulent (acute infective exacerbation) or FEV1 falls
What are the morphological changes in chronic bronchitis
large airways: mucus gland hyperplasia, goblet cell hyperplasia, inflammation and fibrosis is a minor component
small airways: goblet cells appear, inflammation and fibrosis in long-standing disease.
explain globlet cells
Modified epithelial cells that secrete mucus on the surface of mucous membranes of intestines and airways
Their role is to protect the surface of the epithelium, lubricate it, and catch harmful particles. Although protective, goblet cells may be involved in the pathophysiology of certain respiratory diseases, such as chronic bronchitis.
define emphysema
pathological definition: increase beyond the normal in the size of airspaces distal to the terminal bronchiole arising either from dilation or from the destruction of their walls and without obvious fibrosis
what is the acinus?
the gas exchange tissue part of the lunch and is defined by everything distal to the terminal bronchiole
histology emphysema
the air spaces become bigger - loss of alveolar walls
most common form of emphysema
centri-acinar emphysema
middle of acinus - middle disappears - holes surrounded by lung tissue
what is pari-acinar emphysema
holes all alveolar and acinous gas exchange lost. scarring is irregular and has “bullous” emphysema. bullae are spaces under the pleura full of air. This is significant because if they pop, this can cause pneumothorax
mechanisms airway in COPD.
small airways smooth muscle tone and inflammation - will respond to same drugs as asthma - inflammation component will respond. the fibrotic element will not, however.
Why i t isn’t reversible what cannot be treated is emphysema - the loos of alveolar attachment is most important
explain what happens with emphysema and collapsing of airway
when we exhale, the small airways would close/collapse, but there is a radial pull from alveoli elastic fibres which keep them open. in centri-acinal emphysema the alveolar walls are lost
airways likely to collapse when trying to breathe out
the airway will collapse trapping air inside the lung
What are the clinical effects of COPD?
hypoxaemia
airway obstruction
reduces respiratory drive
loss of alveolar surface area
shunting - during acute infective exacerbation
what are the pulmonary vascular changes in hypoxia
- physiological pulmonary arteriolar vasoconstriction - (alveolar tension fails can be a localised effect. or all vessels constrict if there is hypoxaemia - hypertension occurs in the pulmonary vascular system. right ventricle working harder = pathological hypertrophy of right ventricle chronic cor pulmonale then result in congenital heart disease. right heart failure.
a protective mechanism (do not send blood to alveoli short of oxygen)
explain cor pulmonale - pulmonary hypertension
pulmonary vasoconstriction anatomical changes in vessels become hypertrophic and end of vessels become fibrotic = reduction in luminal cross-sectional area of the vessel Makes harder to pump blood through.
emphysema leads to a loss of blood vessel (capillary bed) = fewer blood vessels for the heart to pump blood through = pulmonary vascular resistance increased.
if continuous in hypoxic state bone marrow tries to produce more RBC - blood becomes more viscous = harder to pump through compromised vascularity.
explain the basics of asthma with diagnosing
some chellenges
- no definition
- no tests
- two national guidelines
- symptom-based
- identical to lower respiratory tract symptoms in acuse phases
- relapse and remission
Some key things regarding asthma when diagnosing for children
- no wheeze = no asthma
- tests may help decision although often don’t
if the symptoms affect the quality of life - confirm the diagnosis with a trial of inhaled corticosteroids
if the quality of life is not affected do not rush to treat, watch and see
what is asthma?
chronic condition- with wheeze, cough and shortness of breath
has multiple triggers
variable/reversible
responds to asthma treatment
(child asthma) what causes asthma?
host response to environment
infection important
physiology abnormal response before symptoms
is a syndrome.
different asthma syndromes
infant onset
childhood-onset
adult-onset
exertional asthma
occupational asthma
what can cause asthma
- genes 30-80% causes
- interact with the environment
- epigenetics
allergen stimulated immune system and then an allergy response
what is the best assessment in children for asthma
history
examination not always helpful - if healthy unlilely wheezing, stethoscope wont be important and unhelpful if not wheezing
no diagnostic asthma test for children - peak flow no good,
allergy test irrelevant for asthma only environment allergy, spirometry lacks specificity,
nitric oxide can display affiliation eosinophils are allergic to blood cells - tells inflammation in the lung.
spirometry for asthma (child asthma)
useful don’t with a bronchodilator response to measure lung function - give asthma medicine and see if flow changes
What is nice guideline for asthma diagnosis? (child asthma)
1. spirometry
2. bronchodilator response (BDR)
3.FeNO nitrous oxide test
4 peak flow
yes-no mark of diagnose or test further
what does the BTS/Sign guideline have in classing diagnosis (child asthma)
1. spirometry
2. bronchodilator response (BDR)
3.FeNO nitrous oxide test
4 peak flow
score as high probability, intermediate probability or low probability
where is the main diagnosis problem? (child asthma)
uncertainty in <5 years old
tests are not reliable in < 5-year-olds
the tests cal already be difficult already
(child asthma) cough variant asthma__
not common in children, this is common in adults
(child asthma) when having symptoms described to you about a child, what is important?
to establish if it is actually a wheeze. often it’s a rattle, not a wheeze. Ask “what you mean by wheeze, is it like a whistle or rattling?”
common symptoms of asthma (child asthma)
Wheeze (needed)
shortness of breath at rest - significant difficulties <30% lung function
airway obstruction
“sooking” in of ribs with wheeze ribs sucked in tummy sticks out
coughing - dry, common night, after exercise
other circumstance - parent history asthma, eczema, hayfever, food allergy
responding to asthma treatment how long does it take for steroids to have maximum effect? (child asthma)
two months. must keep using 2 months if it doesn’t work after 2 months then it isn’t working.
(child asthma) when on an inhaler - what is false positive?
a child with transient respiratory symptoms not asthma - symptoms go away. inhaler might not have actually worked. Stop inhaler in spring see if symptoms return if not = false positive.
(child asthma) key to diagnosing asthma
- wheeze without and without upper respiratory tract infection
shortness of breath at rest
parental asthma (helps)
responds to treatment
(child asthma) trialling asthma treatment for children benefit/harm
harm: cost, hassle, loss of height 0.5-1cm, oral thrush
benefit: helps diagnosis, if symptoms respond, improve quality of life, reduces risks of attacks
for children, when is it not asthma usually?
under 18 months, likely infection
over 5 years - likely asthma
but if it sounds like asthma and responds to asthma treatment it is asthma regardless of age
(child asthma) what is differential diagnosis for asthma for under 5 years of age
- congenital ( a disease or physical abnormality) present from birth.
- Cystic fibrosis (CF)
- Primary ciliary dyskinesia (PCD) is a rare genetic condition that can lead to chronic lung,
- bronchitis
- foreign body
(child asthma) what is differential diagnosis for asthma for over 5 years of age
- dysfunctional breathing
- vocal cord dysfunction
- habitual cough
- pertussis (also known as whooping cough)
asthma vs Viral-Induced Wheezing child (child asthma)
treated the same bronchodilators
not separate conditions
in preschool children 99%
should be treated
what are the goals in treatment for asthma (childhood)
- have minimal symptoms during day and night
minimal need for reliever medication
- no attacks (exacerbations)
no limit of physical activity
normal lung function (in practical terms FEV1and or PEF >80% predicted or best
the right questions to ask when reviewing asthma (children)
to see if poorly controlled asthma
SANE - pneumonic
- Short-acting beta-agonist/week (are you using more than 2x week) (if Yes poorly controlled)
- Absence - from school/nursery
Nocturnal symptoms a week if waking >1 night a week = poorly controlled
Exertional symptoms a week
(child asthma) treatment decisions for well-controlled asthma patient
- no change of treatment
- consider reducing dose
(child asthma) treatment decisions for poorly controleld asthma
- are they taking treatment? are they taking it correctly? - no change to asthma treatment
- is this not asthma? stop asthma treatment
none of the above? - increase treatment to….
(child asthma) asthma step up and step down
start on low dose inhaled corticosteroids (as diagnostic process)
review after 2 months
- no routine test to monitor progress, no change is easier to step down
YOU NEED to give them an easter inhaler holiday to check working anyway
classes of asthma medications (child asthma)
- short-acting beta-agonists
- inhaled corticosteroids
- long-acting beta-agonists
leukotriene receptor antagonists
theophyllines
oral steroids
“add ons”
add treatment to short beta-agonists (child asthma)
add preventer - long-acting beta-agonist
leukotriene - montelukast only 1/3 significant improvement 1/3 some improvement 1/3 no improvement, better adherence, granules used for reluctant toddlers
severe asthma approach(child asthma)
when long-acting and short-acting beta-agonist doesn’t work
experimental medicine 50% psychological issues
>50% compliance issues.
question the diagnosis
a minority have a genuine disease
new medication biologics although unproven for children
metered-dose inhaler with spacer why do you need a spacer (children)
you get less than 5% of the drug in your lung
you get around 20% deposition with a spacer
4x as much drug
and SHAKE the inhaler between puffs
also, wash spacer do not rinse
for a parent of a child with asthma how can they improve child’s asthma without medication
stop tobacco smoke exposure
remove environmental triggers: cats, dogs
dust mite levels
no evidence of diet for asthma
alter humidity ionisers increase cough but dehumidifiers or humidifiers don’t improve asthma control
weight reduction good but not evidence for asthma
acute asthma treatment mild (child asthma)
short-acting beta agonists
acute asthma treatment moderate (child asthma)
short-acting beta-agonist via neb + preventer (when a child is a well neb)
acute asthma treatment severe asthma (child asthma)
iv salbutamol
iv aminophylline
iv magnesium (nebuliser)
iv hydrocortisone
intubate and ventilate
how to choose what treatment? (child asthma)
look at the patient - can talk?
respiratory rate
work of breathing
heart rate
o2 saturation
ability to complete sentences
confusion
air entry
for child asthma treating acutely - what is the treatment path?
start treatment chosen, assess in 1 hour
step-up or down as appropriate
for chronic/maintenance treatment = inhaled steroids (_not o_ral)
acute treatment = oral steroids (not inhaled)
(adult asthma) definition
complex disease no universally accepted definition
characterised by increased responsiveness of the trachea and bronchi to various stimuli and manifested by widespread narrowing of airways that changes in severity either spontaneously of as a result of therapy
(adult asthma) - what is it?
history of respiratory symptoms (most marked at beginning or end of the day) such as:
wheezing
shortness of breath
coughing
chest tightness
(adult asthma) why is it important
common 5-10% population 5,4 million at least effected
dangerous 3 asthma-related deaths a day
expensive 70,000 admissions yearly avg stay 4 days
pathophysiology asthma
1 disease of lung airway - airway inflammation mediated by immune system
2 widespread narrowing of airway
3 increased airway reactivity ► airway narrowing can be done spontaneously or to stimuli
risk factors for (adult asthma)
hereditary - recognised genetic basis - disease clusters in families + twin, family and population-based studies
atopy - body predisposition to develop antibody called immunoglobin E (IgE) in response to exposure to the environmental allergen and is an inheritable trait
associated with allergic rhinitis, asthma, hayfever eczema
increased first-degree family member of asthma or atopic disease maternal atopy
proven risk of asthma
smoking - maternal smoking
also grandmother smoking - tobacco on genes.
(adult asthma) occupational asthma
underestimated but 10-15% adult onset asthma)
interaction with smoking and atopy
isocyanates - twin pack paint
colophony - welding solder flux
laboratory animals - rodent urinary proteins
grains - wheat protein grain mites
enzymes - subtilisin, amylase
drugs - antibiotics, salbutamol
crustaceans - prawns and crabs
(adult asthma) links to asthma - prevalence
obesity - increased BMI with asthma - obesity proinflammatory
diet - vitamin e,c and d. selenium. polyunsaturated fatty acids. oily fish, Mediterranean diet, margarine
hygiene hypothesis - reduced exposure to microbes/microbial product
children born on farms less likely to develop asthma
microbial diversity appears to be important in reducing the risk of asthma
(adult asthma) clinical aspects
history important
investigation can be supportive but no single test diagnoses asthma
important to think what else it could be
symptom history of asthma
(adult asthma)
wheeze
short of breath (dyspnoea), and how severe
chest tightness
cough, proximal and usually dry
sputum (occasional)
symptom variation?
(adult asthma)
variable symptoms - daily variation (nocturnal/early morning)
weekly variation (occupation, better at weekends and holidays)
annual variation (environmental allergens)
what can trigger (adult asthma) symptoms
differs for each individual
exercise, cold air, cigarette smoke, perfumes/strong scents, Upper respiratory tract infections, pets, tree or grass pollen, food, drugs (aspirin/NSAID)
another aspect of asthma history
PMH - childhood asthma, bronchitis or wheeze in infancy; eczema; hayfever
drugs - current inhalers (check their technique) other asthma therapy, compliance; beta-blockers, aspirin NSAIDs
Family history - asthma and other atopic diseases
Social history - tobacco, recreational drugs, vaping; pets; occupation (past and present); pathological aspect.
(adult asthma) clinical examination
usually unhelpful in the clinic -; breathless on exertion; hyperinflated chest; wheeze
probably not asthma if; finger clubbing, cervical lymphadenopathy; stridor; asymmetrical expansion, dull percussion note (collapse/effusion); crepitations (bronchiactasis, cyctic fibrosis, Interstitial Lung Disease (ILD) or left ventricular function (LVF)
differential diagnosis (adult asthma)
really trying to differentiate other causes of wheeze, cough, dyspnoea
Generalised airflow obstruction - COPD (irreversible airflow obstruction), bronchiectasis, cystic fibrosis
Localised airway obstruction (inspiratory stridor = large airways) Tumour, Foreign body
cardiac-related
(adult asthma) intermediate suspicion of asthma tests
fev1/fvc <70% lindicates airflow obstruction
normal spirometry may still be asthmatic.
Spirometry > normal > peak flow monitoring > bronchial provocation or nitric oxide
Spirometry > obstructed (fev1/fvc) <70% fev1 <80% predicted > full pulmonary function > reversibility using beta 2 agonist (or oral steroid)
(adult asthma) if obstructed what next test (pulmonary function)
full pulmonary function test - exclude COPD /emphysema
carbon monoxide gas transfer (transfer of co to hb across alveoli)
asthma gas transfer is preserved or even can be increased. in COPD reduced due to alveolar reduction and destruction of lungs by smoking.
(adult asthma) what is a further test (reversibility)
response to bronchodilator
baseline 15 mins post 400 ug inhaled salbutamol
baseline 15 minutes post neb 2.5-5mg salbutamol
interpretation significant reversibility - fev1>200ml + fev1 12% baseline
(adult asthma) reversibility to corticosteroids (anti-inflammatory)
separates COPD from asthma. oral steroids 0.6mh/kg prednisolone 14 days
peak flow chart and meter
baseline + 2-week spirometry peak flow.
Normal spirometry - variable obstruction (adult asthma)
lung function may (usually) be normal
look for variability airflow obstuction
peak flow meter and chart twice daily (best 3 measurements for 2 weeks)
analysis subjective
morning/nocturnal dips, decline over weeks/days variability >20% on > 3 days a week
apart from lung function tests (adult asthma) what other investigations are useful?
Chest x-ray - hyperinflated or hyperlucent (find no effusion, collapse, opacities, interstitial changes)
skin prick testing (atopic status)
total and specified IgE (atopic status)
Full blood count (eosinophilia (atopy)
atopy are likely to have asthma
(adult asthma) assessment of acute asthma
ability to speak
heart rate
respiratory rate
PEF flow
oxygen saturation/arterial blood gas
how is acute asthma graded (adult asthma)
moderate
severe
life-threatening
near-fatal
(adult asthma)
moderate
symptoms
able to speak and complete sentences
RR <25
Ref 50-70% predicted or best
Sao2 >92% no need for ABG
pao2 >8kPa
(adult asthma)
severe
symptoms
Any one of
inability to complete sentences in one breath
hr>110
RR >25
REF 33-50% predicted of best
Sao2>92%
pao2 >/8kpa
(adult asthma)
life-threatening
symptoms
any one of
- grunting; impaired consciousness; confusion: exhaustion; bradycardia/arrythmia/hypotension; PEF <33% predicted or best; cyanosis silent chest; poor respiratory effort
Sao2 <92% (definitely need blood gas!); pao2 <8kPa; Paco2 noemal (4.6-6.0kPa)
(adult asthma)
near-fatal
Symptoms
Raised paCo2
need for mechanical ventilation
for (adult asthma) treatment what is the goal
- no daytime symptomes
no night time wakening
no need for rescue medication
no asthma attacks
no limitation on activity including exercise and normal function (in practical terms fev1 and or pef 80% predicted or best)
minimal side effects from medication
what are non-pharmilogical management of (adult asthma)
- patient education and self-management plans
exercise
smoking cessation
weight management
flu/pneumococcal vaccinations
(adult asthma) inhalers
a small dose of the drug
delivery directly to the target organ (airway and lung)
the onset of effect is faster
minimal systemic exposure
systemic adverse effects are less severe and less frequent
name the inhalers for symptom control
short-acting beta 2 agonists (SABA) relievers
salbutamol - meter dose inhaler andd DPI (side effect tremor and tachycardia)
terbutaline - DPI
Name the oral therapies for (adult asthma)
Leukotreine receptor antagonist (montelucaste prob most common)
Theophylline
prednisolone
treatment for mild/moderate (adult asthma) attack
Increase inhaler use
oral steroid
treat trigger
early follow up
backup plan
how to teat a moderate/severe (adult asthma) acute asthma attack
hospital treatment
- nebulisers - salbutalom ipratropium
oral/iv steroid (hydrocortisone iv short-acting + predisinolone (oral)
magnesium
aminophylline
triggers -infection/allergen
complications - chest xray
review
level 2/3 care (hdu itu)
contract od asthma and COPD
- age of onset
smoking history
response to treatment
treatment goals
trajectory
similar therapies
non-pharmacological interventions the same
what is COPD definition
a lung disease characterised by chronic obstruction of airflow interfering with normal breathing and is not fully reversible
an umbrella term that also takes in to account chronic bronchitis and emphysema
diagnosis of copd - symptoms of chronic bronchitis
cough and sputum for at least three months present in two consecutive years
diagnosis of COPD - symptoms of emphysema
structural changes in the alveoli causing them to disintegrate - lose surface area
what is main cause of COPD
smoking
modifiable and non-modifiable causes of COPD
modifiable - smoking or low-income biomass of fuel cooking and heating, air pollution, geographical, temporal association, occupational
non-modifiable, female sex, increasing age.
symptoms of COPD
cough
breathless
sputum
frequent chest infections
wheezing
weight loss
fatigue
swolen ankles
copd key things to note symptom and factor
smoking history
age
onset/progression
copd examination finding signs
cyanosis
pursed lip breathing
hyperinflated chest
raised jvp
using accessory muscles
peripheral oedema
cachexia severe weight loss
wheeze
mmrc dyspnoea scale
0 - only breathless in strenuous exercise
1- short of breath when hurrying on level ground or walking up a slight hill
2 - on the level ground walk slower than people same age because of breathlessness or have to stop for breath when walking at my own pace
3 - I stop for breath after walking about 100 yards or after a few minutes on level ground
4 - I am too breathless to leave the house or I am breathless when dressing
fev1 and ratio spirometry what indicates an abnormality
fev1<80% predicted normal
fvc <80% predicted normal
ratio fev1/fvc <0.7
fev1 and ratio spirometry what indicates an obstructive disorder
fev1< 80%
fvc usually reduced but to a lesser extent than fev1
fev/fvc ratio <0.7
fev1 and ratio spirometry what indicates a restrictive disorder
fev1 <80% predicted normal
fvc reduced (<80% predicted normal)
fev1.fvc ratio (>0.7)
spirometry when diagnosing the severity: mild
stage 1, mild - FEV1 80% of predicted value or higher (diagnosis can only be made on basis of respiratory symptoms
spirometry when diagnosing the severity: moderate
stage 2, moderate - fev1 50-79% predicted value
spirometry when diagnosing the severity: severe
stage 3, severe - FEV1 30-49% of predicted value
spirometry when diagnosing the severity: very severe
stage 4, very severe - fev1 less than 30% predicted value
spirometry when diagnosing the severity: end-stage
end-stage COPD not part of the staging classification, but a term used in practice
chest x-ray COPD
hyperinflation (more than 6 anterior ribs showing or 10 posterior ribs)
flat diaphragm
small heart
bulla (from emphysema)
It is likely that allergies cause the development of childhood asthma.
Select one:
True
False
False – it is likely that an underlying abnormality in the epithelium leads to the development of both asthma and allergies.
other tests for COPD
spirometry
then pulmonary function tests - lung vol - transfer of gas
radiology (high resolution computed tomography hrct)
where is emphysema usually found in smokers
upper area of lungs due to inhalation injury to tissues
acute COPD exacerbation what will be reported
worsening symptoms - unable to smoke; short of breath; systemic upset (eating drinking ADL); wheeze; tight chest; temperature (if infection); cough; fatigue; sputum purulence and volume
signs of severe copd exacerbation
breathless and resp rate over 25 min
significant decrease in exercise tolerance
using accessory muscles at rest
signs of sepsis (if infection(
purse lip breathing
fluid retention, cyanosis spo2 92% on air; confusion
differential diagnosis for COPD
pneumonia; pulmonary embolism, myocardial infarction, lung cancer, pleural effusion, pneumothorax
management of COPD
change inhalers (technique, device, add bronchodilator, increase or add inhaled steroid)
oral steroid - prednisolone tablet
antibiotics
self-management for select patients
acute exacerbation visual symptoms, test and treatment
confusion; cyanosis; severe breathlessness; flapping tremor; drowsy; pyrexial; wheeze; tripod position
tests - chest x-ray, blood gases. full blood count, u+E, sputum culture, Viral throat swab
treat - o2 therapy, nebulised bronchodilator (beta 2 agonist and antimuscarinic) oral/iv corticosteroid +/- antibiotic
(iv aminophylline, respiratory stimulant NIV)
severe copd exacerbation tests
tests - chest x-ray, blood gases. full blood count, u+E, sputum culture, Viral throat swab
treat - o2 therapy, nebulised bronchodilator (beta 2 agonist and antimuscarinic) oral/iv corticosteroid +/- antibiotic
(iv aminophylline, respiratory stimulant NIV)
severe copd exaverbation - treatment
treat - o2 therapy, nebulised bronchodilator (beta 2 agonist and antimuscarinic) oral/iv corticosteroid +/- antibiotic
(iv aminophylline, respiratory stimulant NIV)
treat other co-existing conditions
Severe disease - respiratory failure cause
cause by reduces v/q match (ventilation/perfusion)
increased physiological dead space due to emphysema
types of respiratory failure
type 1: reduces p02
type 2 reduces po2 and increased pco2 (ventilatory failure)
how often do you have type 2 respiratory failure?
severe cases of COPD
Signs of respiratory failure
flapping tremor - co2 retention hypercapnia
become acidotic and risk death
explain cor pulmonale
right-sided heart failure due to lung disease - comes from smoking and hypoxia
symptom - tachycardia, oedematous, raised JVP, congested liver
ECG shows right axis deviation, p pulmonale, t wave inversion on v1-v4
echo: pulmonary hypertension, tricuspid regurgitation
in severe copd why does oedema occur
cor pulmonale right-side heart failure, cause a backup of blood. causes reduce circulation volume of blood - activates a compensatory system of kidneys RAAS system - leads to fluid retention
Why would COPD have raised harmoglobin?
secondary polycythemia - body produces increased erythropoietin in response to low 02 levels. increases haemoglobin, haematocrit and blood viscosity
what is NOT a cause of COPD in osce
finger clubbing is NOT a symptom of COPD
what is public health measure to prevent COPD
age to purchase tobacco raised from 16 - 18
picture warnings
sale of tobacco banned in vending machines
ban smoking in cars with children
standardised packagine
the treatment plan for COPD goals
improve exercise tolerance
prevent exacerbation
nutrition/weight loss
complications (cor pulmonale, respiratory failure)
anxiety/depression
co-morbidities
dysfunctional breathing
palliative care
non-pharmicological management COPD
SMOKING CESSATION
VACCINATION FLU/PNEUMOCOCCAL
pulmonary rehabilitation
nutritional assessment
psychological support
pharmacological goal of COPD
relieve symptoms
prevent exacerbations
improve quality of life
Inhaled therapy for COPD
Short-acting bronchodilators: SABA salbutamol SAMA ipratropium
long-acting bronchodilators: LAMA long-acting antimuscarinic agents - umeclidinium, tiotropium LABA long-acting beta2 agonist - salmeterol
high dose inhaled corticosteroids ics and laba - relvar - fluticasone/vilanterol; fostair MDI
A child under 5 with a new diagnosis of asthma who is symptomatic more than 3 times a week should be started on a leukotriene receptor antagonist.
Select one:
True
False
True – the initial preventer medication for under 5s is a LRTA. For children over 5, it is a very low dose inhaled corticosteroid.
The correct answer is ‘True’.
Pharmacological treatments (i.e. inhalers) give the best value for money in terms of improvement in quality of life for patients with COPD.
Select one:
True
False
False – the best value for money in QALY (quality-adjusted life-years) is from flu vaccination, smoking cessation and pulmonary rehabilitation. Non-pharmacological interventions in COPD are very effective and very important.
The correct answer is ‘False’.
he hallmark of obstructive lung disease is reduced FVC.
Select one:
True
False
False – although the FVC may be reduced, for a lung disease to be considered obstructive there needs to be reduced FEV1:FVC (less than 0.7).
The correct answer is ‘False’.
Decline in FEV1 over time can be reversed by stopping smoking.
Select one:
True
False
False – Decline in FEV1 is irreversible, however the rate of decline can be slowed.
The correct answer is ‘False’.
It is important to take a history and perform a full respiratory examination before diagnosing a child with asthma.
Select one:
True
False
False – examination findings are likely to be normal. Diagnosis is from the history!
The correct answer is ‘False’.
An excess of alpha-1-antitrypsin can lead to emphysema.
Select one:
True
False
False – alpha-1 antitrypsin is an enzyme which breaks down other enzymes that break down alveolar tissue. A deficiency of this enzyme tips the balance towards tissue destruction and can lead to emphysema
The correct answer is ‘False’.
Respiratory failure in COPD is due to V/Q (Ventilation/Perfusion) mismatch.
Select one:
True
False
False – generally speaking, respiratory failure in COPD is due to matched defect in ventilation and perfusion. Remember that oxygenation will be impaired in any situation where blood is not getting to the alveoli (perfusion) or air is not getting to the alveoli (ventilation). In COPD, both are affected.
The correct answer is ‘False’.
In spirometry, an FEV1:FVC of 0.5 would be considered obstructive.
Select one:
True
False
True – normal FEV1:FVC is about 0.7-0.8.
The correct answer is ‘True’.
Peripheral eosinophilia is not diagnostic of asthma.
Select one:
True
False
True – while a peripheral eosinophilia may be suggestive of atopy (remember this is the cluster of conditions including asthma, eczema, hayfever, allergic rhinitis and other allergies), it’s important to remember that there is NO diagnostic test for asthma. Diagnosis is primarily from the history, and some tests are useful to help you gather additional information.
The correct answer is ‘True’.
Spirometry is required to diagnose COPD.
Select one:
True
False
True – unlike asthma, the diagnosis of COPD requires both typical symptoms and history AND typical spirometry showing airflow obstruction. Spirometry is performed pre- and post-bronchodilator therapy, to demonstrate non-reversible (or partially reversible) obstruction.
The correct answer is ‘True’.
Initial treatment of asthma in adults is with a low-dose inhaled corticosteroid.
Select one:
True
False
True – it is now known that inhaled steroids are the most effective initial treatment, and are given as a trial to assist in the diagnosis of asthma.
The correct answer is ‘True’.
Carbon monoxide gas transfer in asthma can be normal or increased.
Select one:
True
False
True – gas transfer is calculated by measuring uptake of carbon monoxide, and can be helpful to distinguish between COPD and Asthma. It is reduced in COPD due to alveolar destruction. In asthma it should be normal or slightly increased.
The correct answer is ‘True’.
In moderate or severe exacerbations of asthma, the pCO2 is normal.
Select one:
True
False
False – this is really important. In moderate or severe exacerbations of asthma, the respiratory rate goes up, so you would expect more CO2 to be blown off, therefore the pCO2 (measurement of the amount of CO2 dissolved in the blood, shown on a blood gas analysis) should be LOW. If a patient is having an acute asthma attack with a high respiratory rate and their pCO2 is “normal”, this means they are not ventilating adequately, and this is an indication that they require specialist input urgently as their asthma is life-threatening.
The correct answer is ‘False’.
A child >5 on a very low dose inhaled corticosteroid who continues to require their reliever inhaler twice a week should have a long-acting beta-agonist added on to their treatment.
Select one:
True
False
True – the BTS/SIGN guidelines would recommend a long-acting beta agonist (LABA) as the next step, and this would be a reasonable next step as per other guidelines.
The correct answer is ‘True’.
Smoking tends to cause emphysema in the bases of the lungs.
Select one:
True
False
False – as emphysema from smoking is caused by inhaled pathogens, it tends to occur in the region of the lung most easily reached by inhaled smoke: the apex. Contrast this to alpha-1-antitrypsin deficiency, where the resulting emphysema tends to affect the base.
The correct answer is ‘False’.
For a diagnosis of chronic bronchitis to be given, a patient should have a cough productive of sputum most days, for 3 consecutive months, for at least 3 years.
Select one:
True
False
False – it only needs to be for 2 years.
The correct answer is ‘False’.
In an acute asthma attack, steroids should be given via a nebuliser rather than through a metered-dose inhaler.
Select one:
True
False
False – in an acute asthma attack, steroids should be given orally, or sometimes intravenously.
The correct answer is ‘False’.
Hypoxia increases the blood pressure in the lungs in COPD.
Select one:
True
False
True – hypoxia leads to a reflex constriction of blood vessels in the lungs. This increases the vascular resistance, meaning the right side of the heart has to work harder, and the blood pressure rises. This is called pulmonary hypertension.
The correct answer is ‘True’.
Most infections causing exacerbations of COPD are viral.
Select one:
True
False
True – although patients will often receive antibiotics for acute infective exacerbations of COPD, in the majority of cases the pathogen is a virus.
The correct answer is ‘True’.
Centri-acinar emphysema begins with dilatation of the alveoli.
Select one:
True
False
False – centri-acinar emphysema begins with dilatation of the respiratory bronchiole, and then progresses to loss of alveolar tissue.
The correct answer is ‘False’.
Forced Vital Capacity (FVC) divided by the Forced Expired Volume in one second (FEV1) is a useful clinical measure of lung function.
Select one:
True
False
False. That statement is the wrong way round. A useful clinical measure of lung function is FEV1 divided by FVC (not the other way around). This tells you what proportion of the FVC a patient can exhale in one second.
The correct answer is ‘False’.
The saturation of haemoglobin decreases as blood passes through the tissues because of an increase in pH.
Select one:
True
False
False. Haemoglobin saturation decreases as blood passes through the tissue because the tissues have a lower partial pressure of oxygen (40mmHg) than is found in the plasma (100mmHg). As such oxygen moves down its partial pressure gradient into the tissues until equilibrium is reached. Alkalosis (a rise in extracellular fluid pH) actually causes haemoglobin to hang onto its oxygen more – it increases the affinity of haemoglobin for oxygen so would increase saturation.
A pneumothorax (air in the pleural cavity) disrupts the relationship between the visceral pleural membrane and the lungs
Select one:
True
False
False. It disrupts the relationship between the parietal pleural membrane and the visceral pleural membrane. The visceral pleural membrane would remain attached to the lung surface in a pneumothorax.
The haemoglobin-O2 saturation curve is moved to the left by a decrease in body temperature..
Select one:
True
False
True. A decrease in body temperature increases the affinity of haemoglobin for oxygen and thus shifts the binding curve to the left. This is one of the reasons hypothermia is so dangerous – at a body temperature of 20oC the haemoglobin remains fully saturated meaning while the blood is jam packed full of oxygen the peripheral tissues cannot access it because the haemoglobin won’t release it.
lveolar ventilation volume is more than pulmonary ventilation volume.
Select one:
True
False
False. Pulmonary (or minute) ventilation describes the total amount of air breathed in or out per minute (basically tidal volume x respiration rate). Alveolar ventilation accounts for the volume of air that gets stuck in dead space and never reaches the alveoli, so dead space volume must be subtracted from tidal volume before multiplying by respiration rate ((TV-DS) x RR), making alveolar ventilation smaller than pulmonary ventilation i.e. not all the air you breathe in reaches the level of the alveoli and participates in gas exchange!
shift of the oxygen dissociation curve of haemoglobin to the right decreases the oxygen content of blood at a given oxygen pressure.
Select one:
True
False
True. A rightward shift means that for any given value of PO2, less oxygen will be bound to haemoglobin than if that shift had not happened – look at the S shaped curve if you don’t believe it!
The correct answer is ‘True’.
Respiratory acidosis often accompanies severe lung pathology.
Select one:
True
False
True. Most lung pathologies lead to an impairment of gas exchange for one reason or another. This impairment increases CO2 levels in arterial blood. An increase in CO2 leads to an increase in H+ concentration (revise the chemical equation shown in the lectures if you don’t understand why this happens). As the increase in H+ are due to respiratory dysfunction this is called a respiratory acidosis.
Lung compliance is defined as the magnitude of the change in lung volume produced by a given change in transpulmonary pressure.
Select one:
True
False
True. Compliance describes the change in lung volume for any given change in transpulmonary pressure (sometimes graphs show intrapleural pressure rather than TP but the effect is the same).
A pneumothorax (air in the pleural cavity) increases the functional residual capacity.
Select one:
True
False
False. FRC (volume of air left in the lungs after a forced expiration) will decrease in pneumothorax as the affected lung has recoiled and thus has a smaller volume than before.
During quiet inspiration in the upright position, most of the tidal volume is distributed to alveoli at the base of the lung
Select one:
True
False
True. Compliance is greatest at the base of the lung so a greater volume of inspired air ends up at the base of the lung compared to the apex.
The sum of the resting tidal volume and the inspiratory reserve volume is the inspiratory capacity
Select one:
True
False
True. This is the volume of air you are capable of inspiring.
The correct answer is ‘True’.
criteria for long term o2 COPD
quit smoking for at least 6 months
stay hypoxic so blood gas is <7.3
be hypoxic at rest
or pao2 7.3-8kpa if@ polycythaemia; nocturnal hypoxia; peripheral oedema; pulmonary hypertension
what kind of infection is most common in COPD
viral infection
primary care management acute exacerbation of COPD
Short-acting bronchodilators (SABA) salbutamol SAMA ipratropium - nebs if cannot use inhalers
steroids - prednisolone 40mg per day for 5-7 days
antibiotic - most exacerbation viral - if evidence infection (fever, increase volume/purulence sputum)
consider hospital admission if unwell (tachycardia. low spo2 <90-92%) and hypotension
acute exacerbation COPD - investigation
- full blood count - biochemistry and glucose - theophylline concentration (in patients using theophylline preparation) - arterial blood gas documenting amount of o2 given and by what device - ECG - chest x-ray - blood cultures in febrile patients - sputum microscopy, culture and sensitivity
acuse exacerbation of COPD - ward bade management
02 therapy keep spo2 88-92%
nebulised bronchidilators
- corticosteroids
- antibiotics (oral vs Iv)
assess for evidence of respiratory failure - clinical - arterial blood gas (ABG)
acute exacerbation COPD - when in respiratory failure what do you consider
non-invasive ventilation (NIV)
COPD palliative considerations
teach management of breathlessness and dysfunctional breathing - pharmacological help (morphine) - psychological support - palliative care referral
anticipatory care planning - hospital admission planning - ceiling of treatment - ward-based HDU - DNACPR
Emphysema is the dilatation of bronchioles leading to air trapping.
Select one:
True
False
False – emphysema is the increase in size of the airspaces that are distal to the terminal bronchioles (i.e. the respiratory bronchioles and alveoli). This can be due to dilatation or destruction of their walls, and causes obstruction through air trapping.
In assessing severity of acute asthma in adults, subjective parameters (eg. distress) are just as important as observations and blood gases.
Select one:
True
False
False – patients and doctors tend to underestimate asthma severity, and a life-threatening attack may not be associated with significant distress. Objective measurements such as vital observations (pulse rate, oxygen saturations, peak flow) and blood gas analysis are most useful.
The initial treatment for asthma in children over 5 is very low dose oral steroids.
Select one:
True
False
False – very low dose inhaled steroids are the initial treatment for paediatric asthma. Oral steroids are only used by specialists in treatment-resistant asthma.
Omalizumab is a specialist treatment for asthma, and dampens all components of the inflammatory response.
Select one:
True
False
False – omalizumab is a specialist treatment, and is termed a “biologic” because it is an antibody. It specifically targets IgE (an antibody involved in the allergy response), compared to e.g. prednisolone which has a much more generalised anti-inflammatory action.
Washing a spacer device before using it increases the static charge and decreases the drug delivery to the lungs.
Select one:
True
False
False – washing the spacer device leaves a coating of detergent, which will decrease the static charge. This means the drug is less likely to stick to the spacer, and increases drug delivery to the lungs.
Treatment-resistant, severe asthma is relatively common in children.
Select one:
True
False
False – Severe airways disease that does not respond to maximal treatment is extremely uncommon in children. More commonly, there are complex psychological and illness behaviour elements to the presentation, which can include not taking the treatment as prescribed. These should be thoroughly explored as part of the patient-centred management.
Spirometry is required to diagnose chronic bronchitis.
Select one:
True
False
False – it is a clinical diagnosis, meaning there are no specific tests for chronic bronchitis.
Terbutaline is a short-acting beta agonist used as a reliever medication in asthma.
Select one:
True
False
True – although salbutamol is the most commonly-used reliever medication, terbutaline is also used.
The prevalence of COPD is increasing, but the incidence is decreasing.
Select one:
True
False
True – remember that “prevalence” refers to the total number of people with a condition at any given moment, while “incidence” refers to the rate of new diagnoses.
Asthma is associated with low exhaled nitric oxide (FeNO) due to airway inflammation.
Select one:
True
False
False – FeNO works like a breathalyser for airway inflammation. A high degree of inflammation will lead to a high FeNO, which would be suggestive of asthma.
Female sex is a risk factor for COPD.
Select one:
True
False
True – although the prevalence of COPD among males has historically been higher than that among females (due to a higher prevalence of smoking), a female smoker is more likely to develop COPD than a male smoker.
Ipratropium bromide is a long-acting beta agonist.
Select one:
True
False
False – ipratropium bromide is a muscarinic antagonist. It works by relaxing the smooth muscle of the airways.
Patients are eligible for longterm oxygen therapy if they have a PaO2 of <7.3 AND additional complications of chronic hypoxia.
Select one:
True
False
False – patients are eligible for LTOT if they have a PaO2 (measured from an arterial blood sample) of <7.3 regardless of additional features. If they have complications of chronic hypoxia such as polycythaemia, pulmonary hypertension, peripheral oedema or nocturnal worsening of hypoxia, LTOT is offered sooner, at a PaO2 of <8.
More than 50% of long-term smokers will develop COPD.
Select one:
True
False
False – surprisingly, less than half of long-term smokers will develop COPD in their lifetime. This demonstrates the interaction between genetic predisposition and environmental factors in the development of COPD
In moderate or severe exacerbations of asthma, the pCO2 is normal.
Select one:
True
False
False – this is really important. In moderate or severe exacerbations of asthma, the respiratory rate goes up, so you would expect more CO2 to be blown off, therefore the pCO2 (measurement of the amount of CO2 dissolved in the blood, shown on a blood gas analysis) should be LOW. If a patient is having an acute asthma attack with a high respiratory rate and their pCO2 is “normal”, this means they are not ventilating adequately, and this is an indication that they require specialist input urgently as their asthma is life-threatening.
