Chronic Obstructive Pulmonary Disorder Flashcards
What is the definition of COPD?
a disease state characterised by airflow limitation that is not fully reversible
the airflow limitation is usually both progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases
What 2 conditions is COPD usually a combination of?
BRONCHITIS:
- cough & sputum production on most days for at least 3 months during the last 2 years
EMPHYSEMA:
- enlarged air spaces distal to the terminal bronchioles, with destruction of the alveolar walls
What are the usual causes of COPD?
it is caused by long-term exposure to toxic particles and gases
- cigarette smoking accounts for over 90% of cases
- also inhalation of smoke from biomass fuels used in heating and cooking in poorly ventilated areas
What group of conditions is it important to distinguish COPD from?
How are these conditions defined?
COPD needs to be distinguished from the restrictive pulmonary diseases
these are also chronic respiratory diseases that are characterised by decreased lung capacity where FEV1 and FVC are both decreased proportionally
this results in a normal FEV1 : FVC
What is the FEV1 : FVC ratio in COPD usually?
Is this factor essential for diagnosis?
FEV1 : FVC ratio is <70%
COPD can also be diagnosed in patients with FEV1 : FVC >70% on the basis of clinical signs and symptoms
(e.g. cough, shortness of breath)
around 30% of cases of COPD have normal spirometry at diagnosis
What is the general disease course of COPD typically like?
patients typically follow a slowly progressive course with recurrent exacerbations
this involves short periods of increased shortness of breath, with or without infection
In general, what is involved in the long term management of COPD?
- combinations of inhaled steroids and bronchodilators
- smoking cessation
- pulmonary rehabilitation
- important to prevent exacerbations with flu and pneumonia vaccines
How are COPD exacerbations typically managed?
exacerbations are often mild and can be treated in primary care, but COPD patients sometimes present to the hospital with exacerbations
- oral steroids
- increases in doses of inhaled agents
- oxygen therapy
- most cases are also given antibiotics
What is the prevalence of COPD in the UK?
- affects 1.5million in the UK
- affects at least 1 in 7 people over 40
- it is severely under-diagnosed with airway obstruction affecting 10% of the population, but only 5% being diagnosed with COPD
What % of COPD cases are accountable to smoking?
Why is this important to consider?
smoking accounts for 90-98% of all cases
symptoms will improve in 90% of patients with smoking cessation
What are the characteristics of a typical patient presenting with COPD?
Why is it important to ask about how many cigarettes the patient smokes?
- most commonly seen in ex-smokers > 35 years of age
- most patients do not show symptoms until they are in their 50s
COPD is unlikely to develop with a smoking history less than 10 pack years
What factors are involved in the aetiology of COPD?
- smoking
- coal mining
- exposure to air pollution
- particularly in the developing world - indoor fires & cooking
- genetic predisposition
- a1-antitrypsin deficiency causes emphysema
What are 2 predisposing factors to development of COPD?
- low socioeconomic status
- low birth weight
- associated with reduced maximum lung capacity in adulthood
What % of smokers will develop COPD?
10 - 20% of all smokers will develop COPD
up to 50% of those with a >20 pack year history will develop COPD
not all heavy smokers develop COPD, showing there is some individual susceptibility
What are the characteristic symptoms of COPD?
- cough (may or may not be productive, but usually is)
- wheeze
- dyspnoea (breathlessness)
- usually following many years of a smokers cough
- frequent exacerbations producing purulent spputum
What factors can sometimes worsen symptoms in COPD patients?
- cold, foggy weather
- atmospheric pollution
- in advanced disease, breathless becomes severe even after mild exercise, such as dressing
What are the most common clinical signs of COPD?
- in mild disease, there are no signs apart from “wheeze” throughout the chest
- in severe disease, there is tachypnoea with prolonged expiration
- use of accessory muscles of respiration
- intercostal indrawing on inspiration
- pursing of the lips on expiration
- poor chest expansion
- hyperinflation of the lungs
What is the cricosternal distance?
How is this changed in COPD and why?
the distance between the cricoid cartilage and the sternal angle
it is reduced and is < 3cm in COPD due to hyperinflation
the thorax is raised in relation to the cricoid cartilage
What may chest / breath sounds be like in COPD?
- Resonant chest sounds are suggestive of hyperinflation
- Quiet breath sounds over areas of emphysematous bullae
What is wheeze?
What causes it?
an abnormal high pitched or low pitched breath sound heard on expiration
it is caused by abnormal narrowing of the smaller airways
What type of wheeze is usually present in COPD?
What is the other type and what is this more likely to be?
COPD presents with a POLYPHONIC wheeze
this is made up of many different “notes” as it is caused by many abnormal airways
the other type of wheeze is MONOPHONIC
this is caused by a single airway obstruction, and is more likely to be cancer
Why is wheeze sometimes confused with stridor?
What tends to cause stridor?
stridor is the name for a sound heard on INSPIRATION, rather than expiration
it is typically caused by an UPPER airways obstruction such as an inhaled foreign body or mass (cancer) impinging on the upper airway
Why does someone with COPD have a prolonged expiration?
as their FEV1 is low, they have to have a prolonged expiratory phase to allow for adequate respiration
Why do patients with COPD use a pursed lip breathing technique?
- it creates a smaller opening though which air can exit the respiratory system
- this keeps pressure in the airways higher
- this helps to stop smaller airways from collapsing
- there is a larger surface area for gas exchange than in the absence of pursed lip breathing
Why is pursed lip breathing sometimes called Auto-PEEP?
PEEP stands for positive end expiratory pressure
it is a technique used in intubated and CPAP patients to improve ventilation
pursed-lip breathing provides a small amount of PEEP for patients with COPD
What is meant by the “dynamic closure point” in a COPD patient?
in COPD, some of the airways will collapse at a point proximal to many of the alveoli
this point is the dynamic closure point
it occurs due to destruction of elastin tissue that occurs in emphysema
How can pursed-lip breathing alter the dynamic closure point?
What is the overall effect of this on ventilation and reducing dyspnoea?
- high pressure in the lungs created by pursed lip breathing moves the dynamic closure point to a more distal area of the lung
- this means that ventilation can occur in a greater number of alveoli
- VQ mismatch is reduced
- dyspnoea is reduced
What is the difference in the way COPD patients present depending on whether they remain sensitive to CO2?
those who remain responsive to CO2 are usually breathless and rarely cyanosed
heart failure & oedema are rare features except as terminal events
those who become insensitive to CO2 are often odematous and cyanosed, but rarely breathless
What features may a COPD patient present with if they have hypercapnia?
What can severe hypercapnia lead to?
- peripheral vasodilatation
- bounding pulse
- coarse flapping tremor of the outstretched hand when pCO2 is above 10 kPa
- severe hypercapnia leads to confusion and progressive drowsiness
Why does COPD lead to hyperinflation?
Why is this a problem?
COPD leads to gas trapping which increases the amount of dead space and leads to hyperinflation
this reduces the amount of air exchanged with outside air with each breath
it also leads to reduced chest wall compliance
hyperinflation is exaggerated during exercise
How is a diagnosis for COPD usually made?
it is usually clinical and uses the GOLD criteria
there is a history of breathlessness and sputum production in a lifetime smoker
in the absence of smoking, a working diagnosis of asthma is usual unless there is family history of lung disease suggestive of a1-antitrypsin inhibitor deficiency
What would be expected to be seen on lung function tests (spirometry) in a patient with COPD?
- FVC < 80%
- FEV1 : FVC < 0.7 or < LLN (lower limit of normal)
- increased residual volume (but may also be normal)
- gas transfer coefficient of carbon monoxide is low when significant emphysema is present
What would be expected to be seen on a chest X-ray of someone with COPD?
- possible hyperinflation, but often normal
- flattened hemi-diaphragms
- large central pulmonary arteries
- decreased peripheral vascular markings
- bullae
- cylindrical heart (due to cor pulmonale)
- patchy consolidation may be present if there is an ongoing infective exacerbation
What may be seen on an ECG in someone with severe COPD?
if there is right atrial and ventricular hypertrophy suggestive of cor pulmonale, this will produce large p waves on ECG
this is known as P pulmonale
What do blood gases show in someone with COPD?
they are often normal
in advanced disease there is evidence of hypoxaemia (reduced PaO2) and hypercapnia (increased PaCO2)
What may be seen on a full blood count in someone with COPD?
- raised haemoglobin & PVC as a result of persistent hypoxaemia
- this is secondary polycythaemia
- in this case, the haematocrit is measured and is >45
- normocytic normochromic anaemia of chronic disease has a prevalence of 20%
What other test is performed when investigating COPD?
a1-antitrypsin levels
normal range is 2 - 4 g/L
What is involved in the gas transfer coefficient for carbon monoxide test?
it is a measure of the effectiveness of gas transfer across the alveoli
the patient inhales a known value of carbon monoxide, which has a very high affinity for haemoglobin
in emphysema and severe fibrosis, the gas transfer value is reduced
What test is required for a diagnosis of COPD?
When can these values be a bit less reliable?
spirometry is required to confirm a diagnosis of COPD with a cutoff of FEV1 : FVC ratio of <0.7
in patients >65 and <45 this ratio is not as reliable, and specialist spirometry may be required to clarify the diagnosis in borderline cases
Why can it be difficult to diagnose COPD sometimes?
What can it become confused with?
there are no clinical features that are diagnostic and COPD cannot be diagnosed on the basis of CXR and clinical history alone
- COPD cannot be diagnosed from hyperinflation seen in CXR as asthma may also cause this
- there may appear to be a barrel chest in elderly patients that is actually curvature of the spine due to osteoporosis
In what groups of patients should a diagnosis of COPD be considered?
- patients >35 with symptoms of breathlessness and cough and/or sputum production
- all smokers and ex-smokers > 35
Why does spirometry need to be measured both pre- and post- giving a bronchodilator?
if airflow limitation is reversible
(usually an increase in FEV1 of >12% and >200mls)
this is suggestive of asthma or mixed COPD
if FEV1 increase is >400mls this suggests asthma
What is predicted FEV % and typical symptoms in mild COPD?
FEV predicted 60 - 80%
- symptoms are variable and there are typically few symptoms
- breathlessness on moderate exertion
- no effects on activities of daily living (ADLs)
- may be cough and sputum production
What are the symptoms and predicted FEV % in moderate COPD?
FEV predicted 40 - 60%
- breathlessness when walking on flat ground
- exacerbations
- some limitations of ADLs
What is the predicted FEV and symptoms in severe COPD?
FEV predicted <40%
- breathlessness on minimal exertion
- daily activities severely limited
- frequent and severe exacerbations
What is the most consistent pathological finding associated with COPD?
What is the result of this on lung function?
hypertrophy and increase in the number of mucous-secreting goblet cells of the bronchial tree
this is evenly distributed throughout the lung but mainly seen in larger bronchi
this reduces lumen size and increases distances for gas exchange
What is seen on histology of the bronchi in severe COPD?
the bronchi themselves are obviously inflamed
pus is seen in the lumen
Microscopically, what is seen on pathology in COPD?
What is the end result of these changes?
- infiltration of the walls of the bronchi and bronchioles with acute and chronic inflammatory cells and lymphoid follicles
- epithelial layer may become ulcerated
- when ulcers heal, squamous epithelium replaces columnar cells
- inflammation is followed by scarring and remodelling
- this thickens the walls (increased gas diffusion distance) and leads to widespread narrowing of the small airways
What is the difference in the lymphocyte infiltrate in COPD compared to asthma?
in COPD the lymphocyte infiltrate is predominantly CD8+, rather than CD4+
How does the size of the airways affected by inflammation change as COPD progresses?
How can this be reversed?
- initially, only the small airways are affected
- no significant breathlessness has developed at this stage
- initial inflammation of small airways is reversible
- this accounts for the improvement in airway function if smoking is stopped early
- in later stages, larger airways start to become affected and inflammation continues even if smoking is stopped
Following on from inflammation, if COPD continues to progress, what changes are seen?
What is the consequence of this?
- progressive squamous cell metaplasia
- and fibrosis of the bronchial walls
- inflammation and scarring reduces the size of the lumen of the airways and reduces lung elasticity
- the result of these changes is the development of airflow limitation
How can airflow limitation be made even worse in COPD following brochial fibrosis and squamous cell metaplasia?
resulting airflow limitation is made more severe when it is combined with emphysema
this causes loss of the elastic recoil of the lung
What is the definition of chronic bronchitis?
What 2 features are present on histology?
defined as cough and sputum production on most days for at least 3 months during the last 2 years
there will be presence of:
- an increase in the number of mucus secreting glands (hypertrophy)
- an increase in the number of goblet cells (hyperplasia)
- in extreme cases the bronchial tissue itself becomes inflamed and pus is present in the lumen
What is the main cell involved in chronic bronchitis?
NEUTROPHIL
this is opposed to eosinophils in asthma
the main leukocyte infiltrate is CD8+, as opposed to CD4+ in asthma
After the initial inflammation in chronic bronchitis, what happens to the bronchial tissue?
What is the result of this on FEV1 and gas exchange?
there is scarring and fibrosis of the tissue
- this thickens the walls of the airway and reduces the size of the lumen
- this decreases the amount of air that can travel into and out of the lungs quickly (FEV1)
- it increases the distance that gases have to travel in order to diffuse properly
Why can bronchodilators sometimes be used in COPD / chronic bronchitis for symptom relief?
inflammatory processes, like those that occur in chronic bronchitis, also cause bronchoconstriction
in cases of COPD where bronchoconstricition is a factor, bronchodilators can be used for symptom relief
What is the result of emphysema on airspaces in the lungs?
emphysema causes enlarged airspaces distal to the terminal bronchioles
destruction of the elastin alveolar walls causes decreased elastic recoil of the lungs
What structures are affected in centri-acinar emphysema?
How disabling is it?
distension and damage of lung tissue is concentrated around the respiratory bronchioles
the more distal alveolar ducts and alveoli tend to be well preserved
this is very common and is not usually associated with disability when it is modest
severe centri-acinar emphysema is associated with substantial airflow limitation
What is pan-acinar emphysema?
What disease is this associated with and what are the consequences?
distension and destruction appear to involve the whole of the acinus
in extreme forms, the lung becomes a mass of bullae
severe airflow limitation and V/Q mismatch occur
this type of emphysema occurs in a1-antitrypsin deficiency
What is para-septal emphysema?
emphysema that tends to affect the more distal alveoli and alveolar ducts
What is irregular emphysema?
there is scarring and damage affecting the lung parenchyma patchily without regard for acinar structure
What are the 3 main pathological effects in COPD?
- loss of elasticity of the alveoli
-
inflammation and scarring
- reducing the size of the airway lumen and reducing elasticity
-
mucus hypersecretion
- reducing the size of the lumen and increasing the distance that gases have to diffuse
these all cause narrowing of the small airways and trapping of air leading to hyperinflation of the lungs and breathlessness
How does emphysema affect lung capacity and gas transfer?
- emphysema results in expiratory airflow limitation and air trapping
- loss of lung elastic recoil leads to an increase in TLC
- loss of alveoli results in reduced gas transfer
What is important to remember about loss of lung capacity with age?
after the age of 25, an individual naturally loses 30ml of functional lung capacity each year
the process of COPD accelerates this loss
What are emphysematous bullae?
large closed off air spaces with trapped air inside them
the alveoli distend to form exceptionally large air spaces, especially in the uppermost regions of the lungs
Why does V/Q mismatch occur in COPD?
- partly due to damage and mucus plugging of smaller airways from chronic inflammation
- partly due to rapid expiratory closure of smaller airways as a result of loss of elastic recoil from emphysema
- this leads to a _fall in *P*aO2_ and an increase in the work of respiration
How is CO2 excretion changed in COPD?
In what 2 different ways can patients present depending on how they cope with reduced pO2?
CO2 excretion is not impaired to the same extent as the fall in PaO2
some patients try to maintain normal blood gases by increasing their respiratory effort (pink puffers)
some patients fail to maintain their respiratory efforts and their CO2 levels rise (blue bloaters)
What is meant by a “pink puffer”?
What is their PaO2 and PaCO2 like and why?
they have a _near normal *P*aO2_ and a _normal or low *P*aCO2_ (due to hyperventilation)
they “puff” to increase their alveolar ventilation
by increasing their respiratory effort, they are able to keep their blood gases close to normal
What underlying condition do “pink puffers” usually have?
What are they more likely to develop over time?
they generally have EMPHYSEMA
or at least a higher degree of emphysema than bronchitis
they are likely to enter type I respiratory failure
What is meant by a “blue bloater”?
What are their PaO2 and PaCO2 values like?
blue bloaters have _low *P*aO2_ and _high *P*aCO2_
they fail to maintain respiratory efforts
they have decreased alveolar ventilation, and as a result, CO2 levels rise
What condition are “blue bloaters” more likely to have?
chronic bronchitis
they are more likely to develop type II respiratory failure
In a “blue bloater”, what are the results of increased CO2 in the short-term and long-term?
in the short term, the rise in CO2 leads to stimulation of respiration
in the long-term, their respiratory centre becomes sensitised
they become insensitive to raised levels of CO2 and rely on hypoxic drive to maintain adequate ventilation
What is the appearance of a “blue bloater” due to?
- they are not breathless as they run low PaO2 values
- they begin to retain fluid, giving a bloated appearance
- this is also due to cor pulmonale, which they often go on to develop
- they are cyanosed due to polycythaemia (increased production of erythrocytes)
Why is it not always a good idea to administer oxygen to a “blue bloater”?
administering oxygen may be an attempt to abolish hypoxaemia
this can make the situation much worse by decreasing respiratory drive in these patients who rely on hypoxia to drive their ventilation
What have studies shown about the loss in FEV1 in healthy people compared to patients with COPD?
What are the three mechanisms for this?
What is the definition of an acute exacerbation in COPD?
a change in the patient’s baseline symptoms, such as:
- worsening SOB
- increase in cough
- increase in sputum
that is beyond normal day-to-day variation and is acute in onset
In what groups of patients are exacerbations more common in?
- history of previous regular exacerbations
- history of GORD / reflux
- more severe disease (low FEV1)
What are more frequent COPD exacerbations associated with?
frequent exacerbations are associated with an increased rate of decline in respiratory function
this is measured by FEV1
mortality is also directly correlated with the frequency of exacerbations
What are the indications that an acute exacerbation may require hospital admission?
- sats < 92%
- not responsive to outpatient management
- inability to eat or sleep due to breathlessness
- very low exercise tolerance
- confusion (may be due to hypercapnia)
- unable to cope at home
- co-morbidities suggestive of likely poor outcome
What is the aim of oxygen therapy to treat an acute exacerbation?
What needs to be looked out for and how is this acheived?
controlled oxygen therapy should be given to maintain sats at 88 - 92%
beware of CO2 retention - need to monitor for hypercapnia and associated respiratory acidosis
this is acheived by repeating ABGs every 20 minutes to assess for a rise in PaCO2
What should be considered if PaCO2 has risen > 1.5 kPa?
the use of non-invasive ventilation (NIV)
such as CPAP or other assisted ventilation
What are PaO2 and PaCO2 dependent on?
Why is this significant?
PaCO2 is dependent on VENTILATION
this is the volume of air that is inhaled and exhaled
PaO2 is dependent on OXYGENATION
this is that amount of alveolar gas transfer and the percentage of oxygen inhaled
When giving oxygen to a patient with COPD what is important to consider?
What is different about their respiratory drive?
the normal respiratory drive is driven by PaCO2
in COPD this is no longer effective
a patient may be adequately oxygenating due to the quality of oxygen they are being given, but may not be adequately ventilating to get rid of CO2
rising PaCO2 can lead to reduced level of consciousness and over-oxygenation is associated with respiratory failure and death
What types of inhalers are given to patients with COPD who are having an exacerbation?
- salbutamol (e.g. 4-8 puffs via spacer)
- ipratropium (e.g. 4 puffs)
repeat the doses as required and check the patients inhaler technique
What type of anti-inflammatory is given to someone having an exacerbation?
Steroids
This is typically 50mg prednisolone OD for 5 days
tapering is not required after short courses such as this
What other type of medication is considered being given in COPD exacerbations?
antibiotics
these are only prescribed where there is evidence of an infection
What are the 2 most common causes of bacterial exacerbations of COPD?
Streptococcus pneumoniae:
- a Gram-positive diplococcus
Haemophilus influenzae:
- a Gram-negative coccobascillus
What are the antibiotics that are typically prescribed in an exacerbation of COPD?
- first line is typically amoxicillin 500mg tds for 7 days
- second / third line options might include:
doxycycline 100mg PO for 5-7 days
co-amoxiclav and ciprofloxacin (if there is penicillin allergy)
What is a1-antitrypsin and what is its function?
it is an antiprotease enzyme that is produced in the liver, secreted into the blood and diffuses into the lung
it inhibits neutrophil elastase - a proteolytic enzyme that can destroy alveolar wall connective tissue
it also inhibits other proteases such as trypsin and collagenases
What happens if someone has a deficiency of a1-antitrypsin?
neutrophil elastase, collagenases and trypsin in the lung are not inhibited
they break down alveolar wall connective tissue, leading to COPD
How many people are affected by a1-antitrypsin deficiency?
How many people are carriers of the gene?
it is an autosomal dominant condition
about 1 in 5000 people are homozygous dominant for this condition and have COPD
around 1 in 10 people are carriers of the gene
Why does cigarette smoking in someone with a1-antitrypsin deficiency nearly always lead to COPD?
the proteases that act in the lung are often released by inflammatory cells
in smoking, there are more inflammatory cells present in the lungs, so the effect becomes exaggerated
What are the non-pharmacological approaches to management of long-term COPD?
- pulmonary rehabillitation
- advice for smoking cessation
- this is vital in reducing the speed of disease progression
What is involved in pulmonary rehabilitation?
typically it involves a combination of physiotherapy breathing exercises and regular physical activity
exercise guidelines are at least 30 minutes on at least 5 days of the week of moderate intensity physical activity
patients should exercise until they feel too breathless to continue, rest for several minutes and then continue
What vaccinations may be offered to someone with COPD?
- an annual influenza vaccine
- one dose of the polyvalent pneumococcal polysaccharide vaccine
What co-morbidities are the most important to treat along with COPD?
- diabetes
- cardiovascular disease
- hypertension
- dyslipidaemia
- osteoporosis
When might oxygen therapy be prescribed to a patient with COPD?
What does this involve?
LONG TERM OXYGEN THERAPY
- LTOT involves 2L via nasal prongs for at least 15 hours per day
- reserved for severe cases
- LTOT and smoking cessation are the only 2 things that can prolong life expectancy in COPD
What is the goal of pharmacological management in COPD?
What can giving drugs not acheive?
- to reduce the rate of exacerbations
- to provide symptomatic relief
the medications themselves do not improve prognosis
but reducing the frequency of exacerbations can reduce the rate of decline of lung function
What are the 3 types of inhaled medications that are used in COPD?
-
Beta agonists
- can be both long and short acting (SABA / LABA)
-
Antimuscarinic agents
- can be both long and short acting (SAMA / LAMA)
- Inhaled corticosteroids
What is the first step in prescribing an inhaled drug for COPD?
What does this tend to be?
In mild disease, a short-acting bronchodilator is prescribed
- This can be a short-acting beta agonist (SABA)
- e.g. salbutamol 200ug every 4-6 hours
- This can be a short-acting antimuscarinic agent (SAMA)
- e.g. ipratropium 40ug four times daily
What is the difference between prescribing a SABA or SAMA for bronchodilation?
greater and more prolonged bronchodilation is acheived with antimuscarinic agents
What is involved in the second stage of treatment for COPD?
moderate disease involves adding a LABA or LAMA
the recommendation is using a SABA with LAMA
SAMA and LAMA should NOT be used together!!!
Why is it recommended to use SABA and LAMA rather than SABA and LABA?
there is evidence that antimuscarinic agents provide prolonged and greater bronchodilation and are more effective at symptomatic relief
e.g. tiotropium 18 ug daily
What is the third stage in treatment for COPD?
What is recommended before and after starting this treatment?
adding an inhaled corticosteroid
prednisolone 30mg is given for 2 weeks
lung function is measured before and after the prednisolone is started
if there is an increase in FEV1 > 15% this suggests a significant improvement in airflow limitation
If there is an increase in FEV1 > 15% after predisolone is taken for 2 weeks, what should be done?
prednisolone is discontinued and replaced by inhaled corticosteroids
this is beclometasone 400ug twice daily
the dose can be adjusted according to response
What SABA is commonly used and what dose?
SALBUTAMOL
each puff is 100mcg
recommended dose is 2 - 8 puffs PRN
What is an example of a SAMA?
What is the recommended dose?
IPRATROPIUM
each puff is 20mcg
2 puffs should be taken daily (preventative)
4 puffs STAT (instantly) in exacerbations
What are the 2 most commonly used LABAs?
What doses are recommended?
SALMETEROL:
- 50 - 100mcg given BD (twice a day)
FORMOTEROL:
- 12 - 24mcg given BD
What is the most commonly used LAMA?
What is the dose?
What should be stopped when this is started?
TIOTROPIUM
10 mcg is given once a day (OD)
!!! SAMAs should NOT be used with LAMAs !!!
The SAMA being used previously should be stopped immediately as the LAMA is started
What is Ultibro?
a combination of a LAMA and a LABA
the LAMA is indacterol
the LABA is glycopyronium
What inhaled corticosteroids are prescribed for COPD?
- fluctisalone (100 - 500 mcg BD)
- beclomethasone (50 - 200 mcg BD)
What are the indications for giving a patient LTOT?
How is this initially assessed?
it is indicated for patients with proven hypoxaemia:
- PaO2 < 7.3 kPa
- PaO2 < 8 kPa and patient also has polycythaemia, hypoxaemia, peripheral odema or pulmonary hypertension
initial screening test for hypoxaemia is O2 saturations <92% on pulse oximetry
a true diagnosis of hypoxaemia requires low PaO2 on blood gas
What is the most common surgical procedure that patients with COPD sometimes have?
How can this benefit them?
patients who have large emphysematous bullae may benefit from bullectomy
this enables adjacent areas of collapsed lung to re-expand into the space and function again
this improves V/Q mismatch
How does lung volume reduction surgery work?
Why is this not performed that often?
the aim is to increase the elastic recoil of the lung
patients must have a FEV1 < 1 L
it improves symptoms, but does not improve mortality
Why must patients with COPD seek advice from their doctor before air travel?
- within an airliner, PaO2 falls from 13.5 kPa to 10kPa
- oxygen saturation falls by 3%
- this has no effect on a normal individual, but in patients with COPD, it can reduce their O2 saturation to around 6.5 kPa
- oxygen therapy may be needed
What are the 2 potential complications associated with COPD?
- respiratory failure
- cor pulmonale
What are the values of PaO2 and PaCO2 in respiratory failure?
respiratory failure occurs when:
- _*P*aO2 is LESS than 8 kPa_ (60 mmHg)
- OR _*P*aCO2 is MORE than 7 kPa_ (55 mmHg)
Why does respiratory failure eventually occur in COPD?
How are cardiac output and renal function affected?
persistence of chronic alveolar hypoxia and hypercapnia leads to constriction of pulmonary arterioles
this leads to pulmonary arterial hypertension
cardiac output is normal or increased, but salt and fluid retention occurs as a result of renal hypoxia
What is meant by type I respiratory failure?
What is CO2 level and what causes it?
there is hypoxaemia but there is NOT hypercapnia
CO2 level is normal or low
it is caused by a VQ mismatch
What are examples of conditions that can cause type I respiratory failure?
- pneumonia
- pulmonary oedema
- pulmonary embolism
- asthma
- emphysema
- fibrosing alveolitis
- ARDS
What are the treatments for type I respiratory failure?
- treat underlying cause
- give oxygen (35-60%) by face mask to correct hypoxia
- assisted ventilation is given if PaO2 does not rise above 8 kPa
What is meant by type II respiratory failure?
What causes it?
This involves hypoxaemia WITH hypercapnia
CO2 levels are raised as a result of alveolar hypoventilation
There is no V/Q mismatch
What conditions can cause type II respiratory failure?
Pulmonary disease:
- COPD
- asthma
- pulmonary fibrosis
- obstructive sleep apnoea
Reduced respiratory drive:
- due to sedentary drugs, trauma or CNS tumour
Neuromuscular disease:
- cervical cord lesion
- diaphragmatic paralysis
- myasthaenia gravis
Thoracic wall disease
Why is it important to give oxygen therapy with care in type II respiratory failure?
the respiratory centre has become desensitised to CO2 levels and hypoxia is now its main driving force
What is involved in the treatment for type II respiratory failure?
- give controlled oxygen therapy starting at 24% O2
- recheck the ABG after 20 minutes
- if PaCO2 is steady or lower, then O2 can be increased to 28%
- if PaCO2 rises by > 1.5 kPa then consider assisted ventilation or a respiratory stimulant (such as doxapram 1.5-4 mg/min IV)
What is cor pulmonale?
heart disease secondary to disease of the lung
it involves pulmonary hypertension, leading to right ventricular hypertrophy
the end result is right-sided heart failure
What may a patient with cor pulmonale present like?
- patient is centrally cyanosed (due to lung disease)
- ankle oedema and ascites due to fluid retention
- patient becomes severely breathless
What clinical signs may be present in someone with cor pulmonale?
- prominent parasternal heave due to RV hypertrophy
- loud pulmonary heart sound (second heart sound)
- in severe pulmonary hypertension, there is incompetence of the pulmonary valve, which is heard as a diastolic murmur
As cor pulmonale develops into right sided heart failure, what other clinical features may be present?
tricuspid incompetence may develop leading to a greatly elevated jugular venous pressure (JVP)
there may also be ascites and upper abdominal discomfort due to swelling of the liver
