Chronic Obstructive Pulmonary Disorder Flashcards
(136 cards)
1
Q
What is the definition of COPD?
A
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
2
Q
What 2 conditions is COPD usually a combination of?
A
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
3
Q
What are the usual causes of COPD?
A
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
4
Q
What group of conditions is it important to distinguish COPD from?
How are these conditions defined?
A
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
5
Q
What is the FEV1 : FVC ratio in COPD usually?
Is this factor essential for diagnosis?
A
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
6
Q
What is the general disease course of COPD typically like?
A
patients typically follow a slowly progressive course with recurrent exacerbations
this involves short periods of increased shortness of breath, with or without infection
7
Q
In general, what is involved in the long term management of COPD?
A
- combinations of inhaled steroids and bronchodilators
- smoking cessation
- pulmonary rehabilitation
- important to prevent exacerbations with flu and pneumonia vaccines
8
Q
How are COPD exacerbations typically managed?
A
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
9
Q
What is the prevalence of COPD in the UK?
A
- 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
10
Q
What % of COPD cases are accountable to smoking?
Why is this important to consider?
A
smoking accounts for 90-98% of all cases
symptoms will improve in 90% of patients with smoking cessation
11
Q
What are the characteristics of a typical patient presenting with COPD?
Why is it important to ask about how many cigarettes the patient smokes?
A
- 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
12
Q
What factors are involved in the aetiology of COPD?
A
- smoking
- coal mining
- exposure to air pollution
- particularly in the developing world - indoor fires & cooking
- genetic predisposition
- a1-antitrypsin deficiency causes emphysema
13
Q
What are 2 predisposing factors to development of COPD?
A
- low socioeconomic status
- low birth weight
- associated with reduced maximum lung capacity in adulthood
14
Q
What % of smokers will develop COPD?
A
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
15
Q
What are the characteristic symptoms of COPD?
A
- 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
16
Q
What factors can sometimes worsen symptoms in COPD patients?
A
- cold, foggy weather
- atmospheric pollution
- in advanced disease, breathless becomes severe even after mild exercise, such as dressing
17
Q
What are the most common clinical signs of COPD?
A
- 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
18
Q
What is the cricosternal distance?
How is this changed in COPD and why?
A
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
19
Q
What may chest / breath sounds be like in COPD?
A
- Resonant chest sounds are suggestive of hyperinflation
- Quiet breath sounds over areas of emphysematous bullae
20
Q
What is wheeze?
What causes it?
A
an abnormal high pitched or low pitched breath sound heard on expiration
it is caused by abnormal narrowing of the smaller airways
21
Q
What type of wheeze is usually present in COPD?
What is the other type and what is this more likely to be?
A
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
22
Q
Why is wheeze sometimes confused with stridor?
What tends to cause stridor?
A
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
23
Q
Why does someone with COPD have a prolonged expiration?
A
as their FEV1 is low, they have to have a prolonged expiratory phase to allow for adequate respiration
24
Q
Why do patients with COPD use a pursed lip breathing technique?
A
- 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
25
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
26
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
27
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
28
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_**
29
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 *p*CO2 is **_above 10 kPa_**
* severe hypercapnia leads to **confusion and progressive drowsiness**
30
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
31
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**
32
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
33
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
34
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***
35
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)
36
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%
37
What other test is performed when investigating COPD?
a1-antitrypsin levels
normal range is 2 - 4 g/L
38
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
39
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
40
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**
41
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_**
42
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_**
43
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**
44
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
45
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**
46
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_**
47
What is seen on histology of the bronchi in severe COPD?
the bronchi themselves are obviously inflamed
pus is seen in the lumen
48
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_**
49
What is the difference in the lymphocyte infiltrate in COPD compared to asthma?
in COPD the lymphocyte infiltrate is predominantly **_CD8+_**, rather than CD4+
50
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**
51
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_**
52
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
53
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
54
55
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
56
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
57
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
58
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
59
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
60
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_**
61
What is para-septal emphysema?
emphysema that tends to affect the more distal alveoli and alveolar ducts
62
What is irregular emphysema?
there is scarring and damage affecting the lung parenchyma **_patchily_** without regard for acinar structure
63
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_**
64
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_**
65
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
66
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
67
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_**
68
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 *P*aO2
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)
69
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
70
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_**
71
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
72
What condition are "blue bloaters" more likely to have?
**_chronic bronchitis_**
they are more likely to develop **_type II respiratory failure_**
73
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
74
What is the appearance of a "blue bloater" due to?
* they are **_not breathless_** as they run **low *P*aO2 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)
75
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**
76
77
What have studies shown about the loss in FEV1 in healthy people compared to patients with COPD?
What are the three mechanisms for this?
78
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
79
In what groups of patients are exacerbations more common in?
* history of **previous regular exacerbations**
* history of **GORD / reflux**
* more severe disease (**low FEV1**)
80
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
81
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
82
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 *P*aCO2
83
What should be considered if *P*aCO2 has risen \> 1.5 kPa?
the use of **non-invasive ventilation** (NIV)
such as CPAP or other assisted ventilation
84
What are *P*aO2 and *P*aCO2 dependent on?
Why is this significant?
***P*aCO2** is dependent on **_VENTILATION_**
this is the ***volume of air*** that is inhaled and exhaled
*P*aO2 is dependent on **_OXYGENATION_**
this is that amount of ***alveolar gas transfer*** and the ***percentage of oxygen inhaled***
85
86
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 *P*aCO2**
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 *P*aCO2 can lead to reduced level of consciousness** and o**ver-oxygenation** is associated with **_respiratory failure and death_**
87
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
88
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
89
What other type of medication is considered being given in COPD exacerbations?
**antibiotics**
these are only prescribed where there is evidence of an infection
90
What are the 2 most common causes of bacterial exacerbations of COPD?
**Streptococcus pneumoniae:**
* a Gram-positive diplococcus
**Haemophilus influenzae:**
* a Gram-negative coccobascillus
91
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)
92
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
93
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
94
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
95
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
96
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
97
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
98
What vaccinations may be offered to someone with COPD?
* an **annual _influenza_ vaccine**
* one dose of the **polyvalent _pneumococcal_ polysaccharide vaccine**
99
What co-morbidities are the most important to treat along with COPD?
* diabetes
* cardiovascular disease
* hypertension
* dyslipidaemia
* osteoporosis
100
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
101
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 exacerbation*s can reduce the *rate of decline of lung function***
102
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**
103
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
104
What is the difference between prescribing a SABA or SAMA for bronchodilation?
**greater** and **more prolonged** **bronchodilation** is acheived with antimuscarinic agents
105
106
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!!!
107
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**
108
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
109
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
110
What SABA is commonly used and what dose?
**_SALBUTAMOL_**
each puff is 100mcg
recommended dose is **2 - 8 puffs PRN**
111
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**
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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
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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
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What is Ultibro?
a combination of a **_LAMA and a LABA_**
the LAMA is **indacterol**
the LABA is **glycopyronium**
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What inhaled corticosteroids are prescribed for COPD?
* fluctisalone (100 - 500 mcg BD)
* beclomethasone (50 - 200 mcg BD)
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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**
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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_**
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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
119
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
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What are the 2 potential complications associated with COPD?
* respiratory failure
* cor pulmonale
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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)
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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**
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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**
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What are examples of conditions that can cause type I respiratory failure?
* pneumonia
* pulmonary oedema
* pulmonary embolism
* asthma
* **emphysema**
* fibrosing alveolitis
* ARDS
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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**
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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
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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**
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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_**
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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)
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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_**
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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_**
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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_**
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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
