COPD Flashcards
COPD definition
Disease state characterized by airflow
limitation that is not fully reversible but
progressive with an abnormal inflammatory
response of the lung to noxious particles or
gases
COPD is comprised of
Chronic bronchitis + emphysema
difference between bronchitis and emphysema
Bronchitis is inflammation of large airways
emphysema is inflammation of alveoli
Difference between COPD and asthma
COPD- Onset in mid-life
Symptoms slowly
progressive
Long smoking history
Largely irreversible
airflow limitations
Asthma- Onset early in life,
family history of
asthma
Symptoms vary from
day to day
Symptoms at
night/early morning
Allergy, rhinitis,
eczema also present
Largely reversible
airflow limitation
Risk factors of COPD main two categories
Host factors
Environmental factors
Host factors that affects COPD
Genes- alpha 1 antitrypsin deficiency
Gender- female smokers at higher risk
Lung growth- childhood infections, maternal infections
Environmental factors that affect COPD
o Tobacco smoke
o Occupational dust- wood dust
o Pollution
o Infections
o Socioeconomic status
Pathophysiology of COPD - central airways
mucus hypersecretion,
ciliary dysfunction → chronic cough, sputum
production
Pathophysiology of COPD - peripheral airways
Airway remodelling, scar
tissue formation → fixed airway limitation,dynamic hyperinflation → low FEV1, high TLC,
rhonchi, barrel chest
Pathophysiology of COPD - parenchyma
emphysema → loss of elastic
recoil, impaired gas exchange → low DLCO,
hypoxaemia
Pathophysiology of COPD - vasculature
hypoxia →pulmonary
vasoconstriction → pulmonary hypertension
→ right ventricular hypertrophy (RAD< R in
V1, RBBB) → Right ventricular failure
(oedema, raised JVP, hepatomegaly)
Hx in COPD
–
* chronic cough (intermittent or daily-cough
and sputum production for >3months,>2
years),
* chronic sputum production,
* breathlessness (progressive and
exertional),
* wheeze
* minimal day to day variation,
* worsening of symptoms with infections
* exposure to risk factors (smoking,
occupational dusts, smoke from home
cooking)
Physical signs of COPD
- usually late,
- thin wasted person,
- hyperinflation of chest, barrel shaped
chest, reduced cardiac dullness, liver
pushed down - Prolong expiration, B/L rhonchi on
auscultation, - cyanosis and polycythaemia,
- oedema
- cor-pulmonale
Two clinical presentations of COPD
Blue bloaters
Pink puffers
Blue bloaters Sx
Chronic, productive cough
Purulent sputum
Hemoptysis
Mild dyspnea (initially)
Cyanosis
Peripheral edema
Crackles, Wheezes
Prolonged expiration
Obese
Pink puffers Sx
Dyspnea
Minimal cough
Increased minute ventilation
Pink skin, Pursed lip breathing
Accessory muscle use
cachexia
Hyperinflationm Barrel chest
Decreased breath sounds
Tachypnea
Complications of blue bloaters
Secondary polycythemia vera due to hypoxemia
Pulmonary HTN due to reactive vasoconstriction from hypoxemia
Cor pulmonale from chronic pulmonary HTN
Complications of Pink puffers
Pneumothorax due to bullae
Weight loss due to work of breathing
FEV1/FVC ratio of COPD
<70% ( Obstructive disease)
FEV1 level in COPD
<80% predicted
TLC, FRC, RV
Increased
DLCO levels in COPD
Reduced
DDs of COPD
- Long standing breathlessness –
1. chronic persistent asthma, chronic
heart failure - Chronic cough – bronchiectasis,
tuberculosi
Management of COPD
- Diagnose, assess, monitor
- Reduce risk factors
- Manage stable COPD
- Management of exacerbation
o Controlled oxygen through mask
o Nebulized bronchodilators (salbutamol,
ipratropium
o Antibiotics
o Oral prednisolone – 40 mg/day
Pulmonary rehabilitation
Education and
training program to help patient to live an
active life within the limitation of symptoms
Pulmonary rehabilitation
- Stopping smoking
- Controlling breathlessness
o Breathing control
o Pursed lip breathing
o Correct posture - Stopping smoking
- Controlling breathlessness
o Breathing control
o Pursed lip breathing
o Correct posture
Complications of COPD
- recurrent exacerbations by URTI,
- cor-pulmonale,
- type II respiratory failure,
- pneumothorax,
- polycythaemia
- systemic effects (muscle wasting, muscle
fatigue
MMRC dyspnea scale
0 - vigourous exertion
1- rapid walking / climbing uphill
2- normal speed wailking
3- 100m / few minutes of level ground walk
4- Stationary activity – dressing, undressing etc.
Can’t leave home
CAT ( COPD assessment tool)
score each from 0-5 (good - 0 to
worst -5)
1. Cough
2. Sputum
3. Chest tightness
4. Dyspnoea
5. ADL
6. Sleep
7. Confidence in walking out
8. Energy
Dx steps in COPD
- Spirometrically confirmed Dx - Post bronchodilator FEV1/FVC <70%
- Assessment of airflow limitation - Predicted FEV1
GOLD 1 >= 80
GOLD 2 50-79
GOLD 3 30-49
GOLD 4 <30 - Assessment of Sx/risk of exacerbations - table
Assessment of Sx/ risk of exacerbations. Y axis and X axis
Y axis - exacerbation Hx
X axis - Sx
Y axis
0 or 1 (not leading to hospital admission)
>=2 or >=1 leading to hospital admission
X axis
mMRC 0-1 and CAT <10
mMRC >=2 and CAT >=10
Group A in COPD Mx
mMRC 0-1 CAT <10
0-1 exacerbations and no hospital admissions
Group B in COPD Mx
mMRC >=2 CAT >=10
0-1 exacerbations and no hospital admissions
Group C in COPD Mx
mMRC 0-1 CAT<10
>=2 or >=1 w hospital admission
Group D COPD Mx
mMRC >=2 CAT >=10
Group B Drugs COPD
LAMA or LABA
persistent Sx
LAMA+LABA
Group A Drugs in COPD
LAMA or LABA
evaluate the effect
Continue, stop or try alternative class or bronchodilator
Group C drugs COPD
LAMA
further exacerbations
LAMA+LABA or LABA+ICS
Group D drugs COPD
Start w LAMA
further exacerbations
LAMA+LABA or LABA+ICS
further worsening
LAMA+LABA+ICS
further exacerbations
Consider Roflumilast (if FEV1 <50% predicted and pt has chronic bronchitis)
OR
Consider Macrolides (in former smokers)
When to consider LTOT for COPD
if PaO2 <55mmHg
Should be given at least 15h/d
Mortality benefit in COPD
Cessation of smoking
Long term O2 therapy
Lung vol reduction therapy
Indications of NIV for COPD exacerbations
PaCO2 >45mmHg
Persistent hypoxia despite other exacerbation measures
Clinical severe dyspnea w progression to exhaustion
Pack years calculation
(No of Cig smoked per day/ 20) x No of years smoked
Barrel chest
AP diameter > transverse
How does COPD cause the right heart to fail
In alveoli that are not adequately oxygenated, blood supply for perfusion will not happen. BV will undergo vasoconstriction. (Coz there’s no point sending blood to these alveoli)
This causes pulm HTN ( causes RVH coz of extra pressure in RV)
RVH causes RAD ( tall wave in V1)
At some point, R heart will fail ( Ascites, Edema, increases JVP, Hepatomegaly)
meaning behind Pink puffers
usually in people increasing CO2 levels stimulate the respi centre in the medulla. But in pink puffers, hypoxia stimulates the respi centre, so they are always gasping for breaths. Therefore, they are not cyanosed.
meaning behind blue bloaters
they are not sensitive to hypoxia. ( Respi centre is not stimulated by hypoxia) so they are not cyanotic. Kidneys will also undergo hypoxia. Renal hypoxia will trigger RAAS. causing Sodium- water retention giving edema
% of controlled oxygen given in COPD and the target SpO2
25-28%
target SpO2 - 88-92%
