COPD Flashcards
What is COPD?
COPD is a progressive obstructive airway disease that is not fully reversible and encompasses chronic bronchitis and emphysema.
What is chronic bronchitis ?
Chronic inflammation of the airways.
Clinical term relating to a chronic productive cough for at least 3 months over two consecutive years.
What is emphysema?
Typically refers to abnormal airspace enlargement distal to terminal bronchioles with evidence of alveoli destruction and no obvious fibrosis.
Emphysema is characteristically panlobular with a lower zone predominance. This is compared to emphysema from smoking, which is characteristically centriacinar.
Causes of COPD?
- Smoking
- alpha- 1 anti-trypsin deficiency
- Recurrent childhood infections
- Occupational exposure
- Household exposure to burning coal or biomass fuel
What does Chronic bronchitis lead to in the airways?
- Goblet cell hyperplasia
- Mucus hypersecretion
- Chronic inflammation and fibrosis of small airways
- Narrowing of small airways
- Loss of cilial function
Pathophysiology?
Inflammatory processes lead to the production of proteases by inflammatory cells such as macrophages and neutrophils.
The protease elastase causes the destruction of elastin, a protein important to the structural integrity of the alveoli.
Loss of elastin has two effects:
- Collapse: the alveoli are prone to collapse.
- Dilation and bullae formation: alveoli dilate and may eventually join with neighbouring alveoli forming bullae.
How can you get cor pulmonale in COPD?
Chronic hypoxia → vasoconstriction of pulmonary arteries → elevated pulmonary arterial pressure → chronic elevation of pulmonary arterial pressure → right heart failure
Differentials?
- lung cancer
-asthma - fibrosis
- heart failure
- pulmonary embolism
Symptoms
- Chronic Shortness of breath
- Chronic Productive cough
- White sputum
- Frequent episodes of ‘bronchitis’
- Wheeze
Signs?
- Barrel chest
- Dyspnoea
- Pursed lip breathing
- Wheeze
- Coarse crackles
- Loss of cardiac dullness
-Downward displacement of liver - Signs of CO2 retention
- signs of cor pulmonale
MRC dyspnoea score ? 1-5
1- I only get breathless with strenuous exercise
2- I get short of breath when hurrying on level ground or walking up a slight hill
3- On level ground, I walk slower than people of my age because of breathlessness, or I have to stop for breath when walking at my own pace on the level
4- I stop for breath after walking about 100 yards or after a few minutes on level ground
5- I am too breathless to leave the house or I am breathless when dressing/undressing
How to diagnose COPD?
Clinical picture + spirometry
What will Spirometry show ?
- Obstructive picture on spirometry
- FVC:may be normal but often reduced due to air trapping.
- FEV1:reduced
- FEV1/FVC:< 70% (<75%?)
- Spirometry does not show reversibility with salbutamol (bronchodilator)
Bedside investigations
- Obs- pulse oximetry
- ECG
- Sputum culture- infection
- BMI
- ABG- if hypercapnia or hypoxia
Bloods investigations
- FBC - anaemia and polycythaemia
-Alpha-1 antitrypsin levels - U&Es
- CRP
- TLCO-Transfer factor for carbon monoxide
Imaging investigations? what findings
CXR- hyperexpanded, flattened hemidiaphragm,- Hypodense, Saber-sheath trachea
CT scan- only if:
- Symptoms disproportionate to spirometric assessment
- Alternative diagnosis suspected (e.g. bronchiectasis, fibrosis)
- Lung cancer suspected or to investigate abnormalities on chest x-ray
Echo- only if:
cor pulmonale suspected.
Grading of COPD using FEV1
Using predicted FEV1- average FEV1 in a population of similar age, sex and body composition
- stage 1: FEV above 80% of predicted
- stage 2: FEV1 50-79% of predicted
- stage 3: FEV1 30-49% of predicted
- stage 4: FEV1 less than 30% of predicted
Overview of COPD care
- Education: about their condition and check inhaler technique
- Smoking cessation
- Vaccination: seasonal influenza vaccine and the pneumococcal vaccine
- Pulmonary rehabilitation
- Self-management plans
- Management of co-morbidities
- Pharmacotherapy
Pharmacological management
Inhaled therapy:
Step 1- SABA or SAMA
Step 2- LABA +LAMA or if steroid responsive= LABA+ ICS
Step 3- Triple therapy- LABA+LAMA+ICS
If ongoing symptoms or acute exacerbations despite optimal treatment try ORAL treatment options, nebulisers and consider assessment for LTOT
Evidence of steroid responsiveness or asthmatic features? for ICS treatment
- previous diagnosis of asthma or atopy
- a higher blood eosinophil count
- substantial variation in FEV1 over time (at least 400 ml)
- substantial diurnal variation in peak expiratory flow (at least 20%)
For triple therapy in what cases would you try this?
Already on LABA + LAMA:
- 3 month trial of triple therapy if clinical features impact quality of life. If no improvement, revert back to LABA + LAMA only
- offer triple therapy if 1 severe or 2 moderate acute exacerbations within one year.
Already on LABA + ICS:
offer triple therapy if clinical features impact quality of life or 1 severe or 2 moderate acute exacerbations within one year
Severe long term management
- salbutamol (SABA) or ipratropium (SAMA) nebs
-oral theophylline: Many interactions and requires monitoring levels. At risk of toxicity. - oral mucolytics
- long term prophylactic Abx (eg. azithromycin)
- LTOT
What surgical interventions can you have in COPD?
- Lung reduction surgery
- Bullectomy
- Lung transplantation
COPD discharge CARE BUNDLE- 5 points
- Assessment of inhaler technique
- Self-management action plan and an emergency drug pack
- Smoking cessation
- Access to a treatment programme that can help people with a lung condition stay active (pulmonary rehabilitation)
- Follow-up arrangements
Outpatient COPD management
- COPD Care bundle
- Smoking cessation
- Pulmonary rehab
-Diet
Pharmacological:
- Bronchodilators
- Antimuscarinics
- Steroids
- Oral mucolytics
- LTOT
Surgery
- LUNG VOLUME Reduction
What is the role of pulmonary rehabilitation in COPD treatment?
-aims to optimise thephysical and social performance of patients suffering from long-term chronic lung conditions like COPD.
- Break the cycle of avoiding exercise and physical activity due to SOB which leads to weakened muscles and doing less
- This vicious cycle leads to increasing social isolation, depression and worsening of symptoms
What do they do in Pulmonary rehabilitation? Who is it used for and who not?
an MDT 6-12 week programme of
supervised exercise,
unsupervised home exercise,
nutritional advice
disease education
Breathing techniques
Pulmonary rehabilitation is offered to any patient with COPD who feels disabled by their condition.
It isnotsuitable:
- cant walk
- Recent MI
- unstable angina
LTOT -When are patients considered
- very severe airflow obstruction (FEV1 < 30% predicted)
- cyanosis
- polycythaemia
- peripheral oedema
- raised jugular venous pressure
- oxygen saturations less than or equal to 92% on room air
LTOT- Criteria
Long-term oxygen therapy(LTOT) is reserved for patients who meet the following criteria:
- Arterial Pa02< 7.3 kPa,OR
- Arterial Pa02< 8 kPawith any of:
- Pulmonary hypertension
- Peripheral oedema
- Secondary polycythaemia
How many hours a day is LTOT used?
LTOT to be used at least 16 hours/day for a survival benefit
Why may uncontrolled oxygen be potentially dangerous in someone with COPD?
CO2 retention can occur as administering oxygen reverses Hypoxic pul vasoconstriction
This allows blood flow to non ventilated alveoli which increases the V/Q mismatch
This leads to CO2 not having enough ventilated alveoli to allow diffusion out of the blood stream
Hypercapnia caused = Resp acidosis
What is the oxygen in LTOT treating
oxygen is not a treatment for breathlessness; it is a treatment to help prevent organ hypoxia
Complications of COPD
- Respiratory failure
- Pneumonia: often recurrent
- Pneumothorax: rupture of bullous disease
- Polycythaemia or anaemia
- Depression
What interventions alter prognosis (Mortality) of patients in COPD
- LTOT
- Pul rehab
- Smoking cessation
What are the 2 types of COPD exacerbations?
Infective
- Change in sputum volume / colour
- Fever
- Raised WCC +/- CRP
Non-infective
- PE
Clinical features of acute exacerbation
- Worsening breathlessness
- Worsening cough
- Increased sputum production
- Change in sputum colour
Investigations:acute exacerbation
- Arterial blood gas(ABG)
- Cultures: Blood (if pyrexial- ?sepsis), sputum
- Electrocardiogram(ECG): arrhythmias or evidence of heart strain
- Bloods: FBC, U&E, CRP
- Chest x-ray: look for pneumonia, PE
- Theophylline levels(if part of admission medications)
Management : acute exacerbations
- A-E approach
- Give O2 via fixed performance face mask (Venturi masks if non-rebreathe causing retention) due to risk of CO2 retention
- Nebs of salbutamol and ipratropium
- Steroids- Oral prednisolone
- ABx- if raised CRP/WCC or purulent sputum
- CXR
- consider IV aminophylline
- if pH below 7.25 consider referral to ITU
Why is there respiratory acidosis in COPD?
- PaO2< 8 kPa andraised PaCO2 >6.5 KPa
- retained CO2 decreases the pH of the blood, usually seen in acute exacerbation of COPD when the kidney can’t release bicarbonate quick enough in response to the increased CO2
What does raised bicarbonate in COPD suggest?
CO2 is chronically retained causing bicarbonate to be released by the kidneys in response to the acidosis over an extended period of time causing compensation and therefore a normal pH
Describe type 1 respiratory failure
PaO2< 8 kPa or <90% o2 sats on air
low/normal pCO2 (only one affected)
Describe type 2 respiratory failure
PaO2< 8 kPa and raised PaCO2 >6.5 KPa (two affected)
