Lecture 10- Obstructive airway diseases Flashcards
example of obstructive lung diseases
asthma
COPD
COPD
emphyseme and chronic bronchitis
asthma overview
- Chronic inflammatory airway disease
- Affects small airways
- Intermittent and variable airway obstruction and hyper reactivity in the airways
- Usually reversible
- Can be spontaneous
pathophysiology of asthma can be
atopic (more prevalent ) or non-atopic asthma
- Atopic means
Susceptible individual
- Triad of
- Asthma
- Eczema
- Hay fever
atopic asthma lined to
allergens- Type 1 hypersensitity reaction
-
Type 1 hypersensitivity
- *
- Allergen (1st exposure)
- Comes into contact with APC e.g. macrophage
- Process information about allergen to T helper 2 cell
- Causes a cascade of events which involves antibody production–> IgE
- IgE attach themselves to the surface of mast cells which release histamine and leukotrienes when antibodies sense re- exposure to antigen–>cause mast cell degranulation cause inflammation :
- Mucus production
- Bronchoconstriction – parasympathetic nervous system (oedema- sweeling in the airway)
Non-allergic asthma, or non-atopic asthma, is a type of asthma that
- Symptoms of asthma
- Breathlessness
- Chest tightness
- Wheeze –> poor airflow
- May be a symptom or sign
- Dry cough - nocturnal
- Worse at night because parasympathetic NS more prevalent at night
- Atopy
- Intermittent symptoms
- Triggers (allergen)/ hyper-responsive
signs of asthma
- Increase RR, HR and decreased O2 sats
- Wheeze
investigations for asthma
Peak flow (PEFR)
Spirometry
peak flow takes into account
- Sex
- Age
- Height
- not usually race
spirometry results for asthma
- Decreased FEV: FVC ratio <70%
- If you give bronchodilator you will see reversibility in form of bronchodilation which will increase FEV/ FVC ratio
management if low probability of being asthma
- no typical features, other diagnosis more likely
- Want to investigate other causes to rule out
management if intermediate probability of being asthma
-
Intermediate prob -borderline- some not all symptoms. Treatment for other cause isn’t working
- Investigate for definitive diagnosis- spirometry
management if high prob of being asthma
-
High prob- typical presentation
- Start treatment straight away
Long term treatments for asthma
- Patient education- removed triggers
- Pharmacology (inhalers)
- Asthma Patient education- remove triggers
- Say bye to the cat
- Remove dust
- Remove smoke
first line drugs for asthma
- B2 agonists- Salbutamol (blue enhaler)
- Short acting- - relieves symptoms in short term
-
Inhaled corticosteroid- preventor (brown inhaler)
- Dampen down inflammation which causes narrowing of airways
B2 agonists- Salbutamol (blue enhaler) works by
- Promote bronchodilation via the sympathetic NS (B2 receptor in the lungs)
- Asthma long term treatment : If they have to use the reliver 3+ times a week or if they are being woken up at night
- Need to check inhaler technique
- Move to Step 2
- Add-on therapies:
- Inhaled long acting beta agonist (salmeterol)
- Inhaled Cortical Steroid
- Purple inhaler (with both in)
- Inhaled Cortical Steroid
- With blue reliver
Long term asthma treatment: step 3
- Increase dose of ICS to medium dose
- Add leukotriene receptor antagonist
If still not responding… have you made the right diagnosis
- Management will change depending on
- age
- May introduce a spacer–> don’t need to have coordinated breathing technique
emergency managemnt asthma - 2 scenarios
acute severe asthma
life threatening asthma
-
Acute serve asthma
- Assessment when they are brought in
-
A–> E assessment
- A- may not be able to complete sentences
-
B
- O2 sats may be low but O2>92%
- Wheeze
- RR >25
- PEFR – 33-50% of their known best peak expiratory value
- E.g. precited peak flow 400, but only getting 180 –> would qualify in the 33-50% bracket.
-
C
- HR >110
- Life threatening asthma
ABGs in….
Acute serve asthma
- Decreased CO2 (blowing of CO2)
- Increased pH
- Respiratory alkalosis
- Low O2
- Type 1 respiratory failure
ABGs in… life threatening asthma
Life threatening
- Can look normal
- LOOK AT THE PATIENT
- Treatment is working
- Patient deteriorating (rising CO2 due to decreased respiratory rate- may need ventilation if cant support own breathing)
emergency management of asthma
- Oxygen
- Salbutamol nebuliser – short acting
- Steroid (oral or through vein)
- Admit +/- ITU
- CXR
COPD = umbrella term for:
- Emphysema
- Chronic bronchitis
COPD is the
- 4th leading cause of death
- Signif morbidity
Emphysema
- Damage to walls of alveoli
- Rather than lots of small alveoli, they breakdown forming larger alveoli –> unable to support bronchioles
- Bronchioles collapse and trap air inside the lungs
- Changes in emphysema are irreversible
causes of emphyseme
- Smoking (must stop smoking to stop it getting worse)
- Alpha 1- antitrypsin deficiency
- Alpha 1- antitrypsin deficiency
- Not truly a deficiency- malformed alpha 1-antitrypisn–> cant leave the liver, therefore builds up in the liver and can cause liver disease directly
- In the lung main function
- Balance action of protease and elastase enzymes which are produced in the presence of inflammation, infection, or smoking
- If no alpha 1-antitrypsin, then elastase can break down the structure of the lung
Chronic bronchitis
- Chronic inflammation of the bronchioles
- Inflammatory changes like asthma
-
Instead of responding to allergen, it responds to irritants like cigarette smoke
- Not T1 hypersensitivity
- Non-reversible
- Increased mucus and inflammation that causes narrowing of the airway –>not bronchoconstriction
difference between asthma and chronic bronchitis
- Increased mucus and inflammation that causes narrowing of the airway –>not bronchoconstriction
Symptoms of chronic bronchitis
Chronic productive cough
- Risk factors for COPD
- Smoking
- More common in male (cultural)
- Increased age
- Childhood respiratory disease
- Genetic e.g. A1AT deficiency
- Exposure
- Symptoms of COPD
- Breathlessness and wheeze (airway narrowing)
- Chronic bronchitis
- Productive cough
diagnosis of COPD based on
spirometry and CXR
COPD Spirometry
- Will show obstructive airway pattern- reduced FEV: FVC ratio
- <70%
- Poor bronchodilator reversibility (not caused by bronchoconstriction)
- COPD CXR
- Can see bigger alveoli–>air trapping–> shows up as hyperdense
- Hyperinflated chest – how many ribs can you seen
symptomatic test for COPD
MRC dyspnoea scale
severity of COPD based on
- decreased FEV1
prevention of COPD
quit smoking
pharmcological management of COPD
- SABA (short acting beta agonists) /LABA (long acting beta agonists)
- Antimuscarinics (ipratropium bromide or tiotropium- long acting)
- Steroids (ICS)
- Non-pharmacological management of COPD
- Vaccines
- Chest physiotherapy
Acute exacerbation of COPD
- In response to
- Infection- viral/bacterial
- Irritants
Acute exacerbation of COPD symptoms
- Increased dyspnoea
- Cough
- Productive/ green sputum
- Wheeze
Acute exacerbation of COPD signs
- Breathless
- Using accessory muscles-tripoding
- Pursed lip breathing
- Look cyanosed
investigations for acute exacerbations of COPD
- CXR
- ABG
- FBC, CRP
- U&Es
- Cultures
- Sputum
- Blood culture (if fever- sepsis
- Management of Acute exacerbation of COPD
- SABA and SAMA nebuliser
- Steroid orally/ IV
- Antibiotics if bacterial
- +/- O2- 88-92% target
what do we need to consider carefully when managing pts with COPD
giving oxygen
- different response to normal people due to different hypoxic drive
Hypoxic drive in normal people
- Increase pCO2- CO2 retention
- Resets central chemoreceptors in the brain
- Chemoreceptors are sensitive to absolute pH
- Increased pCO2= decreased pH
- Sends a message to respiratory centre to hyperventilate (acute setting)
- Chemoreceptors are sensitive to absolute pH
- Hypoxic drive in COPD pts
- Hyperventilation cannot fix the increased pCO2
- In pts with chronic lung disease, their levels of pCO2 are continually high
- Worse gas exchange (reduced SA)
- Even hyper ventilation will not blow off the CO2
- Need to involve the kidneys
- Retain HCO3- to buffer increased CO2
- Improved low pH in the brain and therefore hyperventilation stops (not sensing levels of cO2, sensing pH)
- H+ still high as well as HCO3- high- brain think this looks normal
- The brain is very sensitive to increased CO2 to drive respiration (main force of resp drive)
- If you have chronically high Co2 levels, brain will not detect changes due to compensation by the kidney
- Back up option
- Peripheral chemoreceptors which detect changes in Oxygen
- Much less sensitive than central chemoreceptors
- O2 has to drop very low for the hypoxia to be the determining driver for respiration
- Peripheral chemoreceptors which detect changes in Oxygen
COPD patients and oxygen
This is why pts with COPD are given very controlled amounts of oxygen- we aim for a lower range of saturation as is normal for them
- If we over correct the oxygen in a COPD patient…
- we will completely remove the hypoxic drive detected by the peripheral chemoreceptors
- Oxygen levels may come back up to normal but the CO2 will still be high
- Respiratory rate will plummet
how do we tightly control pO2 in COPD pts
- venturi marks
- Very heavily controlled oxygen to make sure we don’t damage hypoxic drive
- Aiming for 88%-92% oxygen
However in emergency situation and you don’t know if they have COPD- give oxygen normally and correct later.
longterm complications of COPD
chronic hypoxia
chronic resp failure
polycythaemia
Chronic hypoxia
1.
- State of chronic hypoxia due to under perfused lungs can lead to pulmonary hypertension
- If under perfused area of lung- vasoconstriction to divert blood flow
- If much of the lung is chronically hypoxic- more widespread vasoconstriction
- Pressure in blood vessels goes up- pulmonary hypertension
- Harder for right side of the heart to pump blood into pulmonary circulation
- Right sided heart failure (Cor pulmonale- caused by pathology in the lungs)
Cor pulmonale
Right sided heart failure
- caused by pathology in the lungs- pulmonary hypertension due to vasconconstriction of pulmonary blood vessels
Chronic respiratory failure
Co2 retention can lead to type 2 resp failure due to chronic poor ventilation of the lungs
Polycythaemia
due to chronic hypoxia–> body is doing all it can to increase oxygen carrying capacity –> increases number of RBC–>Polycythaemia
Respiratory failure is divided into type I and type II.
Type I respiratory failure involves low oxygen, and normal or low carbon dioxide levels.
Type II respiratory failure involves low oxygen, with high carbon dioxide.
summary of difference between asthma and COPD
Explanation by Dr Christides:Changes in ventilation in people with chronic CO2 retention with oxygen therapy
- High CO2 because of lung disease
- Initially CO2 diffuses across the BB reacting with H2O increasing carbonic acid- that rapidly dissociates to H+ and HCO3- brain extracellular fluid pH drops because H+ increase
- Choroid plexus increases re-absorption of HCO3—restores HCO3-: CO3 reaction – brain ECF pH restored
- But at a higher PaCO2 levels (Those with COPD)
- Therefore ventilation now adjusted by hypoxaemia triggering peripheral chemoreceptor
- If O2 given and PaO2 increase and Hb increases
- CO2 levels may increase for 2 main reasons
- V/Q mismatch and Haldane (this is the main problem)
- Haldane- oxygenated Hb carries less CO2
- Exacerbation of V/Q mismatch
- If alveoli not well ventilated - O2 levels fall- constriction of pulmonary arteries- decreased perfusion to maintain V/Q as close to 1:1
- Perfusion needs to go to healthy alveoli
- If we give oxygen
- Still poor ventilation to alveoli, but have increased o2
- Therefore we lose the pulmonary vasoconstriction- worsening V/Q mismatch <1
- Still cant get rid of CO2 due to poor ventilation
- Lose diffusion gradient for CO2
- If alveoli not well ventilated - O2 levels fall- constriction of pulmonary arteries- decreased perfusion to maintain V/Q as close to 1:1
- Loss Hypoxia/ hypoxaemia drive minor role (minor role)
- Carrying more CO2
- V/Q mismatch and Haldane (this is the main problem)
- CO2 levels may increase for 2 main reasons
