Resp: FEV, Respiratory failure, Asthma Flashcards
1
Q
What is FEV 1
A
Forced expiratory volume in 1 second
Where a person takes maximal inspiration and then exhales maximally as fast as possible
2
Q
Procedure to measure FEV 1
A
Breathe in to total lung capacity
Exhale as fast as possible in one second
Volume produced is FVC for one second
3
Q
What is FEV 6
A
Forced expiratory volume 6 seconds
4
Q
When is flow of air in res cycle greatest
A
Expiration, and declines in rate as volume decreases
5
Q
What does FEF25 mean
A
Flow at point when 25% of total volume is exhaled has been exhaled
6
Q
Define FVC
A
Forced Vital capacity
7
Q
Name 4 obstructive lung diseases
A
- COPD
- Asthma
- Bronchiectasis
- Bronchitis
8
Q
When is the value of FEV1 normal
A
When it is 80% of the normal predicted value for that patient
9
Q
What indicates airways restriction
A
- Ratio of FEV1/FVC greater than 0.7 AND FVC is lower than 80% of predicted value
- Just a low FVC (less than 80% of predicted value
10
Q
What indicates airways obstruction
A
- FEV1/FVC less than 0.7 (in other words they can breathe fast in the first second but obstruction stops them from fully expelling their total capacity volume)
11
Q
Define type I respiratory failure
A
- Hypoxia but not hypercapnia
12
Q
What causes type I respiratory failure
A
- High altitude
- VQ mismatch
- Shunting
- Diffusion problem (oxygen can’t enter capillaries due to parenchymal disease)
13
Q
What defines type II respiratory failure
A
- Hypoxia
- Hypercapnia
- pH DECREASED
14
Q
What causes type II respiratory failure
A
- Increased respiratory resistance (COPD, asthma)
- Reduced breathing effort (brain stem lesions! Obeisty)
- Guillain-Barré Syndrome
- MND
- Ankylosing Spondylitis
- Decrease in area of the lung available for gas exchange
ANYTHINg that causes inadequate alveolar ventilation
CO2 CAN’T BE ELIMINATED
15
Q
Where in the lungs is V/Q ration higher
A
Apex
Lower in base of lungs
16
Q
Why iS V/Q lower at the base of the lung
A
Because Perfusion increases as we go down the lungs faster than ventilation due to gravity
17
Q
What is a V/Q of 0
A
Area with perfusion and no ventilation = shunt
18
Q
What is dead space
A
Area with ventilation and no perfusion (V/Q of infinity)
19
Q
Effect of pulmonary embolism on V/Q
A
High V/Q
Because there is a decrease in Q, making value bigger
20
Q
What most commonly causes type I res failure
A
Pulmonary embolism
21
Q
What most commonly causes type II resp failure
A
Hypoventilation
22
Q
What neurological conditions can result in reduced ventilation
A
- MG
- Guillain-Barre syndrome
- Encephalitis
- MND
- Space-occupying lesions (increased ICP which can compress brainstem)
23
Q
What conditions can decrease Q in V/Q
A
- Pulmonary embolism
- Cardiac failure
- Shunt (VSD)
- Pulmonary hypertension
24
Q
What conditions can decrease V in V/Q
A
- COPD
- Neurological weakness
- Obesity
- Reduced drive from narcotics
25
Signs of hypercapnia
1. tachycardia
2. Flapping tremour
3. Confusion
4. Drowsiness
5. Reduced consciousness
26
Difference between ASTHMA and COPD
Asthma : airflow varies in obstruction
COPD: Fixed airflow obstruction
27
What is the transfer co-efficient
Measure of ability of oxygen to diffuse across alveolar membrane
28
How do you calculate transfer co-efficient
Inspiring a small amount of CO and hold breath for 10 seconds at total lung capacity, fast transferred measured
29
In what conditions is transfer co-efficient low in
1. Severe emphysema
2. Fibrosing alveolitis
3. Anaemia
4. Pulmonary hypertension
5. COPD
30
When is transfer co-efficient high
Pulmonary haemorrhage (can absorb O2 efficiently as bleeding means more blood cells available)
31
Risk factors for COPD
1. Tobacco smoking
2. Female
3. Secondhand smoke
4. Air pollution
5. Cold mining, silica dust
6. Alpha 1-antitrypsin deficiency
7. Poverty
32
What can exacerbate COPD
1. Cold temperature
| 2. Pulmonary embolus
33
Signs of pulmonary emboli in COPD
1. Heart failure
2. Pleuritic chest pains
NO SIGN OF INFECTION
34
Pathophysiology of COPD
1. Increased numbers of mucus-secreting goblet cells within bronchial mucosa
2. CHRONIC BRONCHITIS occur
1. Airway narrowing and airflow limitation due to HYPERTROPHY AND HYPERPLASIA of mucus secreting glands of the bronchial tress, bronchial wall inflammation and mucosal oedema
2. Infiltration of walls of bronchi and bronchioles with acute and chronic inflammatory cells
3. Epithelial cells ulcerate and squamous epithelium replaces columnar cells when ulcer heals
4. Causes scarring and thickening of walls which narrows airways
35
When can chronic bronchitis be reversed
Early in disease when there is no significant change in breathlessness
Continued inflammation even when smoking is stopped
36
What kind of patients present with COPD
1. Alpha-1 antitrypsin gene deficiency
| 2. Young patients
37
What dies alpha-1 antitrypsin deficiency do in th body
Causes cirrhosis
38
When is airflow worst
Breathing out
39
What is the replacement of columnar epithelial cells with squamous epithelial tissue now called
1. Bullae
Large air pockets (Bulllous emphysema)
40
Why is airflow worst when breathing out
Because the chest is compressing airways at this time
So more air remains in the lungs than should be there = hyperinflation
41
Define emphysema
1. Dilatation and destruction of lung tissue distal to terminal bronchioles
Results in loss of elastic recoil which normally keep airways open during expiration
This makes it harder to breathe out in COPD
42
What emphysema is found in smokers
Centriacinar emphysema
43
What emphysema is seen in alpha 1 - antitrypsin deficiency
Panacinar emphysema
44
What is panacinar emphysema
1. INVOLVES destruction of ENTIRE respiratory acinus from respiratory bronchiole to alveoli is expanded
45
What is centriacinar emphysema
1. Only effects respiratory bronchiole (alveoli are unchanged)
46
What causes V/Q mismatch in COPD
1. Damage and mucus plugging of small airways during expiration and rapid closure in smaller airways lead stop fall in PaO1 and increased work of inspiration
47
Why is CO2 level unaffected in COPD
1. Increase in CO2 increases rate of preparation but patients become insensitive to CO@ and depend on hyperaemia to drive ventilation = eventual increase in CO2
48
Clinical presentation of COPD
1. CHRONIC cough is the first symptom to develop with white sputum production = chronic bronchitis which causes rib fractures
2. History: Have common colds lasting a long time
3. Shortness of breath
4. Chest tightness
5. Wheezing
6. BARREL CHEST (rare)
7. Advanced COPD leads to high pressure eon lung arteries which strains RV = cor pulmonale and ankle oedema
49
Why do patients with COPD develop polycythaemia
1. Renal hypoxia causes fluid retention and increased erythrocyte production
Bloating and cyanosis
50
Clinical presentation of COPD
1. CHRONIC cough is the first symptom to develop with white sputum production = chronic bronchitis which causes rib fractures
2. History: Have common colds lasting a long time
3. Shortness of breath (extended expiration)
4. Chest tightness
5. Wheezing
6. BARREL CHEST (rare)
7. Advanced COPD leads to high pressure eon lung arteries which strains RV = cor pulmonale and ankle oedema
8. Pursed lips on expiration to stop airway collapse
51
What inflammatory mediators are released by cigarettes in COPD
1. IL-1
2. IL8
3. TNF-alpha
52
Systemic symptoms of COPD
```
1. Hypertension
2> Osteoporosis
3. Depression
4. Weight Loss
5. Reduced muscle mass
```
53
Systemic symptoms of COPD
1. Hypertension
2. Osteoporosis
3. Depression
4. Weight Loss
5. Reduced muscle mass
54
Systemic symptoms of COPD
1. Hypertension
2. Osteoporosis
3. Depression
4. Weight Loss
5. Reduced muscle mass
55
What defines chronic bronchitis
1. Cough persists for more than 3 months each year for 2 years
56
What is seen in patients at later stages of COPD
1. PaO2 less than 8kPa
2. PaCO2 greater than 7kPa
3. Pulmonary hypertension (cyanosis)
4. Hypoxic kidney causes peripheral oedema due to failure of excretion of sodium and water
57
Differential diagnosis of COPD
1. Asthma
2. Congestive heart failure
3. Bronchiectasis
4. Allergic fibrosing alveoli's
5. Pneumoconiosis
6. Asbestosis
58
What is bronchiectasis
1. Airways are abnormally widened resulting in build up of excess mucus making lungs more susceptible to infection
59
How is diagnosis of COPD made
1. Anyone over the age of 35 to 40 with shortness of breath or chronic cough
2. Spirometry to measure FEV1 and FVC (FEV1/FVC < 0.7 = COPD and FEV <0.8 predicted value)
3. Transfer co-efficient (less CO will diffuse through alveoli due to decreased SA)
4. CXR
5. CT
6. ABG to determine need for oxygen
7. FBC
60
Characteristics of CXR in COPD
1. Overexpanded lungs
2. Bullae
3. Flattened diaphragm
4. Increased retrosternal space
61
Characteristics of CT in COPD
Shows distribution of emphysema in the lungs
62
Describe how we stage COPD
1. >80% FEV1 predicted value
2. 50-79
3. 30-49
4. <30
63
Results of FBC in COPD
1. PCV and Haemoglobin may be high due to persistent hyperaemia and secondary polycythaemia
64
Treatment of COPD
NO CURE
1. SMOKING CESSATION
2. Pulmonary rehabilitation (exercise and disease management, improved QOL)
3. Bronchodilators
4. Corticosteroids (decrease acute exacerbations)
5. Antibiotics (erythromycin - reduces frequency of exacerbations)
6. Supplemental Oxygen to those with sats less than 88% - decreases risk of heart failure
7. Surgery (lung transplantation or lung volume-reduction surgery - removes parts of the lungs most damaged by emphysema)
8. Antimucolytic agents to reduce mucus viscosity
9. Diuretics for oedema
10. Diet to reduce weight
65
Why is 88-92% oxygen saturation needed for COPD patients
Because over this will increase the risk of hypercapnia
66
Examples of pulmonary rehabilitation exercises
1. Pursed lip breathing
| 2. Tai Chi
67
What bronchodilators are given
B2 agonist and anticholinergics
1. INITIALLY Tiotropium Bromide (long-acting anticholinergic) + Ipratropium (short-acting anticholinergic)
2. INITIAL LABA (Salmeterol)
3. SABA (Salbutamol and terbutaline)
68
Name a SABA
Salbutamol
69
How long do SABAs act for
4 to 6 hours
70
Side effects of anticholinergics
1. UTIs
2. Dry Mouth
3. Heart disease
4. Stroke
71
How does triotropium bromide effect COPD patients
1. Prolonges bronchodilatation
72
When is Salmeterol given to patients
With persistent dyspnoea
73
What corticosteroid is given to mild/moderate COPD
1. Prednisblonedaily for two weeks with measurement of lung function before and after treatment
Improvement seen then discontinue prednisolone and move to inhaled corticosteroid
74
What corticosteroid is given as an inhalation
Beclometasone twice daily
75
How do we prevent infections in COPD patients
1. pneumococcal vaccino e
2. Influenza vaccination
3. Antibiotic treatment
76
When is oxygen therapy given to patients
Once they have stopped smoking
77
How long is oxygen administered for
19 hours every day via nasal prongs
78
Define asthma
Long-term inflammatory disease of the lung airways (REVERSIBLE AIRFLOW OBSTRUCTION and bronchospasming)
79
What causes asthma
Combination of environmental and genetic factors
80
What are some asthma related microbes
1. Chlamoydophila pneumoniae (stops ciliary movement in ciliated bronchial epithelial cells)
2. Mycoplasma pneumoniae
3. Human rhinovirus (cause upper respiratory infections)
ALSO:
dust mite
cockroaches
mold
81
Genetic factors that increase risk of asthma
1. ADAM33
Genes affecting production of IL3,4,5,9 and 13
82
When does asthma begin
1. Childhood between 3 and 5
83
Three characteristics of asthma
1. Airflow limitation
2. Airway hyper-responsiveness
3. Bronchial inflammation with T lymphocytes, mast cells, eosinophils causing epithelial damage and mucus plugging
84
Two main types of asthma
1. Allergic/eosinophilic asthma (caused by allergens)
2. Non-allergic/non-esoniohilic (RARE):
Exercise, cold air and stress
smoking
obesity associated
85
How can allergic/eosinophilic asthma be classified
1. Extrinsic
| 2. Intrinsice
86
What is extrinsic asthma
1. Asthma caused by extrinsic causes like sensitisation to NSAIDs
87
What is intrinsic asthma
1. Starts in middle-age and attacks are triggered by INFECTIONS
2. Shows positive allergic skin tests and history of childhood respiratory symptoms
88
What causes hyper-responsiveness in asthma
ATOPHY
Where individuals easily produce IgE against dust mites, grass pollen etc leading to elevated serum IgE levels
89
Risk factors for asthma
1. HISTORY of atopy
2. Family history of asthma and atopy
3. Obesity
4. Inner-cit environment
5. Premature birth
6. socio-economic deprivation
90
Pathophysiology of asthma
1, 1. During an episode, inflamed airways react to environmental triggers such as smoke or dust
2. Airways narrow and produce excess mucus making it DIFFICULT TO BREATHE
3. The bronchi contract into spasms
4. Inflammation of bronchi further narrow airways leading to coughing
5. Afferent nerve endings under bronchus sne dimpulsen to brainstem vagal centre causing ACh to be released in efferent nerve endings, too much IP3 produced leading to muscle contraction and bronchoconstriction
91
What is the hygiene hypothesis
1. Lack of early childhood exposure to infectious agents can suppress natural development of the immune system
92
Precipitating factors of asthma
1. Wood dust, bleaches and dyes, latex
2. Cold air and exercise
3. Atmospheric pollution and irritant dust
4. Diet (more fruit is protective)
5. Emotions (stress)
6. NSAIDs (aspirin)
7. Allergen induced asthma
8. BETA BLOCKERS
93
How do beta blockers cause asthma
1. They cause bronchoconstriction of the airways
94
Describe how the airways become inflamed in asthma
1. Mast cells increase in epithelium, smooth muscle and mucous gland sin asthma
2. Become sensitised when IgE binds to mast cell receptor
TYPE I hypersensitivity reaction
95
What do mast cells release in response to IgE
1. Histamine (bronchoconstriction via H1 receptor and inflammation)
2. Tryptase
3. Prostaglandin 2
4. Cysteine leukotrienes (more potent than histamine and causes bronchoconstriction and inflammation)
5. Cytokines
96
What do cysteine leukotrienes bind to
cys-LT1 receptor
97
What cytokines are released by mast cells
1. TNF-alpha, IL-3 (increases number of mast cells)
2. IL-4 (causes IgE synthesis)
3. Il-5 (inflammation and airway remodelling)
98
Where are eosinophils found
1. bronchial walls and secretions of asthmatics
99
What cytokines attract eosinophils to the airway
1. IL 3 and IL 5
These also enhance mediator secretion
100
What happens to eosinophils once activated
Release LTC4 and basic proteins such as MBP (major basic proteins) and ECP (eosinophilic cationic protein) and eosinophilic peroxidase (EPX) that are toxic to epithelial cells
101
What medication decreases the number of eosinophils
Corticosteroids
102
Where are dendritic cells and lymphocytes found
Mucous membranes of airways and alveoli
103
Role of dendritic cells and lymphocytes in asthmas
1. Dendritic cells take up and present allergens to lymphocytes
2. T helper cells activate and release cytokines activating mast cells
104
What happens in the lungs after allergen presentation
1. 30 mins after: BRONCHOCONSTRICTION
2. 3 Hours after: Bronchoconstriction decreases then inflammation due to vasodilatation
3. 6 hours after: Worsening of inflammation due to eosinophils releasing mediators = second wave bronchoconstriction
105
What happens to the cells in chronic asthma
They undergo REMODELLING
106
How does remodelling is asthma take place
1. Airway smooth muscle undergoes hypertrophy and hyperplasia
2. Airway is also thickened by deposition of repair collagen and matrix proteins below basement membrane
3. Deposition of metrix proteins, swelling and cellular infiltration expand the submucosa beneath the epithelium causing smooth muscle shortening and excess airway narrowing
4. Swelling outside smooth muscle layer reduces retractile forces exerted by surrounding alveoli so the airways close more easily
5. Epithelium of conducting airway is stressed and damaged will loss of ciliated columnar epithelial cells
6. Metaplasia occurs with increase in number ofmqcus-secreting goblet cells
7. Damage to epithelium make sit more vulnerable to infection
107
Clinical presentation of asthma
1. Dyspneoa
2. Wheezing
3. Nocturnal Cough
4. Sputum
5. Symptoms worse at night
6. Episodic shortness of breath
7. Provoking factors: allergens, infections, cold air and exercise)
```
ATTACK:
Reduced chest expansion
Prolongues expiratory time
Bilateral expiratory polyphonic wheezes
tachypnoea
```
108
Characteristics of uncontrolled asthma
1. PEFR less than 50%
Resp rate less than 25
Pulse less than 110
Normal speech
109
Characteristics of severe attacks of asthma
1. Can't complete sentences
2. Pulse greater than 110
3. Resp rate greater than 25/min
110
What can be seen in a life-threatening attack of asthma
1. Silent chest
2. Confusion and exhaustion
3. Cyanosis
4. Bradycardia
5. PEFR less than 33%
111
Immediate Management of asthmatic attack
1. OXYEGN TEHRPAY
2. Nebuliser 5mg salbutamol (+Ipatropium)
3. Prednisolone (with or without hydrocortisone IV)
4. ABG and repeat within 2 hours
5. CXR if failure to respond to treatment
6. Check PEFR every 15/30 mins
7. Oximetry
112
Differential diagnosis of asthma
1. Pulmonary oedema
2. COPD
3. Large airway obstruction caused by foreign body
4. Pneumothorax
5. Bronchiectasis
113
What is pneumothorax
Abnormal collection of air in the pleural space
114
Describe the asthma control test
1. 25 - well controlled
2. 20-24 on target
3. Less than 20 - off target
115
What lung function tests do we do for asthmatics
1. PEFR (measured when waking BEFORE taking bronchodilator and before bed AFTER bronchodilator)
2. Spirometry
3. CO test is normal
116
What other tests can we do to see severity of asthma after management
1, Exercise test
2. Trial of corticosteroids
3. Exhaled NO
4. FBC and sputum test
5. Skin prick tests
6. History
117
Why is exhaled NO checked
Efficacy of corticosteroids (measure of eosinophilic inflammation)
118
Why is blood test and sputum checked
1. Number of eosinophils can be checked (sputum eosinophilia)
119
How do we distinguish asthma from COPD
1. COPD is a later disease
2. SOB is progressive
3. Less day-to-day variation
4. Sputum production in COPD
