Week 9: Airway Patency, Obstructive and Restrictive Lung Diseases Flashcards
Explain the equal pressure point (using expiration) and what a negative transmural pressure gradient is
During expiration the driving pressure (alveolar pressure – atmospheric pressure) reduces along the airways due to frictional airway resistance Because of this, at some point, this driving pressure reduces so much that the pressure outside [pulmonary pressure] = intra-airway pressure. It is as this point that is the Equal pressure point (EPP) Anywhere above this EPP will result in a negative transmural pressure gradient (when the pressure outside the airway [pulmonary pressure] is greater than the pressure inside the airway) which will result in collapse and/or compression of the airway (only if they don’t have cartilage)
Explain how EPP causes the collapse of airways in emphysema.
- Patients lose their lungs radial traction (Is the elastic and type 4 collagen that helps pull the airways open) - Meaning their airway is going to narrow (not pulled open as much anymore) - This results in increased airway resistance - As the person is now feeling out of breath, they start doing more forced breathing - This increases the pulmonary pressure (pressure outside, from muscles forced breathing), that when combined with the increased airway resistance (from loss of radial traction) results in the EPP dropping below the cartilage supported zone collapsing more and more airways during expiration
What are obstructive diseases and what will they result in (in terms of TLC and FRC etc…)
an increase in airway resistance
- Vital capacity will decrease (this is the maximum amount of air a person can expel after maximum inhalation)
- There will be increased total lung capacity, increased residual volume (amount of air remaining after lungs have fully exhaled), increased functional residual capacity (air present in the lungs are passive expiration) – due to gas trapping
What is the diagnostic spirometry test that is used to diagnose obstructive and restrictive diseases?
- FEV1 : FVC ratio
- FEV1 (the amount of air you can blow out in 1 second) divided by,
- forced vital capacity (the max someone can expel from their lungs after max inhalation)
What are restrictive diseases and what do they result in (in terms of TLC, FRC etc….)
restrictive diseases is a decrease in lung compliance
- Restrictive diseases will result in;
- Decreased VC
- Decreased TLC, RV, FRC
Explain the FEV1 / FVC in restrictive vs obstructive pulmonary disease
- In obstructive disease, patient’s airway resistance is increased, dropping the EPP out of the cartilage supported zone, collapsing the airways. It then takes longer for patients to completely exhale their vital capacity meaning there FEV1/FVC will be reduced
- In restrictive disease, lung compliance drops, making it harder and harder to inflate the stiffened lung meaning they are going to have less than 80% of the lung capacity compared to their predicted (for their age, height, gender, ethnicity)
Define what FEV1 and FVC mean
- FEV1 (the amount of air you can blow out in 1 second) divided by,
- forced vital capacity (the max someone can expel from their lungs after max inhalation)
What effect does fibrosis and emphysema have on lung compliance and why?
- Fibrosis of the lungs;
- Is characterised by a decrease in lung compliance, they become stiff
- This is caused by an increase in collagen fibres within the lung
- Thus, we need a large pressure to maintain a moderate volume - Emphysema of the lungs;
- Is characterised by an increase in lung compliance making the lung overly stretchy
- This is caused by the breakdown of collagen and elastin within the lung
- Whilst the lung may be easier to stretch (which reduces the cost of breathing) the surface area is diminished reducing the ability of the lung to exchange gas (meaning they have to increase minute ventilation to get enough alveolar ventilation to satisfy their metabolic need) – they have to breath more often to get gas diffusion occurring in their lung.
What is emphysema?
- Is a condition characterised by the enlargement of the air spaces distal to the terminal bronchiole, and by the destruction of the walls of the alveolar (it is a presumptive diagnosis in a living person)
What are the major causes of emphysema? (main two)
- Smoking
- Air pollution
- Occupational hazards (mining, asbestos)
- Bacterial infections
- Some genetic factors
Explain the pathogenesis of emphysema:
The destruction of the alveolar walls is caused by something known as the protease-antiprotease mechanism
- Within the lung, there is a balance between the proteases (breaks stuff down) and antiproteases. It is when this balance is shifted that destruction occurs
- The two sides of this balancing act within the lungs are;
1. Elastase (derived from neutrophils)
- which digests elastin and type 4 collagen (is our protease)
- These are very important in providing the structural integrity of the lung (particularly alveolar wall strength
2. Alpha 1 antitrypsin
- Is our Anti-protease
Causes of the imbalance:
Some sort of stimulation (such as smoking) can cause an increase in number of neutrophils
It can also increase the amount of elastase in the neutrophil
Stimulated Neutrophils also release O2 free radicals which inhibit alpha 1 antitrypsin activity
You can also have low alpha 1 antitrypsin levels due to genetic cause
Explain the smoking effects on emphysema
- Smokers have a greater number of neutrophils within their alveoli (as the production of neutrophils is stimulated by smoking)
- Smoking stimulates the release of elastase from neutrophils (neutrophils also contain a greater number of elastase compared to non-smoker neutrophil)
- The oxidants that are present in cigarette smoke also inhibits alpha 1 antitrypsin activity
- The O2 free radicals released from the increased neutrophils also inhibits alpha 1 antitrypsin activity
What is a summary of the effects of emphysema (x3)
- Destruction of the alveolar tissue, especially the septa (the walls)
- Inflammation of the bronchioles due to inhalation of airway pollutants
- Loss of radial traction (which leads to airway collapse leading to gas trapping)
What clinical manifestations of emphysema
- Some patients may also develop a barrel shaped chest, due to over inflation of the lungs (caused by gas trapping)
- Decreased surface area for gas exchange
- Airway collapse due to loss of radial traction
- In a patients x-ray with emphysema, what you will notice is an overinflated lung, and lowered flattened diaphragm (usually sits around the 5th intercostal space)
- Increased Functional Residual Capacity
- Increased Residual volume
- Increased TLC
- Decreased FEV1
- Decreased Vital Capacity
What are the 3 types of emphysema?
- Centriacinar emphysema
- Is the destruction of the central parts of the lobe, without damaging the alveolar
- This results in reduced airflow to the alveolar, as the bronchioles etc. are collapsed
- Most common in the upper regions, and then spreads downwards - Panacinar emphysema
- Is a form of emphysema that destroys the entire region of the lungs
- The terminal airways and the alveolar space is destroyed
- Shows no regional preference - Alpha 1 antitrypsin deficiency
- Is the genetic form of emphysema, resulting in reduced alpha 1 antitrypsin levels
- This results in destruction of the lower lobes (then moving upwards)
- Usually, in a non-smoker this wouldn’t be evident until 40 years of age
What are some treatments of emphysema
- Cessation of smoking
- Inhaled bronchodilators (beta -agonists and anticholinergics)
- Corticosteroids
- Anti-tussives (dextromethophans, codeine)
- Expectorants (bromhexine)
- O2 therapy
- Antibiotics and antiviral agents
What are 4 restrictive diseases
- Diffuse interstitial pulmonary fibrosis
- This is characterised by the fibroblasts down laying far too much collagen in the interstitium of alveolar walls
- Patients with this end up with multiple air filled cystic pouches
- This increases the thickness of the respiratory membrane, making gas diffusion far more difficult
- It is also known as honey comb lung - Pulmonary fibrosis
- Treatment is so hard as there are a number of mechanisms that cause this disease
- It is a disease characterised by the scarring and stiffening of alveolar - Pneumothorax
- Is a restrictive disease involving the pleura and chest wall
- Basically, a pneumothorax is a loss of negative pressure within the pleura cavity, when the chest then expands, the lungs do not move with it
- This negative pressure is affected by air that enter the pleural space or chest wall (usually a penetrating injury)
- There are a number of different types of pneumothorax; - Scoliosis
- This is a restrictive condition that is caused by a problem with the neuromuscular and skeletal elements that relate to ventilation
- Scoliosis is a lateral curvature of the spine and kyphosis (hunchback) to posterior curvature
- In this disorder, the lung function itself is ok, but there instead there is a curvature of the spine which affects the ability of the ribs / diaphragm to move to inflate the lung
- This causes areas of lung compression, with resulting V / Q inequalities
- There is an increase cost of breathing because of the abnormally formed ribs
- There may also be increased pulmonary artery bed on the compressed side (leading to pulmonary oedema
What is a pneumothorax
- Is a restrictive disease involving the pleura and chest wall
- Basically, a pneumothorax is a loss of negative pressure within the pleura cavity, when the chest then expands, the lungs do not move with it
- This negative pressure is affected by air that enter the pleural space or chest wall (usually a penetrating injury)