RESP: Mechanics of breathing Flashcards
What is the consequence of impaired airway function?
Insufficient ventilation
To reach gas exchange surfaces, what must air pass through?
A series of increasingly narrow and numerous airways
What is the rate of airflow dependent on?
Pressure gradient & level of airway resistance
What is Ohm’s law?
Airflow (V) = 𝚫 Pressure (P)/ Resistance (R)
⬆️ 𝚫P = ⬆️ Airflow
⬆️ R = ⬇️ Airflow
What is the Hagen-Poiseuille equation?
The Hagen-Poiseuille equation describes the relationship b/w resistance and the various properties of airways and airflow
When effective constants are removed, it demonstrates that resistance of a gas is inversely proportional to cross-sectional radius to the power of 4.
This means a small decrease in radius will produce a large increase in R.
What is airway resistance further increased by?
Turbulent airflow - This creates eddies, which prevents air from moving through in a laminar fashion
Turbulence occurs where high velocities of airflow are achieved, or if there is a sudden decrease in luminal area such as in obstructed airways.
The vibration generated by turbulent airflow is responsible for the wheezing sound produced in patients with obstructed airways.
What physiological changes can cause airway obstruction and why do they cause obstruction?
- Loss of airway patency due to degradation of structure can cause airway obstruction. The open structure of airways is maintained by elastic fibres within wall of airway + radial traction. Pressure differentials b/w intrapleural space + airways can reduce airway patency during forced expirations. When intrapleural pressure becomes positive (forced expiration), collapsing force will be exerted onto airways and this can be problematic for those with diseases involving impaired airway structure (e.g. COPD)
- Contraction of airway smooth muscle
- Excessive mucus secretion
- Oedema/Swelling of the airway tissue
All of these reduce the size of the airway lumen, increasing airway resistance and decreasing airflow
Describe lung compliance
Lung compliance quantifies the relationship between the level of expansive force applied to the lung and the resulting change in lung volume
Essentially, lungs that are more compliant need less of an expansive force to inflate them
Lung compliance - The change in lung volume produced by a particular change in transpulmonary pressure
Compliance = 𝚫Volume/𝚫Pressure
Higher lung compliance = Less elastic recoil = Less force required to inflate = ⬆️Volume change per pressure change- This will create a steeper gradient on a V-P curve, where compliance is the gradient.
The opposite is true for lower lung compliance
What happens during inspiration in terms of pressure?
Increasing levels of negative intrapleural pressure generated as lung volume increases due to elastic properties of lung tissue.
The increasing negative intrapleural pressure keeps the lungs inflated as it’s less than the transpulmonary pressure
What factors and diseases affect lung compliance?
Number of diseases that affect recoil or structure of lungs + chest wall, leading to altered lung compliance:
- Scoliosis - Affects chest wall mechanics, decreases lung compliance
- Muscular dystrophy - Affects chest wall mechanics, decreases lung compliance
- Obesity - Affects chest wall mechanics, decreases lung compliance
- NRDS - Affects alveolar surface tension, decreases lung compliance
- Fibrosis - Affects elastin fibres, decreases lung compliance
- COPD - Affects elastin fibres, increases lung compliance
How is lung compliance affected by disease? (Specifically emphysema and pulmonary fibrosis)
Emphysema (COPD) involves degradation of the elastin fibres, makes the lungs less stiff, more compliant (but reducing recoil), therefore the lungs can expand more but it also means there’s no elasticity for the lungs to compress and therefore expiration is difficult
Pulmonary fibrosis - Scarring + deposition of structural fibres such as collagen making the lung stiff and less compliant, lungs cannot expand enough
What do air-liquid interfaces (e.g. alveoli) generate and how?
Surface tension, which resists inflation.
Alveoli are lined with fluid to enable gas exchange (the gas molecules dissolve into water before diffusing. The water molecules have a tendency to form H bonds with each other, and this is what generates the surface tension, as they produce force on each other. However, the water molecules on the top of the water layer don’t want to react with air, and so they generate a net force downwards (due to the fact that the H bonds it forms with molecules on its left and right will cancel out), and this makes the water layer get thinner, and a collapsing force is generated towards the centre. As the layer gets thinner, it creates surface tension with the air, and as the tension increases it ‘pulls’ on the alveoli, this is the collapsing force.
The Water-air interface formed b/w the lining fluid and alveolar airspace creates a ‘bubble’
Within the bubble formed by the water-air interface, surface tension arises due to H-bonds between the water molecules, exerting a collapsing force toward the centre of the bubble, hence the alveoli collapses.
What does the law of Laplace describe?
The pressure generated by the surface tension within a bubble.
The collapsing forces generates local pressure. The amount of pressure generated within a specific bubble is described the Law of Laplace:
P = 2T/r (T= surface tension)
If T remains constant, then P ∝ 1/r
Where is more pressure to collapse generated?
More pressure to collapse is generated within a smaller bubble than a larger bubble
What would happen if 2 bubbles of different radius were connected to each other (e.g. different size alveoli connected via airways)?
Pressure gradients would be created between different sized alveoli, resulting in smaller alveoli emptying into larger ones
What is alveolar surface tension reduced by?
The presence of pulmonary surfactant, secreted by type 2 pneumocytes
What is pulmonary surfactant and how does it work to reduce surface tension?
A phospholipoprotein secreted by type II pneumocytes (alveolar cells).
Surfactant molecules are amphipathic, with hydrophilic head and hydrophobic tail regions, so position themselves at the air-liquid interface.
The presence of the surfactant molecules acts to disrupt the attractive forces between water molecules, reducing surface tension, and the collapsing pressure generated.
What are the 2 types of cells that the surface of alveoli primarily consists of?
Type 1 (95% of alveolar surface) = responsible for gas exchange
Type 2 = secrete pulmonary surfactant
What is the action of pulmonary surfactant?
Acts to equalise pressure and volume across varying alveoli.
As alveoli expand, the number of surfactant molecules per surface area (the localised PS “concentration”) decreases, increasing surface tensions.
Now the pressure differences mean larger alveoli tend to collapse into smaller ones, helping consistent inflation of the lungs.
What is neonatal respiratory distress syndrome caused by?
NRDS occurs in premature infants, who develop and produce insufficient levels of pulmonary surfactant. This results in respiratory failure due to the alveoli collapsing, decreasing lung compliance (’stiffer’ lungs)l, alveolar oedema, reducing gas exchange.
Increased forces + pressure involved within lung also damage alveoli and innervating capillaries.
NRDS is treated with either supplementation of artificial surfactant, or by administering glucocorticoids (these increase surfactant production via maturation of type II pneumocytes) to mothers deemed high risk.
What happens when ex vivo lungs are inflated with saline rather than air?
Ex vivo lung perfusion allows for the lungs to be manipulated + characterised in an external environment so the effect of specific ventilation/perfusion variables can be studied independent of other physiological changes.
Compliance increases. Saline-filled lungs required less pressure to inflate (⬆️compliance)
Washing lungs with saline before inflating with air produced lungs that required more pressure to inflate (⬇️compliance).
What is the action of pulmonary surfactant?
Increases lung compliance
