Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
70 Cards in this Set
- Front
- Back
- 3rd side (hint)
What makes up the ventilatory apparatus?
|
The lungs and the surrounding chest wall
|
|
|
What does the chest wall consist of?
|
Rib cage
Diaphragm Abdominal wall |
|
|
Where are the visceral and parietal pleura located?
|
Visceral: Lungs
Parietal: Chest wall |
|
|
Are the lungs attached to the chest wall?
|
No, but they act in series with the chest wall
|
|
|
Why is there negative P?
|
Chest always want to pull out, lungs always want to collapse in
|
|
|
How are the visceral and parietal pleura coupled together?
|
By a thin layer of liquid that fills the intrapleural space
->The liquid lets the lungs slide against theinternal wall of the chest during breathing and to follow the change in thoracic configuration |
|
|
What is Pleural Pressure (Ppl)?
|
The P that can be measured in the liquid filled spcae between the lungs and chest
|
|
|
What i the Ppl at rest? Why?
|
Negative
Due to the opposing forces acting on the lungs and chest wall |
|
|
What happens if there's a pneumothorax?
|
The lungs collapse and the chest springs outwards
|
|
|
How can the elastic properties of the respiratory system be measured?
|
Measure the changes in the recoil pressure of the different structures for a given change of lung volume
|
|
|
How can lung volumes be mesured?
|
Spirometry
|
|
|
What is used to measure respiratory system P?
|
Manometers
Pressure Transducers (they're referenced to atmospheric pressure) |
|
|
What is recoil pressure?
|
Pressure difference between the inside and the outside of the structure (transmural P)
|
|
|
What is negative P?
Positive P? |
Negative: P below atm
Positive: P above atm |
|
|
What is the recoil P of the chest wall, transchest-wall P (Pw)?
|
Difference between Ppl and the P at the body surface
|
|
|
How can Ppl be measured?
|
Using a ballon introduced into the esophagus
->esophagus is between 2 pleural spaces so esophageal P is a close approximation to pleural P |
|
|
What does Pw (chest wall) equal?
|
Pw = Ppl - Pbs
bs:body surface pl: pleural w:chest wall |
|
|
What is the recoil P of the lungs?
|
Transpulmonary P (Pl)
|
|
|
How is Pl measured?
|
Pl = Palv - Ppl
->if no air flow, closed nose and mouth, P alv and P at the mouth are the same |
|
|
How is the recoil P of the total respiratory system , the transrespiraoty system P (Prs) measured?
|
Difference between Palv and Pbs
Prs = Palv- Pbs -> Palv = Pl + Ppl -> Pbs = Ppl - Pw .: Prs = Pl + Pw |
|
|
What does compliance of the lungs/chest wall/total respiratory system refer to?
|
Ease with which each of these structures can be distended
|
|
|
How is the respiratory system compliance determined?
|
Determne the static P-V relationship while lung volume is decreased step by step from TLC
(C= dV/dP) |
|
|
What happens to P to maintain a given volume of gas in the lungs if the volumes increase?
|
P must also increase
(slope of P-V curve decreases with increasing volume) |
|
|
In which diseases is lung compliance altered?
|
Emphysema
Fibrosis |
|
|
What does the P difference between the alveoli (Palv) and the pleural space(Ppl) equal?
|
P drop across the lungs
->P req'd to maintain the lungs at a given inflation volume against their tendency to recoil Cl = dV/ (dPalv-dPpl) |
|
|
How is lung compliance (Cl) related to elastcity (El)?
|
El = 1/Cl
|
|
|
How is the elastic recoil of the lungs produced?
|
Partly by elastic lung tissue
Mostly from properties of the liquid film lining the inside of the lungs |
|
|
Why does the surface tension of this liquid film generate such a force?
|
The SA of the film is so large
|
|
|
What happens during fibrosis?
|
Deposition of fibrotic tissues on alveol surface (makes them stiffer, harder to inflate then the alveoli)
Get smaller change in V for a given P |
|
|
What happens in emphysema?
|
Destruction of the alveolar wall
->Easy to inflate them but not easy to recoil, hard to deflate the alveolu ->FRC will we higher than normal Need to use moe expiratory muscles, but still have a higher volume |
|
|
What happens to the lungs at higher volumes?
|
Harder to stretch the lungs
|
|
|
Is compliance measurement static or dynamic?
|
Static
->Fill lungs then take a measurement |
|
|
Why is the P when measuring the lung compliance always positive?
|
Lungs always tend to collapse
|
|
|
How come the compliance P for the chest wall can be positive and negative?
|
Chest wall tends to collapse only after reaching a volume of 60% vital capacity
|
|
|
What happens when the chest is compressed?
|
It wants to spring out
-> Negative P |
|
|
What happens when cest P is increased?
|
It will want to collapse: Positive P
|
|
|
What is the Prs (P drop across the respiratory systm) at FRC?
|
Zero, because the system is at rest
->stable condition caused by the inward recoil of the lungs (+5cm H2O) which is balanced by the outward recoil of the chest (-5cm H2O) ->At FRC, the lungs are above their resting volume and th echest is below its resting volume (**Pneumothorax**) |
|
|
What happens during a pneumothorax?
|
Air enters the pleural space cuz Ppl < Patm
Lungs collapse to their resting position below RV Chest wall expands towars its resting position (~75% of total lung capacity) |
|
|
Why can a spontaneous/traumatic poneumothorax be life-threatening?
|
Lungs are uncoupled from the chest wall
|
|
|
What happens during inspiration?
|
Diaphragm contracts and the chest wall is pulled open
->Get a more negative Ppl that cause chest expansion |
|
|
What happens if the chest volume is increased?
|
The Ppl is decreased (P becomes more negative)
->Lungs will follow: inflate lungs, decompress air in the lungs |
|
|
Is Palv or Patm greater during inspiration? Expiration?
|
Inspiration: Palv < Patm
Expiration: Palv > P atm |
|
|
What is the equation for flow?
|
F= (Palv-Patm)/R
|
|
|
What happens as the lungs are pulled further and further away from their resting position (which is below Residual volume)?
|
Ppl becomes more subatmospheric
As lung volume increases, gas in the lungs are decompressed Palv drops below atmospheric P This produces neg P gradient btw the alveoli and atm makes air flow to the lungs |
|
|
What happens as inspiration continues?
|
Lungs fill up with air
P gradient and air flow start to decrease At the end of inspiration, airflow stops because Palv=Patm |
|
|
What happens at the onset of expiration?
|
Diaphragm relaxes
Elastic recoil of the respiratory system compresses the gas in the lungs Palv increases Positive P gradient btw the atm and lungs is reversed and air from the lungs to the atm |
|
|
What happens near the end of expiration?
|
Lung volume decreases
Ppl slowly returns to its resting level At the end of expiration (FRC), air flow= 0ml/s and Palv=O cm H2O and Ppl= -5cm H2O |
Look at SLIDE for DYNAMICS of breath
|
|
What is required to get airflow through the airways?
|
P of airway opening (Pao) must be different to that in the alveoli (Palv)
|
|
|
What is the resistance of the airways to gas flow (Raw)?
|
Ratio of Pao to Palv difference and the flow
Raw= (Palv-Pao)/Flow |
|
|
What has more resistance, a large diameter or small diameter?
|
Small diameter
**Air resistance is related to airway caliber and is an important determinant of lung fuction** |
|
|
What happens in asthma?
|
Lumen becomes smaller
Diameter of airway decreases .: less air can come in per unit of time |
|
|
Why is the descending portionof the flow-volume curve independent of effort?
|
Because of the compression of the airways by intrathoracic P
**Pleural P is greater than airway P** |
|
|
What happens to the P's before, during and end of inspiration and then during forced expiration?
|
Before: Airway P=0 and Intrapleral P= -5cm H2O
During: Pleural an airway P fall End: Airway P =0 and airway transmural P = 8cm H2O Forced expiration: Intra-pleural and alveolar P are increased ->because of the P drop along the airways as flow begins, there is a point at which there is a positive P tending to close airways |
|
|
What is an example of a restrictive disease?
|
Fibrosis
|
|
|
What is an example of an obstructive disease?
|
Emphysema
|
|
|
What happens in restrictive diseases?
|
Max flow rate and max volume exhaled are reduced
|
|
|
Wha happens in obstructive diseases?
|
Flow rate is very low and a scooped out appearance is often seen
|
|
|
What happens to the lungs in restrictive diseases?
|
Lungs very stiff
Lungs want to recoil so flow will be greater for a given lung volume, but lower if compared overall) |
|
|
What happens to the lungs in an obstructive disease?
|
Lungs easier to inflate
Hard for lungs to recoil For any lung volume, flow < normal |
|
|
What is an important contributor to the mechanical properties of the respiratory system?
|
The surface tension of the liquid film lining the lungs
|
|
|
How oes this surface tension arise?
|
The molecules in the surface of the film tend to arrange themselves in the configuration that has the lowest energy
->they're mmore attracted to themselves then air molec ->generates tension across the film surface |
|
|
When can this tension produce a pressure?
|
If the surface is curved
->inside n alveolus or airway |
|
|
What is La Place's law?
|
P= 4T/r
(P is inversely proportional to the radius, .: the P inside a smaller bubble is greater than inside a large bubble) |
|
|
What happens to the surfactant that is secreted by epithelial cells?
|
It puts itself between water molecules and decreases the surface tension
|
|
|
What is the difference in surfactant in small alveoli and large alveoli?
|
Many small alveoli: have many layers of surfactant
->decreases surface tension a lot 1 Large alveoli: only has 1 monolayer of surfactant ->Surface Tension decreases by less |
|
|
What would happen if we didn't have surfactant? Why?
|
We wouldn't be able to breathe because the forces of surface tension are so great
(surfactant stabilizes the lungs, but produces more of an effect in small alveoli than large ones) |
|
|
What prevents the collapse of small alveoli into larger ones?
|
Pulmonary surfactant
|
|
|
Which cells secrete pulmonary surfactant?
|
Alveolar type II cells
|
|
|
What are the 2 principle roles of pulmonary surfactant?
|
1) Make surface tension in the alveoli change with lung volume to prevent the P in the small alveoli fom exceeding the P in the large alveoli
2) Reduce overall surface tension so that we can breathe |
|
|
What would happen if the surface tension in the liquid lining layer was the equal to that of water?
|
We wouldn't be able to inflate our lungs
|
|