CVPR Week 5: Mechanics of breathing Flashcards
Objectives
5 listed
Congenital central hypoventilation syndrome genetics
PHOX2B gene
Congenital central hypoventilation syndrome clinical features
if you fall asleep you stop breathing
Identify symbols
Identify
Identify
Identify
The lungs have how many attachments to the body?
1 . . . the Hilum
the lungs are otherwise free-floating in the pleural space
What is in between the chest wall and the lungs?
pleural membranes Parietal pleura of the chest wall and the visceral pleura of the lung
and
intrapleural fluid
Intrapleural fluid function
helps hold the parietal and visceral pleural membrane together providing surface tension and also lubricates them to ease sliding
Intrapleural fluid location
in between the visceral pleura of the lung and the parietal pleura of the chest wall
Gases move in and out of the lung by?
Bulk flow
How are CO2 and O2 exchanged in the lungs?
Diffusion
Gasses dissolved in the blood are transported via?
Bulk flow
How are CO2 and O2 exchanged in the tissues?
Diffusion
~ Surface area of the lung available for diffusion
about one half of a tennis court
Identify
Factors that influence the speed of diffusion
6 listed
- surface area
- distance traveled (thickness of membranes)
- partial pressures
- temperature
- solvent density
- mass of the solute
Identify
A = Alveoli
RB = Respiratory bronchioles
TB = Terminal bronchioles
AD = Alveolar ducts
Macrophage is here also
Type II pneumocytes make surfactant
C = capillary
PA = Pulmonary artery
Pulmonary function testing can measure?
Lung volumes and capacities
What is spirometry?
a pulmonary function test that measure volumes and capacities
What cannot be measured with simple spirometry?
3 listed
- TLC
- FRC
- RV
TLC AKA
Total lung capactity
FRC AKA
Functional residual capacity
RV AKA
Residual volume
What is tidal volume
What is inspiratory reserve volume?
What is the expiratory reserve volume?
What is the residual volume?
What is the vital capacity?
What is the inspiratory capacity?
What is the functional residual capacity?
What is the total lung capacity?
Question 1
C)
Contraction of the diaphragm decreases Pip with increases the transmural pressure gradient, expanding the alveoli, the larger alveoli now has a subatmospheric pressure creating a gradient for air flow
What is the mechanism of normal quiet breathing?
Inspiration is from the contraction of the diaphragm creating a sub-atmospheric pressure change driving air in
Expiration is caused by the relaxation of the diaphragm pushing the air out
What is the transmural pressure gradient?
P alv - Ppl = transmural pressure
It is the pressure gradient and determines the volume of the lung (distending pressure of the alveoli)
Palv = alveolar pressure
Ppl = interpleural pressure
What is the pressure gradient driving air flow?
Palv - Pbs(ao) = the pressure gradient driving air flow
Palv = alveolar pressure
Pbs(ao) = body surface or atmospheric
PV = nRT therefore?
Pα = 1/V
What pressure gradient determines the volume of the alveoli?
Transmural pressure
Palv - Pbs(ao) = the pressure gradient driving air flow
Palv = alveolar pressure
Pbs(ao) = body surface or atmospheric
The chest wall is always pulling in which direction?
out away from the lungs
The lung is always pulling in which direction?
inwards
when cadaver the association with the chest wall is gone and the lungs retract and recoil
Increasing alveolar volume does what?
decreases Palv sucking air into the lung
intrapleural pressure changes
- 5 mmHg to -8mmHg …. etc should be more
What defines these volumes?
TLC
FRC
RV
Mechanical recoil forces of the lung and chest wall establish these volumes
outward forces of the chest wall, muscles of inspiration
vs
how much inward recoil force of the lung
How is the TLC defined?
When the total outward forces match those of the inward recoil force of the lung
(Force out = force in ) = TLC
How is FRC defined?
Functional residual capacity is in between breaths
where the inward recoil of the lung is exactly equal and opposite the outward forces of the chest wall
How is RV defined?
when the recoil of the lung is equal and opposite the forces of the muscles of expiration and chest wall
When does the transmural pressure point become negative?
Just after the equal pressure point (EPP) the transmural pressure becomes negative
Why do the pressures going away from the alveoli decrease?
because there is resistance to flow
Pressures of passive expiration vs forced expiration
trachea cartilage holds it open
Losing some recoil of the lung in?
Emphysema - you lose some elastic tissues so there’s less recoil force
also increasing resistance through a process called (lateral infraction?)
Emphysema EPP
in ephysema, elastic tissues are lost so there is also loss of recoil of the lung
the EPP migrates closer to the alveoli and away from the cartilaginous rings so the air ways collapse
Question 2
increase because the lung can collapse in emphysema
if it decreased then the lung would stiffen and probably not collapse
Compliance curve of the lung
transpulmonary pressure vs volume
ΔV / ΔP =
Compliance
The steeper the compliance slope the. . .
easier it is to expand the lung
Restrictive lung diseases
Interstitial fibrosis (“scar tissue”) make lungs stiffer - more muscular work
Obstructive lung diseases
Diseases that destroy elastic tissue (e.g. emphysema) make the lung more compliant
Compliance of restrictive lung diseases
greater changes in pressure are required to expand the lung
Requires more work
Also
FRC changes to breathe from smaller lung volumes (makes sense so they can do less work)
Compliance of obstructive lung diseases
smaller changes in pressure are required to fill the lungs
less work is required to breath
FRC changes to a higher capacity (because exhaling is a passive process which requires the lung to be an elastic organ, so a higher capacity, also to facilitate expiration in the absence of elastic tissue)
Lung volumes in obstructive and restrictive lung diseases
Explain this graph
in the saline-filled lung, there is no air fluid interface so you don’t have to fight against the forces of surface tension in the lung
In the air-filled lung, there is an air-fluid interface so the surface tension forces must be overcome to inflate the lung
La Place’s Law equation
P = 2T/r
Explain La Place’s Law
helps us relate the pressure inside a sphere to the surface tension and the size of that sphere
smaller spheres would have higher pressure than larger alveoli
Why don’t we just have 1 big alveolus due to smaller alveoli pushing their air into the larger
pulmonary surfactant allows us to have different sized-alveoli and avoid the collapsing alveoli problem
because the surface tension that is produced is area dependent
What happens with surfactant deficiency?
requires a lot of pressure to open the lungs
old term of surfactant deficiency
hyalin membrane disease
Identify
What is surfactant composed of?
mostly DPPC lipid
also have proteins
Where is surfactant made?
in the lung by type II pneumocytes
Identify
Surfactant protein SP-A/SP-D
- Involved in the unraveling of lamellar bodies
- host immune response
Surfactant protein SP-B/SP-C
Optimize rapid absorption and spreading of phospholipids on the alveolar surface
Surfactant small hydrophobic proteins
SP-B and SP-C
Surfactant lung collectins
SP-A and SP-D
Surfactant proteins and functions
Regulation of surfactant secretion
4 listed
- Gestational age
- β-adrenergic and ATP-mediated activation of purinergic receptors
- Signaling pathways involve changes in intracellular Ca2+ as well as activation of PKA and PKC
- Mechanical distention (sigh and exercise)
Question
Total work in the lung
work to overcome recoil (elastic/surface tension) forces (lung and chest wall) + Resistive work (tissue and AIRWAYS) but also friction
friction between the lung and the chest wall (minimized by intrapleural fluid) + frictional resistance of air moving in airways (primary)
Resistance of air moving in airways equation
Where is the site of greatest resistance along the respiratory tree?
in the tertiary bronchi?
Resistance along the respiratory tree
Resistance is low in the terminal bronchioles because
parallel resistances and smaller lengths
Lung volume and airway resistance and why?
as the lung is expanded airway resistance decreases
- the transmural pressure gradient also affects smaller airways
- lateral traction
*
Lateral traction
airway is surrounded by alveoli
when the alveoli expands it wants to return back to its original shape and pulls out on the airway causing lateral traction
this is partly why resistance is increased in emphysema because loss of tissue results in loss of these phenomenon
Bronchial smooth muscle tone and airway resistance
CO2 effect on bronchial smooth muscle
cause the bronchial dilation
innervation bronchial smooth muscle
β2 adrenergic activation causes dilation
vagal cholinergic causes constriction
bronchial smooth muscle reflex
chemical irritants, smoke, dust (reflex response) mediated by parasympathetic cholinergic pathways
Question
Question
To inflate the lung you must over come these intrinsic forces
What can modify airway resistance?
airway obstruction and reduced lateral traction
Elastic work vs frictional work
compliance curves in normal, fibrosis and asthma/chronic fibrosis
Functions of the respiratory system outside of breathing
4 listed
- Vascular reservoir
- Acid-base balance
- Defense mechanisms
- metabolic functions of the lung
The lungs as a Vascular reservoir
can have fluctuations in CO without huge changes in pulmonary pressre
pulmonary arteries are thin walled and distensible and expand their radius to buffer an increase in pressure
also
not every single pulmonary artery are receiving blood so you can recruit or stop using some to buffer changing pulmonary arterial pressures
The lungs in acid-base balance
bicarbonate buffer system to eliminate CO2
the lung eliminates CO2 returning the blood back to steady state pH
The lungs defenses
Filtration
mechanical filter cough or sneeze them out
microcirculation (remove emboli)
Immune defense mechanisms (example is pulmonary alveolar macrophages)
Metabolic functions of the lung
Activation of ACE
Inactivation thorugh Bradykinin (ACE) ET-1 (ETb receptors)
Lungs in speech
need air around vocal cords to make sound
