Flashcards in L06, L07- Mechanisms of Breathing Deck (101):
Definition of Airway?
passageways through which air flows between external environment and alveoli
Definition of Alveoli?
site of gas exchange
Definition of elasticity?
property of matter that causes it to return to its original shape or size after being deformed by
an external force
What two criteria are there for an elastic structure?
1. Deformation of the structure must be caused by an external force
2. When the external force is removed, the structure recoils to its resting position (e.g. original
What is another term for distending pressure?
Distending pressure = recoil pressure
Higher elasticity= higher or lower distending pressure?
High elasticity= high distending/recoil pressure
Does recoil pressure act in the same direction to distending pressure?
No, recoil is opposite in direction to distending pressure, but EQUAL in magnitude
What are the recoil tendencies of the chest wall and the lungs?
Chest wall= outward
How do the recoil pressures of lungs and chestwall interact?
Lungs' inward recoil tendency is countered by the chest wall's outward recoil tendency and vice versa
At End-Expiratory-Position, what in the INTRApleural pressure?
Negative at -4mmHg
when 0mmHg is atmospheric
What happens to chest wall and lungs during pneumothorax?
air leaks into pleural cavity
Pleural pressure raised to atmospheric (but pV = constant)
Lung collapses inward (recoils)
Chest wall springs outward / enlarges (recoils)
At EEP require energy to maintain?
Inward recoil pressure of the lung balances outward recoil pressure of the chest wall (opposite in
direction, equal in magnitude)
What links the recoil pressures of the lungs and the chest wall?
Thin layer of fluid (intermolecular force of water) helps adhering inner surface of chest wall to
outer surface of lung
What are the fundamental pressures? e.g. PB
PB = barometric pressure
PA = Palv = (intra-)alveolar pressure
PPL = Pip = (intra)pleural pressure
Derive pressures? (3)
PTP = transpulmonary pressure = Palv - Pip (=
distention of lungs)
PCW = transchestwall pressure = PPL - PB (=
distention of chestwall)
PTT = transthoracic pressure = PA - PB (=
distention of lungs + chestwall)
What is the Palv/PA at EEP?
At the end of expiration: Palv = 0 because interior of
alveoli is continuous with outside
During inspiration, what muscles contract leading to what?
Diaphragm and inspiratory
intercostal muscles contract
volume of thoracic cage
subatmospheric (-4 > -6 > -7)
What happens to transpulmonary pressure as intrapleural pressure becomes more negative?
is increased (= lung
(4 > 5 > 7)
lungs expand > alveolar pressure becomes subatmospheric
(-1 at mid-inspiration, 0 at end of inspiration)
Pressure difference between inside and outside drives airflow into lungs until no pressure gradient
Palv = 0
Inspiration vs Expiration. Which one is active?
During expiration what happens to intrapleural pressure?
Diaphragm and Inspiratory intercostal muscles cease contracting
chest-wall returns passively to original size (preinspiration position)
Pip back to preinspiration value (-7 > -5 > -4)
As lungs coil during expiration, what happens to transpulmonary pressure?
Transpulmonary pressure (same as distention of the lungs) back toward preinspiration value (7 > 5 > 4)
What happens to Palv during expiration?
Air in alveoli becomes compressed >
raises alveolar pressure (Palv (= 1 at mid-expiration) > Patm (= 0))
air flows out of lungs
When is Palv= PB
During End of inspiration and end of expiration
When is lung distending pressure largest?
Lung distending pressure = Transpulmonary Pressure
Largest at end of inspiration
Run through the entire sequence of inspiration.
Intercostal muscles and diaphragm contract
Increase thoracic volume so intrapleural pressure decreases
Causes the Palv to become negative/ more sub-atmospheric and transpulmonary pressure (Palv-Pip)/ lung distending increases
Air rushes into lungs until Palv= Pb = 0, Pip is largest at end of inspiration
Run through the sequence for expiration.
Diaphragm and intercostal muscles stop contracting
The thorax volume decreases.
Transpulmonary pressure (lung distending pressure) returns to preinspiration value.
Intrapleural pressure decreases back to preinspiration value
Palv becomes above atmospheric (+1) during mid-expiration and air becomes compressed
Air rushed out of lungs until Palv= PB= 0
What does statics involve?
What does dynamics involve?
Static= change in volume
Definition of Statics? (2)
-Study of the stationary properties of breathing apparatus (change in vol.)
- properties INDEPENDENT of movement during breathing
When is lung recoil pressure at maximum?
Total Lung Capacity
What is the volume-pressure slope like in the distention of lungs?
Non-linear slope (due to mixture of tissues having different elasticity):
Steep at 40- 50 %VC
Gentle near TLC
At Residue Volume, is the pressure zero?
No, very small pressure exist because the natural position of lungs is total collapse
Pressure required to inflate air-filled lung is larger or lower than that needed to inflate saline filled lungs?
pressure required to inflate air-filled lung > pressure required to inflate saline-filled lung
What are the components of lung recoil pressure?
1/3 = tissue elasticity (elastance) of the lung
2/3 = surface tension of the fluid lining the alveoli
What is tissue elastance due to?
tissue elasticity (elastance) of the lung
Due to presence of elastin, collagen
Obeys Hooke’s Law: volume change pressure
Explain surface tension in contribution to lung recoil pressure?
Due to presence of air-liquid interface= intermolecular force between water molecules
Surface tension at the air-liquid interface causes what?
Increase in the pressure needed to push against the surface tension because surface tension minimizes/ contracts the surface to the smallest size
What is the resolved direction of surface tension?
What law applies to Surface Tension?
Laplace’s Law: P = 2T/r
P = distending pressure
T = surface tension
r = radius of alveolus
Need to apply bigger pressure if high T or small r
If surface tension is constant, what happens?
assuming T is constant
If there is a difference in radius between two alveoli arranged in parallel, the smaller alveoli with smaller radius would have higher pressure than the larger alveoli
Air would empty from the smaller to the larger alveolar until the smaller one collapses
Causes Alveolar instability
Explain what happens when surface tension is overcome?
When surface tension is overcome:
1. Surface area of lung increases > gas exchange
2. Lengthens tissues > increases volume
In reality how does surface tension vary with volume?
Small alveolar = low T
Large alveolar= high T
How is varying surface tension achieved?
Pulmonary surfactant = protein-carbohydrate-phospholipid complex produced by:
1. Type II pneumocytes and/or
2. Clara cells
Name the 3 advantages of having surfactant.
1. Lowers the surface tension force (increases lung distensibility), decreases work of breathing (spend less energy)
2. Reduces difference between tension in large and small alveoli = promotes alveolar stability
3. Prevent transudation of fluid into alveoli
Explain the varying surface tension due to surfactant.
Small alveolar = high surfactant conc. = reduce intermolecular force between fluid lining alveolar wall = surface tension decreases
Large alveolar = lower surfactant conc. = surface tension decreases
explain the advantage surfactant has for transudation of fluid into alveolar.
Prevents the transudation of fluid into the alveoli
If low [S] > high T > greater tension to contract air-liquid
interface > more fluid is sucked into alveolus from
capillaries > thicker film of fluid > more work needed to distend lungs
Premature babies has insufficient surfactant. Explain consequences and treatment.
Loss of surfactant =
Infant Respiratory Distress
Hyaline Membrane Disease:
1. Stiff lungs (high surface tension to overcome)
2. Areas of collapse
3. Alveolar filled with transudate
Treatment: add surfactant
Tissue elastance. What is the volume- pressure relationship of chest wall?
recoil pressure at 0 at relaxed/ natural position at 60% Vital Capacity (higher than at EEP VC)
Explain change in size causing change in recoil pressure.
Decrease size= compress to RV = chest wall recoil outwards to resting pos.
Increase size = inhale to TLC = chest wall recoil inward to resting pos.
Chest wall recoil due to?
Tissue elastance ONLY, not fluid forces
What are the pressures of CW and L during EEP/ FRC?
Pcw = PL
zero overall recoil pressure
At 60% VC what is the overall recoil pressure?
PL = positive
therefore overall recoil pressure only involves inward lung recoil
Inhalation beyond EEP/FRC depends on which pressures?
To inhale beyond EEP (can be normal breath):
Needs to spend energy to overcome inward recoil of the lungs
Helped by outward recoil of chest-wall
Inhalation beyond 60% VC requires what?
To inhale beyond 60% VC (> normal breath, e.g. to TLC
requires muscle contraction to overcome BOTH lung and chest wall recoil pressures
Exhale down to RV requires what?
Needs to spend energy to overcome outward recoil of
Helped by inward recoil of lungs
Explain changes in FRC/EEP in emphysema patient.
Emphysema = loss of lung tissue elasticity
decreased inward lung
recoil pressure (steeper, shifted to left, easier to
balances outward chest-wall recoil pressure at a higher volume
increased EEP and FRC
(breathe at higher lung position)
No change in chest-wall recoil pressure
Explain changes in FRC/EEP in pulmonary fibrosis.
Pulmonary fibrosis (e.g. after inflammation) = increased lung tissue elasticity
Increased inward lung recoil pressure (flatter, shifted to
balances outward chest-wall recoil pressure at a lower volume
decreased EEP and FRC
Explain changes in FRC/EEp in pneumothorax.
both lung and chest recoil to natural position:
Chest bulges out
Why does airway obstruction e.g. astham lead to higher FRC?
Expiration is passive (depends on lung elastic recoil)
Energy loss in overcoming Raw (high airway resistance)
Air-trapping inside lungs (lesser energy to drive flow)
What 2 definitions are there for compliance?
1) = slope of static volume-pressure curve (∆V / ∆PTM)
2) = volume change per unit change in transmural
pressure (distending pressure)
Relate compliance to elastance.
Compliance= 1/elastance (reciprocal of elasticity / elastance)
so 1/C = elasticity (elastance) or resistance to distension
E.g. stiff lungs have low compliance but high elasticity > harder to distend
Forumula for total compliance (Ct) ? therefore formula for total elastance ?
change in volume / transthoracic pressure GRADIENT
Ct= CL + Ccw
1/Ct = 1/CL =1/Ccw
At EEP, what is Ct, Ccw and CL?
Ct= 0.1 L/cm H20
CL= Ccw = 0.2 L/cm H20
How is compliance affected by Lung Volume?
- At very low or very high lung volumes: ↓CL
(flat slopes of PV curve)
- At moderate lung volumes: ↑CL (steep slope of PV curve)
Compliance affected by Lung Size?
CL (children) < CL (adult)
because adult has more alveoli than children = overall larger change in volume
Specific compliance = compliance / FRC = 0.08/cm H2O (normally)
Posture and Compliance?
Upright to supine position:
↓ lung volume (due to gravity)
↑ pulmonary blood volume = less air volume
Diaphragm pushed forward (because abdominal contents no longer pulled down)
↓CL (less space to distend)
Pulmonary blood volume and compliance?
pulmonary vascular congestion (e.g. left heart failure (does not pump well), or alveolo-capillary
membrane becomes thicker and stiffer
more blood stays in
↓CL (harder to distend)
Age and compliance?
aging (loss of elasticity in emphysema) = ↑CL
Diseases and compliance?
Emphysema (loss of elasticity) = ↑CL
Fibrosis (↑elasticity) = ↓CL
Edema (fluid in alveoli or interstitial space = higher surface tension; stiffer lung or membrane respectively) = ↓CL
Transpulmonary, Transchestwall and trans thoracic pressures equal what distension?
Transthoracic = distension of lungs
Transpulmonary= distension of both lungs and chest wall
Transchestwall= distension of chest wall
What factors affect chest wall compliance? Explain each of the 3 factors.
1. Posture: supine to upright posture = displacement of diaphragm (part of chest wall) and viscera = ↑CCW
2. Skeletal muscle disease: spasticity, rigidity (hard to distend chestwall) = ↓CCW
3. Deformation of chest-wall (e.g. obesity (thick chest = hard to distend), old age,
Formula for chest wall compliance?
change in vol. / transchestwall pressure gradient
value is Calculated, hard to measure
Define airway resistance (Raw)
= Trans- airway Pressure difference divided by flow rate (cm H2O.sec/L)
= (Palv – PB) / V.
V.= instantaneous airflow
Explain the Distribution of airway resistance.
1. Upper airways (nose,
mouth, pharynx and
larynx): 50% Raw
2. Medium-sized airways
(trachea, bronchi): 40% Raw
3.Small airways (bronchioles): <10% Raw
Decrease in diameter of airway correlates with resistance and cross section area how?
decrease in diameter= decrease cross sectional area= increase resistance
Explain silent zone of small airway disease.
Small airways (bronchioles): <10% Raw
Tremendous dichotomous branching of respiratory tract = enormous combined cross-sectional area in small airways = contribute very little to total airway resistance
hard to feel / pick up = silent zone of small airway disease (can be present before detecting abnormal airway resistance)
What is radial traction?
retracting action of surrounding alveoli on the wall of small airways e.g. alveolar ducts
What is radial traction caused by? How does it work?
lung recoil pressure
Always toward centre of alveoli > pull on wall of small airways > keep them open
Similar to upper airways: shape maintained by cartilage
Low lung volume= high or low radial traction? High Lung volume causes increase of decrease in Raw?
Low lung volume > low lung recoil pressure > low
radial traction on airway wall
High lung volume = increase radial traction = low Raw
High Lung volume causes increase of decrease in Raw?
High lung volume > high lung recoil pressure >
inflated alveolar means high radial traction on airway wall > ↓Raw
Emphysema or other obstructive lung
disease . How does it affect Raw? (think elasticity and radial traction)
Emphysema = due to destruction of alveolar
↓ lung elasticity = ↓ radial traction = partially collapse = ↑ Raw
Asthma changes Raw. How?
smaller lumen due to:
1) Increased mucous glands 2) mucus in airway > mucosal edema
3) Contracted hypertrophied bronchial smooth muscle during asthma attack
How does pulmonary fibrosis change Raw?
↑ lung elasticity > ↑ radial
traction > ↓ Raw
P. Fibrosis = restrictive lung disease: hard to inflate / distend
What is Bronchomotor tone?
↑ bronchial smooth muscle tone (constriction) > ↑
What 2 reflexes cause bronchomotor tone?
1) Parasympathetic overactivity (ACh): ↑ tone
2) Sympathetic overactivity (Noreadrenaline), β2 agonists : ↓ tone = ↓ Raw
Asthma drugs can work via 2 pathways on bronchomotor tone. Explain.
Either Anti-Cholinergic to inhibit Ach and inhibit parasympathetic overactivity
or B2 agonist to cause sympathetic overactivity
both lower bronchomotor tone
What 2 LOCAL factors affect bronchomotor tone?
1) decrease in PCO2 in alveolar > increasing pH > affect electrolyte balance> increase in AP in bronchial smooth muscle tone > increase tone > increase Raw
2) Inflammatory mediators e.g. histamine release after inhaling allergen > cause increase tone > increase Raw
How does lumen obstruction affect Raw?
Lumen obstruction (e.g. bronchial mucus secretion, edema, vascular congestion
↑ mucosal layer = ↑ Raw
How does increase in air density affect Raw?
↑ density (e.g. deep dive, surrounding pressure increases) = ↑ Raw
In small tubes flow is? in large tubes flow is?
Small tube= laminar flow
Large= turbulent flow with eddy currents
Laminar flow equation and turbulent flow equation?
Laminar flow: R= 8ηl/πr^4
Turbulent flow: Re=2rvd/η
η is viscosity
What is transmural pressure across wall of intrathoracic airway?
relative pressure between alveoli compared with that in intrapleural space
How does transmural pressure affect Raw?
End-inspiration: ↑ PTM (= 10 cm H2O) > ↑ airway lumen >
End-expiration: ↓ PTM (= 5 cm H2O) > ↓ airway lumen > ↑Raw
What is work of breathing?
product of pressure and volume (simultaneous measurements of intrapleural pressure and change in volume during a breath)
2 types of work during breathing. Explain.
1) Elastic work (EBIDOE): against elastic forces (= energy stored in alveolar wall without airway)
2) Resistive work: against viscous forces (airway and tissue resistances)
Resistive work 2 subtypes. explain.
Inspiratory resistive work (ECIBE): against airway resistance during inspiration (need extra energy to
Expiratory resistive work (EBIAE): against airway resistance during expiration
What other type of work is done during a breathing cycle?
Work dissipated as heat (EAIDOE)
2 factors affecting work of breathing?
1. Frequency of breathing (normal = 12-18 breaths per min)
2. Tidal volume
Total work is lowest during what?
Normal breathing rate 12-18 breathes per minute at rest
Work is high during what?
Slow deep breathes or fast shallow breathes
How does resistive work change with increasing breathes per min?