Mechanics of breathing Flashcards
1ᵒ function of respiratory system?
ventilate gas exchange surfaces by
moving air between alveoli + from atmosphere, via airways
Total Lung Capacity?
volume of air within lungs at end of max inspiration
Vital Capacity?
total volume of air an individual can breath in from max forced expiration to max forced inspiration
Tidal Volume?
air which enters + leaves lungs during normal breathing
Residual Volume?
volume of air remaining in the lungs after a maximum forced expiration
Expiratory Reserve Volume?
air that can be expired from the lungs by determined effort after normal expiration
Functional Residual Capacity?
volume of air within lungs at end of a resting/quiet expiration
Inspiratory Reserve volume?
-Volume of additional air that be forcibly drawn in at the end of normal tidal volume
What does total level of ventilation (total v of air inspired over time period) depend on?
v of air inspired
frequency of breathing per min(respiratory rate)
What’s V̇= Vt x f?
min v (mL) = tidal v (mL) x frequency (min⁻¹)
total v of air inhaled in all breaths over 1 min = v of air inhaled in each breath x number of breaths per min
What’s ‘dead space’ ?
air required to occupy the airways but doesn’t contribute to gas exchange
Why doesn’t 150ml of dead space air reach the alveoli?
1st to leave respiratory system at beginning of expiration
How do you calculate alveolar ventilation rate?
V̇a = (Vt - Vd) x f
Alveolar minute v(mL) = (tidal v - dead space v) x frequency per min
What’s alveolar minute v?
Total v of fresh air entering alveoli across all breaths over 1 min
What’s Boyle’s law?
P ∝ n/V
How’s movement of air between atmosphere + lungs achieved?
changing alveolar p
How’s alveolar p changes achieved?
contraction/relaxation of respiratory muscles
How’s the sealed pleural cavity stretched between the lungs + chest wall?
lungs recoil inwards + chest wall recoils outwards due to elastic properties
What happens if pleural cavity is stretched?
decrease p as greater volume but same number of molecules – gas or liquid cannot enter from adjacent area as the space is sealed
Why does the pleural cavity resist changes in v more?
filled w liquid
What’s negative p?
overall effect of the opposing recoil of the chest wall + lungs –> intrapleural p is naturally subatmospheric
What happens when there’s negative intrapleural p?
pull 2 pleura together - collapsing force
What happens when there’s positive intrapleural p?
pull 2 pleura apart - expanding force
What does chest wall recoil do?
pulls chest wall outwards + expand the thoracic
cavity
What does lung recoil do?
pull the visceral pleura inwards + compress lung
v
What forces determine if lungs expand or compress at
given time?
lung recoil
chest wall recoil
intrapleural p
When should the forces be equal?
between end of expiration + start of next inspiration
How inspiration begins?
-contraction of diaphragm
-pull parietal pleura outwards
-stretches pleural cavity
-decreasing intrapleural p –> negative
-force pulling 2 pleurae together increases > force
lung recoil
-visceral pleura pulled outward, expanding lung
How expiration begins?
- relaxation of inspiratory respiratory muscles
- decreased outward force acting on the parietal pleura -reduces force acting to stretch the pleural cavity,
- increasing intrapleural p < lung recoil
- visceral pleura pulled inward (along with the pleural cavity and parietal pleura)
- decreasing lung v
How forced expiration begins?
- abdominals actively contract to compress v of thoracic cavity
- muscle contraction generates inward force on parietal pleura
- compressing pleural cavity
- more pronounced decline in lung v (speed + magnitude)
Inspiration?
- diaphragm contract
- increase in thoracic cavity v
- more negative intrapleural p
- outward force exerted on visceral pleura > inward recoil force
- lungs expand increasing v
- alveolar p < atmospheric p
- air moves down p gradient via airways to alveoli
- lungs expand
Expiration?
- diaphragm relax, lungs recoil
- decrease in thoracic cavity v
- increase in intrapleural p
- lung v decreases
- alveolar p > atmospheric p
- air moves down p gradient into atmosphere deflating lungs
When does the compression of lungs happen?
forced expiration
What does the speed of airflow depend on?
p gradient
level of airway resistance
How is intrapleural p naturally sub-atmospheric?
opposing recoil of chest wall + lungs
Define pneumothorax
air entering pleural space
Entry of air into the pleural cavity
- loss of negative p
- intrapleural p will increase until = atmospheric p
- expansion of the pleural cavity which decreases lung v (collapses)
- reduces intrapleural p changes during inspiration so lungs can’t expand
What happens if there’s a loss of negative intrapleural p?
elastic recoil of chest wall + lungs no
longer resisted –>affected regions of lungs to collapse
Ohm’s law?
V = P/R airflow = change in p/resistance
What factors determine level of resistance?
cross sectional area of airway lumen
airflow pattern
Hagen-Poiseuille + what does it show?
R ∝ 1/radius⁴
As radius of an airway decreases, resistance increases dramatically –> airflow decreases dramatically
How does air flow in healthy airways?
laminar pattern
How does air flow in obstructed airways?
turbulent pattern
How does turbulence occur?
where high velocities of airflow are achieved (during forced breathing manoeuvres)
sudden decrease in luminal area (obstructed airways)
What causes wheezing sound?
vibration generated by the turbulent airflow
Define airway patency
state of being open/unobstructed
What’s open airways are maintained by?
elastic fibres within airway wall
radial traction
Why’s airway obstruction more noticeable during expiration?
during expiration, lung tissue+airways compressed
What can reduce airway patency during forced expirations?
p differentials between the intrapleural space + airway
What’s Spirometry + role?
measuring FEV₁/FVC ratio
quantifying airflow + level of airway obstruction present during breathing
What does measuring FEV₁/FVC involve?
producing a max forced expiration into a
spirometer- measures v of air passing through over time
What’s FEV₁ + corresponds to?
max v that’s expired during 1st second of a max forced expiration
how quickly air can pass via airways, reflects airway function + health
Values of obstructive airway diseases?
reduction in FEV₁ (<80% expected value)
FEV₁/FVC ratio (<70%)
Values of restrictive lung diseases?
reduction in FEV₁ + FVC (<80% expected value)
relatively normal FEV₁/FVC ratio (>70%)
Why does restrictive lung diseases have a normal FEV₁/FVC ratio?
decrease in FEV₁ reflects an overall decrease in lung v rather than airway obstruction
Define transpulmonary p
Ptp = Palv – Pip
diff between p within alveoli + intrapleural space
Role of transpulmonary p?
determines level of force acting to expand/compress lungs
Define compliance
how easily lungs can be distended
compliance = change in v/change in p
What happens if there’s a higher compliance + eg?
- less elastic recoil
- less force required to inflate
- ↑ v change per pressure change (↑gradient on v-p curve)
- emphesyma (elastic degrades)
What happens if there’s a lower compliance + eg?
- more elastic recoil
- more force required to inflate
- ↓v change per pressure change (↓ gradient on v-p curve)
- pul fibrosis (scar, fibrosis, collagen)
Features of lung v-transpulmonary p curve?
- gradient = lung compliance
- measurements taken when no airflow 0 (STEEP) = static compliance
What’s dynamic compliance?
measurements taken in presence of airflow - gradient between end tidal inspiratory + end tidal expiratory points on v-p curve
Features of v-p loops?
- gradient of overall line from end of expiration to end of inspiration = compliance
- area within loop = proportional to level of airway resistance generated
Why would there be a greater area of v-p loop?
forced inspiration/expiration
airway obstruction
What are the structures affect lung compliance ?
chest wall mechanics ↑
alveolar surface tension ↓
elastic fibres ↓
How’s bubble formed?
water-air interface formed between lining fluid + pseudo-spherical alveolar airspace
What happens within bubble?
surface tension due to H bonds between
water molecules –> collapsing force toward the centre of the bubble –> p
Law of Laplace + what does it show?
amount of p within bubble P = 2T/r if T is constant surface tension of water 0.075N/m P ∝ 1/r smaller alveoli = larger p
Why would the inflation of the lungs be impossible?
p gradients that would be created between diff sized alveoli –> smaller alveoli collapsing into larger
How is smaller alveoli collapsing resolved by?
pulmonary surfactant: phospholipoprotein secreted by type II pneumocytes (alveolar cells)
Features of pulmonary surfactant + how they work?
-amphipathic = hydrophilic head + hydrophobic tail regions
-disrupt H-bonds between water molecules, reducing
surfacing tension: decreases collapsing p + prevent alveolar oedema due to excessive fluid being pulled from capillaries
-equalise p between diff alveoli sizes:
as alveoli expand, conc of pul surfacant decreases, increasing surface tension –> larger alveolar collapse into smaller –> consistent inflation
What does the surface tension at the air-liquid interface do?
- increases collapsing p –> inconsistent inflation
- reduces hydrostatic p in alveolar tissue so pull fluid out surrounding pulmonary capillaries into alveoli + interstitial tissue –> alveolar oedema
Why does Neonatal Respiratory Distress Syndrome (NRDS) occur?
develop + produce insufficient pul surfactant
surfactant production at week 24-28
What does NRDS do?
-respiratory failure due to:
alveoli collapsing, low lung compliance, alveolar oedema
-hypoxia
-pul vasoconstriction, endothelial damage, acidosis, pul + cerebral hemorrhage
How is NRDS treated?
-HIGH RISK MOTHERS:maternal diabetes(insulin affect pneumocyte maturation) + premature birth
-supplementation of affected infants w artificial surfactant and/or administering glucocorticoids (increase surfactant production via
maturation of type 2 pneumocytes)
