Respiratory 4 Flashcards
What does high compliance mean
Easy to inhale
Hard to exhale
Low elastance
What does low compliance mean
Hard to inhale
Easy to exhale
High elastance
What is another important determinant of compliance and lung elastic recoil
Surface tension at air water interface of the airways
What is surface tension
Measure of force acting to pull a liquids molecules together at an air-water interface
What did Von Neergard find
Way easier to inflate if their was liquid
Found fluid lining the inner walls of alveoli
What is structure of alveoli
Alveoli wall then liquid layer then air inside
What would happen if alveoli only had water lining walls
The pull inward would be so strong alveoli would collapse
Where is fluid found in alveoli
Lining the inner walls
What happens when intermolecular force pulls the surface molecules downward
The molecules that remain at surface develop opposing force, surface tension
What is surfactant
Detergent-like molecule secreted by type II alveolar cells
- 90% phospholipids, 10% proteins
What is role of surfactant
Reduce surface tension and disrupt intermolecular bonds
- reduce surface tension to ~25 dynes/cm or less
What are the regions of the surfactant molecules and where do they sit
Hydrophilic end stays in water and hydrophobic goes into air
- sit between adjacent water molecules so they can’t form bonds
What are 2 things surfactant does
- Increases compliances (reduces inward pressure)
- Ensures alveoli of all size inflate (smaller have greater concentration of surfactant)
What do alveoli of different radius have in common
Same surface tension so there’s equal inward pressure and small ones wont empty into large ones
What ensures two alveoli inflate and have adequate surface area for exchange even when one is blocked or smaller alveolus
The rapidly expanding one will put a “brake” on expansion by increasing surface tension and elastic recoil
The slowly expanding one will have less diluted surfactant causing no “brake” in expansion
What is infant respiratory distress syndrome
Premature: insufficiency of surfactant production and immaturity of lungs
- alveoli collapse
- prevalence decreases with gestational age
- decrease compliance, increase elastance
Prevention of infant respiratory distress
Glucocorticoid injection
Treatment of infant respiratory distress syndrome
- artificial surfactant
- continuous positive airway pressure (CPAP)
- intubate
Where does 90% of airway resistance occur in healthy individual
Trachea and bronchi
- is constant
- smallest total cross sectional area
What is airway resistance based on
Poiseuille’s equation
Resistance increases when length and viscosity increase
Resistance decreases when increase in radius
What is air flow determined by
Pressure gradient at start vs end
Resistance (length, viscosity, radius)
Factors that affect airway resistance
- length of system: constant
- viscosity of air: constant (humidity or altitude alter)
- diameter of airways (constant in healthy)
- upper airways: physical obstruction (mucus, etc.)
- bronchioles: bronchoconstriction (parasympathetic, histamine), bronchodilation (CO2, epinephrine)
What is the site of variable resistance
Bronchioles
What is common control of bronchoconstriction/dilation (smooth muscle control)
- paracrine control, CO2 being major one
High levels = dilation (reduce resistance, get rid of CO2)
Low levels = constriction
What does histamine released from mast cells cause
Bronchoconstriction
- large amounts released in response to allergic reaction
- stimulated by irritants and prevent from getting to alveoli
How to parasympathetic nerves affect bronchiole smooth muscle
Constriction
- activate PLC-IP3 pathways via M3 muscarinic receptor
What does not innervate bronchiole smooth muscles
Sympathetic nerves
What is the PLC-IP3 pathway that cause constriction
ACh from postganglionic parasympathetic neurons bind to M3 muscarinic receptors activate G protein complex which activates PLC and converts IP3 and cause release of Ca
What are 2 characteristics of asthma
- Chronic inflammation of airways
- Periods of bronchoconstriction/bronchospasm
What can oppose bronchoconstriction during infrequent and frequent asthma attacks
Infrequent- B2 adrenergic agonist (Inhaler)
Frequent- weekly inhaled corticosteroid
What is effectiveness of ventilation determined by
Total pulmonary ventilation
Total pulmonary ventilation
Volume of air moved into and out of the lungs each minute (minute ventilation)
What is normal ventilation rate and normal tidal volume
12-20 breaths/min
500ml
Total pulmonary ventilation calculation
Total pulmonary ventilation= ventilation rate x tidal volume
Ex) 12 breaths/min x 500ml= 600 ml/min
Is total pulmonary ventilation a good indicator of how much fresh air reaches the alveoli
No
- air remains within conducting air space (pharynx, larynx, trachea, bronchi, bronchioles) and does not take part in gas exchange (anatomic dead space)
- ~150ml
What is the calculation for alveolar ventilation
= ventilation rate x (tidal volume- dead space)
Ex) 12 breaths/min x (500 -150 ml) = 4200 ml/min
What is alveolar ventilation
Total amount of air making it to alveoli and available for gas exchange in 1 minute
At end of inspiration what is dead space filled with
Fresh air (150ml)
If we exhale 500ml and there’s 150ml of fresh air in dead space what leaves the alveoli
350ml leaves alveoli
At end of expiration what is dead space full of
Stale air from alveoli
If we inhale 500 ml of fresh air
First 150ml of air in alveoli is stale air from alveoli
Only 350ml of fresh air reaches alveoli
- dead space is full with 150ml of fresh air
What kind of breathing can increase alveolar ventilation
Slow deep breathing
What kind of breathing can decrease the amount of fresh air to the alveoli
Shallow and rapid
