Respiratory 4 Flashcards

1
Q

What does high compliance mean

A

Easy to inhale
Hard to exhale
Low elastance

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2
Q

What does low compliance mean

A

Hard to inhale
Easy to exhale
High elastance

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3
Q

What is another important determinant of compliance and lung elastic recoil

A

Surface tension at air water interface of the airways

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4
Q

What is surface tension

A

Measure of force acting to pull a liquids molecules together at an air-water interface

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5
Q

What did Von Neergard find

A

Way easier to inflate if their was liquid
Found fluid lining the inner walls of alveoli

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6
Q

What is structure of alveoli

A

Alveoli wall then liquid layer then air inside

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7
Q

What would happen if alveoli only had water lining walls

A

The pull inward would be so strong alveoli would collapse

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8
Q

Where is fluid found in alveoli

A

Lining the inner walls

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9
Q

What happens when intermolecular force pulls the surface molecules downward

A

The molecules that remain at surface develop opposing force, surface tension

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10
Q

What is surfactant

A

Detergent-like molecule secreted by type II alveolar cells
- 90% phospholipids, 10% proteins

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11
Q

What is role of surfactant

A

Reduce surface tension and disrupt intermolecular bonds
- reduce surface tension to ~25 dynes/cm or less

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12
Q

What are the regions of the surfactant molecules and where do they sit

A

Hydrophilic end stays in water and hydrophobic goes into air
- sit between adjacent water molecules so they can’t form bonds

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13
Q

What are 2 things surfactant does

A
  1. Increases compliances (reduces inward pressure)
  2. Ensures alveoli of all size inflate (smaller have greater concentration of surfactant)
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14
Q

What do alveoli of different radius have in common

A

Same surface tension so there’s equal inward pressure and small ones wont empty into large ones

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15
Q

What ensures two alveoli inflate and have adequate surface area for exchange even when one is blocked or smaller alveolus

A

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

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16
Q

What is infant respiratory distress syndrome

A

Premature: insufficiency of surfactant production and immaturity of lungs
- alveoli collapse
- prevalence decreases with gestational age
- decrease compliance, increase elastance

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17
Q

Prevention of infant respiratory distress

A

Glucocorticoid injection

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18
Q

Treatment of infant respiratory distress syndrome

A
  • artificial surfactant
  • continuous positive airway pressure (CPAP)
  • intubate
19
Q

Where does 90% of airway resistance occur in healthy individual

A

Trachea and bronchi
- is constant
- smallest total cross sectional area

20
Q

What is airway resistance based on

A

Poiseuille’s equation
Resistance increases when length and viscosity increase
Resistance decreases when increase in radius

21
Q

What is air flow determined by

A

Pressure gradient at start vs end
Resistance (length, viscosity, radius)

22
Q

Factors that affect airway resistance

A
  • 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)
23
Q

What is the site of variable resistance

A

Bronchioles

24
Q

What is common control of bronchoconstriction/dilation (smooth muscle control)

A
  • paracrine control, CO2 being major one
    High levels = dilation (reduce resistance, get rid of CO2)
    Low levels = constriction
25
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
26
How to parasympathetic nerves affect bronchiole smooth muscle
Constriction - activate PLC-IP3 pathways via M3 muscarinic receptor
27
What does not innervate bronchiole smooth muscles
Sympathetic nerves
28
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
29
What are 2 characteristics of asthma
1. Chronic inflammation of airways 2. Periods of bronchoconstriction/bronchospasm
30
What can oppose bronchoconstriction during infrequent and frequent asthma attacks
Infrequent- B2 adrenergic agonist (Inhaler) Frequent- weekly inhaled corticosteroid
31
What is effectiveness of ventilation determined by
Total pulmonary ventilation
32
Total pulmonary ventilation
Volume of air moved into and out of the lungs each minute (minute ventilation)
33
What is normal ventilation rate and normal tidal volume
12-20 breaths/min 500ml
34
Total pulmonary ventilation calculation
Total pulmonary ventilation= ventilation rate x tidal volume Ex) 12 breaths/min x 500ml= 600 ml/min
35
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
36
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
37
What is alveolar ventilation
Total amount of air making it to alveoli and available for gas exchange in 1 minute
38
At end of inspiration what is dead space filled with
Fresh air (150ml)
39
If we exhale 500ml and there’s 150ml of fresh air in dead space what leaves the alveoli
350ml leaves alveoli
40
At end of expiration what is dead space full of
Stale air from alveoli
41
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
42
What kind of breathing can increase alveolar ventilation
Slow deep breathing
43
What kind of breathing can decrease the amount of fresh air to the alveoli
Shallow and rapid