Respiratory Flashcards

1
Q

what are the functions of the respiratory system?

A

-provides O2 and elimates CO2
- protects against microbial onfection
- regulates blood pH
- contributes to phonation
- contributes to olfaction
- is a reservior for blood

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2
Q

order that air goes down

A

nasal/oral cavity- pharnyx - larynx - trachea - two primary bronchi - bronchi - bronchioles - terminal bronchi - respiratory bronchioles - alveolar ducts - alveolar sacs

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3
Q

divisions of the lungs

A

trachea - primary bronchi
c shaped cartilage + smooth muscle

bronchi
plates of cartilage + smooth muscle

bronchioles
smooth muscle only

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4
Q

conducting zone

A

NO gas exchange, NO alveoli
- leads gas to gas exchanging regions of the lungs “anatomcial dead space”

trachea, bronchi, bronchioles, terminal bronchioles

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5
Q

Respiratory Zone

A

Where GAS EXCHANGE happens ( has ALVEOLIS)
respiratory bronchioles, alveolar ducts, alevolar sacs

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6
Q

how the airways change as you go to another generation of branching

A

diameter and length decrease

number and total surface area increase as you go down (for gas exchange)

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7
Q

what are alveolis?

A

tiny, thin walled capillary rich sac in the lungs where the exchange of oxygen and carbon dioxide takes place

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8
Q

Type I alveolar cells

A

line the alveolar walls
- continuous mono-layer of flat epithelial cells

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9
Q

Type II alveolar cells

A

produce surfactant
- detergent like substance that reduces surface tension of alveolar fluid
- progenitor cells ( can differentiate into Type I cells)

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10
Q

how does the transfer of O2 and CO2 occur ?

A

occurs by diffusion through the respiratory membrane (very thin)

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11
Q

what are the steps of respiration?

A
  1. ventilation: exchange of air between the atmosphere and alveoli by bulk flow
  2. exchange of O2 and CO2 b/w alveolar air and blood in lung capillaries by diffusion
  3. transport of O2 and CO2 through pulmonary and systemic circulation by bulk flow
  4. exchange of CO2 and O2 b/w blood in tissue capillaries and cells in tissues by diffusion
  5. cellular utilization of O2 and production of CO2
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12
Q

i. pump muscles (respiratory muscles)

A
  • makes changes in pressure/volume in lungs

INS: diaphragm, external intercostals, parasternal intercostals

EXP: internal intercostals, abdominal muscles.

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13
Q

ii. Airway muscles

A
  • keep upper airways open
    INS: tongue protruders, alae nasi, muscles around airways (pharnyx, larynx)

EXP: pharnyx, larnyx

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14
Q

iii. accessory muscles

A

facilitate respiration during exercise

INS: sternocleidomastoid, scalene

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15
Q

Diaphragm

A

active during inspiration (contracts)
- seperates lungs from abdominal content
- increases the volume of the thorax

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16
Q

external intercostal muscles

A

contract and pull ribs upwards to increase the lateral volume of thorax
- bucket handle motion

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17
Q

parasternal intercostal muscles

A

contracts and pulls sternum forward to increase anterior posterior dimension of rib cage
- pump handle motion

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18
Q

sleep apnea

A

-reduction in upper airway patency during sleep
when your upper airway muscles go to rest, so there is a reduction in muscle tone

or caused by anatmocial defects

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19
Q

what is filtering action and where does it occur

A

In the conducting airways, it is lined by a superficial layer of epithelial cells which are:

Goblet cells - produce mucous
ciliated cells

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20
Q

how does the filtering action work

A
  1. Goblet cells produce mucous which traps inhaled materials (its sticky and dense)
  2. cilia movements downward or upward (depending on where it is) to eliminate the mucous + materials through esophagus
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21
Q

what do macrophages do in alveoli?

A

filtering action
- act as a last defense as it phagocytizes foreign particles

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22
Q

pulmonary fibrosis

A

caused by silica dust or asbestos kills the macrophages

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23
Q

spirometry

A

pulmonary function test to determine the amount and the rate of inspired and expired air
- measures pressure

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24
Q

TV?

A

Tidal volume

  • the volume of air moved IN or OUT of the respiratory tract during each cycle
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25
Q

IRV

A

Inspiratory Reserve Volume

the additional volume of air that can be forcibly inhaled following a normal inspiration to the maximum inspiration possible

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26
Q

ERV

A

Expiratory Reserve Volume

the additional volume of air that can be forcibly exhaled following a normal expiration. expiring to the maximum voluntary expiration

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27
Q

RV

A

Residual volume

the volume of air remaining in the lungs after a maximal expiration
- it cannot be expired no matter the effort
can’t be measured with a spirometer!!
RV = FRC - ERV

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28
Q

VC

A

Vital capacity

the maximal volume of air that can be forcibly exhaled after a maximal inspiration
VC = TV + IRV + ERV

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29
Q

IC

A

Inspiratory capacity

the maximal amount of air that can be forcibly inhaled

IC = TV + IRC

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30
Q

FRC

A

Functional residual capacity

the volume of air remaining in the lungs after a normal expiration

FRC = RV + ERV
- cannot be measured with a spirometer

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31
Q

TLC

A

Total Lung Capacity

the volume of air in the lungs at the end of a maximal inspiration

TLC = VC + RV
- cannot be measured with a spirometer

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32
Q

total/minute ventilation

A

total amount of air moved into the respiratory system per minute
= tidal volume X respiratory frequency

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33
Q

Alveolar ventilation

A

= amount of air moved into the alveoli per minute
Depends on anatomical dead space ( 150ml, so 350ml is left for gas exchange)

given by the difference of the tidal volume and the anatomical dead space multiplied by the frequency

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34
Q

how much mL is dead space

A

150 mL

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35
Q

how much is tidal volume

A

500 mL

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36
Q

anatomical dead volume

A

Part of the volume of air that enters the lungs does not reach the alveoli/conductive zone
Stays in the region where no gas exchange occurs until the next respiratory cycle
150ml
Remains constant regardless of breath size

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37
Q

How does the breathing pattern affect alveolar ventilation?

A

increased DEPTH of breathing is more efficient in increasing alveolar ventilation than increasing breathing RATE (shallow and fast is bad, don’tget any alveolar ventilation)

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38
Q

FEV1

A

the forced expiratory volume in 1 sec

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39
Q

FVC

A

forced vital capacity
- the total amount of air that is blown out in one breadth after a maximal inspiration as fast as possible

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40
Q

FEV1/FVC

A

proportion of the amount of air that is blown out in 1 second

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41
Q

obstructive pattern

A

shallow breathing due to difficulty in exhaling all the air from the lungs (air comes out more slowly than normal)
- FEV1 is significantly reduced, so FEV1/FVC is reduced (<0.7)

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42
Q

Restrictive pattern

A

have trouble fully expanding their lungs with air - restricted from fully expanding

FEV1 and FVC are reduced, so FEV1/FVC is almost normal (slightly higher)

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43
Q

Static properties of the lungs

A

mechanical properties when no air is flowing
(maintains lung and chest wall volume)

  • Intrapleural pressure, transpulmonary pressure
  • static compliance of the lung
  • surface tension of the lungs
44
Q

Dynamic properties of the lung

A

mechanical properties when the lungs are changing volume and air is flowing in or out

45
Q

what is ventilation

A

exchange of air between the atmosphere and the alveoli
- gas moves from an area of high pressure to low pressure

46
Q

Boyle’s law

A

for a fixed amount of gas at a fixed temp.
Pressure is inversely proportional to Volume

47
Q

INSPIRATION

A

increase in volume of alveoli leads to lower Pressure, so air flows IN

48
Q

EXPIRATION

A

decreased volume in alveoli leads to higher pressure, so air flows OUT

49
Q

Pleurae

A

thin, doubled layered envelope surrounding the lungs
- visceral (covers lung) and parietal (covers thoracic wall) pleura

  • intrapleural fluid reduces friction of lung against thoracic wall during breathing
50
Q

elastic recoil?

A

tendency of the lungs to collapse
and pulls thoracic cage outward

at equilibrium, both recoils are balanced

interaction b/w lungs and chest wall occurs in the intrapleural space between visceral and parietal pleurae

51
Q

Transpulmonary pressure

A

the force responsible for keeping the alveoli open
- static parameter that maintains lung volume
Ptp = Palv - Pip (intrapleural pressure)

52
Q

Alveolar Pressure

A

pressure of the air inside the alveoli
- dynamic element, directly involved in producing air flow

53
Q

Airway resistance

A
  1. inertia of respiratory system (negligible)
  2. friction
    a. Lung tissue past itself during expansion
    b. Lung and chest wall tissue surfaces sliding past each other
    - Intrapleural fluid significantly reduces friction
    c. Frictional resistance to flow of air through airways (major one)
54
Q

Type of airflow patterns

A

laminar (small airways)
transitional (bronchial tree)
turbulent (large airways, pharnyx, trachea, larnyx)

55
Q

Resistance to airflow

A

highly sensitive to changes in airway radius
( poiseuille’s law)

56
Q

Lung Compliance

A

measure of elastic properties of the lung
measure of how easily the lungs can expand

57
Q

static compliance

A

represents lung compliance during periods of no gas flow

58
Q

dynamic compliance

A

represents pulmonary compliance during periods of gas flow
- lung stiffness + airway resistance
-always less than static compliance

59
Q

Hysteresis

A

defines the difference in the inflation and deflation pathways (due to elastic properties of the lungs)
- greater pressure difference is required to open a previously closed airway than to keep an airway from closing

60
Q

what is lung compliance determined by?

A
  1. elastic components of the lungs
  2. surface tension at the air-water interface of the alveoli
61
Q

elastic components of the airways

A

elastin - spring shape = more elasticity

collagen - strong twine = more stiffness

less elastin and collagen = lower lung compliance (floppy lungs)

62
Q

emphysema

A

increased compliance (floppy lungs) with much less elastic recoil due to less elastin

63
Q

surface tension

A

a measure of the attracting forces acting to pull a liquids surface molecules together at an air0liquid interface ( the molecules that the surface of the water make super strong bonds to the other water molecules close to them)
- causes the surface to maintain as small an area as possible

64
Q

alveolar surface tension

A

surface tension acts like a belt, it decreases the volume of compressible gas inside the alveoli increases its pressure

65
Q

Laplaces equation

A

the smaller the bubble’s radius, the greater the pressure needed to keep the bubble inflated

66
Q

Surfactant

A

produced by Type II aveolar cells
1. lowers the surface tension to improve lung compliance
2. makes the alveoli stable against collapse (maintains alveolis of different sizes)

67
Q

how does surfactant reduce the surface tension

A

it breaks the strong forces that occurs between the molecules of water at the surface, which lowers surface tension, increases lung compliance and makes it easier to expand the lungs

68
Q

how does surfactant equalize pressure in alveolis

A

thickness of surfactant decreases with increase of surface area, helps to stabilize pressure of different sized alveolis to prevent collpase of smaller ones

69
Q

which part of the lung receives more inspired air

A

due to gravity and posture making the alveoli at the bottom more deflated (more pressure) they are able to expand more and receive more inspired air)

70
Q

Daltons law

A

the total pressure is the sum of individual pressures (partial pressures)
air = Pn - 593mmHg + Po2- 160 mmHg + Ph2o - 7.6 mmHg + Pco2 - 0.3 mmHg)

71
Q

Diffusion: Fick’s law

A

the rate of transfer of a gas through a sheet of tissue per time is proportional to the tissue area, and the difference in partial pressures between the two sides

and its inversely proportional to the tissue thickness

72
Q

Diffusion constant

A

the amount of gas transferred between the alveoli and the blood/ time
- proportional to the solubitlity of the gas in the tissue/fluid

73
Q

What contributes to partial pressure?

A

only gas that is dissolved in solution contributes to partial pressure
(i.e O2 bound to Hb does not count for partial pressure)

74
Q

Partial pressure of O2 in air, alveoli and blood

A

PO2 in air = 160 mmHg
PO2 in alevoli: 105mmHg
PO2 in blood = 100 mmHg
PO2 in blood (arteries going to the lungs) = 40mmHg

75
Q

partial pressure of CO2 in air, alveoli, and blood

A

PCO2 in air = 0.3mmHg
PCO2 in alveoli = 40 mmHg
PCO2 in blood (veins towards the heart) = 40 mmHg
PCO2 in blood (arteries going to the lungs) = 46mmHG

76
Q
A
77
Q

how does higher alveoli ventilation affect PO2 and PCO2?

A

↑alveolar ventilation ↑PO2 levels (alveoli)
↑alveolar ventilation ↓ PCO2 levels (alveoli)

air is more similar to the atmosphere

78
Q

how does higher metabolic rate affect PO2 and PCO2 ?

A

↑metabolic rate ↓ PO2 levels (alveoli)
↑metabolic rate ↑PCO2 levels (alveoli)

Increasing metabolic rate will decrease alveolar PO2 and increase alveolar PCO2

79
Q

what is cooperative binding?

A

when O2 binds to a HEME group, it deforms the shape of the HEME group which chnages the shaped of the globin chain from tense (T) to relaxed (R) state.
- this then exposes the iron in the other HEME groups and facilitates the binding of the next O2 molecules

80
Q

Sigmoidal dissociation curve

A
  1. plateau/flat portion (60-100mmHg)
    - saturation of Hb stays high over a wider range of alveolar PO2 so it provides a safety factor when their is a limitation of lung function
  2. steep portion (40=60 mmHg)
    - unloading of large amounts of O2 from Hb with only a small decrease in PO2
    - this enhances O2 unloading
  3. steep portion (10-40 mmHg)
    facilitates diffusion of O2 from plasma into periphery
81
Q

effect of carbon monoxide poisoning on Hb-O2 dissociation curve

A

CO has 200x more affinity to Hb than O2
- makes it harder to unload O2 as there is less oxgyen delivered
-makes the Hb O2 saturation decreased when CO is present = reduction in O2 concentration

82
Q

Pulmonary Circulatory system

A

low pressure system
low resistance system (shorter + wider vessels)
high compliance vessels ( very thin walls, can easily expand)

83
Q

Ventilation-Perfusion relationshop

A

the balance between the ventilation (bringing O2 in and removing CO2 from alveoli) and perfusion (removing O2 from alveoli and adding CO2)

V/Q

84
Q

the greater the ventilation the [blank]

A

the more closely the aveolar PO2 and PCO2 approach their respective values in inspired air

85
Q

the greater the perfusion the [blank]

A

the more closely like composition of local alveolar air approaches mixed venous blood

86
Q

Perfused alveoli that are not ventilated

A

caused by an airway obstruction
- lowers PO2 and increases PCO2 in alveoli so they are almost balanced

87
Q

Ventilated alveoli that do not receive perfusion

A

capillary is blocked
- increases in alveolar PO2 and decrease in PCO2 (no CO2 is delivered from blood)

88
Q

How does the ventilation-perfusion ratio change in a lung?

A

The lowest zone has the greatest ventilation
- Starts with more collapsed alveolis

Due to gravity and posture, perfusion is higher at the base of the lungs and falls towards the apex

IN basal, VA/Q = -.6x ideal VA/Q (↓ PO2 ↑PCO2)
IN apical VA/Q = 3x ideal (↑ PO2 ↓ PCO2)

89
Q

ventilation-perfusion matching

A

homeostatic mechanisms exist to limit the mismatch

if there is bronchioconstriction causing less ventilation, then it will cause vasoconstriction to occur to also reduce perfusion.
- blood flow is then diverted to a better
ventilated alveoli

90
Q

hemoglobin

A

Hb is a protein composed of 4 globin (2 alpha 2 beta ) subunits and 4 Heme groups

  • Each heme group contains an Fe2+ which O2 binds to
91
Q

deoxyhemoglobin

A

No O2 bound to the heme group

92
Q

oxyhemoglobin

A

O2 bound to Hb

93
Q

how is oxygen moved?

A

moves throughout the lungs, blood, and tissues by a series of pressure gradients (diffuses from high to low)

94
Q

how does changes in pH, temp, and PCO2 change the O2 dissociation curve

A

shifts the curve to the right
- O2 affinity of Hb is reduced = more unloading

95
Q

how is oxygen carried in the blood

A

dissolved (5%)
bicarbonate (6-65%)
carboamino compounds (25-30%)

96
Q

carbon dioxide movement in lungs and tissues

A

diffuses into the blood
remains in plasma as dissolved CO2 OR:
- enters RBC and remains dissolved as CO2, bound to DeoxyHB, or reacts with water to produce HCO3- and H+

97
Q

transport of H+ between tissues and lungs

A

H+ is produced during HCO3- production
- DexoyHb has a much higher affinity for it than OxyHb (favours unloading of O2)

large portion of H+ is bound to Hb than dissolved in RBC or plasma , so pH in blood is presevred

98
Q

how is breathing initiated

A

rhythm is established in the CNS
- initiated in the medulla by specialized neurons
(Dorsal respiratory group + ventral respiratory group) + pontine respiratory group

99
Q

PreBotzinger complex (PreBotC)

A

In ventral respiratory group:
Generates excitatory inspiratory rhythmic activity that excites inspiratory muscles

100
Q

Parafacial respiratory group (pFRG)

A

in ventral respiratory group
Generates excitatory active expiratory rhythmic activity that excites expiratory muscles

101
Q

where is breathing rate modified ?

A

Modified by higher structures of the CNS and inputs from central/peripheral chemoreceptors and mechanoreceptors in lung and chest wall
a. Higher centres of the brain
- Speech, emotions, voluntary control of beathing
b. Medullary chemoreceptors
- ↓pH ↑ CO2
c. Carotid body chemoreceptors
- ↓pH ↑ CO2 ↓ O2
d. hering -breuer reflex
e. Proprioceptors in muscles/joints
f. Receptors for touch, temperature, pain stimuli

102
Q

chemical control of ventilation

A

peripheral and central chemoreceptors have a key role
- chemoreceptors sense changes in PO2, PCO2, and pH

103
Q

carotid + aortic bodies

A

sense changes in PO2 and pH
- very vascularized

Type I (glomus cells) - the chemosensitive cells

Type II (sustenacular cells) - act as support in CB

stimulation of these cells causes the release of NTs and eventually excited PreBOTc and pFRG to increase respiration + ventilation

104
Q

central chemoreceptors

A

Specialised neurons located close ot the ventral surface of the medulla
- Other chemosensitive sites are in the medullary
raphe and hypothalamus

Come into close contact with capillaries, where CO2 interacts with H2O to form H+ - then
activates chemorecptors
- This then excites the PreBotC and PFRG
to increase ventilation
PCO2 and H+ levels return toward normal

105
Q
A