Respiratory Flashcards

(105 cards)

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
IRV
Inspiratory Reserve Volume the additional volume of air that can be forcibly inhaled following a normal inspiration to the maximum inspiration possible
26
ERV
Expiratory Reserve Volume the additional volume of air that can be forcibly exhaled following a normal expiration. expiring to the maximum voluntary expiration
27
RV
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
28
VC
Vital capacity the maximal volume of air that can be forcibly exhaled after a maximal inspiration VC = TV + IRV + ERV
29
IC
Inspiratory capacity the maximal amount of air that can be forcibly inhaled IC = TV + IRC
30
FRC
Functional residual capacity the volume of air remaining in the lungs after a normal expiration FRC = RV + ERV - cannot be measured with a spirometer
31
TLC
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
32
total/minute ventilation
total amount of air moved into the respiratory system per minute = tidal volume X respiratory frequency
33
Alveolar ventilation
= 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
34
how much mL is dead space
150 mL
35
how much is tidal volume
500 mL
36
anatomical dead volume
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
37
How does the breathing pattern affect alveolar ventilation?
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)
38
FEV1
the forced expiratory volume in 1 sec
39
FVC
forced vital capacity - the total amount of air that is blown out in one breadth after a maximal inspiration as fast as possible
40
FEV1/FVC
proportion of the amount of air that is blown out in 1 second
41
obstructive pattern
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)
42
Restrictive pattern
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)
43
Static properties of the lungs
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
Dynamic properties of the lung
mechanical properties when the lungs are changing volume and air is flowing in or out
45
what is ventilation
exchange of air between the atmosphere and the alveoli - gas moves from an area of high pressure to low pressure
46
Boyle's law
for a fixed amount of gas at a fixed temp. Pressure is inversely proportional to Volume
47
INSPIRATION
increase in volume of alveoli leads to lower Pressure, so air flows IN
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EXPIRATION
decreased volume in alveoli leads to higher pressure, so air flows OUT
49
Pleurae
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
elastic recoil?
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
Transpulmonary pressure
the force responsible for keeping the alveoli open - static parameter that maintains lung volume Ptp = Palv - Pip (intrapleural pressure)
52
Alveolar Pressure
pressure of the air inside the alveoli - dynamic element, directly involved in producing air flow
53
Airway resistance
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
Type of airflow patterns
laminar (small airways) transitional (bronchial tree) turbulent (large airways, pharnyx, trachea, larnyx)
55
Resistance to airflow
highly sensitive to changes in airway radius ( poiseuille's law)
56
Lung Compliance
measure of elastic properties of the lung measure of how easily the lungs can expand
57
static compliance
represents lung compliance during periods of no gas flow
58
dynamic compliance
represents pulmonary compliance during periods of gas flow - lung stiffness + airway resistance -always less than static compliance
59
Hysteresis
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
what is lung compliance determined by?
1. elastic components of the lungs 2. surface tension at the air-water interface of the alveoli
61
elastic components of the airways
elastin - spring shape = more elasticity collagen - strong twine = more stiffness less elastin and collagen = lower lung compliance (floppy lungs)
62
emphysema
increased compliance (floppy lungs) with much less elastic recoil due to less elastin
63
surface tension
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
alveolar surface tension
surface tension acts like a belt, it decreases the volume of compressible gas inside the alveoli increases its pressure
65
Laplaces equation
the smaller the bubble's radius, the greater the pressure needed to keep the bubble inflated
66
Surfactant
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
how does surfactant reduce the surface tension
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
how does surfactant equalize pressure in alveolis
thickness of surfactant decreases with increase of surface area, helps to stabilize pressure of different sized alveolis to prevent collpase of smaller ones
69
which part of the lung receives more inspired air
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
Daltons law
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
Diffusion: Fick's law
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
Diffusion constant
the amount of gas transferred between the alveoli and the blood/ time - proportional to the solubitlity of the gas in the tissue/fluid
73
What contributes to partial pressure?
only gas that is dissolved in solution contributes to partial pressure (i.e O2 bound to Hb does not count for partial pressure)
74
Partial pressure of O2 in air, alveoli and blood
PO2 in air = 160 mmHg PO2 in alevoli: 105mmHg PO2 in blood = 100 mmHg PO2 in blood (arteries going to the lungs) = 40mmHg
75
partial pressure of CO2 in air, alveoli, and blood
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
77
how does higher alveoli ventilation affect PO2 and PCO2?
↑alveolar ventilation ↑PO2 levels (alveoli) ↑alveolar ventilation ↓ PCO2 levels (alveoli) air is more similar to the atmosphere
78
how does higher metabolic rate affect PO2 and PCO2 ?
↑metabolic rate ↓ PO2 levels (alveoli) ↑metabolic rate ↑PCO2 levels (alveoli) Increasing metabolic rate will decrease alveolar PO2 and increase alveolar PCO2
79
what is cooperative binding?
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
Sigmoidal dissociation curve
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
effect of carbon monoxide poisoning on Hb-O2 dissociation curve
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
Pulmonary Circulatory system
low pressure system low resistance system (shorter + wider vessels) high compliance vessels ( very thin walls, can easily expand)
83
Ventilation-Perfusion relationshop
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
the greater the ventilation the [blank]
the more closely the aveolar PO2 and PCO2 approach their respective values in inspired air
85
the greater the perfusion the [blank]
the more closely like composition of local alveolar air approaches mixed venous blood
86
Perfused alveoli that are not ventilated
caused by an airway obstruction - lowers PO2 and increases PCO2 in alveoli so they are almost balanced
87
Ventilated alveoli that do not receive perfusion
capillary is blocked - increases in alveolar PO2 and decrease in PCO2 (no CO2 is delivered from blood)
88
How does the ventilation-perfusion ratio change in a lung?
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
ventilation-perfusion matching
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
hemoglobin
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
deoxyhemoglobin
No O2 bound to the heme group
92
oxyhemoglobin
O2 bound to Hb
93
how is oxygen moved?
moves throughout the lungs, blood, and tissues by a series of pressure gradients (diffuses from high to low)
94
how does changes in pH, temp, and PCO2 change the O2 dissociation curve
shifts the curve to the right - O2 affinity of Hb is reduced = more unloading
95
how is oxygen carried in the blood
dissolved (5%) bicarbonate (6-65%) carboamino compounds (25-30%)
96
carbon dioxide movement in lungs and tissues
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
transport of H+ between tissues and lungs
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
how is breathing initiated
rhythm is established in the CNS - initiated in the medulla by specialized neurons (Dorsal respiratory group + ventral respiratory group) + pontine respiratory group
99
PreBotzinger complex (PreBotC)
In ventral respiratory group: Generates excitatory inspiratory rhythmic activity that excites inspiratory muscles
100
Parafacial respiratory group (pFRG)
in ventral respiratory group Generates excitatory active expiratory rhythmic activity that excites expiratory muscles
101
where is breathing rate modified ?
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
chemical control of ventilation
peripheral and central chemoreceptors have a key role - chemoreceptors sense changes in PO2, PCO2, and pH
103
carotid + aortic bodies
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
central chemoreceptors
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