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Anatomy 403 > Respiratory Physiology > Flashcards

Respiratory Physiology Flashcards

1
Q

functions of respiratory system

A
  1. provides oxygen
  2. eliminates carbon dioxide
  3. regulates the blood’s hydrogen ion concentration (pH) in coordination with the kidneys
  4. forms speech sounds (phonation)
  5. defends against microbes
  6. influences arterial concentrations of chemical messengers by removing some from pulmonary capillary blood and producing and adding others to this blood
  7. traps and dissolves blood clots arising from systemic veins such as those in the legs
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2
Q

mucous membrane function

A
  • moisturizes
  • cleanse
  • warm
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3
Q

mucociliary escalator

A

traps debris / bacteria and propels it up and out of the respiratory tract

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4
Q

trachea

A
  • 16-20 c-shaped rings made of hyaline cartilage

- smooth muscle allows adjustment of airway radius

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5
Q

conducting zone

A
  1. trachea
  2. bronchi
  3. bronchioles (no more cartilage)
  4. terminal bronchioles
  • contraction / relaxation of smooth muscle in these airways determines how easily air can flow (bronchoconstriciton vs bronchodilaton)
  • no gas exchange here
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6
Q

respiratory zone

A
  1. respiratory bronchioles
  2. alveolar ducts
  3. alveolar sacs
  • no smooth muscle
  • no ciliary elevator –> macrophages eat anything that get this far
  • thin walls for gas exchange
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7
Q

types of alveoli

A
  1. squamous alveolar cell
  2. alveolar macrophages
  3. great alveolar cell
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8
Q

respiratory membrane

A

where gas exchange occurs

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9
Q

alveoli large SA

A
  • size of tennis court

- many small alveoli provide lots of surface area for gas exchange

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10
Q

alveoli thin walls

A

alveolar and capillary walls are very thin, permitting rapid diffusion of gasses

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11
Q

type II cell (great alveolar cell)

A
  • make surfactant (decreases surface tension)
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12
Q

type I cell (squamous alveolar cell)

A

very thin / part of respiratory membrane

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13
Q

intrapleural fluid

A

only few mLs

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14
Q

parietal pleura

A

attached to thoracic wall

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15
Q

visceral pleura

A

covers surface of lungs

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16
Q

plural membrane functions

A
  1. reduces friction
  2. compartmentalize lungs
  3. negative intrapleural pressure keeps lungs inflated
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17
Q

balance of forces at rest

A
  1. pleurae stuck together by intrapleural fluid
  2. chest wall wants to expand outward
  3. lungs recoil inward because of elastic tissue
  4. opposing forces create negative instrapleural fluid pressure
    - –> without negative pressure and connection of pleura = lungs *** come back
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18
Q

pneumothorax

A

air in chest

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19
Q

atelectasis

A

collapsed lung

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20
Q

systemic respiration

A
  1. pulmonary ventilation
  2. gas exchange
  3. gas transport
  4. gas exchange
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21
Q

pulmonary ventilation

A

moving air into / out of the lungs

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22
Q

gas exchange #1

A

alveolar (external) respiration

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23
Q

gas exchange #2

A

systemic (internal) respiration

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24
Q

airway

A
  • always flow high pressure to low pressure
  • pressure atm = pressure alv –> no flow of air
  • P alv (inside) < P atm (outside) = air enters the lungs
  • P alv > P atm = air exits the lungs
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25
Q

how does pressure inside (P alv) change?

A

change volume in the lungs

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26
Q

Boyles law

A

pressure is inversely proportional to volume

  • volume of lungs changed by muscle contractions that change volume of thoracic cavity
  • change volume = change pressure = airflow
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27
Q

compression

A
  • decreased volume = increased pressure

- increased number of collisions

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28
Q

decompression

A
  • increased volume = decreased pressure

- decreased number of collisions

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29
Q

quiet inspiration muscles

A
  • diaphragm

- external intercostals

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30
Q

quiet expiration muscles

A
  • passive

- elastic recoil

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31
Q

forced inspiration muscles

A
  • diaphragm
  • external intercostals
  • scalenes
  • sternocleidomastoid
  • pectorals minor
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32
Q

forced expiration muscles

A
  • internal intercostals

- abdominals muscles

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33
Q

quiet inspiration

A
  • muscle contraction = increase volume of thoracic cavity = increase volume of lungs = decrease P alv (<0)
  • air flows IN until Patm = Palv
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34
Q

quiet expiration

A
  • passive
  • muscles relax = lungs relax = lungs recoil (decrease volume)
  • increase Palv
  • P alv > P atm
  • air flows OUT until Palv = Patm
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35
Q

bronchodilators

A
  • increase r = decrease R = increase F

- SNS, Epi/NE (vasoconstriction)

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36
Q

bronchoconstrictors

A
  • decrease r = increase R = decrease F
  • PSNS (vasodilation)
  • Leukotrienes
  • histamines
  • –> these two are inflammation
  • irritants
  • cold air
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37
Q

asthma

A

inflammation and bronchoconstriction triggered by inhaled allergens

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38
Q

asthma treatment

A

treat with anti-inflammatory drugs

  • Advair
  • singulair = leukotriene antagonist or bronchodilators
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39
Q

resistance to airflow

A
  1. airway radius
  2. pulmonary compliance
  3. surface tension
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40
Q

pulmonary compliance

A

“stretchability”

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41
Q

high compliance

A
  • easy inhale

- “floppy”

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42
Q

high elasticity

A

easy exhale

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43
Q

decreased compliance

A
  • “stiff”
  • cystic fibrosis and other fibrotic lung diseases
  • difficult to inhale
  • breaths shallow and more frequent
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44
Q

emphysema

A
  • lung tissue breaks down increased compliance
  • easy inhale
  • hard to exhale
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45
Q

surface tension

A
  • surfactant in the alveoli increases compliance
  • alveoli = water layer = attractive forces between water molecules (surface tension) –> resists stretch (decreases compliance)
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46
Q

type II cells (surface tension)

A

secrete surfactant

–> mingles with water to decrease surface tension (increases compliance)

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47
Q

newborn respiratory distress syndrome

A

premature babies lack surfactant

  • decrease surfactant
  • increase work of breathing
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48
Q

normal cost of breathing

A

about 3% of total metabolism

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49
Q

lung diseases breathing

A

about 30% of total metabolism – requires more calories to breath

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50
Q

dead space

A

air in conducting zone isn’t available for gas exchange

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51
Q

anatomic dead space

A
  • no gas exchange because no alveoli
  • about 1 mL/1 pound of body weight
  • -> 150 lbs = 150 mL of anatomic dead space
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52
Q

physiologic dead space

A

from non-functional or damaged alveoli

- normally = 0

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53
Q

minute ventilation

A

amount air moved per minute

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54
Q

minute ventilation equation

A

Frequency x TV = MV

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55
Q

alveolar ventilation

A

air available for gas exchange per minute

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56
Q

alveolar ventilation equation

A

Frequency x (TV - DS) = AV

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57
Q

changing the rate of breathing affect alveolar ventilation

A

increase rate = decrease alveolar ventilation

- short quick breaths

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58
Q

changing the depth of breathing affect alveolar ventilation

A

increase depth = increase alveolar ventilation

  • increase depth of breathing = most important, more important than rate because dead space is fixed volume = happens in exercise
  • slow big breaths
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59
Q

lung volumes

60
Q

lung capacities

A

calculated

61
Q

vital capacity (VC) calculation

A

TV (tidal volume) + ERV (expiratory reserve volume) + IRV (inspiratory reserve volume)

62
Q

inspiratory capacity (IC) calculation

A

TV (tidal volume) + IRV (inspiratory reserve volume)

63
Q

functional residual capacity (FRC) calculation

A

ERV (expiratory reserve volume) + RV (residual volume)

64
Q

total lung capacity (TLC) calculation

A

TV (tidal volume) + ERV (expiratory reserve volume) + IRV (inspiratory reserve volume) + RV (residual volume)

65
Q

direct measurements

A
  • inspiratory reserve volume (IRV)
  • expiratory reserve volume (ERV)
  • tidal volume (TV)
66
Q

tidal volume

A

amount of air inhaled and exhaled in one cycle during quiet breathing

67
Q

inspiratory reserve volume

A

amount of air in excess of tidal volume that can be inhaled with maximum effort

68
Q

expiratory reserve volume

A

amount of air in excess of tidal volume that can be exhaled with maximum effort

69
Q

residual volume

A

about of air remaining in the lungs after maximum expiration; the amount that can never voluntarily be exhaled

70
Q

vital capacity

A

the amount of air that can be inhaled and then exhaled with maximum effort; the deepest possible breath

71
Q

inspiratory capacity

A

maximum amount of air that can be inhaled after a normal tidal expiration

72
Q

function residual capacity

A

amount of air remaining in the lungs after a normal tidal expiration

73
Q

total lung capacity

A

maximum amount of air the lungs can contain

74
Q

forced expiratory volume (FEV)

A

percent of vital capacity exhaled in 1 second

- typically about 75-85%

75
Q

restrictive disorders

A
  • lungs difficult to inflate
  • decreased compliance
  • decreased VC, TLC
76
Q

examples of restrictive disorders

A
  • TB

- black lung disease

77
Q

obstructive disorders

A
  • narrowing or blockage of airway
  • decreased VC, FEV
  • increased RV
78
Q

examples of obstructive disorders

A
  • asthma
  • chronic bronchitis
  • emphysema
79
Q

chronic obstructive pulmonary disease (COPD)

A
  • chronic bronchitis

- emphysema

80
Q

emphysema (COPD)

A
  • breakdown of lung tissue
  • collapse of smaller airways
  • increase compliance
81
Q

chronic bronchitis (COPD)

A
  • develops as a result of chronic inflammatory response to inhaled irritant
  • chronic inflammation = increased mucus and thickening / narrowing of airway
82
Q

ventilation

A

driven by change in pressure

83
Q

gas exchange

A

driven by diffusion

84
Q

physical properties of gases

A
  1. collisions with walls determine pressure
  2. Daltons Law
  3. Henry’s Law
  4. Only unbound molecules exert pressure
85
Q

collisions with walls determine pressure

A

pressure increases with increasing temperature and concentration of the gas
- more collisions

86
Q

Dalton’s law

A

Total pressure is the sum of individuals “partial pressures”

  • P total = P1 + P2 + P3 …
  • each behaves independently of other gases
  • gases diffuse from high PP to low PP
87
Q

Henry’s law

A

amount of gas dissolved in a liquid with b proportional to the partial pressure of the gas with which the liquid is in equilibrium

88
Q

only unbound molecules exert pressure

A
  • bound O2 does NOT contribute to PP

- only when unbound portion is in equilibrium will net diffusion stop

89
Q

PO2 in air

90
Q

PCO2 in air

91
Q

PO2 in alveoli

92
Q

PCO2 in alveoli

93
Q

PO2 in pulmonary veins

94
Q

PCO2 in pulmonary veins

95
Q

PO2 in systemic arteries

96
Q

PCO2 in systemic arteries

97
Q

PO2 in cells

98
Q

PCO2 in cells

99
Q

PO2 in systemic veins

100
Q

PCO2 in systemic veins

101
Q

PO2 in pulmonary arteries

102
Q

PCO2 in pulmonary arteries

103
Q

factors that affect alveolar gas exchange

A
  1. pressure gradients
  2. diffusion barrier
  3. surface area of respiratory membrane
  4. matching ventilation and blood flow
104
Q

pressure gradient

A
  • decreased Patm = decreased O2
  • decrease PO2 = decrease PO2 art
  • O2 needs increased gradient because decreased solubility
  • change in elevation doesn’t apply to CO2 because no CO2 in inspired air
  • steeper gradient, rapid O2 diffusion
  • reduced gradient, slower O2 diffusion
105
Q

diffusion barrier

A

(thickness of respiratory membrane)

  • normal lung = very thin
  • diseased lung = inflammation, increased fluid
  • -> ex: cystic fibrosis, pneumonia, congestive heart failure
  • increased diffusion time = blood travels through capillaries before equilibrium
  • CO2 no problem because more soluble
106
Q

surface area of respiratory membrane

A

emphysema = breakdown of respiratory membrane

- decrease SA = decrease diffusion / gas exchange

107
Q

matching ventilation and blood

A
  • vasoconstriction to redirect blood flow to well ventilated areas
  • bronchoconstriction to redirect airflow to well perfused areas
108
Q

effects on airflow and gas exchange (emphysema)

A
  1. decrease elastic recoil = increased compliance (air trapped in lungs)
  2. increase airways resistance (smaller airways collapse during expiration)
  3. decreased SA for gas exchange
  4. ventilation perfusion inequality (loss of pulmonary capillaries)
109
Q

total percentage of O2 dissolved in blood

A
  1. 5%

- systemic arterial blood PO2 = 100 mmHg

110
Q

total percentage of O2 bound to hemoglobin

A
  1. 5%

- arterial Hb = about 98% saturated

111
Q

Hemoglobin

A

4Hb-O2 (bright red) –> oxyHb

- 4 global proteins 
\+ 4 heme groups (molecules)
- 1 Fe+2 / heme 
- 1 O2 / Fe+2 
= 4 O2 / Hb
112
Q

systemic venous blood

A

40 mmHg

  • venous Hb = about 75% saturated
    • 3 Hg -O2 (dark red) –> deoxyHb
113
Q

shape of oxygen hemoglobin dissociation curve

A

important for understanding O2 exchange

114
Q

key features of the oxygen-hemoglobin curve

A
  1. plateau is safety if alveolar PO2 falls –> need big decrease in PO2 before saturation decreases
  2. steepness is ideal for unloading O2 at tissues
    - easiest to unload where PO2 is lowest
    - 75% saturation means cells can obtain more O2 when necessary (exercise)
115
Q

when is breathing 100% O2 helpful / harmful?

A
  1. helps with diffusion barrier
    - -> with increased PO2 gradient, can reach a reasonable concentration by end of capillary
  2. doesn’t help with ventilation - perfusion coupling
  3. long term increased O2 causes damage to tissue –> sissiness, nausea, seizures
116
Q

Haldane effect

A
  • O2 unloaded in tissues = increased deoxyHb
  • deoxyHb has higher affinity for CO2 vs. oxyHb
  • -> increases loading of CO2 onto Hb
  • so = in tissues: increases O2 unloading = increases CO2 loading
117
Q

reverse Haldane effect

A
  • O2 binds Hb = increase oxyHb
  • oxyHb has decreased affinity for CO2 = increased unloading of CO2
  • so = in alveoli = increased O2 loading - increased CO2 unloading
118
Q

factors that affect unloading and loading of O2

A
  1. temperature
  2. acidity
  3. fetal hemoglobin
  4. carbon monoxide
119
Q

effect of temperature

A
  • increased temp (active tissues) = increased O2 unloading (curve shifts to right = “releasing”)
  • decreased temp (lungs = cooler) = increased O2 loading (curve shifts to left = “loading”)
120
Q

bohr effect

A

active tissues produce more CO2

  • -> increased H+ (decreased pH)
  • -> Hb affinity for O2 decreases (increase O2 loading)
121
Q

adult hemoglobin

A
  • 2 alpha

- 2 beta

122
Q

fetal hemoglobin

A
  • 2 alpha
  • 2 gamma
  • the saturation curve for fetal Hb shifts to left when compared to adult Hb
  • -> fetal Hb has greater affinity for O2
123
Q

effects of carbon monoxide

A
  • has 210x higher affinity for Hb vs O2
  • PCO = 0.5 –> 50% CO bound
  • CO binds tightly –> Hb doesn’t want to release CO or remaining O2
  • dissolved O2 remains normal (PO2) so no change in ventilation (no compensation mechanism)
124
Q

respiratory rhythm

A

generated in the medulla oblongata, but is modified by many different inputs

125
Q

higher centers

A
  • voluntary control of breathing
  • speech
  • in the brain
126
Q

Hering Breuer reflex

A

increase stretch during inhalation = stop inhale to prevent over stretch

127
Q

proprioceptors in muscles and joints

A

increase respiration rate to being exercise

128
Q

within the medulla oblongata

A
  • Doral respiratory group (DRG)

- ventral respiratory group (VRG)

129
Q

dorsal respiratory group (DRG)

A

integrates modulatory info and communicates with the VRG

130
Q

ventral respiratory group (VRG)

A

generates the pattern of respiration (rate and depth)

131
Q

hypocapnia

A

arterial PCO2 < 37 mmHg

132
Q

hypercapnia

A

arterial PCO2 > 43 mmHg

133
Q

alkalosis

A

blood pH > 7.45

134
Q

acidosis

A

blood pH < 7.35

135
Q

respiratory acidosis/alkalosis

A

problem with ventilation (change in CO2 is causing problem)

136
Q

metabolic acidosis/alkalosis

A

problem other than ventilation

137
Q

hyperventilation

A

decreased CO2 relative to alveolar ventilation

  • ventilation > metabolism
  • decreased CO2 (hypocapnia) = decrease H+ = increased pH = respiratory alkalosis
  • does not mean increased ventilation (ex: exercise)
138
Q

hypoventilation

A

increased CO2 relative to alveolar ventilation

  • ventilation < metabolism
  • increased CO2 (hypercapnia) = increased H+ = decreased pH = respiratory acidosis
139
Q

central chemoreceptors

A
  • medulla oblongata near DRG neurons
140
Q

peripheral chemoreceptors

A
  • communicate with DRG

- carotid bodies and aortic bodies

141
Q

peripheral chemoreceptors increase firing rate in response to:

A
  • increases arterial H+
  • – metabolic acidosis
  • – respiratory acidosis
  • increased arterial PCO2
  • decreased arterial PCO2 (<60 mmHg)
  • peripheral are less sensitive than central
142
Q

central chemoreceptors increase firing rate in response to:

A

–> increased acidic of brain ECF that is derived from rising systemic PCO2 (respiratory acidosis)

143
Q

effect of PCO2 on ventilation

A
  • small changes in arterial PCO2 quickly trigger changes in ventilation rate
  • mediated by both central (70%) and peripheral (30%) chemoreceptors
  • principle modulator of normal (non-emergency) ventilation
144
Q

effect of plasma [H+] on ventilation

A
  • metabolic [H+]

- [H+] from CO2

145
Q

metabolic [H+]

A

peripheral detection

146
Q

[H+] from CO2

A

both peripheral and central detection

147
Q

effect of PO2 on ventilation

A

a server reduction in arterial PO2 (hypoxia) stimulates increased ventilation via peripheral chemoreceptors

  • these receptors only sense changes in unbound (dissolved) O2
  • -> anemia/CO2 poisoning decrease oxyHb but dissolved (unbound) O2 is unaffected
    - –> chemoreceptors not stimulated

Anatomy 403 (13 decks)

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