Respiratory Physiology Flashcards
1
Q
functions of respiratory system
A
- provides oxygen
- eliminates carbon dioxide
- regulates the blood’s hydrogen ion concentration (pH) in coordination with the kidneys
- forms speech sounds (phonation)
- defends against microbes
- influences arterial concentrations of chemical messengers by removing some from pulmonary capillary blood and producing and adding others to this blood
- traps and dissolves blood clots arising from systemic veins such as those in the legs
2
Q
mucous membrane function
A
- moisturizes
- cleanse
- warm
3
Q
mucociliary escalator
A
traps debris / bacteria and propels it up and out of the respiratory tract
4
Q
trachea
A
- 16-20 c-shaped rings made of hyaline cartilage
- smooth muscle allows adjustment of airway radius
5
Q
conducting zone
A
- trachea
- bronchi
- bronchioles (no more cartilage)
- terminal bronchioles
- contraction / relaxation of smooth muscle in these airways determines how easily air can flow (bronchoconstriciton vs bronchodilaton)
- no gas exchange here
6
Q
respiratory zone
A
- respiratory bronchioles
- alveolar ducts
- alveolar sacs
- no smooth muscle
- no ciliary elevator –> macrophages eat anything that get this far
- thin walls for gas exchange
7
Q
types of alveoli
A
- squamous alveolar cell
- alveolar macrophages
- great alveolar cell
8
Q
respiratory membrane
A
where gas exchange occurs
9
Q
alveoli large SA
A
- size of tennis court
- many small alveoli provide lots of surface area for gas exchange
10
Q
alveoli thin walls
A
alveolar and capillary walls are very thin, permitting rapid diffusion of gasses
11
Q
type II cell (great alveolar cell)
A
- make surfactant (decreases surface tension)
12
Q
type I cell (squamous alveolar cell)
A
very thin / part of respiratory membrane
13
Q
intrapleural fluid
A
only few mLs
14
Q
parietal pleura
A
attached to thoracic wall
15
Q
visceral pleura
A
covers surface of lungs
16
Q
plural membrane functions
A
- reduces friction
- compartmentalize lungs
- negative intrapleural pressure keeps lungs inflated
17
Q
balance of forces at rest
A
- pleurae stuck together by intrapleural fluid
- chest wall wants to expand outward
- lungs recoil inward because of elastic tissue
- opposing forces create negative instrapleural fluid pressure
- –> without negative pressure and connection of pleura = lungs *** come back
18
Q
pneumothorax
A
air in chest
19
Q
atelectasis
A
collapsed lung
20
Q
systemic respiration
A
- pulmonary ventilation
- gas exchange
- gas transport
- gas exchange
21
Q
pulmonary ventilation
A
moving air into / out of the lungs
22
Q
gas exchange #1
A
alveolar (external) respiration
23
Q
gas exchange #2
A
systemic (internal) respiration
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
25
how does pressure inside (P alv) change?
change volume in the lungs
26
Boyles law
pressure is inversely proportional to volume
- volume of lungs changed by muscle contractions that change volume of thoracic cavity
- change volume = change pressure = airflow
27
compression
- decreased volume = increased pressure
| - increased number of collisions
28
decompression
- increased volume = decreased pressure
| - decreased number of collisions
29
quiet inspiration muscles
- diaphragm
| - external intercostals
30
quiet expiration muscles
- passive
| - elastic recoil
31
forced inspiration muscles
- diaphragm
- external intercostals
- scalenes
- sternocleidomastoid
- pectorals minor
32
forced expiration muscles
- internal intercostals
| - abdominals muscles
33
quiet inspiration
- muscle contraction = increase volume of thoracic cavity = increase volume of lungs = decrease P alv (<0)
- air flows IN until Patm = Palv
34
quiet expiration
- passive
- muscles relax = lungs relax = lungs recoil (decrease volume)
- increase Palv
- P alv > P atm
- air flows OUT until Palv = Patm
35
bronchodilators
- increase r = decrease R = increase F
| - SNS, Epi/NE (vasoconstriction)
36
bronchoconstrictors
- decrease r = increase R = decrease F
- PSNS (vasodilation)
- Leukotrienes
- histamines
- --> these two are inflammation
- irritants
- cold air
37
asthma
inflammation and bronchoconstriction triggered by inhaled allergens
38
asthma treatment
treat with anti-inflammatory drugs
- Advair
- singulair = leukotriene antagonist or bronchodilators
39
resistance to airflow
1. airway radius
2. pulmonary compliance
3. surface tension
40
pulmonary compliance
"stretchability"
41
high compliance
- easy inhale
| - "floppy"
42
high elasticity
easy exhale
43
decreased compliance
- "stiff"
- cystic fibrosis and other fibrotic lung diseases
- difficult to inhale
- breaths shallow and more frequent
44
emphysema
- lung tissue breaks down increased compliance
- easy inhale
- hard to exhale
45
surface tension
- surfactant in the alveoli increases compliance
- alveoli = water layer = attractive forces between water molecules (surface tension) --> resists stretch (decreases compliance)
46
type II cells (surface tension)
secrete surfactant
| --> mingles with water to decrease surface tension (increases compliance)
47
newborn respiratory distress syndrome
premature babies lack surfactant
- decrease surfactant
- increase work of breathing
48
normal cost of breathing
about 3% of total metabolism
49
lung diseases breathing
about 30% of total metabolism -- requires more calories to breath
50
dead space
air in conducting zone isn't available for gas exchange
51
anatomic dead space
- no gas exchange because no alveoli
- about 1 mL/1 pound of body weight
- -> 150 lbs = 150 mL of anatomic dead space
52
physiologic dead space
from non-functional or damaged alveoli
| - normally = 0
53
minute ventilation
amount air moved per minute
54
minute ventilation equation
Frequency x TV = MV
55
alveolar ventilation
air available for gas exchange per minute
56
alveolar ventilation equation
Frequency x (TV - DS) = AV
57
changing the rate of breathing affect alveolar ventilation
increase rate = decrease alveolar ventilation
| - short quick breaths
58
changing the depth of breathing affect alveolar ventilation
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
59
lung volumes
measured
60
lung capacities
calculated
61
vital capacity (VC) calculation
TV (tidal volume) + ERV (expiratory reserve volume) + IRV (inspiratory reserve volume)
62
inspiratory capacity (IC) calculation
TV (tidal volume) + IRV (inspiratory reserve volume)
63
functional residual capacity (FRC) calculation
ERV (expiratory reserve volume) + RV (residual volume)
64
total lung capacity (TLC) calculation
TV (tidal volume) + ERV (expiratory reserve volume) + IRV (inspiratory reserve volume) + RV (residual volume)
65
direct measurements
- inspiratory reserve volume (IRV)
- expiratory reserve volume (ERV)
- tidal volume (TV)
66
tidal volume
amount of air inhaled and exhaled in one cycle during quiet breathing
67
inspiratory reserve volume
amount of air in excess of tidal volume that can be inhaled with maximum effort
68
expiratory reserve volume
amount of air in excess of tidal volume that can be exhaled with maximum effort
69
residual volume
about of air remaining in the lungs after maximum expiration; the amount that can never voluntarily be exhaled
70
vital capacity
the amount of air that can be inhaled and then exhaled with maximum effort; the deepest possible breath
71
inspiratory capacity
maximum amount of air that can be inhaled after a normal tidal expiration
72
function residual capacity
amount of air remaining in the lungs after a normal tidal expiration
73
total lung capacity
maximum amount of air the lungs can contain
74
forced expiratory volume (FEV)
percent of vital capacity exhaled in 1 second
| - typically about 75-85%
75
restrictive disorders
- lungs difficult to inflate
- decreased compliance
- decreased VC, TLC
76
examples of restrictive disorders
- TB
| - black lung disease
77
obstructive disorders
- narrowing or blockage of airway
- decreased VC, FEV
- increased RV
78
examples of obstructive disorders
- asthma
- chronic bronchitis
- emphysema
79
chronic obstructive pulmonary disease (COPD)
- chronic bronchitis
| - emphysema
80
emphysema (COPD)
- breakdown of lung tissue
- collapse of smaller airways
- increase compliance
81
chronic bronchitis (COPD)
- develops as a result of chronic inflammatory response to inhaled irritant
- chronic inflammation = increased mucus and thickening / narrowing of airway
82
ventilation
driven by change in pressure
83
gas exchange
driven by diffusion
84
physical properties of gases
1. collisions with walls determine pressure
2. Daltons Law
3. Henry's Law
4. Only unbound molecules exert pressure
85
collisions with walls determine pressure
pressure increases with increasing temperature and concentration of the gas
- more collisions
86
Dalton's law
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
Henry's law
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
only unbound molecules exert pressure
- bound O2 does NOT contribute to PP
| - only when unbound portion is in equilibrium will net diffusion stop
89
PO2 in air
160 mmHg
90
PCO2 in air
0.3 mmHg
91
PO2 in alveoli
150 mmHg
92
PCO2 in alveoli
40 mmHg
93
PO2 in pulmonary veins
100 mmHg
94
PCO2 in pulmonary veins
40 mmHg
95
PO2 in systemic arteries
100 mmHg
96
PCO2 in systemic arteries
40 mmHg
97
PO2 in cells
< 40 mmHg
98
PCO2 in cells
> 46 mmHg
99
PO2 in systemic veins
40 mmHg
100
PCO2 in systemic veins
46 mmHg
101
PO2 in pulmonary arteries
40 mmHg
102
PCO2 in pulmonary arteries
46 mmHg
103
factors that affect alveolar gas exchange
1. pressure gradients
2. diffusion barrier
3. surface area of respiratory membrane
4. matching ventilation and blood flow
104
pressure gradient
- 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
diffusion barrier
(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
surface area of respiratory membrane
emphysema = breakdown of respiratory membrane
| - decrease SA = decrease diffusion / gas exchange
107
matching ventilation and blood
- vasoconstriction to redirect blood flow to well ventilated areas
- bronchoconstriction to redirect airflow to well perfused areas
108
effects on airflow and gas exchange (emphysema)
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
total percentage of O2 dissolved in blood
1. 5%
| - systemic arterial blood PO2 = 100 mmHg
110
total percentage of O2 bound to hemoglobin
98. 5%
| - arterial Hb = about 98% saturated
111
Hemoglobin
4Hb-O2 (bright red) --> oxyHb
```
- 4 global proteins
+ 4 heme groups (molecules)
- 1 Fe+2 / heme
- 1 O2 / Fe+2
= 4 O2 / Hb
```
112
systemic venous blood
40 mmHg
- venous Hb = about 75% saturated
- - 3 Hg -O2 (dark red) --> deoxyHb
113
shape of oxygen hemoglobin dissociation curve
important for understanding O2 exchange
114
key features of the oxygen-hemoglobin curve
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
when is breathing 100% O2 helpful / harmful?
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
Haldane effect
- 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
reverse Haldane effect
- 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
factors that affect unloading and loading of O2
1. temperature
2. acidity
3. fetal hemoglobin
4. carbon monoxide
119
effect of temperature
- 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
bohr effect
active tissues produce more CO2
- -> increased H+ (decreased pH)
- -> Hb affinity for O2 decreases (increase O2 loading)
121
adult hemoglobin
- 2 alpha
| - 2 beta
122
fetal hemoglobin
- 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
effects of carbon monoxide
- 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
respiratory rhythm
generated in the medulla oblongata, but is modified by many different inputs
125
higher centers
- voluntary control of breathing
- speech
- in the brain
126
Hering Breuer reflex
increase stretch during inhalation = stop inhale to prevent over stretch
127
proprioceptors in muscles and joints
increase respiration rate to being exercise
128
within the medulla oblongata
- Doral respiratory group (DRG)
| - ventral respiratory group (VRG)
129
dorsal respiratory group (DRG)
integrates modulatory info and communicates with the VRG
130
ventral respiratory group (VRG)
generates the pattern of respiration (rate and depth)
131
hypocapnia
arterial PCO2 < 37 mmHg
132
hypercapnia
arterial PCO2 > 43 mmHg
133
alkalosis
blood pH > 7.45
134
acidosis
blood pH < 7.35
135
respiratory acidosis/alkalosis
problem with ventilation (change in CO2 is causing problem)
136
metabolic acidosis/alkalosis
problem other than ventilation
137
hyperventilation
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
hypoventilation
increased CO2 relative to alveolar ventilation
- ventilation < metabolism
- increased CO2 (hypercapnia) = increased H+ = decreased pH = respiratory acidosis
139
central chemoreceptors
- medulla oblongata near DRG neurons
140
peripheral chemoreceptors
- communicate with DRG
| - carotid bodies and aortic bodies
141
peripheral chemoreceptors increase firing rate in response to:
- increases arterial H+
- -- metabolic acidosis
- -- respiratory acidosis
- increased arterial PCO2
- decreased arterial PCO2 (<60 mmHg)
- peripheral are less sensitive than central
142
central chemoreceptors increase firing rate in response to:
--> increased acidic of brain ECF that is derived from rising systemic PCO2 (respiratory acidosis)
143
effect of PCO2 on ventilation
- 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
effect of plasma [H+] on ventilation
- metabolic [H+]
| - [H+] from CO2
145
metabolic [H+]
peripheral detection
146
[H+] from CO2
both peripheral and central detection
147
effect of PO2 on ventilation
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
