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Respiratory tract anatomy

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Respiratory tract anatomy
fig 13-1
1
Conducting zone vs. respiratory zone
fig 13-2
2
Conducting zone functions
Regulation of air flow
trachea & bronchi held open by cartilaginous rings
smooth muscle in walls of bronchioles & alveolar ducts
sympathetic NS & epinephrine яВо relaxation (яБв receptors) яВояВн air flow
leukotrienes
(inflammation & allergens яВояВн leukotrienes яВояВн mucus & constriction)
Protection
mucus escalator (goblet cells in bronchioles & ciliated epithelium)
inhibited by cigarette smoke
Warming & humidifying inspired air
expired air is 37яВ░ & 100% humidity (loss of ~400 ml pure water/day)
Phonation
larynx & vocal cords
3
Alveolar structure 1
fig 13-3b
4
Alveolar structure 2
fig 13-4a
5
Alveolar structure 3
fig 13-4b
6
Alveolar structure (notes)
Type I epithelial cells
thin, flat; gas exchange
Type II epithelial cells
secrete pulmonary surfactant яВояВн pulmonary compliance (later)
Pulmonary capillaries
completely surround each alveolus; тАЬsheetтАЭ of blood
Interstitial space
diffusion distance for O2 & CO2 is less than diameter of red blood cell
Elastic fibers
secreted by fibroblasts into pulmonary interstitial space
tend to collapse lung
7
Lung pressures
Lungs are inflated by being тАЬpulledтАЭ open
Transmural/transpulmonary pressure = Palveolar тАУ Ppleural = 0 тАУ (-5) = 5 mm Hg
8
Lung pressures during quiet ventilation
9
Lung pressures during ventilation
Purple line:
alveolar pressure (Palv)
-1 mm Hg during inspiration
+1 mm Hg during expiration
Green line:
pleural pressure (Pip)
-4 mm Hg at functional residual capacity
-7 mm Hg after inspiration
Ptp is transpulmonary (transmural) pressure
i.e. Palv тАУ Pip (e.g. at тАЬ2тАЭ, -1 тАУ (-5) = 4 mm
Hg
Lower curve (black):
labeling accidentally omitted
x axis should read тАЬ4 secтАЭ i.e. time
y axis is tidal volume = 500 ml
10
Pleural pressure during ventilation
Quiet ventilation:
pleural pressure (Pip) always negative
as lung expands, Pip becomes more negative because recoil
(collapsing) force increases as lung stretches
Forced ventilation:
Pip negative during inspiration; more negative as lung expands
Pip can be positive during forced expiration (e.g. FEV1 measurement)
11
Airway resistance
Transpulmonary pressure
as lungs expand, pleural pressure becomes more negative
transpulmonary pressure (alveolar pressure тАУ pleural pressure) increases
alveoli expand, bronchioles expand яВояВп airway resistance
result: inhalation lowers resistance, exhalation increases resistance
Lateral traction
alveoli & bronchioles all interconnected
expansion of lungs stretches alveoli & bronchioles яВояВп resistance
net stocking metaphor
12
Lung compliance
Definition: ease of expansion
e.g. balloon is compliant, auto tire is less compliant
i.e. tire requires much greater pressure increase to expand
compliance = ╬Ф volume / ╬Ф pressure
Factors that decrease compliance
surface tension of fluid lining alveolar surface
elastic tissue in alveolar walls
expansion of lungs (stretched lungs are less compliant)
Factors that increase compliance
pulmonary surfactant secreted by type II alveolar cells
reduces surface tension of alveolar fluid
mixture of phospholipid and protein
low levels in premature infants (respiratory distress syndrome)
13
Airway resistance
Epinephrine
relaxes bronchiolar smooth muscle (яБв2 receptors)
Leukotrienes
released during the inflammatory response
contract bronchiolar smooth muscle
important in asthma & bronchitis
14
Lung volumes
Learn in laboratory:
*tidal volume, *inspiratory reserve volume, *expiratory reserve volume,
residual volume, functional residual capacity, *vital capacity, total lung
capacity
*can be measured with a spirometer
FEV1: forced vital capacity in 1 second (~80%)
Functional residual capacity:
lung volume when all muscles are relaxed (or subject is dead)
lung volume at the end of quiet expiration
tendency of lungs to collapse = tendency of thoracic cavity to expand
pleural pressure is negative (~ -4 mm Hg)
15
Alveolar ventilation
Minute ventilation
tidal volume (ml/breath) x respiratory rate (breaths/min)
Anatomic dead space
space in respiratory tract where no gas exchange occurs
fig 13-20
16
Alveolar ventilation
fresh air entering lung with each breath = tidal volume тАУ dead space
Alveolar ventilation rate
(tidal volume тАУ dead space) x respiratory rate
Example calculations
respiratory rate
tidal volume
dead space
alveolar
ventilation rate
14 /min
500 ml
150 ml
4.9 L/min
24 /min
300 ml
150 ml
3.6 L/min
see also table 13-5
17
Partial pressures
DaltonтАЩs law
In a mixture of gases, each gas behaves independently and exerts a
pressure proportional to its concentration in the gas mixture
For example:
Air is 79% N2, 21% O2, 0.4% CO2
Air pressure = 760 mm Hg (dry air at sea level)
P.N2 = 600 mm Hg, P.O2 = 160 mm Hg, P.CO2 = 0.3 mm Hg
Partial pressure in solution
= partial pressure in gas mixture after equilibration with solution
Why use partial pressures?
because gases diffuse down their partial pressure gradients
(in gas or in solution)
18
Partial pressures at various sites
fig 13-22
19
Partial pressure & solubility
because P.O2 plasma = P.O2 blood, putting them in contact, separated
by O2 permeable membrane яВо no net diffusion
20
Alveolar gas composition as AVR varies
Hypoventilation: яВп alveolar ventilation rate
Hyperventilation: яВн alveolar ventilation rate
21
Ventilation (air flow) & perfusion (blood flow) matching
If air flow to an alveolus is blocked:
alveolar gas = venous blood (P.O2 40 mm Hg, P.CO2 45 mm Hg)
The яВп P.O2 signals constriction of blood vessels (hypoxic vasoconstriction)
i.e. donтАЩt send blood to an alveolus with no air flow
If blood flow to an alveolus is blocked:
alveolar gas = atmospheric air (P.O2 160 mm Hg, P.CO2 ~0 mm Hg)
The яВп P.CO2 signals constriction of bronchioles
i.e. donтАЩt send air to an alveolus with no blood flow
22
Ventilation (air flow) & perfusion (blood flow) matching
23
Alveolar O2 яВо pulmonary capillary blood
fig 13-24
Diseased lung: pulmonary edema, interstitial fibrosis
24
Hemoglobin structure
4 subunits (left) form 1 hemoglobin
Iron is ferrous form (Fe++)
Hb + 4 O2 яВо Hb(O2)4 (saturated)
deoxyHb
oxyHb
fig 13-26
25
Oxygen-hemoglobin dissociation curve
fig 13-27
26
Oxygen-hemoglobin dissociation curve (notes)
100% saturation is when every Hb has 4 O2тАЩs bound
Sigmoid (S-shaped) curve indicates that binding of the 1st O2 increases
the affinity of the other Hb binding sites for O2 (an allosteric effect
technically known as тАЬpositive cooperativityтАЭ)
Sigmoid curve means that the curve is steepest in the region of
unloading O2 i.e. in the tissues where P.O2 is < 40 mm Hg
A steep curve means that a small reduction in P.O2 яВояВн O2 unloaded
Curve is flattest in the lung where P.O2 is ~100 mm Hg
A flat curve means that a large reduction in P.O2 яВояВп reduction in O2
saturation of Hb (e.g. at high altitude or in diseased lung)
Also, flat curve means breathing 100% O2 adds little O2 to the blood
27
O2-Hb curve; effect of pH, CO2, DPG, temperature
In working tissue, яВп pH, яВн P.CO2, яВн temperature, яВн DPG
DPG is diphosphoglycerate (now known as bisphosphoglycerate)
DPG is яВн in hypoxic tissue (and in stored blood in blood banks)
28
O2 from alveolus яВо red blood cell in the lung
all O2 movement is by
simple diffusion down its
partial pressure gradient
fig 13-29
29
O2 from rbc Hb яВо cells
all O2 movement is by
simple diffusion down its
partial pressure gradient
highest P.O2 in alveolus
lowest P.O2 in mitochondria
fig 13-29
30
CO2 from tissues яВо blood
CO2 transport:
60% plasma HCO330% carbamino hemoglobin
10% dissolved CO2
CA = carbonic anhydrase
H2O + CO2 яВо H2CO3
fig 13-31a
31
CO2 from pulmonary blood яВо alveolus
CO2 transport:
60% plasma HCO330% carbamino hemoglobin
10% dissolved CO2
CA = carbonic anhydrase
H2O + CO2 яВо H2CO3
fig 13-31b
32
Hemoglobin as a buffer
Notes on next slide
fig 13-32
33
Hemoglobin as a buffer (notes)
In tissues:
CO2 (produced by metabolism) + H2O яВо H2CO3 яВо H+ + HCO3Hemoglobin becomes more basic when it is deoxygenated, i.e. it
binds H+ more tightly
In the lung:
Hemoglobin is oxygenated, becomes more acidic, (i.e. it is a more
powerful H+ donor), and releases its H+
H+ + HCO3- яВо H2CO3 яВо H2O + CO2 (released into alveolus)
34
Rhythmical nature of breathing
Respiratory rhythm generator
located in medulla oblongata of brainstem
During quiet breathing
Inspiration: action potentials burst to diaphragm & inspiratory intercostals
Expiration: no action potentials; elastic recoil of lungs (passive process)
During forced breathing (e.g. exercise, blowing up a balloon)
Active inspiration & expiration
Expiration with expiratory intercostals & abdominal muscles
Breathing is also modulated by centers in pons of brainstem & lungs
35
Control of ventilation (chemoreceptors)
peripheral chemoreceptors
in carotid & aortic bodies
Central chemoreceptors:
in medulla (brain interstitial fluid)
Stimulated by:
1. яВн P.CO2 (via яВп pH: most important)
Peripheral chemoreceptors:
see left (arterial blood)
Stimulated by:
1. яВн P.CO2 (via яВп pH)
2. яВп P.O2
3. яВп pH
fig 13-33
36
Control of ventilation (яВп arterial P.O2)
fig 13-34
Acts on peripheral chemoreceptors
(яВп P.O2 depresses central chemoreceptors)
relatively insensitive (potentiated by яВн P.CO2)
responds to P.O2, not O2 content (i.e. not to anemia or CO poisoning)
37
Control of ventilation (яВп arterial P.O2)
fig 13-35
38
Control of ventilation (яВн P.CO2)
Acts on central & peripheral chemoreceptors
central chemoreceptors are the most
important regulators of ventilation
acts via яВн [H+] (яВпpH)
note sensitivity
fig 13-36
39
Control of ventilation (яВн P.CO2)
fig 13-37
40
Control of ventilation (яВп pH)
fig 13-38
яВн P.CO2 acts via яВп pH, but this is яВп pH from other sources (e.g. lactic acid)
41
Control of ventilation (яВп pH)
fig 13-39
42
Increased ventilation & exercise
You would think that exercise яВояВн AVR by яВн CO2, яВп O2, or яВп pH
However:
fig 13-41
43
Increased ventilation & exercise; possible mechanisms
fig 13-43
Also:
axon collaterals from descending tracts to respiratory centers
feedback from joints & muscles
44
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