1 respiratory tract anatomy fig 13-1. 2 conducting zone vs. respiratory zone fig 13-2
TRANSCRIPT
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Respiratory tract anatomy
fig 13-1
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Conducting zone vs. respiratory zone
fig 13-2
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Conducting zone functions
Regulation of air flowtrachea & bronchi held open by cartilaginous ringssmooth muscle in walls of bronchioles & alveolar ductssympathetic NS & epinephrine relaxation ( receptors) air flowleukotrienes
(inflammation & allergens leukotrienes mucus & constriction)
Protectionmucus escalator (goblet cells in bronchioles & ciliated epithelium)inhibited by cigarette smoke
Warming & humidifying inspired airexpired air is 37 & 100% humidity (loss of ~400 ml pure water/day)
Phonationlarynx & vocal cords
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Alveolar structure 1
fig 13-3b
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Alveolar structure 2
fig 13-4a
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Alveolar structure 3
fig 13-4b
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Alveolar structure (notes)
Type I epithelial cellsthin, flat; gas exchange
Type II epithelial cellssecrete pulmonary surfactant pulmonary compliance (later)
Pulmonary capillariescompletely surround each alveolus; “sheet” of blood
Interstitial space diffusion distance for O2 & CO2 is less than diameter of red blood cell
Elastic fiberssecreted by fibroblasts into pulmonary interstitial spacetend to collapse lung
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Lung pressures
Lungs are inflated by being “pulled” open
Transmural/transpulmonary pressure = Palveolar – Ppleural = 0 – (-5) = 5 mm Hg
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Lung pressures during quiet ventilation
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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) pressurei.e. Palv – Pip (e.g. at “2”, -1 – (-5) = 4 mm Hg
Lower curve (black):labeling accidentally omittedx axis should read “4 sec” i.e. timey axis is tidal volume = 500 ml
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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)
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Airway resistance
Transpulmonary pressure
as lungs expand, pleural pressure becomes more negative
transpulmonary pressure (alveolar pressure – pleural pressure) increases
alveoli expand, bronchioles expand airway resistance
result: inhalation lowers resistance, exhalation increases resistance
Lateral traction
alveoli & bronchioles all interconnected
expansion of lungs stretches alveoli & bronchioles resistance
net stocking metaphor
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Lung compliance
Definition: ease of expansion
e.g. balloon is compliant, auto tire is less complianti.e. tire requires much greater pressure increase to expandcompliance = Δ volume / Δ pressure
Factors that decrease compliance
surface tension of fluid lining alveolar surfaceelastic tissue in alveolar wallsexpansion of lungs (stretched lungs are less compliant)
Factors that increase compliance
pulmonary surfactant secreted by type II alveolar cellsreduces surface tension of alveolar fluidmixture of phospholipid and proteinlow levels in premature infants (respiratory distress syndrome)
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Airway resistance
Epinephrine
relaxes bronchiolar smooth muscle (2 receptors)
Leukotrienes
released during the inflammatory response
contract bronchiolar smooth muscle
important in asthma & bronchitis
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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)
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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
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Alveolar ventilation
fresh air entering lung with each breath = tidal volume – dead space
Alveolar ventilation rate
(tidal volume – 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
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Partial pressures
Dalton’s 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)
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Partial pressures at various sites
fig 13-22
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Partial pressure & solubility
because P.O2 plasma = P.O2 blood, putting them in contact, separated by O2 permeable membrane no net diffusion
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Alveolar gas composition as AVR varies
Hypoventilation: alveolar ventilation rateHyperventilation: alveolar ventilation rate
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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 P.O2 signals constriction of blood vessels (hypoxic vasoconstriction)
i.e. don’t 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 P.CO2 signals constriction of bronchioles
i.e. don’t send air to an alveolus with no blood flow
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Ventilation (air flow) & perfusion (blood flow) matching
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Alveolar O2 pulmonary capillary blood
fig 13-24
Diseased lung: pulmonary edema, interstitial fibrosis
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Hemoglobin structure
fig 13-26
4 subunits (left) form 1 hemoglobin
Iron is ferrous form (Fe++)
Hb + 4 O2 Hb(O2)4 (saturated)
deoxyHb oxyHb
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Oxygen-hemoglobin dissociation curve
fig 13-27
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Oxygen-hemoglobin dissociation curve (notes)
100% saturation is when every Hb has 4 O2’s 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 “positive cooperativity”)
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 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 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
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O2-Hb curve; effect of pH, CO2, DPG, temperature
In working tissue, pH, P.CO2, temperature, DPG
DPG is diphosphoglycerate (now known as bisphosphoglycerate)
DPG is in hypoxic tissue (and in stored blood in blood banks)
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O2 from alveolus red blood cell in the lung
fig 13-29
all O2 movement is by simple diffusion down its partial pressure gradient
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O2 from rbc Hb cells
fig 13-29
all O2 movement is by simple diffusion down its partial pressure gradient
highest P.O2 in alveolus
lowest P.O2 in mitochondria
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CO2 from tissues blood
fig 13-31a
CO2 transport:
60% plasma HCO3-
30% carbamino hemoglobin
10% dissolved CO2
CA = carbonic anhydrase
H2O + CO2 H2CO3
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CO2 from pulmonary blood alveolus
fig 13-31b
CO2 transport:
60% plasma HCO3-
30% carbamino hemoglobin
10% dissolved CO2
CA = carbonic anhydrase
H2O + CO2 H2CO3
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Hemoglobin as a buffer
fig 13-32
Notes on next slide
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Hemoglobin as a buffer (notes)
In tissues:
CO2 (produced by metabolism) + H2O H2CO3 H+ + HCO3-
Hemoglobin 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- H2CO3 H2O + CO2 (released into alveolus)
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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
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Control of ventilation (chemoreceptors)
fig 13-33
peripheral chemoreceptors
in carotid & aortic bodies
Central chemoreceptors:
in medulla (brain interstitial fluid)
Stimulated by:
1. P.CO2 (via pH: most important)
Peripheral chemoreceptors:
see left (arterial blood)
Stimulated by:
1. P.CO2 (via pH)
2. P.O2
3. pH
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Control of ventilation ( arterial P.O2)
fig 13-34
Acts on peripheral chemoreceptors
( P.O2 depresses central chemoreceptors)
relatively insensitive (potentiated by P.CO2)
responds to P.O2, not O2 content (i.e. not to anemia or CO poisoning)
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Control of ventilation ( arterial P.O2)
fig 13-35
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Control of ventilation ( P.CO2)
fig 13-36
Acts on central & peripheral chemoreceptors
central chemoreceptors are the most important regulators of ventilation
acts via [H+] (pH)
note sensitivity
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Control of ventilation ( P.CO2)
fig 13-37
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Control of ventilation ( pH)
fig 13-38
P.CO2 acts via pH, but this is pH from other sources (e.g. lactic acid)
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Control of ventilation ( pH)
fig 13-39
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Increased ventilation & exercise
fig 13-41
You would think that exercise AVR by CO2, O2, or pH
However:
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Increased ventilation & exercise; possible mechanisms
fig 13-43
Also:
axon collaterals from descending tracts to respiratory centers
feedback from joints & muscles