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Respiratory tract anatomy. fig 13-1. Conducting zone vs. respiratory zone. fig 13-2. Conducting zone functions. Regulation of air flow trachea & bronchi held open by cartilaginous rings smooth muscle in walls of bronchioles & alveolar ducts

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Respiratory tract anatomy

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Respiratory tract anatomy

fig 13-1

Conducting zone vs. respiratory zone

fig 13-2

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  relaxation ( receptors)  air flow


(inflammation & allergens  leukotrienes  mucus & constriction)


mucus escalator (goblet cells in bronchioles & ciliated epithelium)

inhibited by cigarette smoke

Warming & humidifying inspired air

expired air is 37 & 100% humidity (loss of ~400 ml pure water/day)


larynx & vocal cords

Alveolar structure 1

fig 13-3b

Alveolar structure 2

fig 13-4a

Alveolar structure 3

fig 13-4b

Alveolar structure (notes)

Type I epithelial cells

thin, flat; gas exchange

Type II epithelial cells

secrete pulmonary surfactant  pulmonary compliance (later)

Pulmonary capillaries

completely surround each alveolus; “sheet” 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

Lung pressures

Lungs are inflated by being “pulled” open

Transmural/transpulmonary pressure = Palveolar – Ppleural = 0 – (-5) = 5 mm Hg

Lung pressures during quiet ventilation

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 – Pip (e.g. at “2”, -1 – (-5) = 4 mm Hg

Lower curve (black):

labeling accidentally omitted

x axis should read “4 sec” i.e. time

y axis is tidal volume = 500 ml

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)

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

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 = Δ volume / Δ 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)

Airway resistance


relaxes bronchiolar smooth muscle (2 receptors)


released during the inflammatory response

contract bronchiolar smooth muscle

important in asthma & bronchitis

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)

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

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

see also table 13-5

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)

Partial pressures at various sites

fig 13-22

Partial pressure & solubility

because P.O2 plasma = P.O2 blood, putting them in contact, separated by O2 permeable membrane  no net diffusion

Alveolar gas composition as AVR varies

Hypoventilation:  alveolar ventilation rate

Hyperventilation:  alveolar ventilation rate

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

Ventilation (air flow) & perfusion (blood flow) matching

Alveolar O2 pulmonary capillary blood

fig 13-24

Diseased lung: pulmonary edema, interstitial fibrosis

Hemoglobin structure

4 subunits (left) form 1 hemoglobin

Iron is ferrous form (Fe++)

Hb + 4 O2 Hb(O2)4 (saturated)

deoxyHb oxyHb

fig 13-26

Oxygen-hemoglobin dissociation curve

fig 13-27

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

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)

O2 from alveolus  red blood cell in the lung

all O2 movement is by simple diffusion down its partial pressure gradient

fig 13-29

O2 from rbc Hb  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

CO2 from tissues  blood

CO2 transport:

60% plasma HCO3-

30% carbamino hemoglobin

10% dissolved CO2

CA = carbonic anhydrase

H2O + CO2 H2CO3

fig 13-31a

CO2 from pulmonary blood  alveolus

CO2 transport:

60% plasma HCO3-

30% carbamino hemoglobin

10% dissolved CO2

CA = carbonic anhydrase

H2O + CO2 H2CO3

fig 13-31b

Hemoglobin as a buffer

Notes on next slide

fig 13-32

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)

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

Control of ventilation (chemoreceptors)

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

fig 13-33

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)

Control of ventilation ( arterial P.O2)

fig 13-35

Control of ventilation ( P.CO2)

Acts on central & peripheral chemoreceptors

central chemoreceptors are the most important regulators of ventilation

acts via  [H+] (pH)

note sensitivity

fig 13-36

Control of ventilation ( P.CO2)

fig 13-37

Control of ventilation ( pH)

fig 13-38

 P.CO2 acts via  pH, but this is  pH from other sources (e.g. lactic acid)

Control of ventilation ( pH)

fig 13-39

Increased ventilation & exercise

You would think that exercise  AVR by  CO2,  O2, or  pH


fig 13-41

Increased ventilation & exercise; possible mechanisms

fig 13-43


axon collaterals from descending tracts to respiratory centers

feedback from joints & muscles

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