OS 213: Circulation and Respiration

LEC 03: REVIEW OF NORMAL STRUCTURE AND

FUNCTION OF THE LUNG:
ALTERATIONS IN
RESPIRATORY FUNCTION
Exam 1 | Dr. Abundio A. Balgos| August 13, 2012
OUTLINE:
I. Objectives
II. Important Physiologic Concepts to Recall
III.Important Things to Recall
A. Alveoli: The Egg
B. Airways: The Pipes
C. Mucociliary Elements: The Broom
D. Lymphatics: The Dust Pan
E. Lung Recoil: The Nylon Stockings
F. Surfactant: The Soap
G. Lung Mechanics: The Balloon
IV. Approach to Lung Disease
A. Problem-oriented approach
B. Normal breath sounds
C. Other Respiratory symptoms

Disclaimer: The focus of Dr. Balgos lecture are the topics

under the second heading. There were some information
omitted from the previous trans because they werent
discussed. However, we retained some parts that were
not discussed and just placed them in boxes.

o Clara cells: cuboidal, non-ciliated

2. Transitional and Respiratory zone
Gas exchange: no more muscularis layer, only simple
epithelium adjacent to rich vascular bed
Respiratory bronchioles Alveolar ducts Alveolar
sacs
Generations from trachea to alveoli may vary from 1027
Question: At which boundary do many changes
occur?
bronchioles:
from
pseudostratified
Terminal
columnar ciliated epithelium, it gradually turns to
cuboidal then to squamous. It also loses its linings
and submucosal serous glands. At this level, gas

OBJECTIVES
1. Review important concepts in pulmonary physiology and
pathophysiology
2. Review chest/lung P.E. findings as they relate to natural
history of pulmonary diseases
3. Integrate knowledge of structure and function into physical
diagnosis and history taking

IMPORTANT PHYSIOLOGIC CONCEPTS TO RECALL

Mucociliary clearance, cough, and other defense
mechanisms
Where is airway resistance highest?
Ventilation/perfusion matching and its effect on gas
exchange
Equal pressure point (important for emphysematous
patients)
Effect of lung volume on ventilation and perfusion

The
The
The
The
The
The
The

IMPORTANT BASIC THINGS TO RECALL

egg (Alveolus)
pipes (Airways)
broom (Mucociliary Elements)
dust pan (Lymphatics)
nylon stockings (Lung Recoil)
soap (Surfactant)
balloon and syringe (Lung Mechanics)

Alveoli: The Egg

Alveoli have a wider total surface than the skin (as
wide as a tennis court: >120 m2)
Sunny side up arrangement of cells to increase
surface area

Figure 1. Transition from trachea to alveolar sac.

Dr Balgos: 0 to 16th gen conducting zone. Try to
remember the terminal bronchiole: beyond the terminal
bronchiole gas exchange already happens. The
epithelium also changes because lung has to promote
gas exchange.

Type 1 for gas exchange (recall: sunny side up

analogy)
Type 2 for surfactant production
Type 3 absorb excess fluid (similar to Clara cells)

Airways: The Pipes

1. Conducting Zone
No gas exchange
Consists of anatomic dead space (air that remains in
the respiratory tract but is not involved in gas
exchange);
~ 1st 16 generations of bronchioles
Trachea bronchi bronchioles terminal
bronchioles
Trachea cartilaginous rings
Bronchi cartilaginous plates
Bronchioles no cartilaginous support
Also, at the terminal bronchiole:
o No more goblet cells
o No more cilia a.k.a. The Broom

KING KUA LACUATA

Figure 2. L-R Comparison of bronchus, bronchioles and

alveolus

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We can then view the airways of the
lung as an inverted funnel with
the trachea as the neck of the
funnel. Because the total crosssectional area of conducting airways
INCREASES dramatically as we
move from the trachea to the
respiratory zone, there is less
resistance in the distal airways
compared to the larger airways.

3. Ventilation
Dynamics of Breathing (Airflow)
o Laminar - linear, found in small airways, relatively
quiet airflow
o Turbulent - characterized by eddy currents; found in
large airways and at bifurcations; breath sounds are
low-pitched and harsh

Figure 4. Inverted Funnel Analogy

Question:
What causes turbulence?
Very fast flow and bifurcation; related to

increasing resistance
In Large Airways: Turbulent flow
In Smaller Airways: Laminar Flow
Therefore, resistance is higher in larger
airways.
Small airways have greater total surface area
than large airways thus, airways resistance is
smaller.

Figure 3. Laminar vs. Turbulent Flow

Airway Resistance Relationships:
o Diameter of the tube - INVERSE (increase in
diameter, lower resistance)
o Length of the tube- DIRECT (increase in length,
increase in resistance)
o Flow- DIRECT (faster flow, more resistance)
o Theoretically, the smaller and longer the airway,
the higher the resistance to airflow; however, the
smaller airways (<2mm in diameter) in the lungs
have
a
parallel
configuration
(pinhead/tubal
configuration).
o This gives them a larger total cross sectional area
and thus lower air resistance than the larger airways
(central airway).

In summary, resistance is higher in larger airways

Dr. B: because youre dealing with tubes in parallel.

Airway resistance affected by volume of lung. When you
inhale, airway diameters get bigger = resistance goes
down.
4. Perfusion
Process by which deoxygenated blood passes through
the lungs and becomes reoxygenated (pulmonary
circulation)
Pulmonary Circulation
o Low Pressure
o High Capacitance
Implication: need to give very high doses of CCB to
bring down pulmonary HPN
o Low Resistance
o Dr B: High compliance - it can easily dilate because
the blood vessels here are thinner (less muscularis
mucosa)
Lung Circulation
o Bronchial
o Pulmonary
Primarily for gas exchange

Figure 5. Vascular Pressures in Systemic and Pulmonary

Circulation. Alveolar PO2 is greater than venous PO2 and
this provides a gradient for the movement of O2 into the
blood; mixed venous PCO2 is greater than alveolar PCO2

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LEC 03: REVIEW OF NORMAL LUNG STRUCTURE AND FUNCTION: ALTERATIONS IN

RESPIRATORY FUNCTION

and this provides the gradient for the movement of CO2

into the alveolus.

are already maximally open. Ventilation is higher at the

base bec of hydrostatic pressure and gravity.

Ventilation-Perfusion Ratio
o V/Q ratio - ratio of ventilation to blood flow
o Can be defined for a single alveolus, a group of
alveoli, or for the entire lung
o In normal resting individuals, alveolar ventilation and
blood flow are each distributed uniformly to the gasexchanging units, and the alveolar ventilation is
slightly less than the pulmonary blood flow.

Questions:
Alveoli are largest at what level of the lungs at
resting?
At apex; due to hydrostatic pressure

What causes the kind of blood flow distribution in

the lungs (greater blood flow at base, less at
apex)?
Because of gravity and because we

walk upright.The hydrostatic pressure

Alveolar ventilation 4.0 L/min

Pulmonary blood flow 5.0 L/min
Overall V/Q ratio 0.8

o V/Q > 1 ventilation exceeds perfusion

o V/Q < 1 perfusion exceeds ventilation
o In individuals with cardiopulmonary disease,
mismatching of pulmonary blood flow and
alveolar ventilation is the most frequent cause
of systemic arterial hypoxemia.
o Because gravity evokes regional differences in
ventilation and perfusion, even in the normal lung,
V/Q ratio in different areas of the lung is greater than
or less than the normal value of about 0.8.
o Upright Subject
Ventilation and blood flow measured sequentially from
the top to the bottom of the lung
Apex V/Q high
Base V/Q low

o A normal V/Q ratio does not mean that ventilation

and perfusion to that lung unit are normal; it simply
means that the relationship between ventilation and
perfusion is normal.
Lobar Pneumonia
Ventilation to affected lobe is decreased
If perfusion remains unchanged, then it will exceed
ventilation (V/Q < 1)
Decreased ventilation hypoxic vasoconstriction
in pulmonary bed supplying the affected lobe
Decrease in perfusion normal V/Q

Summary
o Blood flow increased at base due to gravity
o Ventilation increased at base despite having
larger alveoli at apex since as we could recall from
the graph, alveoli in the base exhibit a greater
change in diameter than those in the apex
o V/Q is increasing because blood flow >
ventilation. In the equation, Q (perfusion) is in the
denominator, thus plot is increasing

Figure 6. V/Q Ratio

Dr B: Theres also an increase in ventilation, but blood
flow increase is higher so V/Q decreases as you go from
apex to the base.
Lung compliance curve is sigmoidal. (compliance
curve) alveoli in bases when you expand have a bigger
increase in size, compare to alveoli in apex, where they

KING KUA LACUATA

Ventilation-Perfusion Mismatch (not discussed)

o Most common cause of hypoxemia
o V/Q < 1 decreased ventilation
o V/Q > 1 increased ventilation
Alveoli will have higher PO2 and lower PCO2
Arterial PO2 and PCO2 will vary depending on the relative
contribution of the alveolar unit to the blood
Relative over-ventilation of one unit does not compensate
for the under-ventilation of another
Increased ventilation raises only PO2 but adds little to
the PO2 of the arterial blood

Oxygen Transport
o Oxygen Carriage and Hemoglobin

A hemoglobin molecule is composed of four protein

globin chains (2 alpha and 2 beta), each centered around
a heme group
O2 combines loosely and reversibly with the heme portion
of the hemoglobin. Hemoglobins affinity for O 2 increases
as successive molecules of O2 bind

Oxygen-Hemoglobin Dissociation Curve (these

factors were not discussed)
o The upper flat portion of the curve allows Hb
saturation to remain relatively constant during
considerable changes in PO2
o At low PO2 levels, where the curve is steep, small
changes in PO2 result in marked changes in
saturation. Increased PCO2, lowered pH, and
increased temperature shift the curve to the
right and facilitate release of O2 to tissues
o Opposite changes in PCO2, pH, and temperature
shift curve to the left
o Usually, the critical PO2 that needs to be maintained
is at least 60 mmHg, because this is the pressure
where the plateau begins. No significant increase in
O2 saturation occurs even after increasing O2
concentration

Figure 7. Dissociation Curve

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LEC 03: REVIEW OF NORMAL LUNG STRUCTURE AND FUNCTION: ALTERATIONS IN

RESPIRATORY FUNCTION
Questions:
Why is the dissociation curve sigmoidal?
Because when one O2 atom is attached,

the other subunits uncoil, making it

easier to bind to the next O2 atom (steep
part). Once all molecules of Hb are
occupied, the curve plateaus.
What factors change affinity of O2 to Hemoglobin?
pH, PCO2, temperature

5. Control of Respiration (not discussed)

Regulation of gas exchange is possible because the
level of ventilation is so carefully controlled
3 basic elements of the control system
o Sensors

Anything that affects the ratio of the two layers (e.g.,

infection or asthma) would affect ciliary movement
o Too much serous secretion (thick sol layer)
prevents tip of cilium from reaching the gel layer,
impairing mucociliary escalation
o Treatment is geared toward equalizing the ratio
between the two layers
o Dr. B: there is no mucociliary clearance once you
reach terminal bronchioles
One stick of cigarette paralyses the cilia for 24 hours
o Smokers cough is due to chronic paralysis of the
cilia and overproduction of mucous (sol layer
where cilia can move is overwhelmed by the
thickening gel layer)

Chemoreceptors, lung receptors, etc.

Gather information and feed it to the central controller

o Central controller

In the brain (Pons, medulla, etc.)

Coordinates the information and in turn, sends impulses
to the effectors

o Effectors

Respiratory muscles which cause ventilation

Figure 9. Cells of the large airways: brush, goblet,

ciliated, undifferentiated
Table 1. Quick Reference to Differentiate Gel and Sol
Layers
Ge Uppe Mucou Mucoi Goblet
l
r
s
d
Cell
Sol Lowe
Serou
Water Serous
r
s
y
Cell
2. Smaller Airways

Figure 8. Regulation of Gas Exchange

Mucociliary Elements: The Broom
1. Large Airways
Mucociliary escalation: has a mucociliary layer
which functions as a secondary defense by bringing
trapped particles in the airways up the trachea to be
expectorated/swallowed
Dr B : This is the most important defense
mechanism. Next to this is cough.
The mucous lining of the airways is composed of two
physically and morphologically distinct layers:
o GEL LAYER (mucoid) above - traps foreign
particles (for movement up the trachea)
o SOL LAYER (serous) below - allows cilia to move
freely at the bottom
Cilia moves unidirectionally due to neurohumoral
communication
o Power stroke / upstroke: tip of cilium touches
the gel layer
o Relaxation stroke: cilium rotates downwards
back to sol layer(recovery phase)
o Dr. B: When you have a lot of mucoid secretion:
the cilia will not be able to move well. The
escalator system only happens because of the
alternating system bet the two strokes. If at all
parts, the gel layer is always touched, atrasabante ung movement.

KING KUA LACUATA

The interstitium between respiratory bronchioles and

capillaries serves as blood-air barriers
It also has membrane pump mechanism similar to
that of the G.I. tract (Na-K-ATPase)
Supported by collagen and elastic fibers (to prevent
collapse since there is no smooth muscle and
cartilaginous support)
Lymphatics: The Dust Pan
Important in the balance of fluid and in the spread
of cancer
In general, the lymphatics on the R side re-enter the
systemic circulation through the R subclavian vein
Pulmonary lymphatics on the L side return to the
systemic circulation through the thoracic duct or by
directly emptying into the subclavian vein
However, recent findings claim that the R
supracervical node/right scalene node (sentinel
nodes Dr B:they are often the ones enlarged.
thats why in pe, you have to palpate this ) also drains
the L lobe and the R upper lobe and there is cross
linking between the R and L lymphatic system, making
it possible for cancer to spread from R to L lung and
vice versa
Knowledge of this comes handy when dealing with
patients having vena caval syndromes and tumor
obstructions

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LEC 03: REVIEW OF NORMAL LUNG STRUCTURE AND FUNCTION: ALTERATIONS IN

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Lymphatics
- Used in determining malignancy (i.e. grading)
- Sentinel Node: usually the right supraclavicular node
(for both lungs)
Human gas exchange is not the most efficient. (Birds have
the most efficient gas exchange.)

Lung Recoil: The Nylon Stockings

1. Elasticity
Nylon is strong but not elastic. What do you do to
make it elastic? You weave them together.
Recall the nylon stocking model. The lung fibers form
a sort of syncytium. If you tug at one part of the
lung, you also tug at the other parts.
Alveolar interdependence- implies that no single
alveolus can change in dimension without affecting
others
Destruction of the elastic fibers (e.g. in smoking,
infection, emphysema) impairs the ability of the
lungs to recoil. (analogy: a run in the stockings)
for the lung to preserve its elastic property: Elastic
fibers are interspersed with the capillaries. When
lungs are expanded, elastic fibers can impinge on
these capillaries, resulting in increased alveolar size,
increased alveolar volume, and increased pulmonary
resistance.
2. Forces that Expand versus Forces that Collapse
The rib cage of the chest has both (+) and (-) effects
on the lungs in terms of pressure. This is dependent
on position.
The resting position of the lungs pertains to the
functional residual capacity (FRC). It is at this
point that the forces that expand and collapse the
lungs are equal and balance each other out

Figure 11. Effect of surfactant in stabilizing lungs

Remember the Law of Laplace: P = 2T/r, wherein P is
the pressure inside the alveoli, T is the surface tension
and r is the radius of the alveoli. The pressure in an
alveolus due to surface tension is inversely proportional
to the radius.
Therefore, the smaller the radius, the greater is the
pressure inside the alveolus, hence the greater the need
for surfactant.
Smaller diameter, higher surface tension. Dr B: by age
10, you have 100-200 alveoli; by age 20, you have 300M
alveoli. After this: downhill damage from smoking,
pollution. Each of these have varying size. Smaller
alveoli collapse first, and air will go to the larger
alveoli.Surfactants have a greater effect in smaller
alveoli because of bipolar molecules. If you increase the
size of the alveoli, molecules become separated more
and the repelling effect is less. What happens if you lose
surfactants? (e.g. in ARDS.) Microatelectasis (collapse of
airways) occurs and you have a big problem with gas
exchange.
Dr. B: Surfactant is continuously produced by type 2
cells, stored in lamellar bodies, and released when
needed. But if there is a pathology in type 2 cells, there
is no immediate replenishment of surfactants. Tx:
artificial surfactants.

Figure 10. Forces during Quiet Breathing

Surfactant: The Soap
Detergent that acts to decrease surface tension to
prevent alveolar collapse
Mixture of phospholipids, neutral lipids, fatty acids,
and proteins
Major phospholipid: phosphatidylcholine, 75% of which
is present as dipalmitoylphosphatidylcholine
(DPPC)
Stored in lamellar bodies
Greater amounts in smaller alveoli
In premature babies: Type II pneumocytes have not
yet developed, leading to neonatal respiratory distress
syndrome
Surfactant has both charged and uncharged ends
(polar molecule) so it acts as a stabilizer on alveolar
surface

KING KUA LACUATA

Figure 12. Effect of surfactant on lung mechanics.

Volume-pressure curves of lungs filed with saline and
with air. Difference between inflation and deflation curve
(hysteresis) is not present in the saline case because
there is no surface tension. Inflection point: the point
of sudden increase in volume per unit pressure which is
important in monitoring patients in ventilators

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o Abdominals (rectus abdominis, external oblique,
internal oblique, transversus abdominis) depress
lower ribs and compress abdominal contents thus
pushing up diaphragm

Role of surfactants
Principle of water tension (Imagine a RAINDROP)
- When water forms a surface with air, the water molecules
on the surface of water have an extra strong attraction for
one another. As a result, the water surface is always
attempting to contract this is what holds raindrops
together
Alveolar surface tension
- The water surface on the inner surface of the alveoli also
attempts to contract
- This attempts to force the air out of the alveoli through the
bronchi, and in doing so, it causes the alveoli (and other air
spaces in the lungs) to collapse
Surfactant and its effect on surface tension
- Surfactant is a surface active agent, which means that when
it spreads over the surface of a fluid, it greatly reduces the
surface tension
- They do not dissolve in the fluid, instead they spread over
its surface because one portion of each phospholipid
molecule is hydrophilic and it is attracted to the water lining
the alveoli, whereas the lipid portion of the molecule is

Figure 14. Expiration

Dr B: Beyond terminal bronchiole, no
cartilaginous support, airways can collapse
during forced expiration.

Lung Mechanics: The Balloon

1. Inspiration
an active process brought about by the contraction
of the diaphragm, which adds to the (-) pressure in
the lungs by increasing the volume of the thoracic
cavity. (balloon-syringe plunger analogy)
Muscles of Inspiration
o Diaphragm is the main muscle for inspiration.
o The external intercostals elevate the ribs thus
increasing width of thoracic cavity
o The interchondral part of internal intercostals
also elevate the ribs
o Accessory muscles: SCM elevates the sternum;
scalenes elevate and fix upper ribs

3.

Equal Pressure Point

point where the pleural pressure is equal to the

airway pressure
o no matter how hard one blows, there wont be
any increase in pressure and flow
In the normal lung, this point occurs at the part
where the airway still has cartilaginous support
to prevent it from collapsing.
Important for patients with emphysema, where the
EPP moves to the higher pressure areas (upstream or
towards the alveoli) causing an increase in extra
alveolar areas. Since airways upstream would no
longer have cartilage to support them, they would
collapse because pleural pressure is already higher
than intra-airway pressure.
(not discussed) The location of EPP is dependent
on Palv-Ppl difference, that is, on the lung recoil
pressure. The lower the recoil, the more peripheral
(upstream) is the EPP. Patients with emphysema
have poor lung recoil.
(not discussed) These patients experience no
problems during inspiration but have difficulty in
expiration. They compensate as thin-puffers by
breathing out using the resistance of their pursed
lips, creating an internal airway splint

Figure 13. Inspiration

Recall: Boyles Law
When the temperature of a gas is held constant,
the pressure it exerts is inversely proportional to its
volume.
The intra-thoracic volume increases with
movement of the inspiratory muscles. Following
Boyles Law, with chest expansion, a negative pleural
(suction) pressure is consequently generated pulling

Dr B: One of the key things you have to

remember is that there must be an intact
thorax.
2. Expiration

a passive process brought about by the relaxation

of the inspiratory muscles and recoil of the elastic
chest wall. These decrease the volume of the
thoracic cavity, hence increasing the pressure.
The positive pressure causes air to move out.
Muscles of Expiration
o Internal Intercostals

KING KUA LACUATA

Figure 15. Normal EPP

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Figure 18: Stages and corresponding symptoms of

Pneumonia.

Figure 16. Abnormal EPP

APPROACH TO LUNG DISEASE
Problem-oriented Approach

Figure 17. Problem-oriented approach to evaluating

lung diseases.
Importance of Understanding Natural History of
Disease
o Symptoms often non-specific
o Symptoms and times may vary over time
o PE findings may also be non-specific
o PE findings may also change as disease progresses
Sample Diseases and varied symptoms
1.
Symptoms of Acute Hypoxia
o Neurologic: headache, mental confusion, anxiety,
agitation,
impaired
judgment,
emotional
excitement, depression, drowsiness
o Cardiovascular:
tachycardia,
hypertension,
arrhythmias
o Respiratory: tachypnea, dyspnea
2.
Symptoms of Fibrosis
o Dyspnea
o Dry, Irritating, and Persistent Cough
o Substernal Discomfort
o Anorexia
o Weight Loss
o Arthralgia
o And High index of Suspicion!!!
3.
Natural History of Pneumonia in Relation to
History and PE Findings

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Dr. B: fremitus solidification of lobe transmission of

sound increased; hepatization maraming plema,
maraming crackles
4.
Natural History of Lung Malignancy in
Relation to History and PE Findings

Dr. B: Ronchi: low pitched obstruction involves larger

airway;
Wheeze: very severe obstruction

1.
2.
3.

Figure 19. Symptoms and corresponding symptoms of

Lung Malignancy.
Dr. B: Wala masyadong pain receptor sa lung. Unless
naginvade na sa mediastina, pleura, chest wall, walang
symptoms. Depending on stage, you have to make use
of all info from hx pe to come up with good dx
5.

Natural History of COPD

4.
5.
6.

Other Respiratory Symptoms

Sputum Production
Hemoptysis: Dr B - Black or red sputum
Chest Pain: Dr. B - Pain receptors are only found
in pleura, chest wall and mediastinal structures.
Even if you prick the lung itself, there is no pain.
You will feel pain when you STRETCH it. The
moment there is pain, you should think pleural,
thoracic wall or mediastinal involvement.
Wheezing
Hoarseness and Snoring
Non-specific Symptoms: anorexia, weight loss,
bone pain
Dr B: increase in volume and viscosity of mucus:
major manifestation of lung disease
END OF TRANSCRIPTION

Figure 20. The COPD Escalator.

Normal Breath Sounds

Figure 21. Normal Breath Sounds (not discussed)

Figure 22. Classification of Adventitious Breath Sounds.

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