The Bronchopulmonary Segments

Lung Anatomy and Physiology

Cardinal function: exchange of gases between

inspired air and blood.

Three lobes on the right, two lobes on the left.

Right main stem bronchus is more vertical and

more directly in line with the trachea
Aspirated foreign materials tend
-

to enter the right lung more than

-

the left.
-

Bronchioles – Progressive branching of the

bronchi. Distinguished from bronchi by lack of -

cartilage and submucosal glands within their

=
walls.

Terminal Bronchioles – further branching of

bronchioles <2mm

Acinus – part of the lung distal to the terminal

bronchiole. An acinus is composed of:
- Respiratory bronchioles – gives

off several alveoli from their

sides
Alveolar ducts
=
Alveolar sacs- blind ends of the
respiratory passages.

Alveoli – Site of gas exchange. Walls are

formed entirely of alveoli

Pulmonary lobule – Cluster of 3-5 terminal

bronchioles, each with its appended acinus.

Entire respiratory tree is lined by

* pseudostratified, tall, columnar, ciliated

[ epithelial cells.
because of arrangement of nuclei

what a ocdudens : tight junctions

passive diffusion by
•

: restriction of
intercellular space
blocking lateral
of cellular Functions
:
polarization
( ione water transport) between
apical & basolateral membranes
*
20 hula adherens
→
Macula densa : des mo some Firmalino
Microscopic structure of the alveolar walls GROSS & SUBGROSS CHARACTERISTICS
consists of the ff:

1. Capillary endothelium •Weight: 900-1000g

Lining the intertwining network –40-50% blood
of anastomosing capillaries.
•Gas volume:
2. Basement membrane and surrounding –end expiration: 2.5L
interstitial tissue
–Max inspiration: 6L
Thin portions of alveolar
septum – basement membranes •Density: (not uniform)

I
of epithelium and endothelium –Near hilum: 1g/ml
are fused.
–Peripheral: 0.1g/ml
Thick portions – separated by
•Blood vessels:
interstitial space (pulmonary
–More distended at base
interstitium)
–Increasing vascular distending
3. Alveolar epithelium – continuous layer of: pressure-1cmH20/cm
- height down the
Type I pneumocytes – flattened, lung
platelike covering 95% of * * FRC : O 30 glml to 0.1401mL @ TLC
.

alveolar surface Interstitial connective tissue compartments (CT):

Type II pneumocytes – rounded
cells that synthesize surfactant -Parenchymal (alveolar) interstitium
contained in an osmiophilic
-Loose-binding connective tissue (extra-
lamellar bodies
alveolar)
- Peribronchovascular sheath
4. Alveolar macrophages
Derived from blood monocytes Interlobular septa
and loosely attached to the
epithelial cells or lying free
= Visceral pleura elastin & retailin ) Form
within the alveolar spaces. * connective tissue fibrils C collagen ,

alveoli airways
basket like structure around the
&
a 3d -

Alveolar walls are perforated by

numerous Pores of Kohn *Bulk of interstitium: ground substance or
o Permit the passage of matrix of glycosaminoglycans
bacteria and exudate
between adjacent
alveoli

more @ Apex so as vascularity

ALVEOLI : ,

: PNEUMOTHORAX ,
more prone @ apex
emphysema
-

↳ develops subcutaneous
-

↳ usually felt as crepitations

 2. ORAL CAVITY
UPPER AIRWAYS
-
smooth muscle tone in large airway$ maintain partial Accessory airway passage
constriction
- MAIN PURPOSE OF THE UPPER AIRWAY o Warms incoming air
– Conduction of gases, no gas exchange occurs, o Saliva wets & provides moisture for
found the majority of the dead space inhaled air
o Tongue

1. NASAL CAVITY

o Gateway to the respiratory system reflex)

o Oral cavity sometimes become mouth
o Alae (rubbery entry ways)
breathers. Although there is a common
o Vestibules (space on each side) pathway in the oral cavity & in the nose
o Conchae (bony plates on each side of o It also humidifies mainly because of
vestibule) saliva
o Nasal septum (divides nasal cavity, o LARYNX – main organ for phonation
extends posteriorly)
o TONGUE – Will also prevent
o Warm & humidify air (moisture comes
aspiration
from mucus produced by submucosal
glands & goblet cells)
3. PHARYNX
- ALAR FLARING – one of the earliest signs that
o Space behind nasal cavity & mouth
the baby is having respiratory distress
o Extends where the larynx & esophagus
- May also trap airway molecules
separate

swallowing)
MUCOSAL LINING:
swallowing)
o Squamous mucosa
When the nasopharynx does not close, some of the
food particles will go to the trachea or the airway.
Sometimes when the patient is swallowing, the
nasopharynx is still open, that’s the time the
Squamous mucosa because it is usually found in patient may manifest with incessant coughing
the skin until the food particles is expelled out of the lungs
unless the food particles are large.
o Tall columnar ciliated epithelium

4. EPIGLOTTIS

o Extends from the base of the tongue

o 2-4cm long, 0.2-0.5cm thick
o Flap valve over the entry to the larynx

with other NM reflexes

 -up o It is a part of the conducting
o Part of the lungs before the vocal airways, still no gas exchange
chords occurs at this area
o Also a guard against aspiration o Main upper airway
o Hollow musclular tube,
cartilagenous tube
5. LARYNX

o Sound production
o Protective valve:
Adam’s apple or laryngeal
prominence (midline of
thyroid cartilage)
Vocal cords
Cricoid cartilage
cartilage
hyaline cartilage
The reason why this does not collapse during
inspiration & expiration would be the 16-20 U
shaped cartilages. Usually they become
compliant because of the cartilages. Problem is
they are C shaped cartilages, the protection is at
the front rather than at the posterior.
When we have phlegm, we take deep coughing,
that’s the time the trachea will collapse a little so
you could expel some of the phlegm in your
lungs but it would not collapse totally because of
its C shaped cartilages & it is usually at air filled
strucutre

tracheostomy

aspiration

When you press the adam’s apple the voice

will change because if you press on the
adam’s apple it’s like pressing on the voice Airway Generations
box

ACUTE LARYNGITIS – patient will

manifest hoarseness

5. TRACHEA

o Extends through into the

mediastinum up to the middle 3rd of
sternum
o 2-2.5cm diameter & 11cm long
o 16-20 U shaped cartilages, 0.4-
0.5cm high
o Posterior w/ thin muscle between
the open ends of the U.
o Support yet allows some
variation in diameter during
expiration & coughing
o Air filled structure
Upper (extrapulmonary) airways
Bronchomotor tone: partial constriction
Most airway resistance
Lower (intrapulmonary) airways
Bronchi
Membranous bronchioles
Respiratory bronchioles or gas exchange
ducts or alveolar ducts
Intrapulmonary Airways
Bronchi: Cartilagenous walls
Membranous bronchioles:
Noncartilagenous, 1mm diameter or less
o Numerous but short
o Tightly embedded in CT
framework, therefore enlarge
passively as lung volume
increases
Respiratory bronchioles:
o serve dual function (airway &
gas exchange)
o Do not contribute to anatomic
dead space
The conducting zones:
Total volume: 150 ml
o 50% in URT
o 50% in LRT (up to terminal
bronchioles)
Anatomic dead space 150mL
o Upper (extrapulmonary) &
cartilaginous airways
No gas exchange
Gas flow is thrpugh convection or bulk
flow
From nasal cavity to membranous
brochioles
- Only function is to conduct air
DEAD SPACE – volume or amount of
air that does not participate in the gas
exchange. Majority of the dead space is
found in the conducting airways
- BULK FLOW – pressure volume will
push the air towards the lower part of
the airways.
- There is still dead space when you
reach the alveoli
CELLULAR COMPLEXITY OF THE
AIRWAYS
1. EPITHELIAL CELLS
o Nearly half are ciliated (down to
bronchioles)
o Majority of the epithelial cells are
ciliated up to the part of the bronchioles
-
2. CILIA
o -6 um in length, 0.3 um in width
o Motile cilia is arranged longitudinally,
in microtubular doublets
o Motility rests on sliding movements of
microtubules
o Cilia move the superficial liquid lining
layer towards the pharynx from deep
within (centripetal)
o Disappears in respiratory bronchioles
Main purpose of the cilia is for motility,
mucus extraction. Mainly mucociliary
transport
Only found at the level of the membranous
bronchioles & usually disappear at the level of
respiratory bronchioles
3. APICAL JUNCTIONAL COMPLEXES
o Between airway epithelial cells
o Impt. for metabolically regulated
secretion & absorption of electrolytes &
water from liquid lining
a. Zonula occludens
Restricts diffusion TIGHT JUNCTION
→
Polarizes cellular functions
between apical& baso-lateral
membranes
 b. Zonula adherens
c. Macula adherens : DES MO SOME
Usually to impede & as far as the entry of
metabolically active secretion & absorption of
water & electrolytes from the liquid lining
=That’s why we don’t easily have pulmonary
edema is because of the zonula occludens
(Restricts diffusion of any type of molecule
either air or fluid)
- In patients with pulmonary edema or ARDS in
adults, one of the problem is in the zonula
occludens
4. GLANDS
o Found in submucosa of cartilaginous
bronchi, none in membranous bronchi
o Secretes water, electrolytes & mucin
into lumen
o Release modulated by neurotransmitters,
inflammatory mediators
7. LYMPHOCYTES
o Intercalated between airway epithelial
cells
o Cytotoxic lymphocytes undergo IgA
class antibody response
o T & B cells in lamina propia beneath
airway epithelium ( accumulation )
o BALT- principally B cells, express IgA
o A reminder that lung is in constant
challenge with airborne immunologic
stimuli
- Lymphocytes are for immune function
- Epithelial cells are usually IgA in response
8. SMOOTH MUSCLES CELLS
o Extends as far as respiratory bronchioles
o Tone altered by
o ANS/mediators from effector cells
o Forced expiration & coughing

- Smooth muscle cells are usually affected

- In asthma, Basophils & mast cells, once they are during asthmatic attacks, during
granulated would stimulate the secretion of bronchoconstriction in cases of COPD.
mucus into the lumen. that’s why there is mucus - Tone altered by ANS mediators esp histamine
plugging as well as hyperemia in patients with & serotonin
asthma because of this glands once stimulated by
different neurotransmitters particularly 9. MAST CELLS
histamine & serotonin.
o Release mediators that may affect
5. GOBLET CELLS smooth muscles stimulate mucus
Excessive mucin production & induce mucosal edema by
o Mucin secreting epithelial cells
*

production lead increasing permeability of vessels

to aimMmm
" o Decreases in number peripherally,
normally disappearing in terminal Cellular components that contain inflammatory
bronchioles mediators. They are usually seen but they are not
comp µ µ w protein
that Forms or"
.MU#t :
major component
in human lungs granulated. But in the presence of basophils in
cases of hyperasthma, they can become
6. BASAL CELLS degranulated releasing inflammatory mediators
particularly histamine & serotonin that would
o Along basal lamina of airways stimulate smooth muscle contraction, mucus
o Precursor cells for other epithelial cells secretion. This is why in patients with asthma,
including ciliated cells once you stimulate the mast cells, there is airway
narrowing mainly because of smooth muscle
When some of the epithelial cells are destroyed, contraction that is aggravated by excess mucus
these basal cells will become precursor cells for production
the formation of other epithelial cells or ciliated
cells
 10. CLARA CELLS o Bronchial blood

* source of : o Primary site of xenobiotic metabolism,

surfactant proteins
-
affected by cytochrome P450
( SP A B , D)
monooxygenase system (metabolizes
-

,
-

lipids
carcinogens & toxicants) CLINICAL SIGNIFICANCE OF BRONCHIAL
-

✓
proteins - -

-
glycoproteins o Source of apoproteins assoc. with CIRCULATION
inFlamm mediators
-
surface active materials
*
For fluid balance
o Synthesis, secretion, & storage of lipids Bronchial artery supplies the ff:
and glycoproteins
1. Long standing inflammatory &
o Progenitors of ciliated and new clara
-

proliferative diseases such as carcinoma,

cells ↳ For response to injury
bronchiectasis.
2. Scar tissue
Only important thing that occurs here is the site
- Primary source of new blood vessels
of xenobiotic metabolism. This is where the after lung injury (enormous growth
metabolims of inhaled carcinogens or the inhaled
potential)
drugs or inhaled toxic agents would occur
- Usually feeds carcinoma cells
- It could also be a source of apoproteins which
is also needed in the production of the surfactant
That’s why in cases of carcinoma &
- It could also be a precursor cell or progenitor bronchiectasis, one of the manifestations is
cells of ciliated & new clara cells
hemoptysis. And one of the treatment in
hemoptysis whether carcinoma or
bronchiectasis is BRONCHIAL ARTERY
BRONCHIAL CIRCULATION (SYSTEMIC)
EMBOLIZATION (blockage of bronchial artery)
- BRONCHIAL ARTERY:
of the somatic circulation
system Formed
also part
the bronchial
-

o Branch out from aorta or upper by vessels PULMONARY CIRCULATION

intercostal artery
o 0.5-1.5% of cardiac output Functions:
o Blood supply to:
o Gas exchange
o Capacitance reservoir between the
right & left side of the heart
lungs o Blood filter
Visceral pleura, interlobular o Endothelial cells:
septa =

terminal bronchioles bradykinins & PGE1

- Pulmonary artery & bronchial artery – dual vasoactivity

circulation

- Majority of the nutrients that is delivered in the
lungs is delivered by the BRONCHIAL ARTERY
- VENOUS DRAINAGE:
o Bronchial veins to azygos &
Mainly gas exchange. Oxygen coming from the
alveoli will go to the pulmonary circulation.
Excess carbon dioxide coming from the body
would be in the pulmonary circulation, once in to
the alveoli will go out into the alveoli that’s why
the carbon dioxide is exhaled.
← - Pulmonary artery:
accompany branching
o Enters the lung at the hilum
of the bronchial tree o Travels adjacent to & branches with
each airway generation down to Schematic representation of anatomic
respiratory bronchioles relationship: pleura, diaphragm, mediastinum,
o Pressure varies by about 24cmH2O lung
over the full length of the lung

- Low pressure or resistance circulation (1/10th

of systemic)

- Under normal conditions, blood volume in

pulmonary capillaries is well below its maximal
capacity

- Small pulmonary arteries supplies a specific

volume of respiratory tissue, veins drains
portions of several such zones

- Most blood volume is in the large vessels, all

surface area is in smaller vessels
- Vasoactive regulation plays a role in the local
regulation of blood flow in relation of TERMINAL RESPIRATORY UNIT (TRU)
ventilation
- All alveolar ducts, together with all
- Pulmonary veins follow Miller’s dictum accompanying alveoli that stem from most
↳ forms in the wide mesenchymal septa proximal respiratory bronchiole
↳ lies more at the periphery
- Respond to different drugs - Both anatomic & functional existence
- 100 alveolar ducts & 2000 alveoli
- 5 mm in diameter with a volume of 0.02ml (at
MILLER’S DICTUM FRC)
- Shape is maintained at FRC & TLC, distorted
- Veins are generally found as far away from the at low lung volumes
airways as possible. - 150,000 TRU’s in human lungs
o ACINUS: 10-12 TRU
- Cells of TRU are predominantly capillary
PULMONARY BLOD VESSELS: 2 GROUPS endothelium of pulmonary circulation:
- ALVEOLAR VESSELS o Type I flat alveolar cells
o Within alveolar walls o Type II granular pneumocyte
o Embedded in parenchymal connective o Alveolar macrophages
tissue
o Affected by alveolar pressure
ALVEOLUS
- EXTRA-ALVEOLAR VESSELS
o Lying in loose-binding connective - Complex geometric structure with flat walls
tissue (peribronchovascular sheath, and sharp curvature at the junctions between
interlobular septa) adjacent walls (not spherical)
 -

- Most distal lung unit LONG UNITS & THEIR CONNECTIONS

- Site of gas exchange
o Respiratory bronchioles, alveolar - LOBULES
ducts, alveolar ducts & sacs, and alveoli
o Flow is primarily diffusion starting o Has small veins and outline polygonal
from generation 17-19 units
- Resting volume of alveolus: 10-14% of TLC o 3-8 centrally placed terminal
- Alveolar walls are composed primarily of bronchioles and accompanying arteries
pulmonary capillaries o Blood enters the lobule centrally and
empties on the sides
o Infections, hemorrhage and aspiration
ALVEOLAR EPITHELIUM: THE respect these boundaries
PNEUMOCYTES
- Interconnections:
- TYPE I 1. Pores of Kohn
* Fried egg appearance o 90-95% of alveolar surface area Between alveolar septa
o Large, thin flat cells 5-15 um in diameter
→ PULMO EDEMA
Explains the partially aerated
,

if impaired o Membranous cells

lung tissue beyond a completely
o Fragile and easily injured obstructed bronchus
o Specialized for gas exchange 2. Interlobular fissures
o Incapable of cell division

- In cases of ARDS – type I are destroyed INNERVATION

- Type II – progenitor or precursor cells
- AFFERENT pathways
o Sensory pathway
- TYPE II
o Myelinated stretch (hering-breuer
- attached to neighboring
o Small, cuboidal reflex) & irritant receptors
type 1 cells via tight o Proliferate in cases of injury: ( implements ep ith repair)
junctions under normal
o Most are non-myelinated C fibers
conditions
o Give rise to new type II cells & new (sense parenchymal tissue distortion,
type I congestion and interstitial edema)
o Cell of origin of surfactant o Travel in the vagus nerve and
o Synthetic, secretory, repair factories terminate in vagal nuclei in the medulla
oblongata
- ARDS – hypoxemic patiens (low oxygen) o Respiratory center – mainly found in
because the type I cells are destroyed which is the the pons & medulla oblongata
main function is for gas exchange. They suffer
-

from prolong hypoxemia. The type II is not easily - EFFERENT pathways

converted to type I (it would take a long process). o Motor pathway
Sometimes patients with ARDS will still have
o Reach the lung through sympathetic
hypoxemia even they recover from respiratory
(T1-4/5 ganglia) and parasympathetic
distress
in endocytosis (brainstem motor nuclei associated with
contain multi vesicular bodies involved
: ,

vagus nerve) nervous system

ABC transporter membrane protein
-

it expresses the
-

of the alveolar
o Pain innervation is mostly in the
- major synthesizing a secreting Factor parietal pleura
epith o PHRENIC NERVE ( CB -
05)

- in front of ant scalene muscle

.

runs ant . to root of lung ( whereas vagus ④

runs post . to the root of the lung
LYMPHATIC SYSTEM 3. Scalene muscle-
-Raise the rib cage & sternum during
- Extensive lymphatic system inspiration
- Excess fluid would be drained in the - Active even during quiet breathing
lymphatics
- If the lymphatics are abnormal in cases of 4. Accessory muscles of inspiration
lymphoma, carcinoma, the patient may develop
pulmonary edema (the fluid is not drained from a. sternocleidomastoid d. erector spinae
the alveoli), patient may develop pleural effusion b. trapezius e. serratus
(fluid in the pleura because excess fluid is not c. pectoralis minor
drained by the lymphatics)
–Used during exercise, labored
- Function: breathing
o Liquid homeostasis
o Respiratory defense mechanism
COMPLIANCE OF THE LUNG
It contains different antibodies.
- Two groups: -volume curve
o Superficial plexus
change in pressure
visceral pleura
o Deep plexus
peribronchovascular sheath follows a different curve than deflation
(expiration) -> HYSTERESIS
•In middle range of pressures,
---------------------------------------------------------- compliance is greater, and lungs
are more distensible
RESPIRATORY PHYSIOLOGY •At high expanding pressures,
compliance is lower, and lungs
are less distensible and curve
flattens
MECHANICS OF BREATHING

CAUSES OF INCREASED & DECREASED

MUSCLES OF INSPIRATION LUNG COMPLIANCE

1. Diaphragm Decreased compliance:

–Most important muscle for inspiration
•High expanding pressures
–When diaphragm contracts, the •Increased pulmonary venous pressures
abdominal contents are pushed •Lack of surfactant
downwards, the ribs are lifted upward & •Fibrosis
outward
Increased compliance:
2. External intercostal and accessory muscles •Emphysema
–Not used for inspiration during normal •Aging
quiet breathing
Surface tension of alveoli & surfactant resistance

Surface tension the flow

molecules of liquid lining the alveoli
alveoli have a tendency to collapse
LAPLACE’S LAW
proportional to surface tension &
inversely proportional to alveolar radius
-P=2T/r
•P-collapsing pressure •Airway resistance
or pressure required to
keep alveolus open
(dynes/cm2)
• T-surface tension
(dynes/cm)
• r- radius of the
alveolus (cm)
SURFACTANT
Q= ΔP/R
•Q-airflow (ml/min or
L/min)
•ΔP- pressure gradient
(mmHg or cmH2O)
•R- airway resistance
(cm/H2)/L/sec)
R=8ηl/Πr4
R- resistance
η- viscosity of inspired gas
l-length of the airway
r- radius of airway
resistance & the size (radius) of the
airway

phosphatidyl choline
the alveoli, reduces surface
tension, thus prevents small alveoli from
collapsing & increases compliance

Neonatal respiratory distress syndrome

• Atelectasis during expiration, difficulty

reinflating lungs (dec compliance) ->
hypoxemia (V/Q mismatch)

AIRWAY RESISTANCE

Airflow (Q)

the pressure difference between the

mouth (or nose) & the alveoli.
 Regulation of pulmonary blood flow

Hypoxic vasoconstriction
–Hypoxia causes local vasoconstriction;
this response is opposite of that systemic
circulation
–Physiologically important bec local
vasoconstriction diverts blood away
from poorly ventilated, hypoxic regions
of the lung and toward well-ventilated
region