Far Eastern University - Nicanor Reyes Medical Foundation
Respiratory Physiology
Carlomagno Mendoza, M.D.
RESPIRATORY SYSTEM
FUNCTIONS:
1. Gas Exchange
- movement of O2 inside the body and elimination of CO2 into the
environment
2. Primary Barrier (Host Defense Mechanism)
- secretes immunoglobulins and inflammatory mediators
- serves as the barrier between the outside world and the inside of the
body
3. Metabolic Organ
- Synthesizes and secretes hormones (e.g. Angiotensin)
LUNGS:
- has a volume of approximately 4L (adult), surface area of 85m2 (two
football fields), weighs approximately 1kg
- are composed of independently functioning respiratory units and
demonstrates functional utility;
- each unit is structurally and physiologically identical
- the lung volume is mostly composed of alveolar spaces divided by a
thin tissue called insterstitium which is primarily composed of
collagen fibers, and a potential space for fluid to accumulate.
• Right Lung
- 3 lobes (Upper, Middle, Lower)
- 2 interlobular fissures (Horizontal & Oblique)
• Left Lung
- 2 lobes (Upper & Lower)
- has lingula, which is an area where the heart lies
- 1 interlobular fissure, Oblique
• Pleura - a thin membrane covering the lungs
• Visceral - membrane adherent to the lungs (LOOV)
• Parietal - membrane adherent to the chest wall (LAPAS)
- these pleurae allow smooth gliding of the lungs as it expands in
the chest and produces potential space
Clinical Significance:
- Pneumothorax - condition where air enters between the two pleurae
- Pleural Effusion - condition where fluid enters the space between the two
pleurae
- Empyema - due to severe infection, a collection of pus in the pleural
UPPER RESPIRATORY SYSTEM (Upper Airways)
- it begins from the nose - sinuses -- pharynx --- larynx.
- the major function is to condition the air that enters the respiratory
system; when air reaches the trachea, it is at body temperature &
fully humidified.
I. NOSE
- functions to filter, entrap, and clear the inspired air from particles larger
than 10 um. [thank you, nose hair]
LoisLane , md
- humidifies and moisturizes the air and provides nasal resistance (50%
resistance during quiet breathing
- the Nasal Resistance increases during infections or with increased
airflow such as during exercise. As the nasal resistance increases, mouth
breathing begins
- the interior of the nose is lined by respiratory epithelium interspersed
with secretory cells that produce immunoglobulins, inflammatory
mediators, and interferons
- nasal area is increased by nasal turbinates
- highest resistance in the respiratory tract (different in the airways)
II. PARANASAL SINUSES: Frontal, Sphenoid, Ethmoid, Maxillary
- empty cavities
- lined by ciliated epithelium that facilitates the flow of mucus from the
upper airways
- 3 major functions:
- Lighten the skull
- Voice resonance
- Protection from frontal trauma
Clinical Significance:
In some sinuses, the ostium is on its upper edge such as that the maxillary
sinus, making them susceptible to mucus retention and obstruction
secondary to nasal edema, resulting to secondary infections of sinusitis
III. LARYNX (Epiglottis, Arytenoid Cartilages, Vocal Cords)
- the epiglottis and arytenoids as a hood for the vocal cords. During
swallowing, they cover the vocal cords to prevent aspiration of food or
fluid into the lower airways
Clinical Significance:
There are patients with neuromuscular disorders that have altered muscle
reflexes which result to non-coordination of swallowing and closing of the
epiglottis, resulting to aspiration of food and fluid in the lungs, posing a risk
for pneumonia
- Arytenoids: framework of the larynx
- Vocal cords: responsible for the sound (only) we produce
- Lips, tongue, palate: articulation
- Pharyngeal tonsils (adenoids): fight infection
- Eustachian tubes: aid in equalizing pressure
LOWER RESPIRATORY SYSTEM (Lower Airways)
- below the larynx to the distal alveolus
IV. TRACHEA AND BRONCHI
- bifurcates into 2 main stem bronchi;
- main stem bronchi divides into lobar bronchi;
- lobar bronchi divides into segmental bronchi;
Page 1 of 16
 Far Eastern University - Nicanor Reyes Medical Foundation
Respiratory Physiology
Carlomagno Mendoza, M.D.
- segmental bronchi further divides into bronchioles;
- bronchioles continuously divide in a dichotomous or
asymmetric manner until they form terminal
bronchioles;
- the smallest bronchi without alveoli
As the bronchi divides further, the diameter decreases. However, the total
surface area increases because as they reach smaller diameter, there will
be presence of respiratory bronchioles containing alveoli.
- as the bronchioles continuously divide, they attach to alveoli and
alveolar ducts forming the respiratory unit
- Anatomical unit: Bronchopulmonary Segment / Anatomic Unit
- Physiological unit: Respiratory Unit
- the bronchi which contain cartilage, and the terminal bronchioles in
which cartilage is absent, both lacking alveoli --- serve to move gas from
airways to the alveoli are referred to as conducting airways;
- 150 mL in volume
- do not participate gas exchange
- form anatomic dead space
- the trachea divides 16 times, after the 16th division, it becomes a
respiratory unit, it now contains alveoli and alveolar ducts and is called
respiratory bronchiole;
- largest volume of a lung at 2500 mL and surface area of 70 m2
(specifically alveolar spaces).
V. ALVEOLI
- polygonal, 250 um in diameter.
- physiologic unit of the lung.
- contains Type I and Type II cells that exist in 1:1 ratio
A. Type I Pneumocytes
- occupies 96 - 98% of the surface area.
- has a thin cytoplasm for optimal gas diffusion.
LoisLane , md
- its basement membrane is fused with capillary endothelium
minimizing the distance for gas diffusion, facilitating gas
exchange
B. Type II Pneumocytes
- cuboidal, 2 -4% of the surface area.
- found in the corners of the alveolus.
- synthesize pulmonary surfactant to reduce surface tension in
the alveolus promoting less resistance during respiration.
- can differentiate into Type I cells in certain cases of Type I cell death or
injury.
VI. ALVEOLAR CAPILLARY NETWORK
- a dense mesh like network of alveoli and capillaries where gas
exchange occurs.
- 1 - 2 um thick barrier, composed of thin epithelial cells;
- Type I alveolar epithelial cells
- Capillary endothelial cells
- Back to back basement membranes
- O2 and CO2 passively diffuse across this barrier into plasma and RBC
(single file) in less than 1 second
- this network also regulates the amount of fluid within the lung;
- balance between hydrostatic and oncotic pressure
- fluid removal is facilitated by the lymphatic system
VII. LUNG INTERSTITIUM
- composed of:
- Fibroblasts - secrete collagen and elastin
- Collagen - limits lung distensibility and rigidity
- Elastin - responsible for elastic recoil of the lungs
- Cartilage - supports conducting airways, disappears at bronchioles
- Smooth Muscles
- Kultschitzky Cells - neuroendocrine cells that secrete dopamine
and 5-hydroxytryptamine (Serotonin)
CIRCULATORY SYSTEMS IN THE LUNGS
- accommodates large volumes of blood at low pressure.
I. PULMONARY CIRCULATION (aka Low Pressure Circulation)
- uptake of O2 and removal of CO2
- arteries are 7x more compliant, easily distensible
- vessels are normally in a dilated state and have larger diameter
- very compliant, low resistance
- major functions:
- reoxygenate blood and release CO2
- aid in fluid balance
- distribute metabolic products to and from the lung
Page 2 of 16
 Far Eastern University - Nicanor Reyes Medical Foundation
Respiratory Physiology
Carlomagno Mendoza, M.D.

- the Pulmonary Capillary Bed is the largest vascular bed in the body; • NONADRENERGIC, NONCHOLINERGIC INHIBITORY
- at rest, 70 mL capillary volume - BronchoDILATION
- during exercise, increases from 75 to 200 mL due to recruitment of
INNERVATION OF
• PARASYMPATHETIC
THE LUNGS (from Medulla - Cranial Nerve X / Vagus Nerve)
new capillaries resulting from increased pressure and flow The lungs - BronchoCONSTRICTION
function automatically and under the control of the Accessory Muscles:
Central Nervous System. 1.) STERNOCLEIDOMASTO
- also innervate the bronchial glands, when stimulated,2.)synthesizes
SCALENE MUSCLES
The lung is innervated by the autonomic nervous system,
• PULMONARY MICROCIRCULATION mucus
composed of 4 distinct glycoprotein increasing mucus viscosity
components. 3.) ALAE NASI causes na
A. Extra-alveolar Vessels (arteries, arterioles, veins, and venules) - PARASYMPATHETIC
Neurotransmitters: Accessory muscles do
- not influenced by alveolar pressure changes but are affected by - Bronchoconstriction
Cholinergic - Acetylcholine and substance P (excitatory)
however during strenu
- SYMPATHETIC contract vigorously.
intrapleural and interstitial pressure (primarily lung Nonadrenergic - Dynorphin and Vasoactive Intestinal Peptide (inhibitory)
- Bronchodilation They serve to pull the
volume and lung elastin) - NON-ADRENERGIC, NON-CHOLINERGIC INHIBITORY
- high lung volumes decrease pleural pressure, increasing the - Bronchodilation • NONADRENERGIC NONCHOLINERGIC EXCITATORYDuring Expiration:
caliber of extra-alveolar vessels and vice versa - - BronchoCONSTRICTION
NON-ADRENERGIC, NON-CHOLINERGIC STIMULATORY Normally, expiration is
- Bronchoconstriction It is accomplished whe
B. Alveolar Capillaries CH
- reside within the alveolar septa and are effected by alveolar CENTRAL CONTROL OF RESPIRATION CENTRAL CONTROL OF RESPIRATION
But during forceful
hyperventilation, it be
pressure. Cerebral
is inn
Muscles involved durin
origin
- positive pressure ventilation increases alveolar pressure and
cortex
spinal
Mechano- 1.) ABDOMINAL
Chemo- MUSC The
receptors receptors extern
compresses these capillaries, blocking blood flow Respiratory
2.) INTERNAL INTERCO
and fo
center, medulla an inc
C. Microcirculation The internal intercos
Nerve impulses
of the
origin
intercostals, they pull
- comprises of vessels that participate in liquid and solute Force
Spinal cord level o
muscl
Nerve impulses
exchange in maintenance of fluid balance in the lung.
displacement respira
FLUIDS LINING THE LUNG
Respiratory is why
muscles
(Participates only. Main regulator of fluid is the Alveolar-Capillary can b
There are 3 significant
above
ventila
Network) Lung and chest 1.) Periciliary Fluid
wall
Acc
2.) Mucus which
Ventilation nasi,
3.) Surfactants
- the respiratory center is composed Alveolar-capillary neck a
II. BRONCHIAL CIRULATION The respiratory center is composed of several group of neurons
barrier Howe
when
- O2 for the lung tissue (systemic arterial blood) of several groups of neurons located
located bilaterally in the medulla oblongata and pons of the Perfusion
Diffusion

BloodPericiliary Fluid the rib

sternu
- does not reach the terminal / respiratory bronchioles brainstem.
bilaterally in the medulla oblongata;
PCO2, PO2, pH
It is a 5 µm layer ofcleswa(
remain

- after supplying oxygen and nourishment: Consist of: • Fig. 20.9 Block Diagram of the Respiratory Control System,
theRespiratory
respiratoryControl tract.
muscl
• Dorsal Respiratory Group - dorsal portion, for inspiration
Demonstrating Relationships Between the
and Muscles of Respiration. The respiratory center neurons, muscl
1.) Dorsal Respiratory Group located in the dorsal Center
portion of
- only 1/3 of the blood volume via the bronchial vein, drains to the dispersed into several groups in the medulla,The
• Ventral Respiratory Group - ventral portion, for expiration
the medulla, for inspiration.
levelspontane-
demonstrate
ous cyclic activity but are strongly influenced by stimuli descending
and in
of the perici
Exh
from the cerebral cortex (volitional control)of andthefrom ions, mainlybecom
two sensory by
right atrium to enter the pulmonary circulation • Pneumotaxic Center - supero-dorsal surface of pons, controls the
loops: mechanoreceptor and chemoreceptor pathways. Ventilation
2.) Ventral Respiratory Group located in the ventrolateral
and perfusion occur together near the endacross theandlining
of the cycle, their
most
epithe
abdom
- the other 2/3 of the blood volume via the pulmonary vein, drains to rate and depth of breathing
portion of the medulla, for expiration.
output determines partial pressures of arterial and alveolar carbon
dioxide (PCO2) and oxygen (PO2) and, in part, arterial hydrogen ion
concentration (pH). These outputs feed back to the respiratory center
obliqu
interc
the left atrium directly to the systemic circulation (less oxygenation 3.) Pneumotaxic Center located in the superior part of the
via chemoreceptor and mechanoreceptor
Mucus sensory pathways. muscl
The in
dorsal surface of the pons which controls rate and depth of norma
though) [aka Physiologic shunt] breathing. MUSCLES OF RESPIRATION
Muscles of Respiration Secreted by surface
muscl
interspersed among th
- Skeletal muscles (diaphragm, external intercostals, scalene muscles)
The major muscles of respiration include the diaphragm,
the external intercostal muscles, and the scalene muscles,
trained
that t
Oxygen saturation in the blood never reaches 100%, instead only up to 97% It can either be serous
all of which are skeletal muscles. Skeletal muscles provide impair
provide the driving force for ventilation
MUSCLES OF RESPIRATION the driving force for ventilation; the force of contraction fatigue
due to the less oxygenated blood supplied by the bronchial circulation. During Inspiration: increases when they are stretched and decreases when failure
• INSPIRATION they are shortened. The force ofMUCOCILIARY
muscles increases at larger lung volumes.
contraction of respiratoryCLEARANC
Principal Muscles: Lung
1.) DIAPHRAGM
A. DIAPHRAGM The diaphragm is the major muscleComposed of respiration, and
divides the thoracic cavity from the abdominal cavity (Fig.
ofitthe peric
Agin
INNERVATION OF THE LUNGS - major muscle for respiration that also divides the thoracic and
20.10). Contraction of the diaphragmServe
contents
A thin, dome-shaped muscle, innervated by the phrenic nerve downward and forward. This
forces theto
increases the
remove partic
abdominal
vertical The e
- lungs function automatically under the control of the Central Nervous (C3-C5). abdominal cavity.
dimension of the chest cavity and creates a pressure difference
between the thorax and abdomen. In adults,
Surfactant the diaphragm
primit
fertiliz

System, specifically innervated by the Autonomic Nervous System with 4 - can generate airway pressures of up to 150 to 200 cm H2O
a thin, dome-shaped muscle innervated by the phrenic nerve
During contraction, the diaphragm protrudes into the abdominal
during maximal inspiratory effort. During quiet breathing
Lipid-based substance
into p
3 weet
(tidal breathing), the diaphragm moves approximately 1 cm; dichot
cavity and moves the abdomen outside, creating ahowever, negative
distinct compositions: (C3-C5) the
during deep-breathing maneuvers
diaphragm can move as much as
Secreted
10 cm. The
by type 2Reid
(vital capacity),
diaphragm
pned
bronch
pressure inside the chest.
• SYMPATHETIC - contraction of this muscle forces the abdominal contents Surfactant is 85 90%
It pushes the ribs outward increasing the transverse diameter of
- BroncoDILATION the thorax, allowing thedownward
expansionand forward,
of the
form of Dipalmitoyl Ph
lungs. increasing vertical dimension of the chest
- heavily innervate mucus glands (stimulation leads to increase in cavity = negative pressure inside the chest
Second most abundan
which accounts for 1-1
water secretion) and blood vessels B. EXTERNAL INTERCOSTALS
2.) EXTERNAL INTERCOSTALS
8% of the surfactant is
Neurotransmitters:
-
Muscles that connect adjacent ribs.
connect adjacent ribs together 8% is neutral lipid (i.e.
During contraction, it pulls the rib upward and forward.
Norepinephrine
- innervated by the intercostal nerves (T1-T2)
It causes an increase in both the lateral and antero-posterior
Dopamine - no effect on lungs diameter of the thorax.

LoisLane , md Page 3 of 17 Page 3 of 16

 unchanged.
Far Eastern University - Nicanor Reyes Medical Foundation
Respiratory Physiology
Carlomagno Mendoza, M.D.

- contraction of this muscle pulls the ribs upward and forward, • Surfactant Proteins
increasing lateral and anteroposterior diameters of the thorax 1. SP - A
- hydrophilic
effect on surface tension. Surface tension is a force cau
C. ACCESSORY MUSCLES
1. STERNOCLEIDOMASTOID - secreted by Type II and Clara cells

by water molecules at the air-liquid interface that te

2. SCALENE MUSCLES
3. ALAE NASI - causes nasal fl aring
- required in the formation of tubular myelin;
- tubular myelin is a term used to describe a precursor stage of

to minimize surface area, which makes inflating the lu

- do not contract during normal breathing, however do contract
during vigorous exercise and when airway is obstructed by
surfactant as it is initially secreted
- participates in regulation of surfactant turnover and immune

• EXPIRATION
more difficult. The effect of surface tension on lung in
actively pulling up the ribcage regulation
2. SP - D

tion is illustrated by a comparison of the volume-pres

- exhalation is passive. Only active during exercise and hyperventilation
A. ABDOMINAL MUSCLES (Rectus & Transversus Abdominis,
- hydrophilic
- secreted by Type II and Clara cells
curves of a saline-filled lung and of an air-filled lung. Hi
Internal & External Oblique)
B. INTERNAL INTERCOSTAL MUSCLES
- most important in host defense (induced glucocorticoids and
inflammation) and surfactant reuptake regulation (surfactant

inwards
pressure is necessary to fully inflate the lung with air t
- oppose external intercostals, pulling the ribs downward and pool)
3. SP - B

with saline because of the higher surface tension force

FLUIDS LINING THE LUNG EPITHELIUM
- hydrophobic
- protein clipped from Type II
I. PERCILIARY FLUID
air-filled
- a 5 um layer of water lungs than in saline-filled lungs. Surface tensio
and electrolyte lining the epithelium of the
- rapid absorption and spreading of phospholipids AND formation
of tubular myelin

- maintained by theamovement
measure of the attractive force of the surface molec
respiratory tract 4. SP - C
of the ions, mainly by chloride secretions - hydrophobic
per unit length of material to which they are attached.
and sodium absorption across the lining epithelium
II. MUCUS
- spreading of phospholipids
- develops airway during gestation

- can be either serousunits of surface tension are those of a force applied per
- secreted by surface secretory cells / goblet cells
or mucous in consistency
• Surface Tension
- it is a measure of the attractive force of the surface molecules per unit
III. SURFACTANTS
length. For a sphere (such as an alveolus), the relation
- lipid-based substance that reduces the surface tension in the alveoli,
length of the material to which they are attracted
- water or fluid molecules in the alveoli tend to stick to each other, without
between the pressure within the sphere (P ) and the ten
making it more stable
- secreted by Type II Pneumocytes
any surfactant, they can make the alveoli collapse by adhering to one
another s
- 85 - 95% lipids;
in the wall is described by the law of Laplace:
- predominantly Dipalmitoyl Phospatidyl Choline (DPPC) - aka,
- example of surface tension is raindrops, water molecules in the air
tend to adhere with one another to form water droplets. The force that
Lecithin makes them stick together is surface tension
- 1 - 10%, Phosphatidyl Glycerol
- 8%, neutral lipid (Cholesterol)
Equation 21.7
• Law of Laplace
Where:
- 8% is protein
• Secretion and Clearance
P = 2T r
s
P = Pressure in the sphere
T = Tension
- occurs via exocytosis of the lamellar body by constitutive and regulated r = Radius
mechanisms where T is the wall tension (in dynes per centimeter) a
- numerous agents like β-adrenergic agonists, activators of protein kinase
- ↑ tension = ↑ pressure; ↓tension = ↓ pressure
- ↑ radius = ↓ pressure; ↓ radius = ↑ pressure
is the radius of the sphere.
C, leukotrienes, etc., stimulate the exocytosis of the surfactant
- Major route of clearance is via:
- if lungs have high surface tension, it may collapse, which is prevented by
surfactants
The alveoli are linedPulmonary
- Reuptake of Type II cells
- Absorption of the lymphatic system
with a predominantly
Clinical Significance: lipid-b
Surfactant Deficiency aka Respiratory Distress Syndrome (RDS)
substance called surfactant.
- Clearance by alveolar macrophage Pulmonary
- observed in mostly in premature newborns (<36surfactant
surfactant or non-mature surfactant
weeks) due to lack of se
several physiological roles, including
- In adults, caused by severe lung injury (due (1) reducing
to toxic gas, pneumonia)
Page 4 of 16
LoisLane , md
work of breathing by decreasing surface tension forces
 g e a ici i ca e a d a ce ai e e a d e e Lung Compliance
the chest from over expanding the lungs by recoiling inwards. It is the measure of the elastic properties of the lungs.
Far Eastern University - Nicanor Reyes Medical
The change Foundation
in lung volume resulting from a -1 cm H20 change in
essures in the lungs and chest wall the distending pressure of the lungs.
Respiratory Physiology
The ease of stretching or expanding is compliance, the ability to
Carlomagno Mendoza, M.D.
return back to its original state is elasticity.
MECHANICS OF BREATHING II. Compliance can be illustrated as change in volume over change
Static Lung Mechanics
in pressure.
• Boyle's Law • Lung Compliance [Elastance = measure of elasticity]
- at constant temperature, the volume of gas is inversely proportional to - ease of stretching is compliance, ability V to return back to its original
the pressure state is elasticity C=
P
- as volume decreases, the pressure increases and vice versa Where:
High lung compliance means that the lung
C = Compliance P =isPressure
readily distensible.
Low lung compliance means V = Volumethat the lung is stiff.
- High lung compliance = lung is readily distensible
- Low
Factors lung compliance
affecting = lung is stiff
lung compliance
Where: Factors
1.) •Elastic affecting Lung Compliance
Fibers
P = Pressure The1. presence
Elastic Fibers
of elastin and collagen in the lung interstitium.
V = Volume These- presence
fibers of
are elastin and collagen
interwoven in the interstitium, interwoven
TWO STRUCTURE THREE COMPARTMENT MODEL The graph shows like during inspiration, as ckithegglottis
. opens air flows
The lung is not attached to the chest wall except where Whenit isappearing
stretched like "nylon
they
inside formstockings"
because of the indecrease
polygonal polygonal of structures
structures. the alveolar and pleural
- decreasing the volume provides less space for the gas to move, making
suspended (in the area of mediastinum).
2. Pulmonarypressure. Surfactants
rathoracicthem collide (Pleural
Pressure to each other
pressure) Instead, the lung in the thoracic cavity is surrounded by a thin
and produce
layer ofmore
pleural pressure
fluid which[Law of it lubricated.
keeps
- make the
2.) Pulmonary
During mid-inspiration, the air that enters the lungs will increase
lungs
Surfactants dry andpressure.
the alveolar lessens the surface tension, making it
Entropy]
It is defined as the pressure of the fluid in the pleural space. easier to expand
Separating the lung and the chest is a potential space called
Makes the lungsWhen dry alveolar pressure reaches back to zero, it is now equal
and lessens the surface tension, making it
I. TwoisStructure
It normally negative- Three Compartment
relative
pleural space
to the atmosphericModel
where the pleural fluid is located.
pressure, - make lungs with more dependent
the atmospheric pressure outside hence airflow will stop.
easier to expand.
around - -5thecmlung,
H2when
O. removed, always has a tendency to recoil inwards due
The lung, when removed, always has a tendency to recoil
3. Interdependence of Alveolar Sacs
The muscles will now relax and decrease the volume of the chest
inwards, due to its structure. wall and increase the pleural pressure.
to its structure. The chest wallupontothe-7other hand, ontends to recoil - alveolar sacs are
During inspiration, it falls down The cm H
chest 2O.
wall the other hand tends to recoil outwards.
3.) Interdependence ofpolygonal
AlveolarinSacs shape and are attached to each
outwards The two structures have opposing movements. The chest wallother STATIC LUNG MECHANICS
tends to pull the lungs outward when we inhale. DueAlveolar to -thewhen sacs are polygonal in shape and are attached to each
oneLung
alveolar sac expands, it tends to pull other alveolar
rapulmonic
The two Pressure
structures(Alveolar pressure)
have opposing movements.
g e a ici The chest
i ca wall
e aoutwards
d a during
ce ai e e a d other. e e Compliance
sacs, making the whole
It is the measure lungofeasier to expand
the elastic properties of the lungs.
Definedinhalation. The lung however,
as the pressure inside thedue alveoli.
tothe
it'schest
elasticity can prevent the chest from
from over expanding the lungs by recoiling inwards.
When - ex.one alveolar
balloons The sac
are change
easier toexpands,
blowvolume
in lung
it
midway tends to pull other alveolar
resulting from a -1 cm H20 change in
Beforeoverinspiration,
expanding therefore recoiling
the alveolar inwards
pressure
Pressures is and
in the lungs equal to the
chest wall sacs, making thethewhole lung
distending easier
pressure of to
the expand.
lungs.
• Measurement of Lung Compliance
atmospheric pressure which is 0 cm H2O.
• Intrathoracic Pressure - lung compliance The ease of stretching or expanding is compliance, the ability to
returnisback
a very difficult
to its originalto measure,
state however, it is done
is elasticity.
When the(Pleural
glottis opens, assuming no air enters the airways, the Measurement of Lung Compliance
Pressure) using an intrapleural
Compliancecatheter
can be illustrated as change in volume over change
pressure - in the alveoli and the outside environment is equal
pressure fluid in the pulmonic in pressure.
meaning there is no net airflow.
space C=
V
- normally
The pressure insidenegative
the alveoli needs
(-5 cm H2O) to go lower than 0 cm H2O P
for air to move inside.
relative to Patm High lung compliance means that the lung is readily distensible.
During inspiration, it decreases Low lung compliance means that the lung is stiff.
• Intrapulmonic Pressure to -1 cm H2O, enough to pull
0.5L of air(Alveolar
into the lungs.
Pressure) Factors affecting lung compliance
- pressure inside the alveoli 1.) Elastic Fibers
anspulmonary - pre-inspiration, is = to the Patm
pressure The presence of elastin and collagen in the lung interstitium.
These fibers are interwoven like cki g .
The pressurewhich difference
is 0 cm Hbetween
2O
the pleura and the alveoli.
When stretched they form polygonal structures.
(no airflow) - volume during expiration is greater than inspiration
[extra info]
TP•= Transpulmonary
Alveolar Pressure Pressure
(P a) Intrathoracic Pressure
Pleural Pressure (Pleural
(P ) pressure)
pl of the fluid in the pleural space.Lung - compliance
graph is not linear because
2.) Pulmonary Surfactants
is very whento
difficult volume
measure,is increased,
howeverit is not
it is done
Transthoracic
It is defined as the pressurePressure
- pressure difference between It- normally is negative relative to the atmospheric pressure, using directly
an intrapleuralMakes the lungs dry and lessens the surface tension, making it
proportional to volume
catheter. that goes inside the lungs
pressure difference between chest and easier to expand.
pleura and alveoli around -5 cm H2O.
the atmosphere
- compliance is greater during mid-inspiration, lowest
age 5 of 17 During inspiration, it falls down up to -7 cm H2O.
during beginning and late
3.) Interdependence respiration
of Alveolar Sacs [ballon example]
TP = Alveolar Pressure (Pa) - Pleural Pressure (Ppl) Alveolar sacs are polygonal in shape and are attached to each
Intrapulmonic Pressure (Alveolar pressure) Clinical Significance:
other.
- Inspiration: air flows inside dieDefined to the as decrease of the
the pressure Pa and
inside Ppl
the alveoli. - Emphysema - the lungWhen is more compliant,
one alveolar the lung
sac expands, distends
it tends withother alveolar
to pull
- Mid-inspiration: air inside the Before lungs will increase the
inspiration, Pa alveolar pressure is equalminimal to the
increase in
sacs, making the whole lung easier to expand.
pressure [no longer elastic tho]
- once Pa reaches 0, it is now equal atmospheric pressure which is 0 cm H2O.
to Patm, airflow will stop. Muscles - airways,
Pulmonary
When the glottis opens, assuming no air enters the the FibrosisMeasurement
- the lung isofnon-compliant/less
Lung Compliance compliant (very
will relax and the volume of chest wall in
pressure willthedecrease and the
alveoli and increase
outsidetheenvironmentstiff
is and
equalcannot distend)
Ppl meaning there is no net airflow.
The pressure inside the alveoli needs to go lower than 0 cm H2O
for air to move inside.

LoisLane , md
During inspiration, it decreases to -1 cm H2O, enough to pull
0.5L of air into the lungs.
Page 5 of 16

Transpulmonary pressure
 (Re) is a dimensionless value that expresses the ratio of
Fartwo dimensionally
Eastern equivalent
University - Nicanor termsFoundation
Reyes Medical (kinematic/viscosity),
as seen in theRespiratory
equation:Physiology
Carlomagno Mendoza, M.D.

III. Dynamic Lung Mechanics Equation

• Reynold's Number
22.3
• Patterns of Gas Flow
2rvd Where:
ow A. Laminar
Re = Re = Reynold's Number

η 𝜂 = Diameter
v = Average velocity
rflow
or patterns of gas flow
major patterns of gas flow in
in the
the airways—
airways— - if value is >2000, the flow is turbulent
ulent. Laminar flow where is d is the to
parallel fluid the density, v is the average velocity, r is the
urbulent. Laminar flow is parallel to the Clinical Significance:
d present
- happens during low-pressure and quiet breathing
is present
- parallelatatgaslow
low
flow flow
radius,
flowrates. rates. and
As the Asflow η is
the flow the viscosity.
- Bronchitis - In
bronchiole straight
inflammation, tubes,
decreasing radius in turbulence
airway

theoccurs when thethe the Reynolds numberresulting is greater than 2000.

(increased resistance, decreased airflow)
nd particularly
particularlyB. Transitional as
as the airways airways divide, divide, - Asthma - bronchoconstriction in decrease in radius (increased
comes unsteady and small eddies develop.
mesratesunsteady
the flow stream and small From eddies
is disorganized
this relationship develop. itresistance,
and
candecreased
be seen airflow) that turbulence is most
CHAPTER 22 Dynamic Lung and Chest Wall Mechanics 457

es the flow streamlikely

urs. to occur when
is disorganized and the average
IV. Airway
increases for a given flow. Overall, gas velocity is blunted
Resistancevelocity of the gas flow is

-flow characteristics
- branching points from of highlaminar and
to smaller flow the
airways, there radius
were is large. In contrast, a low-density gas
because energy is consumed in the process of generating
larger are
eddies and chaotic movement. As a consequence, higher .08
driving pressure is needed to support a given turbulent flow
y the French physician Poiseuille and apply
disturbances in the corners
w characteristics
C. Turbulent such
of
and air. In straight circular tubes the flow
laminar as helium flow
than to support a similar laminar flow.
is
were less
Whether flow through a tube is laminar or turbulentlikely to cause turbulent
.06
flow. This
[extra info]
In normal airway resistance,
Resistance (cm H2O/L/sec)
depends on the Reynolds number. The Reynolds number

he
ned French
by the followingphysician isPoiseuille
equation: clinicallyand relevant apply in states of increased airway
(Re) is a dimensionless value that expresses the ratio of
two dimensionally equivalent terms (kinematic/viscosity),
as seen in the equation:
resistance
the least resistance is found
in the terminal bronchioles
d air. Equation
In straight 22.1 circular where atubes the flow
.04

decrease
Equation 22.3
Re =
2rvd in gas density (e.g., substituting - due to thehelium
dispersed
Conducting zone for
Respiratory
zone

by the- happens
following equation:
nitrogen
πr 4 high-pressure
Pduring inactivities
inspired air) can improve airflow.
η
where d is the fluid density, v is the average velocity, r is the
and strenuous
.02 location

- V
! = radius, and η is the viscosity. In straight tubes, turbulence - they work in parallel

Equation
multidirectional
8η122.1
• Pouiseuille's Equation
gas flow
Although these relationships apply well to smooth cylin-
occurs when the Reynolds number is greater than 2000.
From this relationship it can be seen that turbulence is most
likely to occur when the average velocity of the gas flow is
0
0 5 10 15 20

riving pressure, r is4 the radius drical

Where: of tubes,
the tube,applicationη of these principles to a complicated
high and the radius is large. In contrast, a low-density gas Airway generation

P π r
such as helium is less likely to cause turbulent flow. This
• Fig. 22.1
of the fluid, and l is the length
̇ = Flow rateof the tube.
Airway resistance as a function of the airway generation.

! = -
is clinically relevant in states of increased airway resistance
𝜂 = Viscosity the highest resistance is at the segmental bronchi or medium-sized
V system
V
of tubes such as the airways is difficult. As a result,
In a normal lung, most of the resistance to airflow occurs in the first
where a decrease in gas density (e.g., substituting helium for eight airway generations.
nitrogen in inspired air) can improve airflow.
that driving pressure (P) is proportional to airways
8η1 r = Radius the greater
P = Pressure 𝜄 = Length of tubing
Although these relationships apply well to smooth cylin-
- in bronchioles, the airflow velocity decreased substantially and the
V); thus the greater the pressure, much of the flow in the airways
drical tubes, application of these principles to a complicated
system of tubes such as the airways is difficult. As a result, demonstrates characteristics
The smallest airways contribute very little to the overall total
resistance of the bronchial tree (Fig. 22.1). The reason for

ng pressure,
- flow is directly r is theofradius
proportional to the pressure
both of the tube, η
and radius smaller airways work in parallel, rather than in series, that's why they
much of the flow in the airways demonstrates characteristics this is twofold: (1) airflow velocity decreases substantially as

the flow laminar and turbulent flow. In the trachea, for

of both laminar and turbulent flow. In the trachea, for the effective cross-sectional area increases (i.e., flow becomes
- the higher the pressure, the greater
example, even during quiet breathing the Reynolds numbercontribute less to resistance
laminar), and (2) most importantly, the airway branches in

he fluid,
istance -(R) and
across l is
a setthe of length
tubes is of
defined the tube. -
is greater than 2000. Hence turbulent flow occurs in the
the larger the diameter of the radius, the greater the flow during
each generation exist in parallel rather than in series. The
exercise, the highest resistance is at the largest airways
example, even during quiet because of the increased flow ofthe
breathing air, theReynolds number
trachea even during quiet breathing. Turbulence is also pro- resistance of airways in parallel is the inverse of the sum of

n driving
driving pressure
- it is inversely
pressure (ΔP) (P)
proportional divided is
to the viscosity byand the
proportional flow
moted by the glottis and vocal cords, which produce some
length
to
irregularity and obstruction in the airways. As gas flows
the individual resistances; therefore the overall contribu-
flow becomes turbulent
tion to resistance of the small airways is very small. As an

is greater
- the more viscous the fluid, the lesser the flow
than 2000. Hence turbulent flow occurs in the
distally the total cross-sectional area increases dramatically, example, assume that each of three tubes has a resistance
• Factors affecting Airway
and gas velocities decrease significantly. As a result, gas flow of 3 cm H2O. If the tubes are in series, the total resistance
hus the - thegreater
longer the tube,the the lesser pressure, the greater
becomes more laminar in the smaller airways even during
the flow 1. Lung Volume
(Rtot) is the sum of the individual resistances:

22.2 trachea even during quiet breathing. - greater volume meansTurbulence is also pro-
maximal ventilation. Overall the gas flow in the larger
• Equation
Equation 22.4
Resistance airways (nose, mouth, glottis, and bronchi) is turbulent, less resistance
R tot = R 1 + R 2 + R 3 = 3 + 3 + 3 = 9 cm H2O/L ⋅ sec
whereas the gas flow in the smaller airways is laminar.
- expansion of lungs results to the expansion of the alveoli which
∆P 8η1 moted by the glottis and vocal
Breath sounds heard with a stethoscope reflect turbulent
cords, which produce the alveoli aresome
If the tubes are in parallel (as they are in small airways),

nce (R) R = across = a4 set of tubes is defined

airflow. Laminar flow is silent, which is why it is difficult the total resistance is the sum of the inverse of the individual
to “hear” small airway disease with a stethoscope. also causes opening of the
resistances: bronchioles because
!
V πr
iving pressure
- resistance (ΔP) irregularity
is the inverse of flow divided
Airway Resistance
by and
the obstruction
flow 2.
in theRegulation
Neurohumoral
airways. As gas flows
located in between the bronchioles - causing them to open
Equation 22.5
1 R tot = 1 R 1 + 1 R 2 + 1 R 3 = 1 3 + 1 3 + 1 3
sistance are cm H2O/L•sec. This equation
todistally
the viscosity andthe lengthtotal cross-sectional • Sympatheticarea increases dramatically,
Airflow resistance is the second major factor that determines R tot = 1 cm H2 O/L ⋅ sec
- it is directly proportional rates of airflow in the airways. Airflow resistance in the - decreased airway resistance due to bronchodilation
flow and - thedemonstrates that the
more viscous the fluid, the greater the resistance
radius of
airways (Raw) differs in airways of different size. In moving
•
This relationship is in marked contrast to the pulmonary
Paraympathetic - increased airway resistance, decreased anatomic
and gas velocities decrease significantly. As a result, gas flow
from the trachea toward the alveolus, individual airways blood vessels, in which most of the resistance is located in
most important
- the longer thedeterminant of resistance.
become smaller while the number of airway branches
tube, the greater the resistance
the small vessels (see Chapter 23). Thus as airway diameter
dead space due to bronchoconstriction
theEquation 22.2 increases dramatically. Raw is equal to the sum of the resis- decreases, the resistance offered by each individual airway
- it is inversely by becomes
tube is reduced tohalf,
more laminarAsthmainpatients
the resistance theare given
smaller β2 agonists airways even fibers during
tance of each of these airways (i.e., Raw = Rlarge + Rmedium increases, but the large increase in the number of parallel
proportional the radius
+ Rsmall). From Poiseuille’s equation, one might conclude pathways and cross-sectional area reduces the resistance at
- the larger the radius, the lesser the resistance to stimulate sympathetic and
∆ η
that the major site of airway resistance is in the smallest each generation of branching.
-fold. If, however, P 8 1
tube length
maximal
is increased
is 16x greater; ventilation. Overall the gas flow in the larger
airways. In fact, however, the major site of resistance along During normal breathing, approximately 80% of the
result to bronchodilation
istance =willof the
R[effect
radius is !
= only
radius to resistance
increase
the bronchial tree is in the first eight generations of airways.
twofold. Thus the
resistance to airflow at functional residual capacity (FRC)

V
be is the principal determinant π r 4
major determinant
airways
of resistance]
(nose, mouth, glottis, and bronchi) is turbulent,
of resistance.
way, resistance cm is,H inversely whereas proportional theequationtogas flow in the smaller airwaysPage 6 of 16
is laminar.
ance areLoisLane md 2O/L•sec. This
r of the radius, and it is directly proportional
w and demonstrates that the radius of
 Far Eastern University - Nicanor Reyes Medical Foundation
Respiratory Physiology
Carlomagno Mendoza, M.D.
CHAPTER 21 Static Lung and Chest Wall Mechanics 449

V. Lung Volumes and Capacities [Spirometry] RV/TLC Ratio is used to distinguish pulmonary diseases
6
Normal: less than 0.25 (25% air is left inside the lungs)
TLC IRV IC VC
increase in RV is seen in Obstructive Pulmonary Diseases
4 FVC decrease in TLC is seen in Restrictive Pulmonary Diseases
Volume (L)

VT
VI. Work of Breathing
2 ERV - under resting resting conditions, the lungs normally perform work to
1.2
FRC
cause inspiration, but not expiration because it is a passive process
RV - requires:
0 - to overcome the elastic lungs
0 10 20 30 40
Seconds - to overcome tissue resistance
• Fig. 21.3 The Various Lung Volumes and Capacities. ERV, expiratory reserve volume; FRC, functional - to overcome airway resistance
residual capacity; FVC, forced vital capacity; IC, inspiratory capacity; IRV, inspiratory reserve volume; RV,
residual volume; TLC, total lung capacity; VC, vital capacity; VT, tidal volume. Clinical Significance:
• Lung Volumes [* = most important] - Pulmonary Fibrosis - requires increased work to overcome the stiffness of
1. *Tidal Volume (TV) - 500 mL the lung tissues
lay a major role in- thevolume
work of inspired
breathing and expired during
(see Chapter normal and quiet breathing -
All lung volumes are subdivisions of total lung capac-
TABLE
Normal Values (Average White Male Asthma and Bronchiolitis - also require increased work to overcome
Adult)
21.1
2. Inspiratory
TLC), the total volume of air that is Reserve
contained Volumein the (IRV) - 3,200 mL increased resistance and decreased diameter of airways
- extrainspiration.
at the point of maximal volume ofLung air can
Lung Volumes
be inspired beyond tidal volume
volumes
ported in liters either as volumes or as capacities. A Functional residual capacity (FRC) 2.4 L
ity is composed 3.of twoExpiratory
or more volumes.Reserve Many Volume
lung (ERV) - 1,100
Total mL (TLC)
lung capacity 6 L- too much increase in respiratory work load may lead to fatigue and end
mes are measured -with a spirometer. The patient
extra volume of air left after a forceful is Tidal volume (V )
expiration and a tidal
T 0.5 L
as respiratory failure
to first breathe normally into the spirometer, and the Breathing frequency (f) 12/min
expiration
me of air (the tidal volume [VT]) that is moved into Static Mechanics
ut of the lungs with each quiet breath is measured.
4. *Residual Volume
atient then inhales maximally and exhales forcefully
(RV) - 1,200 mL [get
Pleural O2 in(Pb/w
pressure
pl ), mean −5 VII.
cm H Ventilation
2 O
Chest wall compliance (C ) at FRC 0.2 L/cm H O
0.2 -L/cm
w 2
breathings]
ompletely, and the volume of exhaled air is measured. Lung compliance (C ) at FRC
L process
2 H O by which the air moves in and out of the lungs determined by
-
otal volume of exhaled air,
volume
from
of
a
air
maximal
left
o a maximal exhalation, is the vital capacity (VC).in
inspira-
the lungs after a forceful expiration the volume of air that moves inside (the lungs) per minute
ual volume (RV)- is immeasurable
the air remaining in the lungs - 2 zones: [refer to table on page 2]
a complete exhalation. TLC is the sum of VC and IN THE CLINIC
• Capacities
t is the total volume of air[combicontained ofin2 the
or more
lungs atlung volumes] 1. Conducting Airways
1. Total Lung Capacity (TLC)
nd of maximal inspiration, and it includes the volume Pulmonary function tests are often used to diagnose
= TV +in IRV
abnormalities lung + ERV +andRVto assess the progression
function
- from trachea (divides 16 times) to non-respiratory bronchioles
that can be moved (VC) and the volume of air that
- maximum
ays present (trapped) in the lungsvolume that can be contained
(RV). Functional
of lung disease. They can distinguish the two major types
in thepathophysiologic
of pulmonary lung processes: obstructive 2. Respiratory Airways
ual capacity (FRC) is the volume of air in the lungs lung diseases and restrictive lung diseases. For example, -
2. *Vital Capacity (VC) = TV + IRV + ERV
in normal individuals, the ratio of RV to TLC is less than
as soon as there is alveoli, it is now the respiratory zone
end of exhalation during quiet breathing and is also
the resting volume- ofmaximum
the lungs. FRC amount of air that
is composed of can be expelled
0.25. Thus in aafter a
healthy maximal
individual, approximately 25% of the- area of gas exchange
total volume of air in the lung is trapped. In obstructive
nd the expiratory reserve volume (the volume of air
inspiration
an be exhaled from FRC to RV).
[how good your lungs can inflate
pulmonary andandeflate]
diseases, elevation in RV/TLC ratio is
secondary to an increase in RV out of proportion to any
- volume of air from maximal inspiration increasetowards forceful
in TLC. In contrast, in restrictive lung diseases,
the elevation in the RV/TLC ratio is caused by a decrease in
surement of Lung Volumes
expiration TLC.
nd TLC can be measured - affectedin twoby position
ways: (supine or standing), strength of muscles,
by helium END OF PARTS 1 & 2
on and by body plethysmography. Both methods are
clinically and provide valuablelunginformation
compliance, males
about lung(greater In VC),normal
morbid obesity (heavy
individuals, the FRC measured by helium
on and lung disease. The fat helium dilution technique
= struggle in breathing) is dilution and the FRC measured by plethysmography are
der and simpler method, but it is often less accurate the same (Table 21.1). This is not true in individuals with
3. Inspiratory
body plethysmography, which requires Capacity (IC)
sophisticated = TV +
lung disease. IRVFRC measured by helium dilution is the
The
xpensive equipment. - amount that can be maximally inspired volume of gas in the lung that communicates with the

4. Functional Residual Capacity (FRC) = ERV + RV

- amount of air left in the lungs after normal expiration
- aka resting volume of the lungs [volume at rest]
- immeasurable
5. Timed Vital Capacity / Forced Expiratory Volume in 1
Second (FEV 1)
- amount of air expired by forceful expiration in 1 second
- 80 - 85% of VC

LoisLane , md Page 7 of 16
 Far Eastern University - Nicanor Reyes Medical Foundation
Respiratory Physiology
Ronald Allan Cruz, M.D.

TRANSPORT OF GASES • Ideal Gas Law

• Dalton's Law
- PT = P1 + P2 + P3...
- total pressure of gas = to the sum of the partial pressures of the
individual gases that comprises it
• Henry's Law
- Weight of gas absorbed by liquid is directly proportional to pressure
of gas to which the liquid is exposed [more pressure = more dissolved]
• Graham's Law
- Rate of diffusion is directly proportional to solubility coefficient, and
inversely proportional to √molecular weight

- 2 circuits: pulmonic and systemic circuit SOLUBILITY COEFFICIENT

CO2 0.57
I. ANATOMIC AND PHYSIOLOGIC CONSIDERATIONS
• Capillary Surface Area O2 0.024
- Large surface area [tennis court]
- Respiratory membrane-pulmonary capillary: 70m2 N 0.012
[activation of sympathetics will recruit dormant alveoli and can He 0.008
increase surface are to 100 m2]
- Systemic capillary-tissue: 40m2 • Amount of gas that will be dissolved in H2O
- Partial pressure gradients V = PxS Where: P = Pressure
- Diffusion properties of gases - Pressure of the gas V = Amount of gas
• Respiratory Membrane - Solubility coefficient of the gas S = Solubility coefficient
- Fluid, surfactant
- Alveolar epithelium • Fick's Law
- Epithelial basement membrane Where: A = Area
V = [A D(P1 − P 2)]
- Interstitial space [fused] D = Diffusion Constant
- Capillary basement membrane T P1 - P2 = Pressure Gradient
- Capillary endothelial cell • Diffusing Capacity [important in pulmo function; reflects how
• 0.2 - 0.6 𝜇m thick, 70 m2 [ensure every RBC is in contact with respi membrane allows O2 and CO2 to cross respi barrier]
respiratory membrane] V
DL =
• 60 - 140 ml blood at any given instant, in 0.75 sec [ganon (P1 − P 2) O2 CO2
kabilis]
• 5 𝜇m capillary diameter 21 mL/min/mmHg Not measured
- RBC: 7.8 𝜇m [will renew formation to pass thru capillaries] accurately
PHYSICS OF GAS DIFFUSION - mL/min/mmHg 11 mmHg pressure 400 - 500 mL/min/
• Boyle's Law (constant T) Where: - DLCO: 20 - 30 mmHg
T = Temperature, absolute degrees - DLO2: 21
P = Pressure, mmHg 230 mL/min Diffusing capacity is
- DLCO2: 20x > O2
V = Volume, L 20x more than O2
• Charle's Law (constant P) n = mass of gas
R = constant, 62.36

LoisLane , md Page 8 of 16
 Far Eastern University - Nicanor Reyes Medical Foundation
Respiratory Physiology
Ronald Allan Cruz, M.D.

Clinical Significance: GAS DIFFUSION

In clinics, we do not use O2 and CO2 due to fast diffusion, instead we use CO. • Equilibration < 0.75 sec [equilibrium is "netflux is 0" or
The diffusion capacity of CO assesses if the respiratory membrane allows O2 "inflow = outflow"]
and CO2 to pass through. The patient, for example with pulmonary fibrosis - Perfusion Limited Diffusion Limited
having a thick pulmonary membrane will not let O2 and CO2 pass through. The
Diffusion of insoluble gas in the Diffusion of highly soluble gas
patient will be asked to breathe in a calculated amount of CO, upon exhalation,
plasma
a certain amount of CO is exhaled, the machine determines the amount that
went out. If a patient was administered "100 units of CO" and only 75 units O2, CO2: 0.25 sec equilibration ↑affinity to Hgb
was exhaled, the 25% left can be found in the plasma. Therefore, - prevents equilibration
The lower the diffusion capacity, the ability of the respiratory membrane to
allow gases to pas through decreases. CO

Respiratory membrane is NOT the Respiratory membrane will NOT

• Partial Pressure of Gases [gases will go were pressure is lowest]
main factor that will inhibit/limit allow CO to pass through
O2 mmHg CO2 mmHg equilibration

Atmosphere 159.0 (20.84%) 0.304 (0.04%) The ONLY factor that will determine The ONLY factor that will determine
equilibration is blood flow equilibration is the respiratory
Humidified Air 149.3 (19.67%) 0.300 (0.04%)
membrane
Alveolar Air 104 (13.50%) 40.0 (5.30%)
Clinical Significance:
Arterial Blood 100 40.0 When we exercise, O2 and CO2 slowly shift to Diffusion Limited - this
highlights the importance the function of the pulmonary system with respect
Venous Blood 40 46.0 to exercise. When we have a pulmonary problem, the impairment of the
respiratory membrane now becomes the main factor for limitation of the
Tissures 30 50.0
diffusion of gases.
- 47 mmHg of water vapor will dilute the O2 content in the air we
breathe, which explains the drop of atmosphere air to humidified air TRANSPORT OF O2 AND CO2
1. O2 Diffusion I. OXYGEN, transported MAINLY in two forms: [These 2
- ABG: PaO2: 80 - 100 mmHg 1. Dissolved O2 (dissolved in plasma)
parameters are
different but are
- determined by ABG (PaO2: 80 - 100 mmHg) related]

2. Oxy-Hgb (oxygen bound to hemoglobin)

- majority of O2 is bound to hemoglobin
- 1 Hgb: 4 O2 molecules
[O2 dropped
by 5 (100 to 95)
- 1 RBC: 280 million Hgb
due to the - 1g Hgb: 1.34 mL O2
physiologic shunt] - measured by O2 saturation (determined by Pulse-Oximeter)
2. CO2 Diffusion
- ABG: PaCO2: 35 - 45 mmHg 3. Myoglobin - present in the muscle
4. HgbA - 2𝛼2β [aka Adult Hemoglobin]
5. HgbF - 2𝛼2𝛾 [aka Fetal Hemoglobin]
- the 2𝛾:
- ↓2,3 DPG [a by-product of glycolysis] ,thus ↑ O2 affinity
Significance:
When a pregnant mother breathes, the O2 goes to HgbA, now this blood will go to the
placental circulation which in the placenta, the fetal blood will pass. Since fetal blood
contains 2𝛼2𝛾, it contains less 2,3 DPG compared to HgbA which then allows the transfer of
O2 from HgbA to HgbF due to the latter's higher affinity to O2 [again, thanks to 2,3 DPG

LoisLane , md
found in 2𝛾, found in HgbF] Page 9 of 16
 Far Eastern University - Nicanor Reyes Medical Foundation
6. ↓O2 affinity
- Hgb abnormalities: Sickle Cell Disease, Thalassemia
- Toxicities: CO, NO, CN
- ↓O2 affinity, Fe+++
HEMOGLOBIN
14 - 15g / 100mL blood
(females up to 12, males up to 16)
1g : 1.34 mL O2
OXYHEMOGLOBIN
• O2 DISSOCIATION CURVE
• Oxy-Hgb
• Cooperativity effect
- binding of 1 O2
molecule facilitates
better binding of
other (3) O2
molecules
- dissociation of 1 O2
molecule facilitates
dissociation of other
(3) O2 molecules
• More Sensitive to
ventilation compared
to PaCO2
• PAO2: 100 mmHg
[alveolar 'to ha: A -
alveolar, a - arterial]
• 1g Hgb: 1.34 mL O2
LoisLane , md
Respiratory Physiology
Ronald Allan Cruz, M.D.
• 2,3 DPG
- Allosteric binding - prevents O2 binding by decreasing affinity of O2
to hemoglobin
• CO
- Competitive binding [binds to active site of O2]
O2 IN BLOOD
- Prevents O2 release
19.4 mL O2 / 100 mL arterial blood - Prevents O2 binding
- Hgb-CO < 2% : normal
- Hgb-CO 5 - 7% : highly urbanized area / chronic smoker
14.4 mL O2 / 100 mL venous blood - Hgb-CO 10% : symptomatic
- Interestingly, if a CO is attached to a Hgb with 3 other O2 this
5 mL O2 is given off to the tissues
each cycle prevents the release of O2 molecules, therefore increasing the affinity
- Utilization Coefficient of O2 [clingy af. O2 will not be released as it passes through
systemic capillaries. B A D]
Clinical Significance:
Patients suffering from CO toxicity, do not exhibit cyanosis
• DEFINITION OF TERMS
1. Dyspnea - difficulty in breathing
2. Anoxemia -↓ O2 in body fluids, PaO2
3. Hypoxia - ↓ O2 supply to tissues
- Hypoxic :↓PaO2: <60 mmHg [Hgb sat.↓ drastically]
- Circulatory :↓ blood flow
- Anemic :↓ O2 binding to Hgb
- Histotoxic :↓O2 utilization [CN poisoning]
4. Cyanosis
- bluish discoloration of skin
- observed in the oral cavity: tongue and soft palate [central
circulation]
5. EPO (Erythropoietin) - hormone responsible for RBC production
- Hypoxia is the most potent stimulus for EPO synthesis
1. Bohr Effect (↓O2 affinity)
- shift to the left when:
- ↑ pH
- ↓temperature [occurs in
tissues]
- ↓ PCO2
- ↓2,3 DPG
2. Haldane (↑O2 affinity)
- shift to the right when:
- ↓ pH
[occurs
- ↑ temperature in lungs]
- ↑ PCO2
- ↑ 2,3 DPG
Page 10 of 16
 Far Eastern University - Nicanor Reyes Medical Foundation
Respiratory Physiology
Ronald Allan Cruz, M.D.

II. EXCHANGE OF GASES • CO2 DISSOCIATION CURVE [O2 affects CO2 content in the body]
• Utilization Coefficient - % of blood that gives off O2
- 25% - 5mL given off from 19.4 mL O2
• Respiratory Coefficient (lungs)
- CO2 : O2
- exchange of O2 and CO2
- 80 CO2 molecules expired : 100 O2 molecules into the pulmonary
capillaries
- 0.8 Respiratory Exchange Ratio (tissue) [every 80 C02
molecules given by the cells, will accept 100 O2 molecules]

III. CO2 TRANSPORT, transported in 5 forms: • Deoxy-Hgb

1. Dissolved CO2 (Carbon dioxide found in plasma) - ↑ CO2 H affinity
- 0.2 mL / 100 mL
- determined by ABG (PaCO2 : 35 - 45 mmHg) IV. BLOOD pH AND CO2 TRANSPORT
2. H2CO3 • CO2 is transported in the
- 0.1 - 0.3 mL / 100 mL blood and reduces pH
3. HCO3 [involves Cl- shift: as bicarb enters, Cl goes out]
[venous blood] [arterial blood]
- the more CO2 in the
- 3 mL / 100 mL [CO2 is diffused in/out]
body, the greater
- 22 - 26 mmol / L H2CO3, pH ↓
4. Carbamino-Hgb [arterial blood] [venous blood]
• ABG pH: 7.35 - 7.45
- 1.5 mL / 100 mL
5. CHON-bound (protein-bound)
CONTROL OF RESPIRATION
[FIGURE DESCRIBES CO2 • Respiratory Rate [the younger the px, the faster the rate]
TRANSPORT IN TISSUES, reverse in the
12 - 18 cpm: 12 years - adult 25 - 40 cpm: 6 - 12 mos
lungs]
14 - 22 cpm: 6 - 12 years 30 - 45 cpm: 3 - 6 mos

20 - 25 cpm: 3 - 6 years 35 - 55 cpm: 0 - 3 mos

20 - 30 cpm: 1 - 3 years 40 - 70: premture

lower rates during sleep

• Goal of Breathing
- Minimize work [diaphragm should perform minimal work]
- Maintain blood gases
- Maintain acid-base balance
• Lungs (upon birth)
• Placenta (intra-utero)
• Respiratory Center [collection of several centers]
- Medulla Oblongata
- Ventilatory pattern generator [Inspiratory Ramp]
- Integrator - needs peripheral activity to go to the center
- integrates all signals from periphery

LoisLane , md Page 11 of 16
 Far Eastern University - Nicanor Reyes Medical Foundation
Respiratory Physiology
Ronald Allan Cruz, M.D.

1. Central Chemoreceptors
- ventrolateral surface of the medulla oblongata
- detect pH of CSF and indirectly PCO2
2. Peripheral Chemoreceptors
- Aortic and carotid bodies [NOTE: bodies = chemoreceptors ;
sinus = baroreceptors]
- detect PaCO2, PaO2, pH levels
3. Pulmonary mechanoreceptors (or stretch receptors),
4. Sensory neurons
- Lungs, airways
• Motor Output • Periodic Breathing Maintenance
- C3 - C5: Phrenic nerve - - ->diaphragm - Dorsal Respiratory Group
- T1 - T12: Intercostal nerves - - -> intercostal muscles, accessory - Nucleus tractus solitarius
muscles for respiration - Ventral Respiratory Group
- Ventrolateral tract: Involuntary [passive breathing] - Rostral nucleus retrofacialis
- Corticospinal tract: Voluntary [active breathing] - Caudal nucleus retroambiguus
- Nucleus paraambiguus
- these centers have overlapping functions
• Inspiratory Ramp - a series of action potentials that will excite the
diaphragm and suddenly stop, repetitively
- always active, unless inhibited
- Nucleus tractus solitarius
- Rostral nucleus retroambiguus
- Nucleus paraambiguus
• Group A is for inspiration. It
generates the Inspiratory
Ramp with excitatory AP to
the diaphragm --> contract
1. PaCO2 --> we inhale
- most potent regulator, and most important • Group A also activates Group
- 40 mmHg B, once activated will send
- ↑:900% ↑ventilation ↓ excitatory signals to Group
2. pH C.
- 7.4 • Once Group C is on, will
- ↓: 400% ↑ventilation send inhibitory signals to
3. PaO2 Group A hence AP cessation
- 80 - 100 mmHg -->relax --> we exhale
- ↓:75% ↑ventilation • Exhalation
- Rostral nucleus retrofacialis
- Caudal nucleus retroambiguus
- Nucleus paraambiguus

LoisLane , md Page 12 of 16
 Far Eastern University - Nicanor Reyes Medical Foundation
Respiratory Physiology
Ronald Allan Cruz, M.D.

- breathing is slower and deeper

Inspiratory Ramp
stops firing, the
excitatory AP to Group B
are curtailed, Group B
will then be off. If Group
B is off, then Group C is
off. If Group C is off, the
inhibitory signals by
Group C to A is stopped,
hence the ramp fires
again signaling a new
series of breath
• Hering-Breuer Reflex - an explanation in which ventilation is regular /
rhythmic
- evident among neonates, due to immature respiratory centers
- will rely on signals from periphery
• Apneustic Center - found in the Lower Pons
- prevents the "switch off" of inspiratory signals going to the DRG
- controls intensity of respiration
- inspiration is deep, short excitatory gasps
- prolonged inspiratory gasps interrupted by transient expiratory
efforts if transected
CENTRAL CHEMORECEPTORS
- found in the Medulla oblongata, surrounded by CSF
- it detects CSF pH (H2CO3) and once activated will stimulate ventilation
• Ventrolateral surface of
medulla
• CSF pH
• BBB
- permeable to CO2
- combines with
H2O to form H2CO3
- H2CO3 is detected
by central
chemoreceptors
- impermeable to H,
HCO3

CSF Plasma

pH 7.33 7.4

PCO2 44 mmHg 40 mmHg

HCO3 22 mEq / L 24 mEq / L

Of these junctional proteins, claudins appear to be important in determining

PERIPHERAL CHEMORECEPTORS
the permeability characteristics of the tight junction, especially with regard to
- Carotid and aortic bodies
cations and anions.. To date, 27 mammalian claudin genes have been
- Type I glomus cells
identified, and 26 are found in the humans. Certain claudins serve as.
- PaCO2, PaO2, and pH
jbcnciwncuwbci
- 40% of the ventilatory response to CO2
- Asphyxia
- ↑PaCO2, ↓ PaO2, ↓pH
- detect PaCO2, PaO2, and pH or arterial blood
• Pneumotaxic Center - found in the Upper Pons
- inhibits respiration
- regulates inspiratory volume and rate by "fine-tuning" the
respiratory rhythm
- more active when there are pathological issues present: Double
vagotomy
- sends excitatory signals to Group C, therefore Group A is off,
inhibiting respiration

LoisLane , md Page 13 of 16
 Far Eastern University - Nicanor Reyes Medical Foundation
Respiratory Physiology
Ronald Allan Cruz, M.D.

- ↑diffusing capacity of gases

- ↑ventilation (maintain blood gases and pH), perfusion, O2
utilization
O2 diffusing capacity mL / min / mmHg
Non-athlete at rest 23
Non-athlete at maximal exercise 48
Skater at maximal exercise 64
• Reflexes Swimmer at maximal exercise 71
- Hering-Breuer reflex
Oarsman at maximal exercise 81
- Diving reflex: when cold water touches the face, ventilation stops
- Aspiration reflex: when an irritant is present in the airways
• Receptors • Anaerobic threshold
- Rapidly adapting pulmonary stretch receptors - level of exercise at which
- irritant receptors sustained metabolic
- Slowly adapting pulmonary stretch receptors acidosis begins
- augment inspiratory drive, lung inflation in COPD • We never cross the threshold
- Juxtaalveolar receptor cos we we do reach it, we
- present in blood vessels just adjacent to the alveoli reach fatigue = we will not
- stimuleted during pulmonary congestion [blood vessels in experience metabolic acidosis
pulmonary capillaries will dilate and w/ a sensation of
dyspnea] • Decompression Sickness
- Somatic receptors - bends
- present in thoracic wall - rapid ↓in total pressure of ambient gases
- modulate lung inflation [signals respiratory center if over- - formation of gas bubbles in tissues and blood
inflating] - N2 bubbles, air embolus
- Hyperbaric therapy
SPECIAL SITUATIONS • Abnormal Control of Breathing
• Exercise and Respiration - Kussmaul's breaathing - metabolic acidosis
- ↑minute ventilation - Apnea - blood gases fl uctuate [cure: CPAP]
- cortical radiation [conditioning in anticipation] - <10 sec
- joint, muscle proprioceptors - Sleep apnea
[ventilatory drive during exercise is NOT mainly CO2, it's also due - OSA
to cortical radiation and AP from proprioceptors] - Central sleep apnea - central alveolar hypoventilation
- SIDS [respiratory center doesn't work]
O2 consumption mL / min
At rest 250
Untrained at maximal conditions 3600
Athlete 4000
Marathon runner 5100

LoisLane , md Page 14 of 16
 Far Eastern University - Nicanor Reyes Medical Foundation
Respiratory Physiology
Ronald Allan Cruz, M.D.

- Apneustic breathing - Control of H concentration

- Chemical buffer systems (phosphate, urate, citrate) : first to react
- least potent
- Respiratory system : second to react (seconds, minutes, to hours)
- Renal system : last to react (3 to 5 days)
- most important because the kidneys can handle a wide variety
of acids and bases
- Lungs
- Controls extracellular CO2
- H2CO3: regulate volatile acid
- Alveolar ventilation modulates PCO2
- 50 - 75% effectiveness
- 1 - 2x buffering power than the chemical buffer systems

- Cheyne-Stokes Ventilation BASIC ACID-BASE DISORDERS

1. Respiratory acidosis
- ↓ventilation
- ↑ CO2, H2CO3
- ↓pH
• Acute
- ↓pH, ↑ PaCO2
- Depression of the respiratory center [sedative overdose]
- Neuromuscular disease
- Airway obstruction
• Chronic
- N pH, ↑ PaCO2 [normal pH due to renal compensation]
- COPD
- Pickwickian syndrome [morbidly obese. Struggle in chest
expansion due to fat]
- Restrictive ventilatory defects
ACID-BASE BALANCE 2. Respiratory alkalosis [secondary to anxiety attack]
- Control of H concentration - ↑ ventilation
- Extracellular concentration: 0.00004 mEq / L - Loss of CO2, ↓ H2CO3
- pH = -log [H] - ↑ pH
- pH = 7.35 - 7.45 - Excessive mechanical ventilation
• Acid : releases H ions - Anxiety, Hysteria, Excitation, Stroke, CVA, Meningitis, Drugs, High
• Base : accepts H ions Altitudes, Fever [increases RR], Pregnancy
• H2CO3 H + HCO3 3. Metabolic acidosis
pH = 6.1 + l og[HCO 3] - ↑ ventilation due to stimulation of chemoreceptors
0.03x PCO 2 - removal of CO2, ↓ HCO3
- ↓ pH, ↓ H2CO3
- ↑lactic acid production, ketoacidosis, Renal pathology, Chronic
diarrhea
4. Metabolic alkalosis
- ↑pH, ↑HCO3
- ↓ ventilation - retention of CO2, ↑H2CO3

LoisLane , md Page 15 of 16
 Far Eastern University - Nicanor Reyes Medical Foundation
Respiratory Physiology
Ronald Allan Cruz, M.D.

- Vomiting [excessive vomiting will expel H+, what's left is

bicarb], Renal pathology

• RESPIRATORY ALGORITHM

pH 7.35 - 7.45
H+ 35 - 45 nmol / L
PO2 80 - 100 mmHg
PCO2 35 - 45 mmHg
HCO3 22 - 26 mmol / L

SHORT ACTIVITY: DIAGNOSE WITH THESE RESULTS

pH 7.47 pH 7.30
H+ 32 nmol / L H+ 48 nmol / L
PO2 91 mmHg PO2 95 mmHg
PCO2 31 mmHg PCO2 43 mmHg
HCO3 24 mmol / L HCO3 19 mmol / L

RESPIRATORY ALKALOSIS METBOLIC ACIDOSIS

END

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