What is the function of the upper respiratory tract?

Raises
Warm incoming air to
Humidify 37 Celsius Forms
mucociliary
Filter escalator
Raises
Vocalize incoming air to
100% humidity
Nonrespiratory Functions of Respiratory System
Route for water loss and heat elimination
Enhances venous return (Cardiovascular Physiology)
Helps maintain normal acid-base balance (Respiratory and
Renal Physiology)
Enables speech, singing, and other vocalizations
Defends against inhaled foreign matter
Removes, modifies, activates, or inactivates various materials
passing through the pulmonary circulation
Nose serves as the organ of smell
Functions of the Respiratory
Passageways
trachea, bronchi, and bronchioles.
Respiratory passageways must be kept open 
allow easy passage of air to and from the alveoli.
multiple cartilage rings extend about five sixths
of the way around the trachea.
In the walls of the bronchi, less extensive curved
cartilages .
These become progressively less extensive in the
later generations of bronchi and are gone in the
bronchioles.
The bronchioles are not prevented from
collapsing by the rigidity of their walls. Instead,
they are kept expanded mainly by the same
transpulmonary pressures that expand the alveoli.
Muscular Wall of the Bronchi and Bronchioles
with the exception of the most terminal
bronchiole, called the respiratory bronchiole 
pulmonary epithelium, fibrous tissue, few smooth
muscle fibers.
Many obstructive diseases of the lung result
from narrowing of the smaller bronchi and larger
bronchioles, often because of excessive
contraction of the smooth muscle itself.
Resistance to Airflow in the Bronchial Tree.
greatest amount of resistance to airflow occurs
larger bronchioles and bronchi near the trachea.
reason  few of these larger bronchi in
comparison with the approximately 65,000
parallel terminal bronchioles  only a minute
amount of air must pass.
In Disease conditions, the smaller bronchioles
often play a far greater role in determining
airflow resistance  small size
 easily occluded by (1) muscle
contraction in their walls, (2) edema occurring in
the walls, or (3) mucus collecting in the lumens of
the bronchioles
Nervous and Local Control of the Bronchiolar
Musculature—
Direct control of the bronchioles by sympathetic
nerve fibers is weak because few of these fibers
penetrate to the central portions of the lung.
norepinephrine and epinephrine released into the
blood by sympathetic stimulation of the adrenal
gland medullae.
Both these hormones— especially epinephrine,
because of its greater stimulation of beta-
adrenergic receptors—cause dilation of the
bronchial tree.
Parasympathetic Constriction of the Bronchioles.
A few
parasympathetic nerve fibers derived from the
vagus nerves penetrate the lung parenchyma.
These nerves secrete acetylcholine and, when
activated, cause mild to moderate constriction of
the bronchioles.
If asthma has already caused some bronchiolar
constriction, superimposed parasympathetic
nervous stimulation often worsens the condition.
When this occurs, administration of drugs that
block the effects of acetylcholine, such as
atropine, can sometimes relax the respiratory
passages enough to relieve the obstruction.
Local Secretory Factors Often Cause Bronchiolar
Constriction.
histamine and slow reactive substance of
anaphylaxis.
released by mast cells during allergic reactions 
pollen in the air.
Causes the airway obstruction in allergic asthma
smoke, dust, sulfur dioxide, initiate local, non
nervous reactions that cause obstructive
constriction of the airways.
Mucus Lining the Respiratory Passageways, and
Action of Cilia to Clear the Passageways
All the respiratory passages, are kept moist by a
layer of mucus that coats the entire surface. The
mucus is secreted by mucous goblet cells in the
epithelial lining and by small submucosal glands.
the mucus traps small particles out of the
inspired air.
The respiratory passage is lined with ciliated
epithelium, with about 200 cilia on each epithelial
cell which beat continually at a rate of 10 to 20
times per second
 ALVEOLAR
VENTILATION
Some of the air a person breathes never reaches
the gas exchange areas but simply fills
respiratory pas-sages where gas exchange does
not occur,
such as the nose, pharynx, and trachea.
This air is called dead space air because it is not
useful for gas exchange.
all the space of the respiratory system other
than the alveoli and their other closely related
gas exchange areas; this space is called the
anatomic dead space.
When the alveolar dead space is included in the
total measurement of dead space, this is called
the physio-logic dead space
•Pulmonary Ventilation:
Is the volume of air breathed in and out per minute

•Alveolar Ventilation:
Is the volume of air exchanged between the
atmosphere and alveoli per minute
This is more important as it represent new air available for
gas exchange with blood.
Some inspired air remains
Pulmonary Ventilation
in the airways (anatomical
dead space) where it is not
& Alveolar Ventilation
available for gas exchange
Pulmonary Ventilation =
Fresh air
tidal volume (ml/ breath) x from inspiration
Respiratory Rate (breath/min)
= 0.5 L X 12 breath/min = 6 Airway dead-space
L/min under resting volume (150 ml)
conditions
Alveolar Ventilation is less
than pulmonary ventilation
because of the presence of Alveolar air
anatomical dead space.
Alveolar Ventilation = (tidal
volume – dead space
volume) x Respiratory Rate
= (0.5 – 0.15) x 12 = 4.2 L/min After inspiration,
under resting conditions. before expiration
Fig. 13-22, p. 472
Pulmonary Ventilation:
Is the volume of air breathed in and out per minute

Alveolar Ventilation:
Is the volume of air exchanged between the
atmosphere and alveoli per minute
This is more important as it represent new air available for
gas exchange with blood.
 Pulmonary Ventilation
To increase pulmonary & Alveolar Ventilation
ventilation (e.g. during
exercise) both the depth
(tidal volume) and rate of Fresh air
breathing (RR) increase. from inspiration
Airway dead-space
volume (150 ml)
because of dead space:
It is more advantageous
to increase the depth of
breathing Alveolar air

After inspiration,
before expiration
t is more advantageous to increase the Depth of Breathing
Respiratory Minute Volume
Amount of air moved per minute
Is calculated by:

respiratory rate  tidal volume

Measures pulmonary ventilation
Alveolar gas concentrations
[O2] in the alveoli averages 104 mmHg

[CO2] in the alveoli averages 40 mmHg

Gas Exchange
Partial Pressure
Each gas in atmosphere contributes to the entire
atmospheric pressure, denoted as P
Gases in liquid
Gas enters liquid and dissolves in proportion to its
partial pressure
O2 and CO2 Exchange by DIFFUSION
PO2 is 105 mmHg in alveoli and 40 in alveolar capillaries
PCO2 is 45 in alveolar capillaries and 40 in alveoli
Partial Pressures
Oxygen is 21% of atmosphere
760 mmHg x .21 = 160 mmHg PO2
This mixes with “old” air already in alveolus to arrive at
PO2 of 105 mmHg
Partial Pressures
Carbon dioxide is .04% of atmosphere
760 mmHg x .0004 = .3 mm Hg PCO2
This mixes with high CO2 levels from residual volume
in the alveoli to arrive at PCO2 of 40 mmHg
Diffusing capacity of Respiratory Membrane
Oxygen under resting conditions
21 ml/min/mmHg
mean pressure gradient of 11 mmHg.
230 ml/min (21 X 11)
increases during exercise
Carbon dioxide diffuses at least 20X more readily than
oxygen
Expired

Air
As one expires a normal tidal volume of 500 ml the
concentrations of oxygen and carbon dioxide
change
O2 falls from about 159 to 104 mmHg
CO2 rises from O to 40 mmHg
1st 100 ml of expired air is from dead space
last 250 ml of expired air is alveolar air
Middle 150 ml of expired air is a mix of above
 (dead space + alveolar air)
Alveolar air turnover
Each normal breath (=tidal volume) turns over only a
small percentage of the total alveolar air volume.
350/2150 mls
Approximately 6-7 breaths for complete turnover of
alveolar air.
Slow turnover prevents large changes in gas
concentration in alveoli from breath to breath
 Gravity, Alveolar Pressure and Blood Flow
Pressure in the pulmonary arterioles depends on both
mean pulmonary artery pressure and the vertical position
of the vessel in the chest, relative to the heart.

Driving pressure (gradient) for perfusion is different in

the 3 lung zones:
 Flow in zone may be absent because there is inadequate pressure
to overcome alveolar pressure.

 Flow in zone 3 is continuous and driven by the pressure in the

pulmonary arteriole – pulmonary venous pressure.

 Flow in zone 2 may be pulsatile and driven by the pressure in the

pulmonary arteriole – alveolar pressure (collapsing the capillaries).
Typically no zone 1
in normal healthy
person

Large zone 1 in
positive pressure
ventilation + PEEP
Ventilation-Perfusion ratios
Normally alveolar ventilation is matched to
pulmonary capillary perfusion at a rate of 4L/min of
air to 5L/min of blood
4/5 = .8 is the normal V/P ratio
If the ratio decreases, it is usually due to a problem
with decreased ventilation
If the ratio increases, it is usually due to a problem
with decreased perfusion of lungs
Ventilation-Perfusion ratios
A decreased V/P ratio as ventilation goes to zero
Not enough ventilation for the amount of
pulmonary blood flow (perfusion)
Alveolar PO2 will decrease toward 40 mmHg
Alveolar PCO2 will increase toward 45 mmHg
Results in an increase in “physiologic shunt blood”-
blood that is not oxygenated as it passes the lung
Ventilation-Perfusion ratios
An increased V/P ratio due to a decreased
perfusion of the lungs from the RV
Not enough pulmonary blood flow (perfusion) for
the amount of ventilation
Alveolar PO2 will increase toward 149 mmHg
Alveolar PCO2 will decrease toward O mmHg
Results in an increase of physiologic dead space- area
in the lungs where oxygenation is not taking place
 includes non functional alveoli
 Lung Ventilation/Perfusion Ratios

Functionally:
Insert fig. 16.24
Alveoli at
apex are
underperfused
(overventilated).
Alveoli at the base
are underventilated
(overperfused).

Figure 16.24
 Ventilation Perfusion
Both blood flow and ventilation vary from bottom to
top of the lung
The result is that
the average arterial
and alveolar partial
Blood Flow 2 pressures of O2 are
Flow
not exactly the
V/Q Ratio same. Normally
Ventilation 1 this effect is not
significant but it
can be in disease.

Bottom Lung Position Top

 Alveolar Dead Space
 The match between air in the alveoli and the blood in the
pulmonary capillaries is not always perfect

 Ventilated alveoli which are not adequately perfused with

blood are considered as alveolar dead space

 In healthy people, the alveolar dead space is very small and

of little importance (note: the physiological dead space =
the anatomical dead space + the alveolar dead space)

 The alveolar dead space could increase significantly in

disease
 Ventilation Perfusion Match in the Lungs

Local controls act on the smooth muscles of airways

and arterioles to match airflow to blood flow

Accumulation of CO2 in alveoli as a result of

increased perfusion decreases airway resistance
leading to increased airflow

Increase in alveolar O2 concentration as a result of

increased ventilation causes pulmonary
vasodilation which increases blood flow to match
larger airflow
 Area in which blood flow (perfusion)
is greater than airflow (ventilation)

Helps Helps
balance Large blood flow balance
Small airflow

CO2 in area O2 in area

Relaxation of local-airway Contraction of local pulmon-

smooth muscle ary arteriolar smooth muscle

Dilation of local airways Constriction of local blood vessels

Airway resistance Vascular resistance

Airflow Blood flow

 Area in which airflow (ventilation)
is greater than blood flow (perfusion)

Helps Helps
balance Large airflow balance
Small blood flow

CO2 in area O2 in area

Contraction of local-airway Relaxation of local pulmonary

smooth muscle arteriolar smooth muscle

Constriction of local airways Dilation of local blood vessels

Airway resistance Vascular resistance

Airflow Blood flow

Note the Different Effects of O2
COUGH REFLEX
The bronchi and trachea are so sensitive to light touch
 foreign matter
 or other causes of irritation initiate the cough reflex.
The larynx and carina (the point where the trachea
divides into the bronchi) are especially sensitive,
and the terminal bronchioles and even the alveoli are
sensitive to corrosive chemical stimuli such as sulfur
dioxide gas or chlorine gas.
Afferent nerve impulses pass from the respiratory
passages mainly through the vagus nerves to the
medulla of the brain.
There, an automatic sequence of events is triggered by
the neuronal circuits of the medulla, causing the
following effect.
First, up to 2.5 liters of air are rapidly inspired.
Second, the epiglottis closes, and the vocal cords
shut tightly to entrap the air within the lungs.
Third, the abdominal muscles contract forcefully,
pushing against the diaphragm while other
expiratory muscles, such as the internal
intercostals, also contract forcefully.
Consequently, the pressure in the lungs rises
rapidly to as much as 100 mm Hg or more.
Fourth, the vocal cords and the epiglottis
suddenly open widely, so that air under this high
pressure in the lungs explodes outward.
Indeed, sometimes this air is expelled at
velocities ranging from 75 to 100 miles per hour.
Importantly, the strong compression of the lungs
collapses the bronchi and trachea by causing their
noncartilaginous parts to invaginate inward, so
that the exploding air actually passes through
bronchial and tracheal slits.
The rapidly moving air usually carries with it any
foreign matter that is present in the bronchi or
trachea.
Sneeze Reflex
The sneeze reflex is very much like the cough
reflex,
except that it applies to the nasal passageways
instead of the lower respiratory passages.
The initiating stimulus of the sneeze reflex is
irritation in the nasal passageways; the afferent
impulses pass in the fifth cranial nerve to the
medulla, where the reflex is triggered.
A series of reactions similar to those for the
cough reflex takes place; however, the uvula is
depressed, so that large amounts of air pass
rapidly through the nose,
 thus helping to clear the nasal passages of foreign
matter.
Vocalization
Speech involves not only the respiratory system
but also
(1) specific speech nervous control centers in the
cerebral cortex,
(2) respiratory control centers of the brain; and
(3) the articulation and resonance structures of
the mouth and nasal cavities.
Speech is composed of two mechanical functions:
(1) phonation, which is achieved by the larynx, (2)
articulation, which is achieved by the structures
of the mouth.
Phonation.
The larynx, is especially adapted to act as a vibrator.
The vibrating element is the vocal folds, commonly called
the vocal cords.
The vocal cords protrude from the lateral walls of the
larynx toward the center of the glottis; they are
stretched and positioned by several specific muscles of
the larynx itself.
During normal breathing, the cords are wide open to
allow easy passage of air.
During phonation, the cords move together so that
passage of air between them will cause vibration.
The pitch of the vibration is determined mainly by the
degree of stretch of the cords, but also by how tightly
the cords are approximated to one another and by the
mass of their edges.
Vocal folds have mucous epithelial lining.
Immediately inside each cord is a strong elastic
ligament called the vocal ligament.
This is attached anteriorly to the large thyroid
cartilage, which is the cartilage that projects
forward from the anterior surface of the neck
and is called the “Adam’s apple.”
Posteriorly, the vocal ligament is attached to the
vocal processes of two arytenoid cartilages.
The thyroid cartilage and the arytenoid
cartilages articulate from below with another
cartilage , the cricoid cartilage.