Introduction to Respiratory System

Internal Respiration: Metabolism, ATP production; has influence on CO2

and O2 levels
External Respiration: gas transport and exchange
1) Ventilation: movement of air into and out of the lungs
(mechanical process)
- pressure and volume
2) Diffusion of O2 and CO2 between air in alveoli and blood within
the pulmonary capillaries
3) Blood transport O2 and CO2 between lungs and tissues
4) Diffusion of O2 and CO2 between lungs and tissues
Also need to consider feedback
- CO2 is the primary afferent information that
control respiratory
Lungs are divided into lobes and the lobes are divided into segments;
segments can function independently of each other
Alveoli- very end
Consists of elastic connective tissue
Compliance is an inspiratory process
Elasticity is an expiratory process
- snap back
Lungs are physically attached to the chest wall
Conducting Airways
- Move air by volumes
- Anatomic Dead Space (No Exchange) aprx 150
Alveoli
- Where most of the gas exchange takes place, but not all
of it
- High surface area
Bronchi
-

Contains cartilage

NO cartilage

Bronchiole
Terminal Bronchiole: NO gas exchange
Respiratory Bronchiole: where you start to see the beginning of gas
exchange

Conducting Zone
Globlet cells secreting mucus around the cilia
Mucociliary Escalator: as you breathe in, the dust particles get
trapped and the cilia move them along
Respiratory Zone
NO Cilia; Host defense involves alveolar macrophages
Upper Airway: Nose to Larynx
Warm the air (better for diffusion)
Humidify air (add water)
Clear larger particles (diameter > 3um)
Trachea
Non-muscular; C-shaped rings of cartilage prevent collapse
Physiological Dead Space
- When we start to have respiratory problems
- Normally equal to anatomical dead space, but can
increase
- If I have more dead space, then less exchange
Bronchi
We have two bronchi
They are not symmetrical
More likely to aspirate something on the right side because it is
more vertical
Bronchioles
NO Cartilage
Smooth muscle
Sensitive to chemicals
Sympathetic Nervous system: Dilates bronchioles
Parasympathetic Nervous system: Constrict bronchioles
Alveoli
Site of gas exchange
Thin walled end sac (one cell tick)
Tons of capillaries
Two types of cells
1) Type I: Make up the actual wall of the alveoli (regular cells)
2) Type II: Produce a chemical called pulmonary surfactants

Pores of Kohn: - Allow alveoli to connect to each other to allow gasses

to be distributed
- Prevent alveoli from collapsing (Help keep them inflated)

Pleural Sac
Visceral pleura: sits on the surface of the lung
Parietal pleura: lines the chest cavity
Between the two is a pleural cavity thats filled with fluid
This is how the chest wall and lungs are connected to each other
During Inspiration
- Expanding chest lungs expand
Pulmonary Circulation
- More distensible and more compliant than systemic
vessels
- More likely to expand
- Flow distribution in the lung is affected by gravity
- Very low resistance
- To allow blood to flow very easily
- It makes it easier for heart to push blood to lung
- Increased pressure reduces resistance (they
accept blood)
- Blood moving very quickly
- Hypoxic vasoconstriction
Pulmonary Artery: Deoxygenated blood from right heart goes to alveoli
Bronchial Artery: Oxygenated blood from left heart that is supplying
the lung with oxygen
Pulmonary Vascular Resistance and MAP
Increases in blood pressure cause vessels diameter to increase,
decreasing the resistance (NO myogenic response)
- Trying to accept as much blood as possible

Pulmonary Vascular Resistance and Lung Volumes

When you inspire Extra-alveolar blood vessels get bigger
Resistance
decrease
Intra-Alveolar blood vessels become compressed
Resistance
increase
- As alveolar is expanding, it is causing those
vessels to constrict
Functional Residual Capacity (FRC)
- Volume where the Total Resistance is at its lowest point
- Starting Point
- Amount of air in lungs before taking a breath

1.

The
a.
b.
c.

conducting zone of the lung

Represents 50% of the total lung capacity
Includes airway generations 17-23
Is the portion of the lung where gas exchange occurs, i.e.,
where oxygen is conducted into the blood
d. Includes airways from the trachea to the terminal
bronchioles

e. Includes airways from the trachea to the segmental

bronchi only
2. In the alveolar region of the lung
a. Alveolar macrophages are part of the alveolar epithelium
and are involved in gas exchange
b. Type II cells make up the largest portion of the alveolar
epithelial surface
c. Type I cells make up the largest portion of the alveolar
epithelial surface
d. Fibroblasts are part of the alveolar epithelial surface
e. Type II cells are alveolar interstitial cells which produce
surfactant

3. In the pulmonary circulation

a. Deoxygenated (venous) blood is carried by the pulmonary
arteries
b. Deoxygenated (venous) blood is carried by the pulmonary
veins
c. Oxygenated (arterial) blood is carried by the pulmonary
arteries
d. Deoxygenated (venous) blood is carried by the bronchial
arteries
e. None of the above

4. The conducting zone of the respiratory tract

a. Includes 0-23 generations of airways
b. Includes airways from the trachea to the terminal
bronchioles
c. Normally is 500 mL in volume
d. Has surface area of 85 m2
e. None of above

5. The anatomical dead space

a. Increases in bronchitis
b. Is the volume of the conducting zone
c. Is the volume of airway generations 0 16
d. Is approximately 150 ml
e. All except A

6. Compared to the systemic circulation, the pulmonary circulation

is a
a. Low flow system
b. Low resistance system
c. High pressure system
d. System more strongly influenced by sympathetic
stimulation of vasoconstriction of the arterioles
e. System unaffected by exercise
7. The mucociliary escalator
a. Is located in the alveolar region of the lung
b. Acts to clear inhaled particles which deposit at the bronchi
and bronchioles of the conducting zone
c. Requires secretion of mucus by clara cells
d. Is involved in xenobiotic metabolism
e. None of the above

8. Alveolar type II cells

a. Are involved in preventing edema
b. Are involved in repair of oxidant damage of the alveolar
epithelium
c. Are involved in xenobiotic metabolism
d. Are involved in production of interferon in response to viral
exposure
e. All of the above

Important Pressures
Atmospheric pressure
- Unless otherwise stated, its 760 mm Hg
Intra-alveolar pressure
- Pressure inside the alveoli
Intrapleural pressure
- Space between the chest wall and the lungs
- Always less than the pressure inside the lungs

Helps keeps the lungs inflated

Normal breathing is considered negative pressure breathing

Roles of Pressures
Air flow = (Lung gas pressure Atmospheric pressure) / Resistance
- For air to flow, you need a pressure gradient
- Diameter of Bronchioles plays an important role in resistance
Compliance: how easy it is to change lung volume
Elastance: how readily the lungs return to resting volume after
inhalation ceases
Resistance: how easily it is for air to move through the airways
The lungs want to naturally collapse and the thoracic wall to expand;
when they are at equilibrium, those are static forces: air is not
flowing
Lung Volumes and Capacities
Tidal Volume (TV)
- Volume of air entering or leaving lungs
during a single breath
- about 500 mL
Inspiratory Reserve Volume (IRV)
- how much additional air they can
breathe in above the tidal volume
- Measure of compliance
Expiratory Reserve Volume (ERV)
- Additional volume of air that can be
Expired after a normal expiration
- Measure of elastance
Residual Volume (RV)
- Amount of air remaining in the lung after a maximal expiration
- Due to chest wall pulling back
Functional Residual Capacity (FRC)
- Starting point
- How much air is in the lungs before taking a breath
- Equilibrium point for respiratory system

Determined by the relationship between compliance and

elastance
It acts as a buffer for continued gas exchange during these
periods

Inspiratory capacity (IC)

- Volume of air that can be inspired after a normal expiration
- TV + IRV
Vital Capacity (VC) *
- Maximal volume that can be expired after a maximal inspiration
- TV + IRV + ERV
Forced Expiratory volume in one second (FEV1)
- How much air they can exhale in one second

Respiratory Mechanics I
Recoil Forces
Lung Recoil
- The inward force that the lungs want to do
- Their natural position is to collapse
Chest Wall Recoil
- Recoil is the outward force
FRC is determined by those two
Intrapleural Pressure (IPP)
Created by the balance between the lungs and the chest wall
- As one pulls one way and the other one pulls a different way, a
negative pressure is created compared to inside the lungs

Transmural Pressure (TMP) gradient

-

Ptm = Pinside Poutside

Always positive
This just means that the inside is more positive than the outside
- Helps keep the lungs inflated (Atelectasis)
- The positive TMP gradient counteracts lung elastic recoil

Traumatic pneumothorax
- In a collapsed lung, the TMP is negative
- Making the IPP greater than inside the lungs
- Puncture wound
Tension pneumothorax
- Air enter IPP space from damaged alveoli
- They will get a tracheal deviation
- Can occur on positive-pressure ventilator

Atelectasis
An area of collapsed or non-expandable lung (regional)
Compliance
V/ P
The less compliant your lungs are, the more work you have to do to
breathe
High Compliance means low elastic recoil force and vice versa
- The easier to get air in, then the harder to get air out
When do you have the best lung compliance?
- Low lung volumes
- Compliance decreases with increasing volume
- Due to elastance (they want to snap back)

Fibrosis (scarring of lung tissues)

Stiff tissue
Lower compliance
Harder to get air due to decreased of compliance
Lung volume will be lower then normal
Expiratory will be good

Emphysema, Aging
- Higher compliance
- Easier to get air in, but harder to get air out
- They are trapping air in the lungs
- Lung volumes will be higher
- Residual volume will be higher
Slopes represent
compliance

Three Components of Lung Recoil

Tissue: collagen and elastin fibers
Surface Tension
- Created in the alveoli
- Alveoli are lined with a liquid (humidified)
- H2O attract to each other and collapse the alveoli because the
H2O molecule are pulling on top of each other
- Surfactants in the lungs reduce the surface tension to keep
alveoli open
Law of LaPlace:
- Relationship between the surface tension and the pressure inside
a bubble
- If one alveoli collapse, then the air in there is going to flow to
another alveoli and increase the surface tension pressure in that
one, causing it to collapse; this will eventually propagate to
another ones
- Regional collapse of alveoli: Atelectasis
Surfactant
Produce by the Type II cells
-

Lowers surface tension

Helps maintain the volume of small alveoli and prevent the law
of LaPlace from happening
It reduces capillary filtration forces and limits pulmonary
edema

Keeps Alveoli open and reduces the risk of pulmonary edema

Respiratory Distress Syndrome (RDS)
Surfactant is lost
- Elastance goes up and compliance goes down
- Decrease lung volume
- Increase risk of edema
- You have to work harder to get air in
Curve A: The person is fighting it
Curve B: The alveoli have collapsed (flat line) and have to get a much
higher pressure

Pressure at FRC
-

At FRC, the alveoli at the apex (top of the lung) are larger than
the alveoli at the base
- Because the at the trop, there is a higher transmural
pressure so they are going to be more inflated
- Alveoli at the top have a lower compliance than at the
bottom

Compliance-Chest /Lung
The chest wants to naturally expand. Therefore, what do you have to
do to make the chest smaller?
- You have to make the pressure less inside the chest (you would
have to suck the air out)
When the lungs start at minimum volume (take them out and put then
on the table)
- its initially easy to put air in, but as you put more and more it
gets more difficult (compliance goes down as you put more air
in )

Here we have maximal

inhalation and muscular
force is needed to keep
lungs inflated. If stop
exerting muscular force,
then system return to
FRC
Here is the rest
point, where lung
elastic recoil pulls in
on chest and chest
pulls out on lungs
FRC

Harder to exhale to
smaller volumes because
recoil of chest pulling
back on lungs
overcomes recoil of
lungs pulling in on
chest. Volume left in the
lungs at the end of a
maximal forceful

Respiratory Mechanics II
Inspiratory Muscles
Diaphragm
- Controlled by phrenic nerves (originate from cervical 3rd, 4th,
and 5th)
External intercostal muscles
- Muscles between the ribs
- Intercostal nerves supplied by thoracic spinal roots from 1st
to 12th
You want to move the diaphragm down and elevate the ribs
- This increases volume and decreases pressure

Before Inspiration
-

You are at FRC and no air is flowing because Patm is equal to Plungs

During Inspiration
-

Muscle contraction expands chest wall

Thoracic volume increases and intrapleural pressure becomes
more negative
The more negative IPP causes TMP to be more positive, resulting
in expansion of the lungs
The expansion of the lung increases alveolar volume and
lowers alveolar pressure to subatmospheric
Air enters lungs

IPP changes first and everything else then follows

Airflow is fastest during the middle
Any disease that interferes with ability of lung to develop more
negative IPP during inspiration is restrictive disease
- Compliance is the problem
Any disease that interferes with ability of lung to develop more positive
IPP during expiration is obstructive disease
- Connected to increase in resistance of the conducting zone
End of Inspiration
As soon as air moves in, it equilibrates with atmospheric pressure and
you are back at a point where there is no movement of air; you are at
the Tidal Volume
Expiration
Relax the diaphragm and snap back to FRC.
You dont work to expire under normal circumstances
Expiratory muscles are only active during forced exhalation
Pressures Important for Breathing
Pao = pressure at airway opening
Pbs = pressure at body surface

Ppl = Intrapleural pressure

PA = alveolar pressure, pressure inside alveoli
What is the pressure gradient for driving airflow?
- The difference between the airway and intrapleural pressure
In order to move air, two forces need to be overcome:
1) The elastic recoil of the lung
2) Frictional resistance forces of air flow
1) Pel is the elastic recoil pressure of lung; pressure necessary to
counteract the elastic recoil of the lungs. This helps keep lungs
inflated
PA - Ppl
- Pel is Ptm
2) Pfr is flow resistive pressure; pressure necessary to overcome the
frictional resistance to airflow
- Pao - PA
Transpulmonary Pressure (Ptp)
- Driving force to move air in
- Is pressure gradient between airway opening pressure pleural
pressure (Pao- Ppl)

9. At FRC (functional residual capacity)

a. The force on the chest wall acts to decrease the volume of
the thoracic cavity
b. The force on the lung is to collapse the lung due to elastic
recoil and surface tension
c. Inspiration does not use muscle contraction
d. Expiration from FRC to residual volume does not use
muscle contraction
e. Intrapleural pressure is 0

10.
At FRC, the forces on the chest wall are in equilibrium with
the forces on the lung. Therefore,

a. At FRC the force on the chest wall is to decrease the

volume of the chest cavity
b. At FRC the force on the lung is to increase lung volume
c. To expire air from TLV to FRC requires contraction of the
abdominal and internal intercostals muscles
d. To inspire air from FRC requires contraction of the
diaphragm and the external intercostals muscles
e. None of the above

11.

Using a spirometer to measure static lung volumes,

a. Residual volume can be determined
b. Vital capacity is the volume of air inhaled in normal
breathing
c. Inspiratory capacity is the volume from maximum
expiration to normal inspiration
d. Tidal volume is normally 80% of vital capacity
e. Functional residual capacity cannot be determined without
measuring residual volume with the He equilibration or the
nitrogen washout technique

12.

Normally, inspiration is negative pressure breathing:

a. According to Boyles Law, as one expands the thoracic, the
intrapleural pressure becomes more negative
b. This negative intrapleural pressure would suck open the
lung
c. As lung volume increases, Boyles Law predicts that
alveolar air pressure would decrease
d. According to Poseuilles law, air would flow from higher
pressure (atmosphere) to lower pressure (alveoli). As air
enters the lung; the number of moles of gas in the alveoli
increase, and according to the ideal gas law alveolar
pressure would increase until it equaled atmospheric
pressure and inspiration would end.
e. All of the above

13.

Surfactant is
a. Composed of mainly lipid with lesser amounts of protein
and carbohydrate
b. Produced by alveolar macrophages

c. Found in the interstitial space of the alveolar wall lining the

pulmonary endothelium
d. A lipoprotein complex which raises the surface tension of
the lung
e. None of the above
14.
a.
b.
c.
d.
e.

15.
a.
b.
c.
d.
e.

16.
a.
b.

c.

d.
e.
17.

Surfactant prevents alveoli from collapsing because

It makes the alveoli throughout the lung a uniform size
It decreases the compliance of the lung
DPPC decreases the attraction between water molecules
It increases filtration of fluid from the pulmonary capillaries
Surfactant apoprotein increases the osmolarity of the
hypophase
Which are properties of surfactant apoproteins?
To increase bacterial killing by alveolar macrophages
To decrease surface tension at the air/liquid interface
To enhance the surface spreading of surfactant lipids
Only a and c are correct
A, b, and c are correct

Using a spirometer
Residual volume can be measured as total lung capacity
minus vital capacity
Residual volume can be measured as total lung capacity
minus the sum of inspiratory reserve volume, tidal volume,
and expiratory reserve volume
Residual volume can be measured as total lung capacity
minus the sum of inspiratory capacity and expiratory
reserve volume
Residual volume cannot be measured
All except D are correct
Emphysema

a. Increases the volume of alveolar sacs, thus increasing the

area available for gas exchange
b. Increases lung compliance
c. Increases the transpulmonary pressure required to inflate
the lung
d. Causes a pneumothorax of the upper lung lobes
e. Causes a pneumothorax of the lower lung lobes
18.
a.
b.
c.
d.
e.

Surfactant
Causes surface tension to be equal in both large and small
alveoli
Enhances the filtration of nutrient-rich fluid from the
pulmonary capillaries
Decreases lung compliance
Decreases muscle work required to inflate the lung
All of the above

Pel counterbalances the elastic recoil of the lung

During inspiration, the velocity maximizes about the middle of the
inspiration. The intrapleural pressure (Ppl) becomes more negative.
The Pel increases to counter the elastic recoil force
Anytime the air is moving, the Ppl changes more than the Pel; At a
static point, they are equal and opposite of each other
- The Ppl is compensating for the resistance and inertia forces
Between inspiration and expiration, there is a point in time where the
air is not moving
During expiration, the Ppl becomes more positive

Work of Breathing
Three factors must be overcome
1) The elastic recoil of the chest and lung
2) Frictional resistance to gas flow in the airways
3) Tissue frictional resistance
Resistance Forces
Wherever we have turbulent flow, we are going to have a lot more
resistance
- Greatest resistance in the bronchus
- However, point of control is in the bronchioles
At high lung volumes, the resistance is very low because your airways
are opened up

Bronchoconstriction (decreased radius, increased resistance to airflow)

- Allergy
- PNS
- Decreased CO2 causes bronchoconstriction
Bronchodilation (increase radius, decrease resistance)
- Epinephrine
- High CO2

Restrictive Disease

Normal

Pathological
- More work (lungs are
stiff)
- Decrease in compliance
- Fibrosis
- Trouble getting air in, but
easy to get air out
- Slope represents compliance
- Width represents work to move air (it tells us about airway
resistance)
Obstructive

Compliance is the same

Increase in resistance
- You have to work harder to move

air
- Difficulty getting air out (larger
lung volumes)
- Expiration is affected more than
inspiration
Forced Expiratory Test
FEV1
- How much air they get out in the first second, relative to the force
FVC
Expiration has two components: effort-dependent and effortindependent
During forced expiration, airflow is property of the patients respiratory
system
- This is the effort-independent part

COPD Pathology
Bronchitis
- There is an increase in blood flow resistance due to blockage of
bronchus in the lung. Therefore, right side of the heart has to
work harder and right heart failure can occur (cor pulmonale)
Emphysema
- Elastic tissue is lost
- Compliance goes up
Asthma
- Airways constrict
- Status asthmaticus: a severe allergic reaction

Larger volumes
Expiration is mostly affected
FEV1/FVC = 50%
Restrictive Patterns
-

Increase in elastic recoil and a decrease in lung compliance

Stiff tissue
Fibrosis (stiff tissue)
IRDS and ARDS (increase in elastic recoil due to loss of
surfactant)

Starting at a lower volume

FEV1/FVC = 88% due to increase in
elastance

Flow Volume Loop Curves

Flow rate peaks at the middle of inspiration
For expiration:
- Effort dependent
- Effort independent
- it doesnt matter how much you squeeze, since air is
coming out on its own

- Its a reflection of your airway resistance

Much larger volume (trapping

volume)
Expiration is much greatly affected
- Especially the effort
independent part ( scalloping
is seen (a dip))

Everything is smaller
Restricting their ability to inspire air

A patient with respiratory issues does PFT and FEV1 is 53%

- Diagnosis? : Obstructive disorder
- Differential: Bronchitis, emphysema or Asthma
- give B2 agonist, if better asthma, if not one of the others

Hemoglobin/Oxygen Transport
Partial pressure
- Is the total pressure times the fractional composition of the gas
PatmO2 = 0.21(760) =160 mm Hg
PupperO2 = 0.21(760 47) = 150 mm Hg
PAO2 (alveolar air) = 100 mm Hg
- goes down due to the abundance of CO2
Alveolar PCO2 (PACO2)
If amount of CO2 in alveolar has increased then alveolar ventilation has
decreased

Hyperventilation
- When PACO2 is lower than normal
Hypoventilation
- When PACO2 is higher than normal
- Shallow breathing
Hyperventilation and hypoventilation is associated with CO2, not how
fast or slow
Alveolar Air Equation- PAO2
PAO2 = [Patm PH2O ]x FIO2 (PaCO2/RQ)
PAO2 = Amount of O2 taking in amount of CO2 that gets built up based
on metabolism
Assume RQ = 0.8
PAO2 determined mostly by Patm and FIO2
Fickss Law of Diffusion
Vgas = A/T x D x (P1 P2)
- With exercise, the alveolar area increases
- In emphysema, the alveolar area decreases
- Thickness across the alveoli (it increases in fibrosis and pulmonary
edema)
- CO2 is more soluble than O2
- Partial pressure gradient is the main driving force for
diffusion
Limitations on Gas Exchange
A gas can be perfusion limited or diffusion-limited
Perfusion limited
- Exchange of O2 and CO2 under normal conditions (diffusion takes
place under normal circumstances)
- You are reaching a state of equilibrium across the membrane
- What is limiting perfusion is blood flow
- The rate of gas exchange can only be increased by increasing
blood flow

Diffusion-limited
- Substance does not reach state of equilibrium
- The rate of exchange can only be increased by increasing the
partial pressures
- This is whats happening under strenuous exercise, high altitude,
and in pathologic conditions such as emphysema and pulmonary
fibrosis
- For Example: CO
Normal physiology is perfusion limited
Weird physiology is diffusion limited
DLCO: Diffusion Capacity of lung
Allows to measure surface area and membrane thickness
- A small sample of gas containing CO is given
- Under normal circumstances, it should go directly into
blood
- If there is damage (a decrease in surface area), then less CO will
go into blood
Total Oxygen Content
- How much O2 is bound to Hb and O2 dissolved in plasma
- 20 volume percent (20 ml oxygen/100 ml of blood)
The PaO2 represents how much is dissolved in the plasma
The amount of O2 dissolved in the plasma influences the % saturation
of Hb
O2 dissolved in plasma represent only a 0.3 volume percent
Most of the O2 is in the Hb
Oxygen in the plasma is what goes into the tissue
As the oxygen content in the plasma goes down, Hb starts releasing
oxygen

Alveolar-arterial (A-a) oxygen gradient

Pulmonary artery carries deoxygenated oxygen (PO2 = 40 mm Hg) to

the capillaries in the lung where it equilibrates with the alveolar to a
PO2 of 100 mm Hg. It goes out the pulmonary vein and into the
systemic arterial with a PO2 of 95 mm Hg (due to shunt)
A-a gradient = 100 95 = 5

Hemoglobin Oxygen Transport

Under normal physiology, Hb in blood leaving the lung is 97%
saturated

The amount of oxygen in the plasma

(PO2) influences amount of saturation
Site 4: Hb in blood leaving the lungs (arteries)
Site 3: Hb in veins (75% saturated)
Site 2: P50
- PO2 when Hb is 50% saturated
- Minimum de-saturation

O2 combines with Fe+2 in heme and is not oxidized to Fe+3

Methemoglobin
- In this case, the F+2 is actually oxidized
- It has a blue tint to it

Amount of O2
that went into
tissues

19.
a.
b.
c.
d.
e.

Forced expiratory volume in the first second (FEV1)

Is normally approximately 80% of forced vital capacity
Is normally approximately 80% of total lung capacity
Is a static lung volume
Is measured using a Wright flow meter
Decreases in restrictive lung disease

a.
b.
c.
d.
e.

An example of a restrictive lung disease is

Bronchitis
Asthma
Emphysema
Fibrosis
All of the above

20.

21.
a.
b.
c.
d.
e.

In obstructive lung disease

Resistance in the airways of the respiratory zone increases
Radius of the airways in the conducting zone increases
Diffusion capacity decreases
FEV1
Resistance in the airways of the conducting zone
increases

22.

The diffusion capacity of the lung (DL)

a. Decreases in disease states such as emphysema where
surface area for gas exchange decreases
b. Decreases in edema where the diffusion distance increases
c. Decreases in asthma
d. Is slightly greater for O2 than CO because the solubility of
O2 is greater than CO
e. All except C

23.

DLCO is measured
a. With a body plethysmograph
b. By dividing the difference between CO inspired into and
expired from the respiratory zone by the partial pressure of
CO in the respiratory zone
c. By determining the alveolar minute ventilation

d. To determine the diffusion capacity of the lung because the

movement of CO across the air/blood barrier of the lung is
perfusion limited
e. All except C

1. Diffusion capacity
a. Is measured using the nitrogen washout technique
b. Is measured using a Wright flow meter
c. Is a dynamic lung volume
d. Measures the resistance of the airways in the conducting
zone
e. Is determined by measuring the net flux of carbon
monoxide from the alveolar space to the pulmonary blood
2. Expired air
a. Has a higher PH2O than room air because it has been
humidified by passage through the nasal cavity and
airways
b. Has a higher PO2 than alveolar gas because some expired
air comes from the airways in the conducting zone
c. Has a lower PCO2 than alveolar gas because some expired
air comes from the airways in the conducting zone
d. All of the above
e. None of the above
3. Ventilation is stimulated by
a. An increase in arterial PCO2
b. An increase in arterial PO2
c. An increase in blood pH
d. Barbiturates
e. Edema of the brain

Oxygen Delivery (DO2)

- Cardiovascular system is important in oxygen delivery
- Q (CO) x total oxygen content
- Normally 1200 ml oxygen/min under normal physiology

Oxygen Exchange
1) Oxygen dissolved in plasma moves into tissue
2) This causes oxygen to be released from Hb
3) It eventually equilibrates
4) Blood enter the venous blood
- PO2 in venous blood is a reflection of gas exchange
If you sample venous blood, that tells you what the tissues did
The alarm is usually set at 90% Hb saturation because the oxygen
content starts to fall pretty quickly below that saturation
The blood that comes in gets oxygenated pretty quickly. This is
important so that it can act as a buffer (more time to saturate blood)
in case something goes wrong
Lung functions are reflected in arterial gas values (since blood had
just left the lungs)
Tissue status is reflected in venous gas values
Oxygen Delivery To tissue
A right sift of the dissociation curve lowers the affinity of Hb for
oxygen, which means more oxygen is going to the tissue
A left shift means less oxygen to the tissues
-

Increase CO2, acid, temperature shifts curve

To the right (more O2 delivered to tissues)
- Reflection of active tissue
- Extracting more O2 from blood
- Blood flow also increases
2,3-BPG is stimulated by hypoxia
P50 has increased

Carbon Dioxide Transport and Neural Regulation of Breathing

CO2 and Blood

1) Dissolved in plasma in about 5%

- More soluble than O2
2) Bound to proteins and Hb in about 5% (CO2 binds to a different
site in Hb so it doesnt compete with O2
3) 90% is converted to HCO3CO2 goes into the RBC and combines with H2O and turns it into H2CO3.
That dissociates into H+ and HCO3-.
- HCO3- leaves the RBC and goes into the plasma (acting as a
buffer). At the same time, chloride goes into the RBC (Chloride
shift)
- This in an electro neutral shift to ensure RBC maintains
neutrality
H+ binds to Hb, so Hb is acting like a buffer
- Curve is shifted to right and oxygen is released
- Bohr effect (takes place at tissues)
- Helps unload O2 at tissues

Tissue tells how much oxygen you need

- if you have local high levels of CO2, then the vessels are going to
dilate (more flow)
- CO2 kicks in Bohr effect, releasing more oxygen
Haldane Effect
- Opposite of the Bohr effect
- Takes place at the lungs
-

As oxygen is picked up in the lungs, CO2 is released so that is can

be excreted
When oxygen levels are high, CO2 levels are low

Reminder:

Phrenic nerve controls the diaphragm (Cervical 3, 4 and 5)

- Activated by dual pathways
- Voluntary (corticospinal tracts)
- Involuntary tracts
Medullary Respiratory Center
The medulla is the primary respiratory centers
The pons fine-tunes it
Pre-Botzinger complex
- Where the pacemaker cells are (inherit rate is 14-15 times a
minute)
- They send info to the Dorsal Respiratory Group
Dorsal Respiratory Group
- Active only during inspiration
- Primary inspiratory center
- Send info to the phrenic nerve and thoracic nerve (external
intercostal)
- When they become inactive, you go into expiration
- Cells are modulated by impulses from Vagus (X) and
glossopharyngeal nerves (IX)
- They are afferent (they are sensory and bringing in
information to the medulla)
- Either from peripheral chemoreceptors or
mechanoreceptors
Ventral Respiratory Group
- Active during forceful inspiration and expiration (ex. Exercise)
Pontine Respiratory Centers (fine-tunes)
Apneustic Center
- Prolongs inspiration
Pneumotaxic Center
- Terminates inspiration so that it doesnt get too long
- Shortens duration of inspiration
Inputs to Respiratory Centers
-

PCO2, PO2 and pH are the three main things that influence
respiratory activity

Central and Peripheral Chemoreceptors

Central chemoreceptors are located in the CNS
- Are sensing whats happening in the arterial system via
changes in the cerebral spinal fluid. The cerebral fluid is
going to be influenced based on whats happening in the arteries
- Sensitive to pH (influenced by CO2)
- Acidity stimulates respiratory activity
- Primary receptors that control respiration
Peripheral receptors are located in the aortic and carotid bodies
- Have the ability to sense PCO2, PO2 and pH
- They act first because they are directly in contact with blood
They are sending information to the medulla. The medulla then sends
information through the dorsal root and down the phrenic nerve
The strongest response is through the central receptors and the
quickest response is through peripheral receptors
Why CO2 to influence respiration and not O2
- The oxygen dissociation curve is flat on the top so by the time I
get to the top, it would be too late

Normal arterial PCO2 = 40 mm Hg

As oxygen levels drop, respiratory rates go up
- If arterial PO2 falls below 60 mm Hg then other
systems kick in and ventilation goes up
They work synergistically

Central Chemoreceptors
-

CO2 diffuses into cerebrospinal fluid from arteries

- Once in the fluid, it is converted to H+, where they interact
with the receptors and increases ventilation
There are no receptors for O2 in the brain. The brain is
strictly a pH monitoring system
The cerebrospinal fluid is limited in its buffering capacity

H+ cant cross into the brain

If the levels of CO2 go to 70 or 80 mm Hg, then the central receptors
become depressed (CO2 narcosis)
Therefore, there is a point where it stimulates activity and a point
where it
inhibits activity
Peripheral Chemoreceptors
-

Sensing whats in the blood

pH and CO2 of blood are being monitored by those receptors
There are also PaO2 receptors, but they are only active when the
PaO2 falls below 60 mm Hg
They respond first, but they are weak

The peripheral receptors respond to changes in blood pH and that is

going to be involved in acid/base physiology
Acute Responses to inhaled CO2
As CO2 goes up, respiratory activity increases. It increases even more if
PO2 is low
- Synergistic effect
Hypercapnia
- Elevated CO2
- Usually due to a decrease in alveolar ventilation
(respiratory issue)
Increases in cerebral blood flow and intracranial pressure
Brain metabolism starts to change

Chronic Hypercapnia
In patients COPD
- Oxygen levels low
- CO2 levels high
The central chemoreceptors become adapted after 12-24 hours
- The increased ventilation in these patients is due to
hypoxia stimulation of peripheral chemoreceptors
The peripheral receptors are now there to kick in if you have problems
- Sensitive to low levels of O2
- During low levels of oxygen, these receptors tell the brain to
breathe
- If you give them 100%O2, then they strop breathing
because that stimulus is gone
Input Integration and Sleep
During sleep, respiratory drive is reduced and CO2 levels rise just a bit
Central sleep apnea
- They have an increase in drive from the brain, blow off more
CO2 and stop breathing
Obstructive sleep apnea
- Obstruction
Abnormal breathing
Apneustic breathing
- Periods of long inspirations followed by periods of short
expiration
- Usually associated with lesions to pons
Cheyne-Stokes breathing
- Rapid periods of ventilations then nothing
- Usually associated with congested heat failure
- When someone is dying

Respiratory Mechanics and Airway Physiology

Total (minute) ventilation = VT x frequency
Dead Space
-

Regions in the respiratory system where there is air, but no gas

exchange
The anatomic dead space is the conducting zone

At end of expiration
- Contains oxygen and carbon dioxide
- Representative of the respiratory zone
At end of inspiration
- Contains oxygen but NOT carbon dioxide
Alveolar Ventilation (VA)
VA = volume of gas that participates in gas exchange
(VT VD) x respiratory rate
If dead space is increased, then alveolar ventilation decreases
Alveolar Dead Space
- Alveoli containing air but without flow (no gas exchange)
- Pulmonary embolus (blocking blood flow in a particular
area)
Physiologic dead space = Anatomic dead space + Alveolar dead
space
In pulmonary embolism, oxygen will be high and carbon dioxide
will be low (zero) in those particular alveoli because there is no blood
flow for gas exchange

The body compensates by bronchial constriction, decreasing

air flow to that particular region and making air go to regions
where there is adequate blood supply
- The low carbon dioxide is what causes the bronchioles
to constrict

If someone has alveolar dead space, then they are going to be

breathing out less carbon dioxide
VD =

PaCO 2PECO 2
PaCO 2

Normally, it is 20%
Lung is not uniform
Alveoli at the top of the lung are bigger than at the bottom because
they have a greater transmural pressure
- The ones at the top have a lower compliance and the ones at the
bottom a larger compliance
- Therefore, more air flows to the bottom when taking a breath

More blood flows to the base of the lung than

the apex due to gravity

Ventilation-Perfusion Relationship
In order to get gas exchange then the ventilation-perfusion
matching has to be normal
Normal value of V(how much air Im moving into and out of
lungs)/Q(blood flow [CO]) is 0.8
Ideal is 1.0
The V/Q ratio is not uniform throughout the lung
- Ventilation increases from apex to the base (alveoli at the top are less
compliant)

- Blood flow also increases, but more rapidly (perfusion)

As a consequence, there is going to be a mismatch where the V/Q ratio
is high at the top of the lung and lower at the bottom, and perfect
match at the middle
At the base, alveoli are under-ventilated because blood flow is larger
than ventilation
- PCO2 > 40
- PO2 < 100
At the apex, alveoli are over-ventilated because ventilation is greater
than perfusion
- PCO2 < 40
- PO2 > 100

2
1(base) (obstruction)
If ventilation is zero, then PO2 will be low and PCO2 will be high
- PCO2 will be high because you still have blood flow
- Blood comes out with low oxygen and high carbon dioxide
2 (pulmonary embolism)
Blood flow is 0, but there is ventilation
- High PO2 and low PCO2
Hypoxic vasoconstriction
Anytime in the lung where there is a region of hypoxia, the blood
vessels will vasoconstrict in order to send blood to areas where
you have good ventilation
- Compensation mechanism

A-a gradient
- Normally there is an Alveolar-arterial (A-a) gradient due to
anatomic shunts (100-95) = 5
Normal A-a = (Age +4)/4
Hypoxia: inadequate oxygen delivery to the tissues
Hypoxemia: refers to low PaO2

Causes of Hypoxemia
1.
2.
3.
4.
5.

Hypoventilation
Altitude breathing or low inspired
Diffusion impairment
V/Q mismatch, low VQ unit
Intrapulmonary shunts, R-L shunts

Normal A-a
gradient

O2

Elevated A-a
gradient

Hypoventilation
- Increase in PCO2
- As PCO2 goes up, PAO2 goes down
- Lung is NOT the problem
- A-a is normal
- Give them oxygen to treat
High Altitude breathing or low inspired O2
- High altitude means PatmO2 is reduced so PAO2 is reduced
- PaCO2 is decreased due to hyperventilation in response to
hypoxemia
- Give them oxygen to treat
------------------------------------------------------------Diffusion impairment
- The problem is getting oxygen into the blood
- Thickness increases (pulmonary edema, fibrosis)
- Elevated A-a gradient
- Enriched oxygen can relieve hypoxemia but A-a gradient
still exists

Ventilation-Perfusion (V/Q) Mismatch: Low V/Q units

- If low ventilation, then oxygen levels fall
- There are some areas in the lung that are unaffected so
administration of O2 can alleviate the hypoxemia
- Problem is in the lung itself
- For instance, a mucus plug
- Lung compensates by vasoconstriction
Intrapulmonary (R-L) shunt
- We are taking deoxygenated blood from the RV and sending it
to the lung without picking any oxygen and dumping it to
the left side
- Diluting the blood
- Supplemental oxygen does not fix the problem
- This is an extreme low V/Q mismatch

Non-Respiratory Lung Functions and Respiratory Response to

Stress
Pulmonary Capillary Exchange
Risk of edema is minimized by
- Low capillary hydrostatic pressure
- Surfactant decreases risk of pulmonary edema
- Alveolar surface tension is pulling fluid away from capillary
- This can be minimized by using surfactant to reduce
surface tension
- Extensive lymphatic system
Cardiogenic Pulmonary Edema
Congestive heart failure can cause pulmonary edema due to an
increase in LAP, which increases capillary pressure. First sign is often
orthopnea (difficulty breathing in a supine position)
- LAP can be treated using diuretic
Pulmonary wedge pressure can be used to measure LAP
Non-Cardiogenic PE
The key thing that triggers this is inactivation of surfactant
Pulmonary Edema

Lung compliance is decreased (restrictive disease)

Hypoxia
Hypoxic hypoxia
- Hypoxemia (low arterial PO2)
Anemic hypoxia
- Decreased total amount of O2 bound to hemoglobin
Ischemic hypoxia
- Everything is normal except for a reduced blood flow
Histotoxic hypoxia
- Failure of cells to use O2 because cells have been poisoned
Tissue status is reflected in venous gas values, lung functions are
reflected in arterial gas values
Altitude Stress
- Peripheral chemoreceptors kick in when oxygen levels fall below
60 mm Hg
- You start hyperventilating and you get a decrease PACO2
(hypocapnia) and PaCO2
- This increases arterial pH (respiratory alkalosis)
- Increased hematocrit due to increased EPO
- [2,3-BPG] increases to enhance oxygen release from Hb
- This decreases the Hb% sat
You get acclimated by increasing Hb concentration (polycythemia) (in
takes about 7 days) your blood gets thicker
You also get pulmonary vasoconstriction
The increased pulmonary vasoconstriction and polycythemia causes
pulmonary hypertension and makes it harder for your heart to pump
blood and leads to right heart failure
The extreme hypoxia causes local vasodilation of cerebral blood
vessels and your brain swells

High Pressure Environment

Normally nitrogen has a low solubility, but it increases under water
with extra pressure. Nitrogen is forced into the blood
- If you start to go up too rapidly, it bubbles out due to a lower
pressure
- Hyperbaric chamber to force nitrogen back into blood and
then forcing it out by slowly decreasing the pressure
Hb concentration effects
In anemia, what only changes is the total O2 content
P50 is the same and saturation is also the same
Carbon monoxide poisoning
-

CO binds with Hb on the same binding site as O2

Once CO binds, it doesnt come off. Therefore, the functional
concentration of Hb decreases
What you get is a reduced arterial O2 content. The arterial PO2 is
the same since the amount that is dissolved in the plasma
doesnt change
When Hb binds to CO, the curve shifts to the left, P50 decreases
(Hb doesnt unload O2)
Venous PO2 is reduced, reflecting an increased tissue
utilization of oxygen (they have to extract more oxygen than
normal since they see less oxygen)

Ischemic Hypoxia
-

Due to low blood flow

If cyanosis is seen in lips and tongue then it is a generalized
hypoxia (due to cardiac issues)
If cyanosis is seen in extremities (fingers) then it is a localized
hypoxia (due to intense vasoconstriction; e.g exposure to severe
cold)

Histotoxic Hypoxia
-

CN poisoning blocks enzymes in the ETC

Tissues cant extract oxygen, therefore,
elevated

Oxygen Therapy

venous

PO2

is

When breathing pure oxygen, you are primarily changing the

amount of free O2, not the storage

Acid-Base Physiology Clinical Emphasis

Changes in lung, kidney or metabolism can produce acidosis
Buffers are the first line of defense but can be overwhelmed quickly.
Buffers just bind H+; they dont get rid of them.
Closed Buffer system
- In a compartment (like Hb inside the RBC)
- How well that buffer can do depends on the concentration of the
buffer
A single buffer works best at a particular range
Open
-

Buffer System
Allows a wide range of options to deal with a situation
Allows to get rid of the problem
CO2 + H2O H+ + HCO3-

- CO2 can then be get rid of it

How well this buffer system works depends on the
concentration of HCO3- . Whos controlling HCO3-? The kidney
PCO2 controlled by lung function

Urinary Buffering
- Although the extracellular pH is the primary physiologic regulator
of net acid secretion, in pathophysiologic states, the effective
circulating volume, aldosterone, Ang II, and the plasma K+
concentration all can affect acid excretion, independent of the
system pH
Lungs
- When we are dealing with plasma pH changes, the peripheral
chemoreceptors are responsible since H+ doesnt cross the
brain barrier
The respiratory system kicks in very quickly (within minutes). If this
cant fix it, then the kidney kicks in (3-4 days before maximum
response is reached)
Acid- Base Imbalances
-

Acidosis and alkalosis are processes that alter the pH. What we
get is either acidemia or alkalemia
In a mixed acid base disorder, multiple acid base processes are
coexisting and may lead to a normal pH

Respiratory vs. Metabolic

1. Respiratory acidosis
- Too much CO2; you are holding on to too much CO2
2. Metabolic acidosis
- Addition of H+ (not coming from CO2) and/or loss of bicarbonate
- Any acidosis that is not respiratory
3. Respiratory alkalosis
- Not enough CO2
- Hyperventilating
4. Metabolic alkalosis
- Loss of H+ (not coming from CO2) and/or addition of bicarbonate
- Vomiting
Normal Values:
pH= 7.4

HCO3- = 24 mEQ/L
PCO2 = 40 mm Hg
Respiratory Acidosis
Anything that causes an increase of CO2 because of reduced alveolar
ventilation
Treat underlying disorder
Supply oxygen since a high CO2 means a low oxygen level
Respiratory Alkalosis
- Due to low CO2 levels
- Hyperventilation
- Can cause cerebral vasoconstriction and leads to reduced cerebral
blood flow
- Can cause secondary hypocalcemia
- H + and Ca+2 compete for binding sites on proteins; decreased
H+ means more Ca+2 is bound to proteins resulting in
hypocalcemia
Treat by re-breathing into paper bag
If intubated, reduce minute ventilation by adjusting rate
Metabolic Acidosis
- Characterized by a reduction in HCO3- If you put acid in the body, then HCO3- is going to be used up
- Loss of HCO3- via urine or GI tract
Plasma Anion Gap
Major players:
Cations:
Na+
=

Anions:
ClHCO3PAG(Plasm
a Anion
Gap)

PAG: anions that are there, but you are not measuring them in the
hospital

PAG = Na+ - (Cl- + HCO3-)

122
With Normal AG
- If the anion of the acid added to the plasma is Cl -, the anion gap
will be normal because the decrease in [HCO 3-] is matched by an
increase in [Cl-]
With Increased AG
- If the anion of the acid is not Cl -, then the anion gap will increase
because the decrease in [HCO 3-] is not matched by an increase in
the [Cl-] but rather an increase in an unmeasured anion
Metabolic Acidosis - Normal Anion Gap
1. Diarrhea (loss of base)
- Since you are losing fluids, your body is going to try and retain
NaCl
2. Type 1 (distal)
- They are normally excreting hydrogen; if they cant excrete
them then you are going to be in a state of acidosis
3. Type 2 (proximal)
- They are normally absorbing HCO3-; if you cant reabsorb them,
then you are in a state of acidosis
4. Type 4
5. Toxic ingestions (if they contain Cl-, then anion gap will be
normal)
If you have a specific kidney dysfunction, then you are going to
have a normal anion gap

Metabolic Acidosis- Increased Anion Gap

1. Increased acid production (ketoacidosis, lactic acid acidosis)
2. Toxic ingestions (salicylate, methanol, ethylene glycol)
3. If you have a generalized renal failure; the kidneys are failing
in general and you have a retention of unmeasured anions
(sulfate, phosphate and urea)
Anion Gap Pneumonic

Metabolic Alkalosis
- Characterized by an elevation in [HCO3-]
Can be caused by:
- Vomiting
- Diuretic use results in water loss and an increase in [HCO 3-] due to
water loss
- If ECF reduction, then you will see an increase of angiotensin then
Ang II and aldosterone will be secreted. This leads to an increase in
[HCO3-] reabsorption and increased H + and K+ secretion, leading to
hypokalemia
Hypokalemia and Alkalosis go together. If you see one, then you have
to look for the other one
Contraction alkalosis
- Caused by the loss of fluid (resulting in concentration of
bicarbonate), which results in the increase of aldosterone
- What perpetuates the alkalosis is angiotensin II that is released by
the fluid loss

Acid-Base Imbalances
Steps
1. What is the osis? Check pH
2. What is the cause of the osis? Look at the bicarbonate
3. Calculate the appropriate compensation

In Respiratory acidosis, the pH is down since there is an increase

in CO2
- This shifts the reaction to the right and HCO3- goes up
- When compensating, HCO3- will be way up

In Metabolic acidosis, the extra H+ being added binds to HCO3-,

decreasing [HCO3-] way down and blowing off more CO2
- Predicted fall in CO2: 1.5 x bicarb +8
(compensating)

In respiratory alkalosis, your are getting rid of CO2, shifting the

reaction to the left and losing HCO3- a fall of 0.2 of bicarb for every 1mm fall of CO2
(acute)
- a fall of 0.5 of bicarb for every 1mm fall of CO 2
(chronic)

In metabolic alkalosis, there is an increase of [HCO3-]

- Predicted rise in CO2: (0.7 x rise in HCO3-) + 40

Compensation
- In a respiratory disorder, the kidney is going to fix it by adjusting the
bicarbonate to match the CO2 change
- Acute (uncompensated): a rise of 0.1 of bicarb for every
1mm rise in CO2
- Chronic (compensated): a rise of 0.35 of bicarb for every
1mm rise in CO2

- In a metabolic disorder, the respiratory system will adjust the CO 2

levels to match the bicarbonate
In compensation, bicarbonate and CO2 move in the same direction. If
they move in the opposite direction you have a mixed disorder.
Compensation for Respiratory Acidosis
PaCO2 = 60 mm Hg
This is 20 mm Hg greater than the normal 40 mm Hg
If acute, then HCO3- will be (20 x 0.1) + 24 = 26
If chronic, then HCO3- will be (20 x 0.35) + 24 = 31
Compensation for Metabolic Acidosis
First calculate the predicted PaCO2
Predicted fall in CO2: 1.5 x bicarb +8
-

If the patients PaCO2 is within the predicted value then

respiratory compensation has occurred
If PaCO2 is higher than calculated then there is also respiratory
acidosis
If PaCO2 is lower than predicted, then patient also has respiratory
alkalosis

Dont forget to check AG

Compensation for Metabolic Alkalosis
First calculate the predicted PaCO2
Predicted rise in CO2: (0.7 x rise in HCO3-) + 40
-

If the patients PaCO2 is within the predicted value then

respiratory compensation has occurred
If PaCO2 is higher than calculated then there is also respiratory
acidosis
If PaCO2 is lower than predicted, then patient also has respiratory
alkalosis

Davenport Diagram

Compensati
ng
(Chronic)
acut

For compensating, we shift towards the green line (Normal values)

Here is an example of a patient having both respiratory acidosis and
metabolic acidosis:
PCO2 = 60 mm Hg
[HCO3- ]= 14 mEq/L

1. Alveolar minute ventilation is

a. (tidal volume)(breathing rate)
b. (tidal volume physiological dead space) (breathing rate)
c. (vital capacity dead space) (breathing rate)
d. (vital capacity residual volume) (breathing rate)
e. (tidal volume residual volume) (breathing rate)
24.
a.
b.
c.
d.
e.

The binding of O2 to hemoglobin

Increases with increasing temperature
Increases as [H+] in the blood increases
Increases with increasing PO2
Only accounts for a small amount of O2 carried by blood
Increases in the presence of CO

a.
b.
c.
d.
e.

Most CO2 is transported in blood

As dissolved CO2
Bound to hemoglobin
As bicarbonate in plasma
As bicarbonate in red blood cells
As CO2 bound to hemoglobin

25.

26.
CO2 and O2 equilibrate between the alveolar and the
pulmonary capillaries but not between the systemic capillaries
and the muscle tissue because
a. Blood flow is greater in the muscle than the lung
b. Solubility of gases is greater in the lung tissue than in
muscle tissue
c. Systemic capillaries are further apart than pulmonary
capillaries
d. Pulmonary blood pressure is lower than systemic blood
pressure
e. None of the above
27.
a.
b.
c.
d.

Pulmonary blood flow

Is only 25% of cardiac output
Is high because pulmonary vascular pressure is high
Is greater in the apex than the base of the lung
Increases in the apex of the lung with exercise

e. None of the above

28.
a.
b.
c.
d.
e.

29.

Ventilation
Is greater in the base of the lung than the apex
Is greater in the apex of the lung than the base
Is highest in the region of the lung with the lowest
perfusion
Is measured by DLCO
Is measured by injecting Xe133 into the peripheral vein and
counting the radioactivity in the thorax during breath
holding

Oxygen chemoreceptors
a. Are located in the medulla
b. Measure the PO2 of cerebrospinal fluid
c. Are more important in controlling ventilation than carbon
dioxide chemoreceptors
d. Send stimulatory signals to the cortex
e. Are located in the carotid bodies and aortic bodies

30.
Input from the pulmonary sensory receptors,
chemoreceptors, and other regions of the brain are integrated
a. In the medulla
b. In the pons
c. In the midbrain
d. In the cerebellum
e. Throughout the brain

31.
a.
b.
c.
d.

Mark the one incorrect statement:

A primary fall in plasma HCO3- is indicative of metabolic
acidosis
A primary fall in plasma PCO2 is indicative of metabolic
alkalosis
In a primary in metabolic acidosis, the compensatory
response is to decrease the respiration
In a respiratory acidosis, the tubular secretion of H+ is
increased

32.

Mark the one CORRECT statement:

a. If the plasma pH is 7.4, then the acid base balance must be
normal
b. A buffer is usually a salt of a strong acid
c. A buffer acid is completely dissociated when the pH = pKa
d. Hemoglobin is an important blood buffer

4. During exercise, a subject has a breathing rate of 20 breaths/min

and inhales 1000 ml/breath. Minute ventilation would be
a. 7500 ml/min
b. 20000 ml/min
c. 5250 ml/min
d. 2 L/min
e. 10 L/min
5. During an accident, an individual punctures the chestwall
between the 7th and 8th right ribs. The pneumothorax would
cause
a. The right lung to collapse
b. Hyperinflation of the right lung
c. Collapse of the right and left lungs
d. Collapse of only the upper lobes of the lungs
e. Apnea
6. Blood flow in the base of the lung
a. Is greater than ventilation
b. Is greater than in the apex of the lung
c. Is lower than in the apex of the lung
d. Is measured by inhaling radiolabeled Xe
e. All of the above
7. During exercise
a. Perfusion increases in the apex of the lung
b. Gas exchange of O2 and CO2 increases in the lung
c. Ventilation increases
d. All of the above
e. None of the above

8. The pneumotaxic center

a. Is located in the dorsal medulla
b. Acts to prolong inspiration
c. Acts to shorten inspiration
d. Is a voluntary control of ventilation
e. Responds to an increase in PCO2
9. Peripheral chemoreceptors
a. Are located in the carotid bodies and aortic bodies
b. Are sensitive only to PCO2
c. Are sensitive only to PO2
d. Are located in the ventral medulla
e. None of the above
10.

In a simple metabolic acidosis

a. Acidemia occurs due to a fall in plasma HCO3concentration
b. The compensatory response includes a reduction in the
rate of respiration
c. The compensatory response includes an increase in the
rate of renal hydrogen ion secretion
d. Both a and c are true
e. The anion gap is always elevated

11.
In the kidney, the long term maintenance of acid-base
balance is due to the renal excretion of H+ and the renal
replenishing of the bodys buffer stores. Renal hydrogen ion
excretion has the following characteristics:
a. When aldosterone is present, the secretion of H+ in the
proximal tubule is stimulated
b. Hydrogen ion secretion in the collecting duct is responsible
for most of the reabsorption of the filtered HCO3-.
c. Renal hydrogen ion secretion is stimulated when PCO2 falls.
d. For every hydrogen ion excreted as ammonium or
titratable acid, a new bicarbonate ion is formed.
e. Hydrogen ion secretion in collecting duct occurs in the
principal cells by the Na-H exchanger.

12.
From the laboratory values given below, choose the most
likely acid-base disturbance in this patient. Plasma pH = 7.5;
plasma potassium = 2.8 meq/l; Plasma chloride = 110 meq/l;
Plasma sodium = 140 meq/l; Plasma HCO3- = 24 meq/l; PCO2 =
30 mmHg.
a. Simple metabolic acidosis
b. Acute respiratory alkalosis
c. Mixed disorder: combined metabolic and respiratory
alkalosis
d. Mixed disorder: respiratory alkalosis and high anion gap
metabolic acidosis