Respiratory Physiology

Fellow/Masters
LESSON 1
 Volumes and Gases
• We can use O2 and CO2 to Understand
Volumes:
 Helium Dilution Test : FRC
Start and End at FRC
The helium-dilution technique makes use of the following relationship:
Amount of solute = concentration of solute x volume of solvent

In the helium-dilution technique, helium is inspired and dissolved in the gas

in the lungs. The concentration of helium is determined with a helium meter.
allowing calculation of the patient lung volume.
Helium is used for this test because it is not taken up by the pulmonary
capillary blood. The total amount of helium does not change during the test.
The helium concentration is monitored continuously with a helium meter until
its concentration in the inspired air equals its concentration in the subject's
expired air.
At that point the concentration of helium is uniform in the spirometer and the
patient's lung.

The test is stopped at the end of a normal tidal volume (Start also from
FRC), FRC and the volume of FRC is calculated:
Initial Concentration of helium x Initial Spirometer Volume =
Final Concentration of Helium x (Final Spirometer Volume + FRC)
The helium dilution technique measures the FRCl
A closed-circuit system where a spirometer is filled with a mixture of helium (He) and oxygen.
The amount of He in the spirometer is known at the beginning of the test (Concentration ×
Volume = Amount).
The patient breathe in the mixture starting from FRC. The spirometer measures helium
concentration. The helium spreads into the lungs and settles at a new concentration (C2).
Because there is no leak, the amount of helium remains constant and the FRC is calculated by
using the following equation:

C1×V1 = C2×V2
C1×V1 = C2×(V1+FRC)
FRC = ((C1xV1)/C2) - V1
V2 = Total gas volume ( FRC + volume of spirometer).
V1 = Volume of gas in spirometer.
C1 = Initial (known) Helium Concentration.
C2 = Final Helium concentration (Measured by the spirometer).

Note: To measure FRC we connect the patient to the spirometer after a normal breath: end of
normal expiration (when the lung volume equals FRC), if the patient is initially connected to
the spirometer at a different lung volume (like TLC or RV) the measured volume will be the
initial volume we started from and not FRC.
In patients with obstructive pulmonary diseases helium dilution technique are not reliable
because of incomplete equilibration of the helium in all areas of the lungs. In such cases it is
more accurate to use a Body Plethysmograph.
 FRC

Between breaths, there is a reservoir of gas over 8 fold larger

than the portion of the TV reaching the alveolus continuing
to absorb CO2 and provide O2 to the blood flowing through
the lung.
This arrangement also helps mitigate the drop in oxygen
content and rise in carbon dioxide content that occurs in the
alveolus and blood with brief cessation of breathing.
 FRC
DEFINITION
Volume remaining in lung after a normal expiration
RV plus Expiratory reserve volume
Equilibrium volume when the tendency of the chest wall to spring
out is balanced by the tendency for the lungs to collapsed inwards.
2.2L or 30mls/kg

FUNCTIONS
1. Buffers O2
2. Avoid atelectasis
3. Resistance: reduces Pulmonary Vascular Resistance
4. Resistance: reduces Airway Resistance
5. O2 Reservoir
6. Work: Decreases Work Of Breathing
7. V/Q mismatch: Minimises
Measurement of the Residual Volume - Helium Dilution
START/END AT RV

The residual volume cannot be measured with a spirometer.

Therefore, to measure RV, several techniques have been described.
In one such technique, an individual breaths into a closed circuit,
which contains a known amount of Helium.
Helium does not cross the blood-gas barrier and is not excreted by
the lungs.
Thus, decrease in the concentration of Helium is brought about by
the increase in the volume of the circuit by connecting the circuit to
the respiratory system.

When, the concentration of Helium is measured following a deep

maximal expiration (end of Forced Expiratory Volume), the total
volume is the volume of the breathing circuit + the residual volume.

Since concentration = amount of a substance / volume of

distribution, the residual volume can be calculated.
Total Body Plethysmograph: TLC
 TLC
• Pbox x Vbox = Pbox f x (Vbox i -∆V)
• Once V has been solved for we can then go on to
solve for the thoracic gas volume in the following
equation:
• PMi x VLi = PMf x (VLi + ∆V)
• This equation follows from the Boyle's Law and tells
us that the initial pressure measured at the mouth
(PMi) times the lung volume at which that pressure
is measured (VLi) will be equal to the new mouth
pressure (PMf) x the new lung volume (VLi + ∆V)
while the patient is making small changes in their
lung volume by panting against the closed shutter.
 Dead Space
Definition - the volume occupied by gas which
does not participate in gas exchange in lung.
A few different types, including:
• anatomical dead space
• physiological dead space
• alveolar dead space
• apparatus dead space
Anatomical dead space
Anatomical dead space is the volume of the conducting airways.
=> about 150mL in an average adult
=> or 2.2mLs/kg
Anatomical dead space is constant regardless of circulation.
Physiological dead space
Physiological dead space is the part of the tidal volume which does not
participate in gas exchange.
Includes:
anatomical dead space
alveoli with no perfusion (i.e. infinite V/Q) (e.g. West's zone 1)
The difference between anatomical dead space and physiological dead
space is alveolar dead space.
With increased cardiac output (e.g. during exercise), physiological dead
space is reduced (due to reduction in alveolar dead space).
Alveolar dead space
Alveolar dead space is the part of the inspired gas which passes through
the anatomical dead space to mix with gas at the alveolar level, but does
not participate in gas exchange. (i.e. infinite V/Q)
Apparatus dead space
When using mask or anaesthetic circuit tubing, this adds to the conducting
zone.
 Alveolar Ventilation
• Anatomic Dead Space → Fowler’s method
• Physiological (Total) Dead Space = Anatomical DS +
Alveolar DS → Bohr Equation
• Healthy : Anatomical DS=Physiological DS
Breathing and Ventilation
 Measurement of anatomical dead space
Fowler's method (Anatomical Dead Space & CV)

• Based on rapid dilution of gas already existing in lung (N2 or

CO2) by inspired gas (100% O2).
• Single breath of 100% O2
• During the following expiration, [N2] increases from 0% (pure
dead space gas) to equilibrium (pure alveolar gas) (i.e.
plateau)
=> as per [N2] vs time graph
• Using [N2] vs expired volume graph, anatomical dead space
is taken to be at the mid-point of the transition from
conducting zone to gas exchange zone.
 Volumes and Gases

• Fowler’s Method –
Anatomic Dead Space

• If you inhale a pure

gas (O2), you will exhale:
– Pure Dead Space Gas (N2 0%)
– Mixed Gas
– Pure Alveolar Gas (plateau)
 Volumes and Gases
• Fowler’s Method – (Single Breath N2 Curve)
Anatomic Dead Space

• Approximately 150 cc
in a “regular man”
• Equal weight in lbs
• 2.2 ml/kg
 Dead Space

• PCO2 curve as 500 cc TV is exhaled, initially it is about zero

representing gas in the conducting airways and then it rises
rapidly to 40 mmHg and plateaus representing alveolar gas.
• The rising portion represents a mixture of alveolar and dead
space gas. The approximate delineation between alveolar and
dead space gas is the mid-point of the rising portion of the
curve
Factors influencing anatomical dead space
•Size of subject
=> increases with body size
•Age
=> at infancy, anatomical dead space is higher for body weight
(3.3mL/kg)
•Posture
=> sitting 147mL, supine 101mL
•Position of neck and jaw
•Lung volume at the end of inspiration
=> anatomical dead space increases by 20mL for each L of lung
volume
•Drugs
=> bronchodilator will increase dead space
Factors influencing alveolar dead space
Low cardiac output can increase alveolar dead space (increasing West's
zone 1)
Pulmonary embolism
Measurement of physiological dead space
By using Bohr's equation and Bohr's method

Bohr's method (Conservation of Mass)

Based on "all expired CO2 comes from alveolar gas", and dead space doesn't eliminate CO2.
VT x FECO2 = VA x FACO2
Also, VT = VA + VD
=> VT x FECO2 = (VT - VD) x FACO2
=> VT x (FACO2 - FECO2) = VD x FACO2
=> VD/VT = (FACO2 - FECO2)/FACO2
VA = ventilated alveolar volume
VT = tidal volume
VD = dead space volume
FECO2 = fractional concentration of CO2 in mixed expired air
FACO2 = fractional concentration of CO2 in alveolus

Bohr equation: VD/VT = (PACO2 - PECO2)/PACO2

Normal value: 0.2~0.35
NB: PECO2 is the partial pressure in MIXED expired gas, NOT end-tidal gas

Enghoff modification - using measured arterial PaCO2 as an estimate of the ideal alveolar PACO2
=> modified: VD/VT = (PaCO2 - PECO2)/PaCO2
 Volumes and Gases
• Bohr Equation – Physiologic Dead Space
• (Fowler: Anatomical DS)
• All CO2 comes from alveolar gas
(not dead space : No CO2 in Inspired air))

• Arterial CO2 is almost always equal to Alveolar CO2

Enghoff modification

• There is conservation of mass.

Volumes and Gases
 Volumes and Gases
• Bohr Equation – Physiologic Dead Space

• VT x PECO2 = Pa CO2 x (VT – Vd) + PICO2 x Vd

Vd Pa CO2  PECO2

VT Pa CO2
 Single Breath N2 Curve
• NOTE: Closing Volume : Lung volume above RV above which
airway in the dependent part of lung start to close. Lower
transmural pressure. Same experiment
 Alveolar Ventilation
• “Residual Volume?”

• The amount of air left in the lung after

maximal exhale

• It’s purpose: Keep the Alveoli Open, No total

collapse
 Alveolar Ventilation
• At low volumes, alveoli would collapse by:

– Absorbing the last air left behind

– Emptying to a larger alveoli

(Surface Tension experiment)
Alveolar Ventilation
 Alveolar Ventilation
• What is surfactant?
– Mainly dipalmitoyl phosphatidylcholine
– Produce by Type II alveolar cells

Protein
B

Protein
D
 Alveolar Ventilation/ Surfactants
At low lung volumes:
• In the small alveoli
– The lipophilic tails of surfactant
are crowded and push each other away

– This keeps the alveoli open.

At large lung volumes:

• In the large alveoli
– The viscosity of surfactant
resist over-distension

– This keeps the alveoli from over expanding/pneumothorax

 Alveolar Ventilation
• Thus, surfactant acts to

• 1) keep airways and alveoli open during end

expiration. (lipophilic tail)

• 2) cause even distribution of air and prevent

over expansion during late inspiration.
(viscosity)
 Alveolar Ventilation
Surfactant resists LaPlace
(LaPlace is Collapsing pressure)
 Law of Laplace

• Pressure in alveoli is
directly proportional to Insert fig. 16.11
surface tension; and
inversely proportional to
radius of alveoli.
– Pressure in smaller alveolus
greater.

Figure 16.11
 Hysteresis
• This gives lung a special property

• The pressure-volume curve is different during

inspiration and expiration.
• Output not same as input: Some lag
• The inflation and deflation curves are not the same

• This is known as Hysteresis

Hysteresis
Hysteresis
 Hysteresis
• There are a variety of factors that influence the
pressure-flow curve and cause hysteresis.
• There are TWO main factors:
– Surfactant
– Collapse of Airways

• Surfactant causes the inspiratory portion of the

hysteresis loop.

• And collapse of airways causes the expiratory

portion of the hysteresis loop (LaPlace)
 Alveolar Ventilation
• Atmospheric Air has mostly nitrogen

• Air in the nose, mouth, or trachea has water

vapor

• Air that has been in the alveoli has water

vapor, CO2, and less O2
 Alveolar Ventilation
• Alveolar Ventilation is affected by:

– Total Flow in and out

– Anatomic Dead Space
– Physiological Dead Space
– Gas Mixing
Ventilation
 Oxygen
• Atmospheric Pressure is 760 mmHg (at sea level)
• Atmospheric Fraction of Oxygen is 21%
• When Air goes through our upper airways, it
becomes humidified and heated.
• The partial pressure of water rises to 47mmHg.
• Alveolar Oxygen concentration?
 P Alveolar Oxygen
ALVEOLAR GAS EQUATION
PAO2 = PIO2 - PACO2 / R

R = Respiratory Quotient

PAO2 = 150 - PACO2 / 0.8 (760-47)/0.21=150

(just before mixing, arterial CO2 equals alveolar CO2)

PAO2 = 150 - PaCO2 / 0.8

(Alveolar Gas Equation)

 Factors Determining Alveolar PO2
• O2 is diluted by the addition of water vapour as gas
moves down the airways.
• Upon arrival to the alveolar space the PO2 = FiO2 (Pb -
PH2O).
• There, the PO2 will drop further due to the exchange
of CO2 for O2 across the alveolar capillary membrane.
• The average exchange of CO2 for O2 is determined by
metabolism at the cellular level (1-1 ratio for carbs,
~0.7-1 for lipids).
• If the exchange is equal (R=1), the alveolar PO2 will
drop by the same amount as the PCO2 rises
 Alveolar Gas Eqn when R=1

• The increase in PACO2 is our marker for the decrease in

the PAO2. For every 1 mmHg rise in PACO2 the PAO2 will
drop by one mmHg → PO2 = FiO2 * (PB-47) - PACO2
 Respiratory Quotient, R
• The Respiratory Quotient, R, is the number of moles of CO2
produced per mole of O2 consumed. ( CO2/O2)
• For a person eating a regular diet, it is approximately 0.8
– It decreases with fat metabolism
– It increases with sugar metabolism

• The range of respiratory coefficients for organisms in metabolic

balance usually ranges from 1.0 (representing the value expected
for pure carbohydrate oxidation) to ~0.7 (the value expected for
pure fat oxidation).
• In general, molecules that are more oxidized (e.g., glucose)
require less oxygen to be fully metabolized and, therefore, have
higher respiratory quotients (CO2/↓O2). Conversely, molecules
that are less oxidized (e.g., fatty acids) require more oxygen for
their complete metabolism and have lower respiratory quotients.

• CHO: 1, Protein: 0.8-0.9, Fat: 0.7

Alveolar Ventilation for Oxygen-Oxygen Cascade
Alveolar Ventilation for Oxygen
OXYGEN CASCADE
 Alveolar Ventilation- Oxygen Cascade
• Thus, the things that reduce oxygen:
– Barometric Pressure
– Initial Inspired Fraction of Oxygen
– Humidification (before and after)
– Alveolar Mixing
– Diffusion Limits
– Mixing with Deoxygenated Blood
– Extraction by Tissue
The oxygen concentration is lowest at the
MITOCHONDRIA : 1.5 kPa (Pasteur Point)
 Oxygen Cascade
• Dry air: PO2 = 0.21x(760) = 159 mmHg
• Saturated air at 37 0C = 0.21x(760-47) = 149mmHg
• Alveolar gas: alveolar gas equation
• Arterial blood: 95mmHg (venous admixture)
• End capillary blood: 40mmHg
• Mitochondria: 4-22mmHg
– Pasteur Point: critical pO2 for oxidative phosphorylation:
1mmHg/ 1.5 kPa
• Oxygen concentration below which oxidative
phosphorylation CANNOT occur
• Below Pasteur point: beginning of anaerobic metabolism.
 A-a Gradient

• The alveolar pO2 is higher than the arterial pO2

• A-a gradient = PAO2 - PaO2

• The A-a O2 gradient (or difference) is < 10-15

mmHg in normal subjects
• (Age/4) + 4
 A–a gradient
• The A–a gradient is useful in determining the source of hypoxemia. Isolate
the location of the problem as either intrapulmonary or extrapulmonary

• A normal A–a gradient for a young adult non-smoker breathing air, is

between 5–10 mmHg.
• A–a gradient increases with age.
• For every decade of life, their A–a gradient increase by 1 mmHg.
• An estimate of normal A–a gradient is less than [age in years/4] + 4.

• Hypoxia with an abnormally increased gradient suggests (intrapulmonary)

– defect in diffusion,
– V/Q (ventilation/perfusion ratio) mismatch,
– right-to-left shunt.

• Hypoxia with a Normal gradient (extrapulmonary)

– Low Fi02
– hypoventilation:
Interpretation: Hypoxemia causes differentiated by A-a Gradient

Increased A-a Gradient Intrapulmonary

Right to Left Intrapulmonary Shunt (due to fluid filled alveoli)
Congestive Heart Failure
Adult Respiratory Distress Syndrome (ARDS)
Lobar Pneumonia
V/Q Mismatch (due to lung dead space)
Pulmonary Embolism
Atelectasis
Pneumonia
Obstructive Lung Disease (e.g. Asthma, COPD)
Pneumothorax
Diffusion Defect
Interstitial Lung Disease

Normal A-a Gradient Extrapulmonary

Hypoventilation
Neuromuscular disorders
Central nervous system disorder
Low inspired FIO2 (e.g. high altitude)
 Carbon Dioxide
• Tissue metabolism produces CO2

• Pulmonary Artery brings in CO2

• CO2 rapidly equilibrates with alveolar CO2

• During exhalation, alveolar gas mixes with dead

space gas and then displacing dead space gas (initial
No CO2) first and then mixed gas.

• By end exhalation, dead space gas is gone and CO2

measured is equivalent to alveolar CO2
 Carbon Dioxide
Capnogram = measurement of exhaled pCO2
• Phase 1: Baseline-initial Expiration (Dead Space) - No CO2
• Phase 2: Expiration - Mixed dead space plus alveolar gas
• Phase 3: Alveolar plateau – Peak call End Tidal CO2
• Phase 4: Inspiration
The CO2 waveform can be analyzed for 5 characteristics:
–Height
–Frequency
–Rhythm
–Baseline
–Shape

NORMAL CAPNOGRAM:4 phases

Phase I (inspiratory baseline) reflects inspired gas, which is normally devoid of carbon dioxide.
Phase II (expiratory upstroke) is the transition between VDanatomy, which does not
participate in gas exchange, and alveolar gas from the respiratory bronchioles and alveoli.
Phase III is the alveolar plateau. PCO2 of the last alveolar gas sampled is called the PETCO2.
Phase 0 is the inspiratory downstroke, the beginning of the next inspiration

Other features:
Normal end-tidal PCO2 is approximately: 38 mmHg or 5%
the alpha angle is the transition from Phase II to Phase III
the beta angle is the transition from Phase III to Phase I (the start of inspiration)
an additional phase IV (terminal upstroke before phase 0) may be seen in pregnancy
ETCO2 represents alveolar CO2 when a relatively horizontal plateau phase (phase III) is seen.
 Pulmonary Gas Exchange

• How does gas get from air to blood and back

again?

• It must cross the membrane which divides the

alveoli and the capillary.
 Diffusion of Gases
• Is Described by Fick’s Law

• Flow (amount of gas transferred) is

proportional to
• Cross sectional area,
• Diffusion constant,
• Pressure gradient,
• The inverse of the thickness of the membrane.
Diffusion of Gases
 Diffusion of Gases
Thus, to maximize gas flow:
• Lung
– the lung increases cross sectional area by extensive
branching, 23 generations: 80m2
– the lung makes the membrane as thin as possible: 3μm

• Blood
– the blood has mechanisms to increase rates of uptake
or removal of gas
Diffusion of Gases: Diffusion Capacity
2 components
 Diffusion of Gases
• Each Gas (O2 , CO2 , CO, NO2 , N2O, Halothane)
diffuses at a different rate.

• Blood flows by at a (relatively) constant rate.

• Thus, the total gas uptake can be limited by either

blood flow or diffusion.
 Diffusion of Gases

Severe exercise reduces the time for oxygenation

Gradient still exit
 Perfusion limitation vs diffusion limitation
Solubility determines the limitation to the rate of gas diffusion:
1. Diffusion limited
• e.g. carbon monoxide (CO)
• CO forms strong bond with Hb
• => increases in CO content result in very minimal increase in partial
pressure (plasma)
• => partial pressure difference still exists (ie. equilibrium is not reached)
when blood finishes its passage through the alveoli
• => transfer of CO is limited by the rate of diffusion, not the amount of blood
available.

2. Perfusion limited
• e.g. nitrous oxide (N2O)
• N2O doesn't form bond with Hb
• => increase in N2O content results in rapid rise in partial pressure (plasma)
(equilibrium within 0.075 second)
• => equilibrium is reached very early on
• => transfer of N2O is limited by the amount of blood available.
Transfer of O2 lies between CO and N2O.
Overall resistance to diffusion of O2 is made up of:

•Diffusion of O2 through blood-gas barrier (including plasma

and RBC interior)
•Reaction time of O2 with haemoglobin
RBC spends about 0.75 seconds in pulmonary capillary.
O2 reacts with haemoglobin within 0.2 seconds.
=> equilibrium for O2 is reached in 0.3 seconds.
due the short transit time, reaction time can still be a
limiting factor.

Normally O2 is perfusion-limited.
(Oxygen:Diffusion limited in pulmonary disease & severe exercise)
 Oxygen versus Carbon Dioxide

• Differences between these gases:

• Solubility constant of CO2 is 24x O2
• MW O2 is 16, less than CO2 28
• Overall:Carbon Dioxide Equilibrates Quickly 20X
• Oxygen Equilibrates Slowler

• (N2O also 20X faster compare O2 and N2)

Diffusion of Gases: CO2
 Diffusion of Gases
• In general GASES are:

– PERFUSION LIMITED (N2O, O2,CO2)

in healthy lungs

– DIFFUSION LIMITED
in disease lung.(O2 in severe exercise)
• CO2 still perfusion limited in disease compare to O2 because of high
solubility of CO2 (20X )
• Therefore commonly in pulmonary disease, patient will develop
hypoxemia WITHOUT hypercarbia.
 Alveolar Ventilation

• Is alveolar ventilation even

across different regions of the lung?

• No.
Regional Ventilation
 Regional Ventilation
• Findings:
– Decreased air flow to the upper lung
– Increased air flow to the lower lung

• How do we explain regional differences in air

flow to the lung?
Regional Ventilation
 Regional Ventilation
• Thus, net differences in ventilation are based on
differences in intra-pleural pressure.
• (less negative at the base compared to apex : due
to the weight of the lung)
• Ventilation is more at the bases.
– Alveoli start off smaller, therefore can expand more.
 BLOOD FLOW
Lung blood flow increases towards bases
Alveolar
Alveolar
vessel
vessel
Zone 1
Zone 1

Lung height above base (cm)

lung height above base (cm)
Zone
Zone2 2

Zone 3
Zone 3

Blood flow
Blood flow
Ventilation Perfusion
Matching
 Ventilation:Perfusion Ratio
• An important measure of gaseous exchange.
• Basic concept.
– Alveolar gas partial pressure dictated by-
• Alveolar perfusion (Q)
• Ventilation (V)
– However neither is uniformly distributed in lung
– Both increase towards base.
– Increase is more marked for blood
• The ratio of pulmonary ventilation (V) to
pulmonary blood (Q) for the whole lung at rest is
about 0.8
– (4L/min vent divided 5L/min perfusion)
• V/Q values are bordered at either end by extremes
numbers
– V/Q = 0 , no ventilation (V = 0) , call a SHUNT
– V/Q = ∞, no perfusion (Q = 0) , call DEAD SPACE
Mixed Venous Point (Shunt) Vs Inspired Gas
Point (Dead Space)
Ventilation Perfusion Matching
O2-CO2 diagram: V/Q Ratio Line
 Ventilation Perfusion Matching

Mixed Venous
Point (Shunt)

Inspired
Gas Point
(Dead
Space)
Shunt: Shunt Equation
 SHUNTS (V/Q =0)
• Refers to mixed venous blood bypassing
ventilated regions of lung
• 2 types of shunts– physiological
- pathological
PHYSIOLOGICAL SHUNTS
– Blood from (POST pulmonary shunts): bronchial,
mediastinal, pleural veins & thebesian vein drain directly
into pulmonary vein and left heart ,AVOIDING pulmonary
capillaries.
– Consequence of adding this volume of mixed venous blood
(called Venous Admixture) directly into the pulmonary end
capillary blood is a small ↓PaO2 & a small ↑PaCO2 as the
shunt accounts for 2- 5% cardiac output
– Venous Admixture calculated from shunt equation
– The larger the Qs/Qt, the greater the shunt , the more
blood that is not fully oxygenated
PATHOLOGICAL SHUNTS
1) Intrapulmonary shunts; unventilated alveoli that
are perfuse: V/Q=0. (< 1% in normal individual)

2) Anatomical shunts ;R→L shunts

– Structural abnormalities of heart eg septal defects
– Mixed venous blood (R ), mix directly with arterial
blood (L)
SHUNTS (O2 & CO2 levels)
• All shunts, larger than normal venous admixture
will reduced concentration of O2 & PaO2
• PaCO2 is not grossly elevated due to
chemoreceptors sensing initial elevated PaCO2 and
respond by hyperventilating
• PaO2 only stimulate peripheral chemoreceptor
when PaO2 drop to 60mmHg
• PaO2 is NOT corrected by 100% O2
– Un-shunted blood already max sat with O2 (ODC).
– Hypoxic shunt – no gaseous exchange
 Causes of Abnormal Oxygenation (HYPOXIA):
ESSAY
Answer: Use oxygen cascade

• Low FIO2 : A-a : Normal

• Hypoventilation : A-a : Normal
• Diffusion block : A-a: High
• V/Q mismatch : A-a: High.
• R to L Shunt : A-a : High
 Response to Breathing 100% Oxygen
• Alveolar hypoventilation or V/Q mismatch responds to
100% oxygen breathing.

• Nitrogen will be washed out of low ventilation lung units

over time: lead to absorption atelectasis

• PaO2 will rise to > 550 mmHg.

• Limited response to oxygen in shunt.

• Use this characteristic to diagnose shunt.