PULMONOLOGY, MED II - 3RD YEAR

Disturbances of Respiratory
Function
( DR CONSTANTINO/ DR LEE TRANS, PRELIMS February 2017)

THREE MAJOR ASPECTS OF DISTURBED RESPIRATORY

FUNCTIONS:
1. Disturbances in ventilatory function – Ventilations to
continually supply the body heat masses Relationship between the volume of gas contained in the
2. Disturbances in the pulmonary circulation – perfusion lungs and the distending pressure (the transpulmonary
to transfer unoxygenated blood to the lungs and exchange
pressure, or PTP, defined as alveolar pressure minus pleural

CAYRAPF – MED II, PULMONOLOGY - JANUARY 2017, 2ND SEMESTER

it with oxygenated blood so perfusion is very important.
pressure) is described by the pressure-volume curve of
3. Disturbances in gas exchange – Gas exchange which
occur within the lung for the elimination of CO2 and create
the lungs.
oxygenation to the blood
 These 3 functions (ventilation, perfusion, gas exchange)
should be working perfectly together in order for the
respiratory system to fulfill its function of oxygenating the
blood and elimination of CO2.
COMPONENTS OF THE RESPIRATORY FUNCTION
 Lungs
 CNS – which controls respiration

PRIMARY FUNCTION OF RESPIRATORY SYSTEM

 Primary function of the respiratory system is to
oxygenate blood and eliminate carbon dioxide and
to fulfill this function, there has to have adequate
ventilation, perfusion and normal diffusion of gases.
 This would be the most important function of the respiratory
system.
VENTILATION
 Three independently functioning components of the
respiratory system:
1. The Lung, including its airway
2. The neuromuscular system
3. The Chest wall
 Each of the 3 component has mechanical properties that
relate to its enclosed volume as for the neuromuscular
system, the respiratory volume to which it is operating and
to the rate of change of volume, which is the flow. We are
talking about volume and flow.
 In ventilation, it is assumed there is flow in and flow out of air.
That is ventilation or flow of air. What would affect the
ventilation of the lung? The lung is dependent on what
structures for complete ventilaton? The lungs, neuromuscular
system and the chest wall. The muscle itself is included in the
chest wall but the action of the muscle would be under
neuromuscular system. So the airway, the lung parenchyma
would all be under the lung..
PHYSIOLOGIC FEATURES
 The lungs are elastic structures, containing collagen
and elastic fibers that resist expansion.
 For normal lungs to contain air, they must be
distended either by:
- A positive internal pressure – i.e, by a pressure in
the airways and alveolar spaces or
- By a negative external pressure – i.e, by a
pressure outside the lung. - That is provided for by
the chest wall which has a tendency for outward
elastic recoil. When the chest wall expands it creates a
negative pressure that pulls at the lung making it
expand.
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 At Functional Residual Capacity (FRC), defined as the
volume of gas in the lungs at the end of a normal
exhalation, the tendency of the lungs to contract is
opposed by the equal and opposite tendency of the
chest wall to expand – So when you are at FRC, the lung
is at equilibrium so there is no movement at this point.
 At TLC, the maximal force applied by the inspiratory
muscles to expand the lungs is opposed mainly by
the inward recoil of the lungs – So much so that it would
be very difficult to expand it further because you have
already reached the maximum total lung capacity
 As a consequence, the major determinants of TLC
are:
- The stiffness of the lungs and inspiratory muscle
strength – So the more stiff the lung is the TLC would
be less because it cannot expand further and if your
inspiratory muscles are weak, the TLC would be
decreased so it would be very difficult to try to expand
the lung.
- If the lungs become stiffer – i.e., less compliant
and with increased inward recoil – TLC is
decreased – as mentioned previously
 If the lungs become less stiff (more compliant and
with decreased inward recoil), TLC is increased.
 If the inspiratory muscles are significantly weakened,
they are less able to overcome the inward elastic
recoil of the lungs, and TLC is lowered. – as mentioned
again previously.
 At RV (RV is the volume of air left inside the lung after
maximal expiration), the force exerted by the expiratory
muscles to decreasing lung volume further is balanced
 by the outward recoil of the chest wall, which
becomes extremely stiff at low lung volumes. – So much
so that it would be difficult again to further decrease the
residual volume once you have reached that residual
volume
 Two factors influence the volume of gas contained in
the lungs at RV
1. The ability of the subject to exert a prolonged
expiratory effort, which is related to muscle
strength and the ability to overcome sensory
stimuli from the chest wall. – So you can only try to
reduce further the residual volume if you prolong
expiration. Actually it is a technique to remove trapped
air by patient with COPD. You do that by pursed lip
breathing. It prolongs the expiratory phase. If you are
able to overcome sensory stimuli in the chest wall you
can further reduce the RV but that is very difficult to do
because of the feedback mechanisms.
2. The ability of the lungs to empty to a small volume.
– Again, this is very difficult to do.
 In normal lungs, as PTP is lowered, lung volume
decreases.
 In lungs with diseased airways, as PTP is lowered, flow
limitation or airway closure may limit the amount of
gas that can be expired. It means you can, in diseased
airways, if PTP is lowered, you develop airway trapping
because the airways collapse. Even before you are able to
fully complete inhalation or expiration ibig sabihin may
naiwan na air.
 Consequently, either weak expiratory muscles or
intrinsic airways disease can result in an elevation in
measured RV. – That is the mechanism in COPD especially
in Emphysema because of early airway closure, you have
increases in the RV so you call that air trapping or dynamic
hyperinflation. It is dynamic because as time goes on you
have more air trapped inside the lung as you breathe
further.
VOLUME-RELATED MECHANICAL PROPERTIES – STATICS
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This is an example of a spirometric tracing. The Tidal Volume (TV),
the one on your left side, you see maliit lang. Tidal Volume is the
volume of air going in and out of the lung with normal breathing.
So makikita niyo very minimal.
When you try to inhale maximally, you have the Vital Capacity.
Vital Capacity is the volume of air that goes into the lung with
maximal inspiration compared to the TLC. Total Lung Capacity
(TLC) is the volume of air inside the lung after maximal inspiration.
TLC = VC + RV.
If you look you have the Residual Volume. Residual Volume is the
volume of air left inside the lung after maximal expiration.
CAYRAPF – MED II, PULMONOLOGY - JANUARY 2017, 2ND SEMESTER
Function Residual Capacity is the volume of air left inside the
lung after normal expiration. That is with tidal breathing. The FRC
is composed of the Residual Volume and the Expiratory Reserve
Volume.
In conditions like for example, Bronchial Asthma or Emphysema,
the RV is increased. Actually, in Bronchial Asthma it can increase
by as much as 400% because of airway trapping due to
expiratory outflow obstruction but the mechanism is somewhat
different it is bronchoconstriction rather than early airway
closure.
The anatomic dead space is the volume of air that does not
participate in respiration so yun yung wala yung mga alveoli so
andun yung trachea, yung nasal passages.
The movement of the lung would be dependent on the resistance
of the lung to deflate or inflate. The lung in static conditions, if you
remove or separate the lung to the chest wall what would
happen to the lung? What is the tendency of the lung, normally?
Deflated. Because the lung is stiff in high volume and it is
compliant in a low volume. If the lung is inflated already and you
try to inflate it further it would be very difficult. This is because of
the elastic recoil of the lung. The tendency of the lung is to
collapse. This elastic recoil is due to the surface tension between
the gas and the fluid in the alveolar level. You have to exert an
effort to inflate the lung and the pressure that would be able to
inflate the lung is the elastic recoil pressure.
At the Tidal Volume or usually before we inhale and exhale, the
lung is really compliant. At the extreme, at Total Lung Capacity,
the lung is stiff because the movement of expansion further has
already plateaud here.
When the lung deflates, there is always a Residual Volume this is
due to the collapse of the very small airways in the lung as the
lung deflates. The patency of this very small airway is dependent
on the lung volume. Because these small airways are pulled open
by the attachment of the lung to the adventitia of the lung. When
you inhale, the lung increases in volume and this very small airway
will be pulled open. As you exhale into very near residual volume
some of this airways will be closed because the tithering of the
lung will already disappear. There are certain
MEASUREMENT OF LUNG VOLUME
 Inert gas dilution Test (Helium/Neon)
 Oxygen Wash-Out Test
 Plethysmography (Body Box) – you use a device that
encloses the whole body. We have discussed this before.
You inhale a certain amount of Helium and it is mixed with
the inspired air and then you compute.

FLOW-RELATED MECHANICAL PROPERTIES – DYNAMICS
 The dynamic airflow of the lung determines
substantially the ability to ventilate and contribute to
the work of breathing, and is often deranged by
disease. You have positive and negative pressures.
 Maintenance of gas flow within the tube requires a
pressure gradient that falls along the direction of the
flow so you have positive pressure within the airways, the
magnitude of which is determined by flow rate and
the frictional resistance to the flow. The magnitude of gas
flow within the airway is affected by the flow rate and the
resistance to flow. If you have more resistance then you have
a decrease in the magnitude of flow obviously kasi binabara
niya eh. If you have a narrower airway, you have a decrease
in the magnitude of flow.
 During tidal breathing, the pressure gradients driving
the inspiratory or expiratory flow are small owing to
the very low frictional resistance of normal pulmonary
airways (<2 cm H2O/L per seconds) – Because of the
low resistance, you have decreased pressure gradients, you
have maximal flow.
 But during rapid exhalation another phenomenon
reduces flow below that which would have been
expected, were frictional resistance the only
impediment to the flow. (Normally only the frictional
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resistance restricts the flow rate. However during rapid
exhalation, you have dynamic airflow limitation). This
phenomenon is called the dynamic airflow limitation,
and it occurs because the bronchial airways are
collapsible rather than rigid. In the pressure within the
airways, the airway collapses and this is more magnified in
patients with lung or airway disease, like for example,
Emphysema. Normally the airways are held open by radial
traction. Radial traction pulls the airway apart and keeps it
open. However, in emphysema since you have a disease
affecting the airways and you have destruction of the
alveolar septa, the radial traction decreases. When the
positive pressure in the airway decreases during exhalation,
you have more negative pressure, it is sucked inward.
CAYRAPF – MED II, PULMONOLOGY - JANUARY 2017, 2ND SEMESTER
Because of the decrease in radial traction, it cannot keep
the airway open so it collapses. So you have bronchial
compression or airway collapse and that will lead to
destruction and Incomplete emptying of the alveoli. You
have air trapping or dynamic hyperinflation.
 Basically in airflow dynamics: Airflow is constant along
the airway.
 Flow = volume/time
 Velocity of flow = Flow/summed X-sectional area
 Velocity of flow is much greater in the central airways
than in the peripheral airways.
 The maximum value of flow is related to
- Gas density: the more dense the gas is, the flow rate
decreases.
- Airway cross- section and distensibility
- Elastic recoil pressure of the lungs
- Frictional pressure loss to the flow limiting airway
site
SPIROMETRY
Information of: Most useful is FVC, FEV1, and FEV1/FVC ratio.
These 3 are more important.
 FVC* - Forced Vital Capacity. Volume of air that goes
in and out of the lungs in forced expiration or forced
breathing.
 FEV1* - Forced Expiratory Volume. During the 1st second
of expiration. This is one of the important information.
 FEV1/FVC* - These *3 are the most important.
 PEFR – Peak Expiratory Flow Rate. Just a reflection of the
FEV1.
 FEF25-75 – also called midexpiratory flow rate. It is a
measure of the flow in the small airways. If it is decreased
you have small airway obstruction. There is probability of
restrictive respiratory impairment.
 Now, the FEV1 is very important because it determines the
possibility of the presence of obstructive ventilatory
impairment. If your FEV1 is decreased, if it is less than 80% of
the predicted value then you have the possibility of
obstructive ventilatory impairment. If your FEV1/FVC ratio is
decreased also, it definitely proves that you have obstructive
ventilatory impairment. However, if your FEV1 is decreased
and your FEV1/FVC is normal or decreased, there is a
possibility of restrictive ventilatory impairment. Why is this so?
In restrictive ventilatory impairment, you can inhale only a
small amount of air. Diba? Kasi may lung restriction e sa
expansion so therefore you only exhale a small amount of air
also. So the FEV1 will be decreased. Yun yung explanation.
When you get a reading of restrictive ventilatory impairment,
you need to do lung volume studies and that will be
confirmed by the residual volume.
 If your residual volume is increased, ano yun? It is more of
obstructive ventilatory impairment.
 If your residual volume is decreased, it confirms the presence
of a restrictive ventilatory impairment. Of course there are
also other conditions that will result in these findings pero
basically that is that.
Flow Volume Loop
 This is a flow volume loop. In the normal flow volume loop, we
have a very arcuate line in inspiration. And then during
expiration you have a sharp upward rise and then you get a
gradual downward sloping.
 In obstructive lung disease, the blue line you will see the same
sharp upward stroke during expiration but you have a smaller
volume. Because you have less air that is coming out due to
the obstruction. And then you have scooping of the slope.
 The red line is restrictive ventilatory impairment due to
extraparenchymal disease (outside of the lung). It shows the
same rapid rise during expiration and then you have the
same, as in parang normal downward slope but you have
lesser volume because of the restrictive lung disease. Less air
coming in, less air coming out.
 The restrictive lung disease due to parenchymal lung disease,
iyan yung may mga Interstitial Lung Disease or Congestive
Heart Failure so increase thickness of the lung, you have the
same rapid rise but a very steep downward slope in your flow
volume loop. You do not need to memorize this.
 In obstructive airway disease, you have less steeper slope.
 Restrictive parenchymal disease approximates the normal
slope.
WORK OF BREATHING
 Normal state – minimal. You do not get tired during
normal breathing unless you have a disease.
 Increase
- Increase need of ventilation (increase
metabolism/ metabolic acidosis), If you have
metabolic acidosis, the compensatory mechanism is to
hyperventilate, in order to maintain the pH back to normal. So
you blow out CO2 to increase pH
- Increase in mechanical load (stiffness of the
lung/chest wall/airway resistant) Kunwari obesity,
you have a mechanical load to lung expansion, puro
taba e so hirap mag expand or if you have increase
airway resistance like Bronchial Asthma that would
increase the work of breathing
ADEQUACY OF VENTILATION
 PaCO2:
- determined by carbon dioxide production and
alveolar ventilation – For patients with COPD, they do not
use a high carbohydrate diet because carbohydrates provide
a substrate for the production of CO2. So sila high protein diet
sila. Also if your alveolar ventilation decreases, you retain CO2.
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 Minute Ventilation (VE) = VT x RR
- is determined by Tidal Volume multiplied by the Respiratory
Rate. If your Tidal Volume is decreased, for example, your Minute
Ventilation will decrease also. If your RR decreases again, your
Minute Ventilation will decrease. For example, from an RR of 18 it
became 10, definitely your PCO2 will rise and you will have
hypercapnia.
 Tidal Volume (VT) = VD + VA
 PAO2 = FIO2 x (Pbar-PH2O) – PACO2/R
GAS EXCHANGE
 DIFFUSION
- Diffusion membrane surface area and thickness
diffusion coefficient (The bigger the surface area , the
CAYRAPF – MED II, PULMONOLOGY - JANUARY 2017, 2ND SEMESTER
better the diffusion. The thicker the diffusion coefficient,
the lesser the diffusion) of the gas/substance in the
lung diffusion is usually “perfusion dependent” – It
is dependent on blood flow.
- “Diffusion dependent” on in high altitude,
maximal exercise or interstitial lung disease (some)
– However in high altitude, maximal exercise or interstitial
lung disease, so gas exchange is not dependent on
perfusion anymore. It becomes diffusion dependent.
 In gas exchange you have 2 abnormalities:
(1) Shunt (2) Ventilation-Perfusion Mismatch.
1. SHUNT – is a condition wherein you have absent or minimal
ventilation in the presence of intact perfusion. In this side, you
have an alveolus wherein it is blocked, so you have no
ventilation. On its right, you have an open alveolus.
 Venous blood which is unoxygenated would have a PO2 of
about 40 mmHg and then since it is not oxygenated as it
passes through the alveolocapillary membrane which is
obstructed, you do not have oxygenation. It remains 40
mmHg.
 The one on the right you would have intact ventilation, it
would be oxygenated and the mixture would be a very low
level of oxygen saturation. Here, you have a PO2 of 55 mmgH
and the saturation is about 87.5% so it’s below normal (90%)
so that’s what happens in a shunt. A shunt is determined
when you have high fractions of inspired oxygen but still you
are unable to correct the PO2 or the oxygenation of the
patient.
 On your right, you still have the same condition. But instead,
the patient is given 100%, yung isa room air e 21%, ito kasi
100% FiO2 and despite the 100%. In the normal alveolus, you
have very good oxygenation, the saturation is 100% but in the
abnormal alveolus, you have still 75% and then the outcome
would still have 56 yung PO2, yung saturation is 88%. That is
essentially what a shunt is so clinically it is determined by the
inability to correct the oxygenation even in high fractions of
inspired oxygen which is 100% It is produced by the absence
of ventilation in the presence of intact perfusion.
2. VENTILATION-PERFUSION HETEROGENEITY – You have 2
kinds. You have a (1) High ventilation-perfusion mismatch and (2)
Low ventilation-perfusion mismatch.
 In a high ventilation-perfusion mismatch, you have an intact
ventilation with abnormal perfusion.
 In a low ventilation-perfusion mismatch, you have an
abnormal or decreased ventilation with intact perfusion.
 For example, in your left, you have a partially obstructed
alveolus. It means your ventilation is impaired. It is not absent.
It is present but it is decreased because of a partial
obstruction. So it represents what? LOW ventilation-perfusion
mismatch. So here, at room air 21% FiO2, you have
hypoxemia. Unoxygenated blood passing through the
alveolus would get a small amount of oxygen. Naging 45
mmHg tapos saturation is 79%. In the normal you have 40
mmHg passing through the alveolus it becomes 99 and what
comes out would be still hypoxemia, 58 mmHg but a
saturation of 89.5%. However, when you give 100% FiO2, you
are able to correct the oxygenation. If you look with 100%
FiO2, the partially obstructed alveolus would be able to raise
the oxygenation to 200 mmHg with a saturation of 100% and
then the outcome would be a very high PO2 350 mmHg. So
in ventilation-perfusion mismatch, you are able to correct
oxygenation even with moderate amounts of oxygen. Kasi
yan 100% sobra-sobra e. So you assume at 50% normal parin
siguro yung PO2. So that is the difference between a shunt
and ventilation-perfusion mismatch. Both are causes of
hypoxemia by the way.
Figure 306e-5 Influence of air versus oxygen breathing on mixed arterial oxygenation in
shunt and ventilator/perfusion heterogeneity. Partial pressure of oxygen (mmHg) and
oxygen saturations are shown for mixed venous blood, for end capillary blood (normal
versus affected alveoli), and for mixed arterial blood FO2, fraction of inspired oxygen;
V/Q, ventilation/perfusion. Harrison’s 19th Ed.
FUNCTIONAL MEASUREMENTS
Measurement of VENTILATORY FUNCTION
1. Lung Volumes – lung volume studies is measured as
mentioned earlier (plethysmography, helium dilution)
2. Airway Resistance - spirometry
3. Respiratory Muscle Strength – by using a device to
measure the maximal inspiratory pressure (MIP) and maximal
expiratory pressure (MEP). This is also part of spirometry
examination but you can measure them separately by using a
manometer, a negative pressure manometer.
 Maximal Inspiratory Pressure (MIP) or Peak Negative
Pressure measures inspiratory muscle strength while the
 Maximal Expiratory Pressure (MEP) measures the expiratory
muscle strength.
 Your (MVV) Maximal Voluntary Ventilation which is also part
of spirometry examination, measures respiratory muscle
endurance – the ability to sustain adequate ventilation for a
long period of time.
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Measurement of GAS EXCHANGE
1. Diffusion Capacity (DLCO) – measures integrity of
alveolocapillary membrane because it measures the ability of
the gases to diffuse across that membrane. It could be
increased/decreased in certain conditions.
2. Arterial Blood Gas (ABG) – measures PO2, PCO2, HCO3,
Oxygen saturation, blood pH and it provides useful information
of gas exchange abnormalities
3. Pulse Oximetry – uses a device which is placed on the
fingertip and it measures pulsations of the capillaries and is only
an estimate of the oxygen saturation. It doesn’t tell about the
PO2. The oxygen saturation is also affected by a lot of factors
such as temperature, pH.
CAYRAPF – MED II, PULMONOLOGY - JANUARY 2017, 2ND SEMESTER
DLCO
 Single breath diffusing capacity
 Uses small amount of carbon dioxide (10 sec. breath
hold)
 Diffusion increases in increase surface area available
for diffusion, amount of Hgb within the capillaries and
inversely related to the thickness of alveolar
membrane
 DLCO maybe increase in: acute CHF, asthma,
polycythemia, and pulmonary hemorrhage
 Diffusion decreases in:
1. Thicken/destroyed alveolar membrane
(pulmonary fibrosis, emphysema)
2. Problem in pulmonary vasculature (pulmonary
hypertension)
3. Reduced alveolar capillary hemoglobin
(anemia)
 Clinically DLCO is important in distinguishing certain disease
conditions. For example, emphysema and bronchial asthma
are obstructive lung diseases. Sometimes we have grey
zones. Sometimes it would be difficult to determine if the
patient has asthma or emphysema especially if it is late onset
or they have a history of smoking. So DLCO will be able to
differentiate. DLCO in Emphysema would be decreased
while in Bronchial Asthma increase or normal because the
pathology in Bronchial asthma is bronchoconstriction,
mucosal edema. It does not affect the alveolocapillary
membrane.
 How about in Emphysema and Bronchitis? Is there a
difference? Again in Emphysema, DLCO is decreased. How
about in Chronic Bronchitis? Ang tip ko diyan if you don’t
know the answer, you go back to the pathophysiology. What
is the problem in Chronic Bronchitis? Hypertrophy and
hyperplasia of the mucosal glands. Does it have to do with
alveolocapillary membrane? Wala. So DLCO is normal.
ARTERIAL BLOOD GAS (ABG)
 Able to determine the blood:
- pH
- PaO2
- Hgb O2 saturation (O2 Sat)
- PaCO2
- Bicarbonate
 CaO2 (ml/dL) = 1.34 (ml/dL/g) x Hgb (g) x O2 Sat +
0.003 (mL/dL/mmHg) x PaO2(mmHg)
PULSE OXIMETRY
 Continuous monitoring of O2 saturation
 Cannot use to predict PaO2
 Cannot determine PaCO2
 CAUSES OF ARTERIAL HYPOXEMIA
 Low inspired oxygen tension
 Alveolar hypoventilation
 V/Q mismatch
 Shunt
 Diffusion defect can also lead to hypoxemia but it is a minor
cause of hypoxemia. Those above are the major causes.
CLINICAL CORRELATION
 Ventilatory Restriction due to Increased Elastic Recoil
– Idiopathic Pulmonary Fibrosis
o Decreased TLC, FRC & RV
o Decreases FEV1 – there is a decrease in the
volume of air going in the lung

CAYRAPF – MED II, PULMONOLOGY - JANUARY 2017, 2ND SEMESTER

o Normal/above normal FEV1/FVC – because this
is a restrictive defect
o Normal airway resistance
o Marked reduction of DLCO – involvement of the
alveolocapillary membrane
Figure 306e-6. Common abnormalities of pulmonary function. Pulmonary function
o Hypoxemia values are expressed as a % of normal predicted values, except for Raw, which is
o Flow/volume loop like a miniature normal loop expressed as cmH2O/L per sec (normal <2 cmH2O/L per second). The figures at the
bottom of each column show the typical configuration of flow-volume loops in each
 Ventilatory Restrictuion due to Chest Wall condition, including the flow-volume relationship during tidal breathing. b.d.,
Abnormality – Moderate Obesity bronchodilation; D1CO3, diffusion capacity of lung for carbon monoxide; FEV1, forced
o Decrease FRC – restrictive defect expiratory volume in 1 sec; FRC, functional residual capacity; Raw, Airways resistance;
RV, residual volume; TLC, total lung capacity.
o Normal TLC & RV
o Mild hypoxemia
o Normal flow/Volume Curve
o Normal DLCO – alveolocapillary membrane is not
involved
 Ventilatory Restriction due to Reduced Muscle
Strength – Myasthenia Gravis
o FRC normal
o Decrease TLC & Increase RV – because of the
weakness you cannot exhale the air you have
Black – Powerpoint
inhaled
Blue - DR CONSTANTINO
o FEV1 reduced – because of reduced inspiratory Red - DR LEE
muscle strength
o Normal airway resistance and DLCO
o Normal oxygenation unless weakness is severe
 Airflow Obstruction due to Decreased Airway
Diameter – Acute Asthma
o Scooped flow-volume loop – expiratory limb has
a downward slope that is scooped yung medyo
palubog
o Normal TLC
o Elevated FRC & RV – as mentioned this can go as
high as 400% increase
o Elevated Airway Resistance
o Mild Hypoxemia
o Normal or mildly increased airway DLCO – I
forgot to mention earlier, in asthma there is initially
decreased PCO2 because of hyperventilation due
to hypoxemia. Initially, you have respiratory
alkalosis.
 Airway Obstruction due to Decrease Elastic Recoil –
Severe Emphysema
o Increased lung volume – because of dynamic
hyperinflation
o Decreased FVC & FEV1 – due to obstruction
o Airway resistance normal in pure emphysema
o Scooped flow-volume loop
o Decrease DLCO – involvement of alveolocapillary
membrane

Page 6 of 7
 ABG EXERCISES: pH 7.38 ↓ Normal (acidotic side)
NORMAL ↓Value ↑Value PCO2 60 ↑
pH 7.35-7.45 Acidosis Alkalosis PO2 70 ↓
PCO2 35-45 Alkalosis Acidosis HCO3 28 ↑
PO2 80-100 Hypoxemia --- pH is normal but is considered acidotic (pointing down), and
HC03 22-26 Acidosis Alkalosis PCO2 is pointing upwards oppsite the pH while HCO3 does not
have the same arrow pointing down the pH. Since pH is within
Note to self: ROME = normal range and HCO3 is alkalotic (pointing upward), it is fully
Respiratory Opposite (pH & PCO2 arrows are opposite) compensated.
pH ↓ PCO2 ↑ = Respiratory Acidosis FULLY COMPENSATED RESPIRATORY ACIDOSIS WITH MILD
pH ↑ PCO2 ↓ = Respiratory Alkalosis HYPOXEMIA

Metabolic Equal (pH & HCO3 have same arrows) pH 7.4 Normal
pH ↓ HCO3 ↓ = Metabolic Acidosis PCO2 60 ↑ (60 from normal 45 = 15)

CAYRAPF – MED II, PULMONOLOGY - JANUARY 2017, 2ND SEMESTER

pH ↑ HCO3 ↑ = Metabolic Alkalosis PO2 70 ↓
HCO3 28 ↑ (28 from normal 26 = 2)
pH 7.25 ↓ Computation is needed kung saan mas Malaki yung change.
PCO2 80 ↑ Since mas mataas ang difference from normal value sa PCO2.
PO2 70 ↓ pH is considered acidotic (pointing down, remember if
HC03 24 Normal respiratory PCO2 is ↑ then pH must be OPPOSITE or pointing ↓). It
pH is acidotic pointing downwards while your PCO2 is pointing is fully compensated because HCO3 is alkalotic and pH has a
upwards (acidosis) and is opposite your pH, so it is respiratory normal value.
acidosis. Since your HCO3 is still in normal range, therefore there is FULLY COMPENSATED RESPIRATORY ACIDOSIS WITH MILD
no compensation. If HCO3 is alkalotic or pointing upward, then HYPOXEMIA
there is compensation.
UNCOMPENSATED RESPIRATORY ACIDOSIS WITH MILD HYPOXEMIA

pH 7.25 ↓
PCO2 80 ↑
PO2 70 ↓
HCO3 28 ↑
pH is acidotic pointing downwards while your PCO2 is pointing
upward (acidosis) and is opposite your pH, it is respiratory acidosis.
Since HCO3 is alkalotic pointing up, so there is compensation. pH
is not normal so it is partial.
PARTIALLY COMPENSATED RESPIRATORY ACIDOSIS WITH MILD
HYPOXEMIA
-LIGHT-
pH 7.45↑ - Considered Alkalotic (Normal, compensated) Please do not rely on this. Double check for any mistakes. Read
PCO2 55 - ↑ the book and study well. God bless, doctors! Thank you.
PO2 70 - ↓ (Mild Hypoxemia) CAyraPF
HCO3 28 - ↑ (Normal)
IF MORE THAN 7.4 IT IS IN THE ALKALOTIC SIDE. pH is considered
alkalotic (pointing up) and HCO3 is also alkalotic (pointing up), there is
metabolic alkalosis. Since PCO2 is acidotic (pointing up), there is
compensation. Your pH is also in normal range so it is fully compensated.
FULLY COMPENSATED METABOLIC ALKALOSIS WITH MILD
HYPOXEMIA

pH 7.5 ↑
PCO2 55 ↑
PO2 70 ↓
HCO3 28 ↑
pH is alkalotic (pointing up) and HCO3 is also alkalotic (pointing
up), there is metabolic alkalosis. PCO2 is acidotic (pointing up)
so there is compensation. The pH does not have a normal value
so it is partially compensating only.
PARTIALLY COMPENSATED METABOLIC ALKALOSIS WITH MILD
HYPOXEMIA
pH 7.5 ↑
PCO2 40 Normal
PO2 70 ↓
HCO3 28 ↑
pH is alkalotic (pointing up) while HCO3 is also alkalotic (pointing
up), so there is metabolic alkalosis. PCO2 is normal so there is no
compensation.
UNCOMPENSATED METABOLIC ALKALOSIS WITH MILD HYPOXEMIA

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