Disturbances of Respiratory Function

Note: This lecture is almost totally the same with all thats
written in Chapter 252: Disturbances of Respiratory
th
Function, Harrisons Principles of Internal Medicine 18 Ed.

Disturbances of the respiratory system are

divided into:

elastic recoil pressure of the lungs. This causes

increase in lung volume. The lung becomes very
stiff, very hard to expand at high volume, so
that relatively small volume change is
accomplished even with high transpulmonary
pressure.

disturbances of ventilation
disturbances of perfusion
disturbances of gas exchange

Problems with these three would cause

derangement of respiratory function, because
the primary function of the respiratory system
is to oxygenate blood and to eliminate C02, and
to fulfill this function, there must be adequate
perfusion, ventilation and normal diffusion of
gases = O2 and CO2.
There are three interdependent functional
components of the lungs. the airways, the
neuromuscular system and the chest wall.

First, the lungs including the airways;

the neuromuscular system including the
muscles that would contract and relax
to help you inhale or exhale;
the chest wall including all that is not
lung or neuromuscular system meaning the mass of the respiratory
muscles, the abdomen (especially in
obese individuals), and the heart
(especially if it is large).

These three components have mechanical

properties that relate with the lung volume, or
in the case of the neuromuscular system, the
volume at which it is operating, and the rate of
change of its volume.

VOLUME-RELATED MECHANICAL PROPERTIES

STATICS
Due both to surface tension at the air-liquid
interface between alveolar wall lining fluid and
alveolar gas and to elastic recoil of the lung
tissue itself, the lung requires passive
transmural pressure to inflate, to expand, and
to stay expanded. The expanding pressure is the
Love, bbf.

In contrast, lung is compliant at low lung

volume as the graph shows. Because the lung is
compliant, it is very easy to inhale or exhale,
hardly any effort is needed.
And at zero, there is still a normal amount of air
in the lungs. This is because the small peripheral
airways are tethered/helped open by the
radially outward pulling of the lungs. This air
intention is exaggerated in patients with
obstructive airway disease resulting in the
increase of the tidal volume.
Chest Wall
- Encloses a large volume at atmospheric
pressure
- Compliant at high enclosed volume &
even at small negative transmural
pressure
- At very small lung volume in response
to large negative transmural pressure,
chest wall becomes stiff due to:
squeezing together of ribs &
intercostals
muscles;
diaphragm
stretch; displacement of abdominal
contents & straining of ligaments &
body articulation
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Disturbances of Respiratory Function

The chest wall differs markedly from the lungs.
The lung tends to deflate, but the chest wall
tends to go outwards.
Because the lung and chest wall function in
mechanical series, the pressure required to
displace the passive respiratory system (lungs +
chest wall) at any volume is simply the sum of
the elastic recoil pressure of the lungs and the
transmural pressure across the chest wall. So
thats why it becomes a sigmoid curve.
There is stiffness at high lung volume and low
lung volume. At high lung volume, the stiffness
is caused by the stiffness of the lung, while at
low lung volume, the stiffness is caused by the
chest wall. The respiratory system is very
compliant at the middle portion.
We have a passive resting point when the
alveolar gas and the transmural pressure is
zero. This is the volume at your FRC wherein the
outward pull of the chest wall is equal to the
inward pull of the lung. This is at the zero
resting volume of the respiratory system.
The maximal pressures these sets of muscles
can generate varies with the lung volume at
which they operate, due to the length-tension
relationship of striated muscles and the changes
of the mechanical advantage as the angles of
insertion change with lung volume.

The respiratory muscles are more than

adequate to generate force to inhale or drive
the respiratory system up to the total lung
capacity (TLC) and up to the residual volume
(RV). RV is the volume that remains within the
lungs no matter how hard you try exhale. The
excursion of the chest wall is from the TLC up to
the RV. The vital capacity (VC) is the difference
between the TLC and RV.
Measurement of Lung volume

Inert gas dilution test

The O2 washout test you let the
patient inhale -instead of He, give your
patient pure O2. Washout all the N2
because the air that we breathe in is
98% N2. Then after several minutes of
breathing pure O2, this pure O2 is
diluted with N2, then check the
concentration, and calculate for the RV.

Body box
Plethysmograph

**The problem with the washout test or

dilution test: there may be some areas
which are poorly ventilated, which cannot
be measured.
Measurement of Muscle Strength
To measure the muscle strength of the
neuromuscular function, request for the
maximal inspiratory pressure, or maximal
expiratory pressure. Try to ask patient to inhale
or exhale maximally through a closed circuit/
closed mouthpiece, then measure the pressure
the patient is able to generate.
Inhalation = generates a negative pressure =
maximal inspiratory pressure = - 60cmH2O
At - 25cmH2O, you can already generate an
effective cough.
Exhalation = positive pressure = pressure above
atmospheric pressure = + 60cmH2O

Love, bbf.

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Disturbances of Respiratory Function

FLOW-RELATED MECHANICAL PROPERTIES
DYNAMICS
The dynamic airflow properties of the lung
substantially determine the ability to ventilate
and contribute importantly to the work of
breathing, and are often deranged by disease.
Understanding these properties is, therefore,
well worthwhile.
As with flow of any fluid (gas or liquid) in any
tube, maintenance of airflow within the
pulmonary airways requires a pressure gradient
that falls along the direction of flow, the
magnitude of which is determined by the flow
rate and the frictional resistance to flow. During
quiet tidal breathing, the pressure gradients
driving inspiratory or expiratory flow are small
owing to the very low frictional resistance of
normal pulmonary airways (normally <2
cmH2O/L per second). However, during rapid
exhalation, another phenomenon reduces flow
below that which would have been expected,
were frictional resistance is the only
impediment to flow. This phenomenon is called
dynamic airflow limitation, and it occurs
because the bronchial airways through which
air is exhaled are collapsible rather than rigid.

During exhalation, gas leaving the alveoli must

therefore gain velocity as it proceeds toward
the mouth.
The maximum value of flow is related to:
- Gas density
- Airway cross-section & distensibility
- Elastic recoil pressure of the lungs
- And the frictional pressure loss to the
flow-limiting airway site.

A. Normal.

B. Airflow obstruction.

Airflow is constant along the airway

Flow = volume / time
Velocity of flow =
flow summed cross-sectional area
Velocity of flow is much greater in the central
airways than in the peripheral airways

C. Fixed central airway obstruction.

RV, residual volume; TLC, total lung capacity.
*Flow-volume loops.

Love, bbf.

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Disturbances of Respiratory Function

The maximum expiratory flow is relatively
elevated when considered in relation to lung
volume. Conversely, in emphysema, lung recoil
pressure is reduced, which is a principal
mechanism by which maximal expiratory flows
fall.
The Bernoulli effect also acts during inspiration,
but the more negative pleural pressures during
inspiration lower the pressure outside of
airways, thereby increasing transmural pressure
and promoting airway expansion. Thus,
inspiratory airflow limitation seldom occurs due
to diffuse pulmonary airway disease.
Conversely, extrathoracic airway narrowing (as
due to a tracheal adenoma or posttracheostomy stricture) can lead to inspiratory
airflow limitation
Ex. Comparison of the plastic straws we use for
drinking
- the hard, strong one (in fastfoods/restaus)
- the soft, pliant one (in softdrinks)

Work of breathing also increases when disease

reduces the compliance of the respiratory
system or increases the resistance to airflow.
The former occurs commonly in diseases of the
lung parenchyma (interstitial processes or
fibrosis, alveolar filling diseases such as
pulmonary edema or pneumonia, or substantial
lung resection), and the latter occurs in
obstructive airways diseases such as asthma,
chronic bronchitis, emphysema, and cystic
fibrosis.
Sometimes, even in patients with obstructive
lung disease, there would be added stiffness to
the lung, not because of the airway resistance,
but there would be added work of breathing
due to the thickening of the lung. Because in
patients with obstructive lung disease, they may
develop dynamic hyperinflation.
When you inhale, the flow is better.

*When you inhale very deeply, the soft straw

will compress and collapse, thus air/fluid is
more difficult to flow through

Ex. When you inhale, lets say 500, then you

exhale 400. You retain 100 because of the flow
limitation site. Even if you havent exhaled all
the air you inhaled, the lung will already retain
more air and build your residual volume.

Work of Breathing

Adequacy of Ventilation

Normal state minimal

- need of ventilation
( metabolism / metabolic acidosis)
in mechanical load
( stiffness of the lung /chest wall/airway
resistant)

Minute volume = amount of air that moves in

and out of the lungs in one minute

The work required of the respiratory muscles is

minimal. However, the work of breathing can
increase considerably, due either to
requirement for substantially increased
ventilation,
an
abnormally
increased
mechanical load, or both. The rate of ventilation
is primarily set by the need to eliminate carbon
dioxide.

Love, bbf.

Tidal volume = amount of air that you inhale or

exhale during tidal breathing. This is made up of
dead space ventilation and alveolar ventilation.
Alveolar ventilation is more important as this is
the one that would participate in your gas
exchange.
Minute ventilation (VE) = VT x RR
Tidal volume (VT) = VD + VA
- Dead space ventilation
Alveolar ventilation participate in gas
exchange

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Disturbances of Respiratory Function

REMEMBER!

PA02 = FI02 x (P bar PH20) PAC02 / R

CO2 is used to know whether your patient has
adequate ventilation or not.

Why CO2?
- Because we hardly inhale CO2
20.9% = O2
78% = N2
1% = all other gases including CO2
CO2 in the body inadequate
ventilation
CO2 is a waste product. It is the amount of
metabolism that our body has.We blow off CO2.
We do not inhale it. If there is a build-up of CO2
in the body, there isnt enough ventilation.
If this is not the cause of inadequate ventilation,
it means the body has produced excessive
amounts of CO2.

Diffusion coefficient of the

gas/substance in the lung diffusion is
usually perfusion dependent
diffusion dependent on in high
altitude, maximal exercise or interstitial
lung disease (some)

O2 and CO2 have good diffusion coefficients.

There is no problem on the transport of these
gases through the alveolar surface membrane.
The problem on gas exchange is with perfusion.
The lung has a very big surface area as big as a
football field. Problems with perfusion affect
problems of oxygen levels in blood.

In patients with shunt, there is perfusion, but

no ventilation. There is blood flow, but no
ventilation.

PaCO2
- Determined by CO2 production &
alveolar ventilation
PaCO2 = vCO2 / VA
If you have increased CO2 production, you have
increased CO2 in the blood. It is directly
proportional.
On the other hand, it is inversely proportional
to the alveolar ventilation.
Gas Exchange
Diffusion
- Diffusion membrane surface area &
thickness
Gas exchange involves diffusion. Diffusion is
affected by the surface area. The larger the
surface area, and the thinner the membrane,
the better the diffusion.

Love, bbf.

For the blood to be completely saturated with

O2 as it passes through the pulmonary
circulation, it only needs 1/3 of the 0.75%. So
even when you exercise, the blood flow through
pulmonary circulation is cut short.
The diffusion problem will only occur if you
have problems with the surface - if it is
destroyed or is very thick.

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Disturbances of Respiratory Function

Measurement of gas exchange
-

Diffusion capacity (DLCO)

Pulse oximetry
Arterial blood gas (ABG)

False low O2 saturation:

- Hypotensive
- Cold tip of finger
*If you request for a complete PFT, you should
include a diffusion study.

ABG
-

Able to determine the blood:

pH
PaCO2 (N)= 35-45
PaO2 (N) = 80-100
Bicarbonate level (N) = 24 (+/-) 2
Hgb O2 saturation

*unit: mmHg/TORR
Serial ABG measures the partial pressures of
O2 and CO2.
ABG get from artery bright red, not maroon
(vein)
The effectiveness of gas exchange can be
assessed by measuring the partial pressures of
oxygen and carbon dioxide in a sample of blood
obtained by arterial puncture.
The oxygen content of blood (CaO2) depends
upon arterial saturation (%O2Sat), which is set
by PaO2, pH, and PaCO2 according to the
oxyhemoglobin dissociation curve; CaO2 can also
be measured by oximetry:
CaO2 (ml/dl) = 1.34 (ml/dl/kg) x Hgb (g) x O2 sat
+ 0.003 (ml/dl/mmHg) x PaO2 (mmHg)
Pulse Oximetry
Pulse oximeter used to determine the oxygen
saturation of the blood. Patients who are
critically ill need monitoring of their oxygen
levels. This can be placed on the earlobe,
fingertips, as a patch.
-

Continuous monitoring of O2 saturation

Cannot use to predict PaO2
Cannot determine PaCO2

Love, bbf.

Diffusion study
DLCO
- Single breath diffusing capacity
- Uses small amount of CO2 (10 sec
breath hold)
- Diffusion increase in increased surfaced
area available for diffusion, amount of
hgb within the capillaries & inversely
related to the thickness of alveolar
membrane
-

DLCO maybe increased in:

o acute
CHF,
polycythemia &
hemorrhage

asthma,
pulmonary

Diffusion decreases in:

1. Thickened/destroyed
alveolar
membrane
(pulmonary fibrosis, emphysema)
2. Problem in pulmonary vasculature
(pulmonary hypertension)
3. Reduced
alveolar
capillary
hemoglobin
(anemia)

Diffusion is very efficient in the respiratory

system. There is hardly any problem with
diffusion.
Primary function of the lung: to oxygenate the
blood and eliminate CO2
Needed for lung to function normally:
- Normal perfusion
- Normal ventilation
- Normal diffusion

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Disturbances of Respiratory Function

Causes of Arterial Hypoxemia
-

Low inspired O2 tension = O2 tension is

less than air inhaled ( < 20.9 or 21%.)
This is true in high altitudes.
Ex. Riding airplanes = O2 tension
decreases

Alveolar hypoventilation
PaCO2 reflects ventilation
CO2 in blood = excessive ventilation
CO2 in blood = lack ventilation

Computation
-

V/Q mismatch
slight increase in ventilation lack of
oxygen
Tx: increase O2 to improve condition

Shunt
blood does not come in contact with O2
no chance to improve

Diffusion defect
(the respiratory system has very good
diffusing capacity so this is not
considered)

A alveolar
a arterial
P bar barometric pressure
R respiratory quotient (metabolism of
whatever you eat)
FiO2 fraction of inhaled O2
PAO2

= 0.21 x (760 - 47) 40 / 0.8

= 0.21 x 713 50
= 149.52 50
= 99.52

PAO2

= 0.21 x (760 47) 60 / 0.8

= 0.21 x 713 75
= 149.52 75
= 74.52

Clinical Correlations
Ventilatory Restriction Due to Increased Elastic
Recoil - Idiopathic Pulmonary Fibrosis
-

TLC, FRC & RV

FEV1
Normal/above normal FEV1/FVC
Normal airway resistance
Marked reduction of DLCO
Hypoxemia
Flow/volume loop like a miniature
normal loop

Ventilatory Restriction Due to Chest Wall

Abnormality - Moderate Obesity
-

Love, bbf.

FRC
Normal TLC & RV
Mild hypoxemia
Normal flow/volume curve
Normal DLCO

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Ventilatory Restriction Due to Reduced Muscle
Strength - Myasthenia Gravis
-

Normal FRC
TLC & RV
Reduced FEV1
Normal airway resistance & DLCO
Normal oxygenation unless weakness is
severe

Airflow Obstruction Due to Decreased Airway

Diameter - Acute Asthma
-

Scooped flow-volume loop

Normal TLC
Elevated FRC & RV
Elevated airway resistance
Mild hypoxemia
Normal or mildly DLCO

Airflow Obstruction Due to Decreased Elastic

Recoil - Severe Emphysema
-

Severe emphysema
lung volume
FVC & FEV1
Airway resistance normal in pure
emphysema
Scooped flow-volume loop
DLCO

Love, bbf.

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