Download Ventilation workshop pre-reading

TELEFLEX Academy
Ventilation Clinical Workshop
Pre-Reading Package
IMPORTANT NOTE:
Every effort has been made by the author to ensure the information presented in this package is accurate
and up to date. New research and experience in the medical field however, results in necessary changes to
treatments and therapies. It is the responsibility of the professional, relying on experience and knowledge
of the patient, to determine the best treatment for each individual patient. The author accepts no liability for
any consequences from the application of the information in this package.
Prepared by Chris Ridgway
© 2014 Teleflex Academy
4 Secombe Place • Moorebank
New South Wales • 2170
Ph 1300 360 226
TELEFLEX Academy Ventilation Workshop Pre-Reading Package
Table of Contents
INTRODUCTION ..................................................................................................................................... 5
CHAPTER 01
RESPIRATORY PHYSIOLOGY
Breathing ............................................................................................................................................. 7
Inspiration .................................................................................................................................... 7
Expiration ..................................................................................................................................... 8
Active Breathing ........................................................................................................................ 9
Lung Volumes ........................................................................................................................... 10
Respiration ........................................................................................................................................... 11
External Respiration .............................................................................................................. 11
Internal Respiration ................................................................................................................ 14
Cellular Respiration ................................................................................................................ 10
Gas Transport.......................................................................................................................................... 14
Oxygen Transport .................................................................................................................... 14
Carbon Dioxide Transport.................................................................................................... 16
Control of Breathing .......................................................................................................................... 17
Central Control of Breathing................................................................................................ 17
Local Control of Breathing................................................................................................... 18
Review Questions ................................................................................................................................ 19
CHAPTER 02
PATHOPHYSIOLOGY
Pathophysiology ...................................................................................................................................23
Oxygenation Impairment ..................................................................................................... 23
Ventilation Impairment ......................................................................................................... 23
Acute Respiratory Failure .................................................................................................... 24
Common Respiratory Disorders ..................................................................................................24
Atelectasis.................................................................................................................................... 24
Acute Pulmonary Oedema ................................................................................................... 25
Pneumonia ................................................................................................................................. 25
Asthma ......................................................................................................................................... 25
Chronic Bronchitis .................................................................................................................. 26
Emphysema ............................................................................................................................... 26
Chronic Obstructive Pulmonary Disease (COPD) ...................................................... 26
Acute Respiratory Distress Syndrome (ARDS) ........................................................... 26
Review Questions ................................................................................................................................27
GLOSSARY ...........................................................................................................................................29
REFERENCES ....................................................................................................................................... 35
4 | 5
TELEFLEX Academy Ventilation Workshop Pre-Reading Package
Introduction
This package provides an introduction to
the concepts and principles of ventilation.
It has been designed to be used as a prelearning package, prior to attendance at a
Teleflex Academy ventilation workshop.
There are practical application notes and review questions located throughout the
package to help you apply the information presented. They can be identified by an
icon from the key on the right. A glossary of common respiratory and ventilation
terminology has also been included to assist you in your learning.
During the workshop it will be assumed that all participants have read and have
a good understanding of the content included in the pre-learning package. If you
have any questions whilst completing the package, please bring your questions
along to the training.
We look forward to seeing you soon.
Regards,
The Teleflex Academy Team
Icon Key
Application note
Test your knowledge
6 | 7
TELEFLEX Academy Ventilation Workshop Pre-Reading Package
Respiratory Physiology
01
Cells within the body require oxygen in order
to access the energy they need from nutrients
(during cellular metabolism). The body is unable
to store oxygen for long periods of time; therefore
it needs a continuous supply of oxygen.
CHAPTER
A REVIEW OF THE PHYSIOLOGY OF THE RESPIRATORY SYSTEM
Metabolism produces carbon dioxide, which becomes an acid in the blood and must be removed
from the cells. Respiration is the process of gas exchange between the atmospheric air and the
blood and between the blood and the cells of the body to provide oxygen to and remove carbon
dioxide from the cells. In order to work effectively it requires:
• Patent airway system to transport air to and from the lungs.
• Effective alveolar system in the lungs to allow diffusion of gases into and out of the blood.
• Effective cardiovascular system to carry nutrients and wastes to and from the body cells
The process of gas exchange has five components:
• Breathing
• External Respiration
• Internal Respiration
• Cellular Respiration
• Gas Transport
Negative pressure generated during
inspiration also assists in the venous
return of blood to the heart
BREATHING
Breathing, or ventilation, is the movement of air through the airways between the atmosphere
and the lungs. The air moves through the passages because of pressure differences between the
atmosphere and the gases inside the lungs that are produced by contraction and relaxation of the
diaphragm and thoracic muscles. There are two phases of breathing; inspiration and expiration.
INSPIRATION
Inspiration is the process of taking air into the lungs. It is the active phase of ventilation because
it is the result of muscle contraction. During inspiration, the diaphragm and intercostal muscles
contract, enlarging the thoracic cavity. The diaphragm, doing most of the respiratory work during
quiet breathing, moves downwards increasing the volume of the thoracic (chest) cavity, and the
intercostal muscles pull the ribs up expanding the rib cage, further increasing this volume (see
Figure 1.1). This increased capacity lowers the air pressure in the alveoli to below atmospheric
pressure. This decrease in intra-alveolar pressure draws air into the lungs as air, like other gases,
flows from a higher pressure region to a lower pressure region.
8 | 9
FIGURE 1.1 Process of inspiration (Image from Marieb, 2004)
EXPIRATION
Expiration is the process of letting air out of the lungs during the breathing cycle. During expiration the diaphragm and intercostal muscles relax. This returns the thoracic cavity to its original volume, increasing the
air pressure in the lungs (see Figure 1.2) . The increase in intra-alveolar pressure pushes air out of the lungs.
Expiration normally takes twice as long as inspiration.
FIGURE 1.2 Process of expiration (Image from Marieb, 2004)
TELEFLEX Academy Ventilation Workshop Pre-Reading Package
ACTIVE BREATHING
The body needs to be able to rapidly respond to changes in activity and therefore demand for energy. This
means that when there is an increased demand for oxygen due to increased cellular metabolism, for example
during exercise or illness, there also needs to be a corresponding increase in supply of oxygen. The increased
metabolism will also result in increased production of carbon dioxide, which must also be removed. In order to
increase gas exchange to meet the increased demand, extra muscles are used to increase the capacity of the
respiratory system. The use of these extra muscles is often referred to as active breathing.
During active breathing accessory muscles are used during
inspiration to lift the rib cage, creating a larger space within the
thorax, further decreasing the pressure and causing a more rapid
flow of air into the lungs. Expiration during active breathing
becomes an active rather than passive action, with contraction
of muscles to rapidly decrease the size of the thorax, thereby
increasing the pressure and forcing air out of the lungs.
The use of accessory muscles in
the absence of exercise can be an
indication of respiratory failure
ic
FIGURE 1.3 Muscles used during quiet and active breathing. (Image from Ingraham, 2004)
10 | 11
LUNG VOLUMES
Air movement in and out of the lungs is determined by the pressure gradient between the atmosphere and
the alveoli. The volume of air inhaled and exhaled with each breath is called the tidal volume. The pressure
gradient, and therefore respiratory effort, required to obtain a particular tidal volume may be affected by the
lung compliance and the resistance of the airways.
Lung compliance is the distensibility or “stretchability” of the lung and the elastance, or elastic recoil back
to its original shape. Lung compliance is affected by connective tissue and alveolar surface tension. A highly
compliant lung will expand easily when pressure is applied;
however a poorly compliant lung requires a greater than normal
pressure, and therefore effort, to expand it.
Lung volumes will be affected by the
compliance & resistance of the airways
The resistance of the airways refers to the opposition to gas flow
through the airways. It is primarily determined by the radius of
the airway, with a smaller bronchial diameter increasing the resistance or opposition to air flow, therefore
slowing down the air flow for a particular pressure gradient. An airway with high resistance will therefore
require greater than normal pressure gradient and effort to achieve normal levels of ventilation.
APPLICATION NOTE
When using an artificial airway a small diameter tube will increase the resistance to airflow causing higher
airway pressures to deliver the same volume or, if the pressures are being controlled, will result in a reduced
volume being delivered
FIGURE 1.4 Normal lung volumes and capacities for an adult male (Image from Marieb, 2004)
MEASUREMENTS OF LUNG VOLUMES AND CAPACITY
Individual components of the mechanics of ventilation can be measured to allow the evaluation of lung function. Lung volumes are measured during normal quiet breathing and then during maximal inspiration and
expiration. From the four volumes measured (tidal volume, inspiratory reserve volume, expiratory reserve
volume, and residual volume), the lung capacity in relation to inspiration and expiration can be calculated (see
Figure 1.4).
TELEFLEX Academy Ventilation Workshop Pre-Reading Package
Respiration
EXTERNAL RESPIRATION
Once the air has reached the alveoli gas exchange between the air and blood, known as external respiration,
can occur. In order for effective gas exchange, there not only needs to be good ventilation but also good perfusion, or circulation, to the ventilated alveoli.
The movement of oxygen and carbon dioxide between the alveoli and capillaries is controlled by diffusion,
with gas moving across the alveolar membrane from areas of high concentration to areas of low concentration.
Gas diffusion is affected by:
• Concentration gradient
• Thickness of barrier
• Surface area available for exchange
• Ventilation-Perfusion matching
• Solubility of gas
CONCENTRATION GRADIENT
Gas concentrations are expressed as partial pressures. In a mixture of gases, each gas contributes to the total
pressure according to its concentration. For example if a gas is 50% of total, it produces 50% of the pressure.
The pressure of room air, or atmospheric pressure, at sea level is 760 mmHg. This pressure is made of different
concentrations of gases – with approximately 78% nitrogen, 21% oxygen, 0.03% carbon dioxide and 0.05%
water vapour. The partial pressure of oxygen in room air is therefore 21% of 760 mmHg, or 160 mmHg.
When air enters the trachea it is humidified, becoming
fully saturated with water vapour. The water vapour,
now taking up approximately 6% (47 mmHg) of the
pressure, displaces other gases and reduces their
concentrations (Smeltzer & Bare, 1992). In the alveoli
there is some residual carbon dioxide, which further
alters the balance of concentrations, with the resulting
partial pressures within normal alveoli:
•
•
•
•
Nitrogen, 569 mmHg (74.9%);
Oxygen, 104 mmHg (13.6%);
Carbon dioxide, 40 mmHg (5.3%);
Water vapour, 47 mmHg (6.2%).
FIGURE 1.5 Diffusion of oxygen and carbon dioxide accross the
alveolar membrane (Image from Marieb, 2004)
The speed of oxygen and carbon dioxide diffusion
across the alveolar membrane is affected by the size of the concentration gradient. The bigger the difference
between concentrations on either side, the faster the gas will move. The biggest gradient, and therefore fastest
diffusion of gas, occurs when fresh gas is brought in to the alveoli during inspiration.
In the alveolar capillaries the blood is returning, through the right side of the heart, from the tissues, where
oxygen has been used and carbon dioxide produced during cellular metabolism. The capillary oxygen levels
are therefore usually low, and the carbon dioxide levels high in comparison to the alveolar gases. The differences in concentration, or concentration gradients, cause movement of oxygen from the alveoli into the blood,
and carbon dioxide from the blood into the alveoli.
12 | 13
GAS EXCHANGE SURFACE
The alveolar-capillary membrane is ideal for diffusion as it has a thin membrane, as thin as 0.3 micrometers in
some areas, and a large surface area of 50-100 m 2 in a normal lung. For gas to get between the air and the red
blood cells it must diffuse through the following layers (see Figure 2.5):
Alveolar space
Surfactant
Fused basement
menbranes
Nucleus of
endothelial cell
Alveolar
epithelium
0.1-1.5µm
Capillary
Endothelium
•
•
•
•
•
•
•
Alveolar fluid
Alveolar epithelium
Alveolar basement membrane
Interstitial space
Capillary basement membrane
Capillary endothelium
Plasma
Any changes to the surface area or layers will affect
the diffusion of gases.
FIGURE 1.6 Layers of the alveolar-capillary membrane
SURFACE AREA FOR GAS EXCHANGE
The total amount of diffusion that occurs accross the membranes is proportional to the size of the surface
through which it can diffuse, or the surface area for gas exchange. The more gas that can come in to contact
with the blood, the more gas will be able to move into and out of the blood. As discussed previously, the gas
exchange units in the lung provide an environment for efficient gas exchange. The alveoli have a huge surface
area of around 160m², each surrounded by a mesh of pulmonary capillaries, with as many as 1000 capillaries
coming in to contact with each alveoli.
In order to minimise the distance for gas diffusion, each capillary is only big enough to fit one red blood cell
at a time. As the red blood cell travels the full length of the capillary (from the pulmonary arterial to venous
system) it may have come into contact with several alveoli. In a normally functioning body at rest the haemoglobin (Hb) on the red blood cells will be fully saturated by the time it has travelled a third of the way along
the pulmonary capillary. There is therefore extra reserve capacity for diffusion, which means that the Hb may
still have time to be fully saturated despite mild problems with the alveolar-capillary membrane that slow
diffusion, or a high cardiac output that reduces red blood cell contact time with the alveoli.
The small capillary diameter and thinness and compliance of the avleolar-capillary walls means that alveolar
pressures can affect capillary blood flow. If the pressure within the alveoli exceeds that of the pulmonary capillary, it can compress or collapse the capillary, blocking blood flow through that capillary.
VENTILATION-PERFUSION MATCHING
For gas exchange to be optimized the body must match the distribution of ventilation with perfusion, or blood
flow in the pulmonary capillaries. Ideally each gas exhange unit would have an equal ratio of ventilation and
perfusion. In a normal upright person however, the ventilation and perfusion are not equally distributed in the
lung, with the average alveolar ventilation 4 L/min and perfusion 5 L/min. The healthy body is however able to
compensate and redirect blood flow to maximise ventilation perfusion matching.
The pulmonary circulation is a low-pressure system, able to vary its resistance to accommodate the blood
flow received and alter the direction of blood flow to well ventilated areas. Due to the low pressures however,
the distribution of blood is greatly affected by gravity, with minimal perfusion to the lung apices when in an
upright position. It is also affected by alveolar pressure, as high alveolar pressures will cause compression of
TELEFLEX Academy Ventilation Workshop Pre-Reading Package
the capillaries and therefore restrict pulmonary blood flow
to the area.
Pathological changes to the airways or pulmonary
circulation can further affect the balance, with two main
types of mismatch occuring:
• A blockage of ventilation to gas exchange units that
still have good perfusion is referred to as a shunt.
The alveoli cannot get any fresh gas and therefore
blood travels past the alveoli without any gases being
exchanged.
• A blockage of perfusion to gas exchange units that
still have good ventilation is referred to as dead space
ventilation. Gas is able to get in to the alveoli, but it
doesn’t have contact with blood, and therefore can not
diffuse accross.
• An absence of both ventilation and perfusion is
referred to as a silent unit. Rather than there being
a mismatch of ventilation and perfusion (as they are
both equally absent) there is a reduction in surface
area available for gas exchange.
FIGURE 1.7 Matching of ventilation and perfusion. (Center)
Normal matching of ventilation and perfusion; (Left) perfusion
without ventilation (i.e. shunt); (Right) ventilation without
perfusion (i.e. dead space). (Image from Porth, 2005)
Monitoring of blood and exhaled gas concentrations in combination with assessing the affect of changes in
inspired oxygen concentrations can help in identifying the cause, and therefore treatment, of a mismatch.
In order to improve the matching of ventilation (represented by the letter V with a dot over it, v̇) to perfusion
(represented by the letter Q), or the v̇/Q match, the pulmonary capillaries can constrict and dilate to help to
direct blood flow toward well ventilated and away from poorly ventilated areas. The capillaries respond to
localised changes in oxygen and carbon dioxide levels.
• In areas with good ventilation there will be effective diffusion and therefore high levels of oxygen and
low levels of carbon dioxide. The high oxygen and low carbon dioxide concentrations will cause the
pulmonary capillaries to dilate, increasing blood flow to these well ventilated areas.
• In areas with poor ventilation there will be limited diffusion and therefore low levels of oxygen and high
levels of carbon dioxide. The low oxygen and carbon dioxide levels will cause the pulmonary capillaries to
constrict, diverting blood away from these areas and towards better ventilated lung units.
GAS SOLUBILITY
The diffusion of a gas is also affected by the gas’s solubility. Oxygen and carbon dioxide must be able to
dissolve into the alveolar fluid and then the blood in order to be transported to and from the tissues. When
gas is exposed to a liquid, the gas will dissolve in the liquid until the concentration, or partial pressure, of
the gas is the same in the liquid and the gas. This means that
oxygen and carbon dioxide are exchanged across the alveolar
membrane until the partial pressure is the same in the alveoli
Carbon dioxide levels are largely
and the blood.
controlled by minute ventilation
whereas oxygen is affected by
Some gases dissolve more quickly and easily than others.
surface area
Carbon dioxide, for example, dissolves approximately 20 times
faster than oxygen. It is therefore relatively unaffected by
increased fluid in the alveoli or interstitial space, whereas oxygen diffusion may be affected. As carbon dioxide
diffuses and equalises so quickly, the best way to remove more from the blood is to replace the air in the
alveoli with new air to re-establish the concentration gradient and therefore restart the diffusion process.
14 | 15
INTERNAL RESPIRATION
The process of gas exchange between the blood and the cells, or internal respiration, is the same as for external
respiration. Movement of the gases is primarily affected by the concentration gradient between the blood and
the cells. When oxygen-enriched blood comes in contact
with tissue with a lower PaO2, oxygen will move from the
blood into that tissue. Also, when the partial pressure of
carbon dioxide (PaCO2) in the tissue exceeds that of the
blood, carbon dioxide will move from the tissue into the
blood to be transported to the lungs. Metabolic changes,
as well as increases in interstitial fluids may affect the
diffusion of oxygen into the cells, and therefore impair cell
function.
CELLULAR RESPIRATION
Cellular respiration, or cellular metabolism, is the process
of deriving energy, in the form of ATP, from molecules
such as glucose. The cells break down glucose either with
or without oxygen. When a glucose molecule is broken
down without oxygen (anaerobic metabolism) 2 ATP
molecules are produced, however in the presence of oxygen
(aerobic metabolism) most cells can produce a further 34
ATP molecules. Oxygen is therefore essential for energyefficient metabolism to produce enough energy to maintain
normal cell function.
FIGURE 1.8 Layers of the alveolar-capillary membrane
Gas Transport
Oxygen and carbon dioxide are transported between the lungs and the cells in the blood stream. Some of the
gas is transported dissolved in the plasma; however the majority is transported combined with some of the
elements of the blood (see Figure 1.8). Gas transport is therefore reliant on the adequate functioning of the
cardiovascular system. Changes to circulation (such as poor cardiac output) or components of the blood (such
as anaemia) will affect the ability of gas to be transported to and from the lungs and cells.
OXYGEN TRANSPORT
The oxygen that is dissolved in the plasma of arterial blood, measured as a partial pressure or PaO2, is in a
form that is readily available for diffusion to the tissues. The poor solubility of oxygen, however, limits the
amount of oxygen that can be dissolved in the blood. The body
therefore needs to have a reserve of oxygen that can be made
available in periods of increased demand, such as exercise
The average red blood cell contains
or illness. Haemoglobin (Hb), found in the red blood cells,
approx 250 million Hb molecules, each
significantly enhances the oxygen carrying capacity of blood
capable of carrying 4 oxygen molecules
and providing a reserve supply. For every 100ml of blood,
approximately 0.3mls of oxygen is physically dissolved in the
plasma, however approximately 20mls of oxygen is present combined with haemoglobin (which becomes
oxyhaemoglobin). At rest only 30% of the oxygen on the haemoglobin is normally used by the tissues.
TELEFLEX Academy Ventilation Workshop Pre-Reading Package
Haemoglobin is made up of iron-containing haem molecules combined with the protein globin. The iron in
haem is able to reversibly bind an oxygen molecule. This means that oxygen can bind to Hb in the lungs and
then be released at the tissues. There are four iron atoms in each Hb molecule comprising four haem groups.
Each Hb molecule can therefore bind with four oxygen molecules. When oxygen is bound to all 4 haem groups,
the Hb is said to be fully saturated.
APPLICATION NOTE
Pulse oximetry measures the oxygen saturation of arterial blood (SaO2 ), i.e. the percentage of oxygen carried
by the available haemoglobin rather than the total oxygen available to the tissues. Hb levels and the PaO2 are
not taken into account.
In the loading and unloading of oxygen, there is cooperation between the four haem groups. When oxygen
binds to one of the groups, the others change shape slightly and their attraction to oxygen increases. The
loading of the first oxygen results in the rapid loading of the next three (forming oxyhaemoglobin). At the
other end, when one haem group unloads its oxygen, the other three rapidly unload as their groups change
shape again having less attraction for oxygen.
This method of cooperative binding and release can be seen in the dissociation curve for
haemoglobin (see Figure 1.9). Over the range of oxygen concentrations where the curve
has a steep slope, the slightest change in concentration will cause haemoglobin to load or
unload a substantial amount of oxygen.
OXYHAEMOGLOBIN DISSOCIATION
PaO2
SaO2
150mmHg
100%
100mmHg
97%
60mmHg
90%
40mmHg
70%
TABLE 1.1 Relationship
between PaO2 and SaO2
The major factor that determines the movement of oxygen onto the haemoglobin is the
amount of oxygen dissolved in the plasma (PaO2). As the concentration of oxygen in the plasma increases,
more oxygen combines with the haemoglobin, until it is fully saturated i.e. oxygen is bound to all 4 haem
groups. Haemoglobin usually becomes 100% saturated, under normal conditions, at a PaO2 of 150mmHg. In
healthy person breathing room air, the expected arterial oxygen levels would be a PaO2 100mmHg (achieving
equalisation with alveolar oxygen concentration) and a corresponding SaO2 of 97%.
Table 1.1 shows the relationship between PaO2 and
SaO2 at various levels:
•
At PaO2 150mmHg, even though the PaO2 has
been increased by nearly 50%, there is minimal
change in the SaO2 as the haemoglobin is almost
completely saturated and cannot combine with any
more oxygen.
•
PaO2 60mmHg, when the symptoms of hypoxia
normally begin, although there is a drop of nearly half
the dissolved oxygen concentration, the haemoglobin is
still 90% saturated at this level. Small changes in SaO2
at this level correspond with large changes in PaO2.
FIGURE 1.9 Oxyhaemoglobin dissociation curve
(Image from Marieb, 2004)
16 | 17
APPLICATION NOTE
In most clinical situations there is minimal benefit in increasing supplemental oxygen concentrations to achieve
a SaO2 >97%. Delivering high concentrations of O2 may in fact cause oxygen toxicity,damaging the airways
and impeding gas exchange.
It is vital to the delivery system for the oxygen to bind and release from the haemoglobin at the right time and
the right place. The oxyhaemoglobin dissociation system is designed to facilitate loading of oxygen onto the
haemoglobin in the lungs, and offloading of oxygen in the systemic capillaries to supply the tissues. Factors
such as the temperature, pH and carbon dioxide differ from the systemic to the pulmonary capillaries.
The systemic capillaries provide oxygen for and carry wastes from cellular metabolism. It is here that we
need oxygen to easily leave the haemoglobin. The conditions in the systemic capillary are greatly affected by
the cellular metabolism that is occurring around it. There are low levels of dissolved oxygen (PaO2) as it is
consumed by the cells, but high levels of carbon dioxide (and therefore a low, or acidic, pH) and heat produced
during the metabolism. These factors, low oxygen, high CO2 and high temperature all affect the binding of
oxygen to the haemoglobin, helping it to release easily.
The pulmonary capillaries allow release of carbon dioxide into the atmosphere and
bring oxygen into the circulation. The blood, having returned from the tissues, has
low oxygen levels, however as carbon dioxide quickly and easily diffuses into the
alveoli, the plasma CO2 level in the pulmonary capillary is low, as is the temperature
as heat is lost over the membrane. In these conditions, oxygen binds more strongly to
the haemoglobin, allowing the haemoglobin to be saturated with oxygen to then be
transported back to the cells.
Increased
O2 affinity
Decreased
O2 affinity
pH
pH
CO2
CO2
Temp
Temp
2, 3 - DPG
2, 3 - DPG
Changes to the level of 2,3-diphosphoglycerate (2,3-DPG), which is produced in the red blood cell, also affects
the affinity of oxygen to haemoglobin. Low levels of 2,3-DPG can be found during sepsis as well as in blood
transfusions, which makes oxygen bind more strongly to the haemoglobin, reducing its availability to the
tissues.
APPLICATION NOTE
Sepsis can not only affect the ability to transport oxygenated blood to the cells, but can also affect the cells
ability to receive and use the oxygen in the systemic capillaries, resulting in organ failure.
CARBON DIOXIDE TRANSPORT
Carbon dioxide created during cellular metabolism diffuses into the blood plasma with over 90% then
entering the red blood cells. Once in the red blood cell approximately 23% binds to the multiple amino
groups of haemoglobin to form carboxyhaemoglobin, whilst the majority (approximately 70%) is converted to
bicarbonate ions and released into the plasma.
The amount of carbon dioxide being transported in the blood is one of the major determinants of the acidbase balance of the body. When carbon dioxide enters the plasma, it reacts with water to form carbonic acid.
Carbonic acid is a strong acid and readily donates its hydrogen ions. An increase in carbon dioxide levels
within the blood will therefore cause an acidosis. As discussed previously, the carbon dioxide diffuses easily
across the alveolar membrane, equalising quickly with the alveolar gas. The arterial carbon dioxide level is
therefore usually equivalent to the partial pressure of carbon dioxide in the alveoli, i.e. 40 mmHg.
TELEFLEX Academy Ventilation Workshop Pre-Reading Package
Control of Breathing
Breathing is controlled both centrally and locally
in response to the stimulation of receptors
located within the brain stem and the lungs.
CENTRAL CONTROL OF BREATHING
The respiratory centre is found in the brain stem. The
pons and medulla oblongata are both integral to the
control of breathing (Figure 1.10). The medulla oblongata
rhythmically stimulates the intercostal muscles and
diaphragm - making breathing possible. The pons also
participates in the reflexes that regulate breathing.
The brain stem receives signals from various organs
in order to detect changes and respond to changes in
physical demands of the body. It receives positive and
negative stimuli to determine the respiratory rate and
depth required.
The rate of cellular respiration (and hence oxygen
consumption and carbon dioxide production) varies
with the level of physical activity. Vigorous exercise
can increase tissue oxygen demand by 20-25 times that
at rest. An increase in physical activity, and therefore
cellular metabolism, will result in increased carbon
dioxide levels and acidity, which is detected by peripheral
and central chemoreceptors which, provide a positive
stimulus to the brainstem to cause an increase in
ventilation, i.e. increase in rate and depth of breathing.
Stretch receptors in the lungs detect over distension,
resulting in a negative stimulus to the brain stem,
reducing the rate and depth of breathing, protecting
against trauma to the airways. Irritant receptors in
the bronchi and lungs will also cause a reduction in
ventilation, to help prevent deep inhalation of irritants
into the lower airways.
FIGURE 1.10 The Respiratory Center is located in the medulla
oblongata & pons of the Brain Stem (Image from Marieb, 2004)
Breathing may be affected by emotional factors, such as fear, anxiety, or pain. Signals are transferred through
the hypothalamus to the brain stem to affect ventilation. We are also capable of voluntary or conscious control
over breathing. The brain stem receives signals from the higher brain centres to increase or decrease ventilation
accordingly.
18 | 19
The most important factor in regulating ventilation
is a rising concentration of carbon dioxide - not a
declining concentration of oxygen. The concentration
of carbon dioxide is detected by cells in the medulla
by changes in the pH of the CSF. If the carbon dioxide
level rises, the medulla responds by increasing the
activity of the motor nerves that control the intercostal
muscles and diaphragm.
Carbon dioxide concentration is the
primary stimulus to breathe
However, the carotid body in the carotid arteries
does have receptors that respond to a drop in
oxygen. Their activation is important in situations
where oxygen supply is inadequate but there has
been no increase in the production of CO2 , for
example at high altitude in the unpressurised
cabin of an aircraft, or in situations of long term
hypercapnia.
FIGURE 1.11 Negative and positive stimuli to the brain stem
affecting ventilation (Image from Marieb, 2004)
Local Control of Breathing
In addition to central control affecting the rate and
depth of breathing, there is also a local control
within the lungs. The smooth muscle in the walls of
the bronchioles is very sensitive to the concentration
of carbon dioxide. A rising level of CO2 causes the
bronchioles to dilate. This lowers the resistance in
the airways and thus increases the flow of air in and
out.
FIGURE 1.12 Primary mechanism for control of breathing
(Image from Marieb, 2004)
TELEFLEX Academy Ventilation Workshop Pre-Reading Package
TEST YOUR KNOWLEDGE
Try to answer the questions below without initially referring to the chapter. The short answer questions should
be completed in your own words.
MATCHING EXERCISES
A. Affinity1.
Alterations in this pulmonary function may be the result of airway obstruction, changes in lung compliance, and gravity
B. Compliance
2.
The capacity of haemoglobin to combine with oxygen that may be described as high or low
C. Resistance
3.
Alterations in this pulmonary function may be the result of changes in pulmonary artery perfusion, alveolar pressure, and gravity
D. Ventilation
4.
A property of the lung that is a measurement of dispensability or how easily a tissue is stretched
E. Perfusion
5.
A property of the lung that is determined mainly by the radius or the size of the airway through which the air is flowing
TRUE/FALSE
Please indicate whether the following statements are true or false.
1. Normal expiration takes twice as long as normal inspiration
2. In the erect adult, more air exchange occurs in the lower regions of the lungs than
in the higher regions of the lungs because of gravity
3. The diffusing power of a gas is directly proportional to its partial pressure
4. Hypothermia, alkalosis, a decreased PaCO2 level, and a decrease in 2,3
diphosphoglycerate (2,3-DPG), result in an increased affinity of the haemoglobin for
oxygen at any given PaO2 value, resulting in less oxygen released to the tissues
5. Central chemoreceptors located in the medulla respond to a low CSF pH by
increasing, through medullary stimuli to the muscles of inspiration, both rate and
volume
6. Hypoxia is the primary stimulus to breathe
TRUE / FALSE
20 | 21
SHORT ANSWER/FILL-IN QUESTIONS
1. Describe the mechanism for spontaneous breathing.
2. Identify four conditions or situations that reduce pulmonary compliance.
a.
b.
c.
d.
3. Name four conditions that cause increased airway pressure.
a.
b.
c.
d.
4. Name four factors affecting alveolar–capillary gas exchange.
a.
b.
c.
d.
TELEFLEX Academy Ventilation Workshop Pre-Reading Package
SHORT ANSWER/FILL-IN QUESTIONS
5. Name four factors that affect the affinity of haemoglobin and oxygen.
a.
b.
c.
d.
6. Describe how oxygen and carbon dioxide are transported around the body.
7. What is internal and external respiration?
8. Draw or describe the movement of oxygen and carbon dioxide during internal and external respiration.
22 | 23
TELEFLEX Academy Ventilation Workshop Pre-Reading Package
Pathophysiology
02
Effective gas exchange relies on each part of
the respiratory process to be functioning. An
interruption at any point will affect the ability
of the body to supply oxygen to the tissues and
remove carbon dioxide.
CHAPTER
Impaired pulmonary function can be classified into two main types:
•
•
Oxygenation impairment – inadequate arterial oxygenation, or hypoxia.
Ventilation impairment – inadequate carbon dioxide removal, or hypercapnia, in the presence of
normal alveolar-arterial (A-a) gradient.
OXYGENATION IMPAIRMENT
Diffusion of oxygen, as previously discussed, is greatly affected by any
changes to the air-blood barrier in the alveoli. Due to its poor solubility,
any changes in the surface area, thickness of the barrier or increased
fluid can result in inadequate oxygenation of the arterial blood.
Not all of the oxygen can diffuse into the capillaries, with a higher
concentration still left in the alveoli (called an A-a gradient).
Treatment of oxygenation impairment requires supplementing oxygen
(which increases the concentration gradient, speeding up oxygen
diffusion) to ensure tissue hypoxia doesn’t occur, whilst treating the
cause; e.g. increase surface area, reduce alveolar/interstitial fluid,
improve ventilation-perfusion match.
FIGURE 2.1 Oxygenation impairment in early
ARDS (Image from Morton et al, 2005)
VENTILATION IMPAIRMENT
Ventilation impairment, or inadequate exchange of gas through the airways between the atmosphere
and the lungs, is characterised by high arterial carbon dioxide levels, respiratory acidosis and
increased work of breathing. The inadequate spontaneous ventilation may be caused by a reduced
drive to breathe, as is found in CNS disorders; or a reduction in tidal volumes from neuromuscular,
musculoskeletal, pleural, or conducting airways disorders.
As carbon dioxide excretion is dependent on the amount of air it can exchange with, any changes to
the respiratory rate or tidal volume (and therefore the minute ventilation) affects the arterial carbon
dioxide level, resulting in hypercapnia.
24 | 25
Treatment of ventilation impairment is focused on increasing the respiratory rate by minimising any central
respiratory depressants or improving tidal volumes by reducing the work of breathing and supporting the
inspiratory effort.
ACUTE RESPIRATORY FAILURE
Respiratory failure is a syndrome in which the respiratory system fails in one or both of its gas exchange
functions: oxygenation and carbon dioxide elimination. The lungs cannot maintain adequate alveolar
ventilation. Hypoxic failure, characterised by low oxygenation, is also known as Type 1 Failure, and hypercapnic
failure, characterised by high carbon dioxide levels, is also known as Type 2 Failure.
Respiratory failure may be acute or chronic. Acute respiratory failure is characterised by life-threatening
alterations in arterial blood gases and acid-base status and is the most common indication for mechanical
ventilation in the Intensive Care Unit Acute respiratory failure can be defined as a PaO2 value of less than
60 mmHg while breathing air, or a PaCO2 of more than 50 mmHg. The manifestations of chronic respiratory
failure are less dramatic and may not be as readily apparent.
Common causes of acute respiratory failure include pneumonia, apnoea, neuromuscular dysfunction, head
trauma, cardiac arrest, or drug-induced central nervous system (CNS) depression.
Common Respiratory Disorders
ATELECTASIS
Atelectasis refers to the collapse of an area of lung, which could be an alveoli, lobule or larger lung unit.
Atelectasis may result from:
• Airway obstruction (eg. from sputum blocking a bronchiole), preventing airflow into the alveoli. The gas
remaining in the alveoli eventually gets absorbed into the capillary, and with no fresh air to replace it,
the alveoli collapse. Failure to adequately remove secretions, due to neurological or respiratory disorders,
commonly causes atelectasis.
• Compression of the lung tissue, limiting expansion and restricting air movement into the alveoli. The
lung tissue may be compressed by air or fluid in the pleural space (i.e. pneumothorax or pleural effusion),
enlarged heart, pericardial effusion, thoracic tumor, patient positioning preventing adequate lung
expansion, or abdominal distension pushing the diaphragm upward.
•
Failure of the normal splinting mechanisms:
- Loss or dilution of surfactant in the alveoli will increase
the surface tension, causing collapse of the alveoli.
- Loss of nitrogen in the alveoli due to inhaling high
concentrations of oxygen. Nitrogen normally comprises
approx 75% of the gas in the alveoli. It is a large molecule that does not diffuse across the alveolar membrane,
assisting in splinting the alveoli open. If high concentrations of oxygen are delivered, there will be a consequential drop in the percentage of nitrogen. If all the alveolar
oxygen diffuses into the capillary the alveoli before it is
refreshed with new gas, the alveoli can collapse.
- Decrease in alveolar pressure, which may cause collapse
FIGURE 3.2 Atelectasis caused by airway obstruction on
of the terminal bronchioles, which do not have any
left, and compression on right (Image from Porth , 2005)
cartilage to splint them open.
TELEFLEX Academy Ventilation Workshop Pre-Reading Package
ACUTE PULMONARY OEDEMA
Acute pulmonary oedema (APO) is the abnormal
accumulation of fluid in the lungs, either in the
interstitial spaces or in the alveoli. An increase of
fluid at the air-blood interface impairs the ability
of oxygen to diffuse into the capillaries (with
carbon dioxide being largely unaffected due to
its high solubility). An increase in fluid within the
alveoli causes a dilution of the alveolar surfactant,
which may result in collapse of the alveoli. APO
may be caused by left heart failure (cardiogenic
APO) which results in increased pulmonary blood
flow and pressure, causing fluid to leak out of the
capillaries into the interstitial airways.
Non-cardiac APO may also be caused by conditions
that increase the pulmonary pressures, affect
the colloid osmotic pressure (e.g. in nephritis),
increase the permeability of the pulmonary
capillaries (e.g. systemic inflammation) or damage
to the capillary walls (e.g. inhalation of noxious
gases, pneumonia and ARDS).
FIGURE 3.3 Asthmatic bronchus
(Image from Morton et al, 2005)
PNEUMONIA
Pneumonia is an infection of the alveoli. It can be caused by many kinds of bacteria (e.g., Streptococcus
pneumoniae) and viruses. Fluid accumulates in the alveoli, reducing oxygen diffusion as well as diluting the
surfactant causing collapse of the alveoli and therefore reducing the surface area exposed to air. Treatment
includes clearance of secretions, and antibiotic treatment, if appropriate. If enough alveoli are affected,
oxygenation is impaired and the patient may need supplemental oxygen.
ASTHMA
In asthma, periodic constriction of the bronchi and bronchioles makes it more difficult to breathe in and,
especially, out. The swollen walls and increased secretions narrow the airways, increasing resistance and
reducing air flow. During inspiration the airways are pulled open, however during expiration, the elastic
recoil causes some obstruction of the airways, trapping air in the alveoli. The resultant ventilation impairment
causes a rise in carbon dioxide levels. Attacks of asthma can be triggered by:
•
•
•
Food and environmental allergies ; eg. dust mites, pollens, animal dander
Air borne irritants; e.g. chemical fumes, pollution, cigarette smoke
Exercise Drugs; e.g. aspirin, β-blockers, NSAIDs
26 | 27
CHRONIC BRONCHITIS
Any irritant reaching the bronchi and bronchioles will
stimulate an increased secretion of mucus. In chronic
bronchitis inflammation and thickening cause narrowing
of the airways, with increased mucous secretions leading
to a persistent cough. Oxygenation is impaired as diffusion
is difficult through the secretions and due to alveolar
collapse. Chronic bronchitis is usually associated with
cigarette smoking.
FIGURE 3.4 Inflammation & secretions seen in bronchitis
(Image from Morton et al, 2005)
EMPHYSEMA
FIGURE 3.5 Lung changes in emphysema
(Image from Morton et al, 2005)
In emphysema, the delicate walls of the alveoli break
down, reducing the gas exchange area of the lungs. They
are grouped into three types according to where in the
alveolar unit the tissue break down occurs. The condition
develops slowly and is seldom a direct cause of death.
However, the gradual loss of gas exchange area forces the
heart to pump ever-larger volumes of blood to the lungs
in order to satisfy the body’s needs. The added strain can
lead to heart failure.
CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)
Irritation of the lungs can lead to asthma, emphysema, and chronic bronchitis; in fact, many people develop
two or three of these together. This combination is known as chronic obstructive pulmonary disease (COPD).
ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS)
Acute respiratory distress syndrome is the clinical manifestation of severe, acute lung injury. It is
characterised by the acute onset of diffuse, bilateral pulmonary infiltrates secondary to non-cardiogenic
pulmonary edema, refractory hypoxia, and decreased lung compliance. Acute respiratory distress syndrome
can result from direct chest trauma, prolonged or profound shock, fat embolism, massive blood transfusion,
cardiopulmonary bypass, oxygen toxicity, or acute hemorrhagic pancreatitis. Most of these patients have no
previous lung disease.
At the onset of ARDS, lung injury may first appear in one lung, but then quickly spreads to affect most of both
lungs.
When alveoli are damaged, some collapse and lose their ability to receive
oxygen. With some alveoli collapsed and others filled by fluid, it becomes
difficult for the lungs to absorb oxygen and get rid of carbon dioxide. Within
one or two days, progressive interference with gas exchange can bring about
respiratory failure requiring mechanical ventilation. As the injury continues
over the next several days, the lungs fill with inflammatory cells derived from
circulating blood and with regenerating lung tissue. Fibrosis (formation of
scar tissue) begins after about 10 days and can become quite extensive by the
third week after onset of injury. Excessive fibrosis further interferes with the
exchange of oxygen and carbon dioxide.
FIGURE 3.6 Late stage ARDS
(Image from Morton et al, 2005)
TELEFLEX Academy Ventilation Workshop Pre-Reading Package
TEST YOUR KNOWLEDGE
Try to answer the questions below without initially referring to the chapter. The short answer questions should
be completed in your own words.
MATCHING EXERCISES
A. Atelectasis
1.
A pulmonary disease triggered by inhaled irritants, exercise, cold air, and viral infections that causes bronchospasm, which is usually reversible, and produces airway inflammation and increased airway responsiveness
B. Chronic bronchitis
2.
A pulmonary disease often caused by cigarette smoking or chronic
infection during which mucus-secreting glands of the
tracheobronchial tree become thickened and encroach on the
diameter of the airway lumen
C. Emphysema
3.
A common postoperative pulmonary problem resulting from
decline of volume or collapse of alveolar lung units that can lead to
increased shunting of unoxygenated blood back to the left ventricle
D. Asthma
4.
An infection of the alveoli causing collapse of alveoli and
impairment of oxygen diffusion
E. Pneumonia
5.
An irreversible pulmonary disease of the alveolus accompanied
by destructive changes of alveolar walls with resultant loss of
elastic recoil of the lung, resulting in over distension of alveoli
TRUE/FALSE
Please indicate whether the following statements are true or false.
1. Passive atelectasis can occur if communications between the alveoli and trachea are
obstructed
2. Ventilation impairment can be caused by a loss of surface area or change in alveolar
membrane and is assessed by low arterial oxygen levels
3. Hypoxia can be treated by increasing the surface area for gas exchange, decreasing
excess alveolar fluid whilst supporting the patient organ function by supplementing
their oxygen intake
4. Acute respiratory distress syndrome often occurs in patients with no previous lung
disease
TRUE / FALSE
28 | 29
SHORT ANSWER/FILL-IN QUESTIONS
1. Name four causes of atelectasis.
a.
b.
c.
d.
2. Describe how atelectasis impairs gas exchange.
3. List four common triggers of asthma
a.
b.
c.
d.
4. Describe how acute pulmonary oedema affects gas exchange.
TELEFLEX Academy Ventilation Workshop Pre-Reading Package
Glossary
ACCESSORY MUSCLES OF VENTILATION
Muscles other than the diaphragm or the internal and external intercostals, which are used in ventilation.
Most visible are the sternocleidomastoid muscles on either side of the neck. The other accessory muscles are
the scalenes. Activity of these muscles is assessed to determine a patient’s breathing effort.
ACIDOSIS
A pathologic condition resulting in the accumulation of acid or loss of base in the body. Respiratory acidosis is
the state of excess retention of carbon dioxide.
ACUTE
Having severe symptoms and a short course.
AEROPHAGIA
The swallowing of air.
AFFINITY
An attraction or force between substances that causes them to interact or combine.
AIR FLOW
Air will flow from an area of higher pressure to one of lower pressure; during inspiration, the pressure in the
alveoli must be less than the pressure at the mouth for air to flow in, and during expiration, the reverse is true.
Air flow may be laminar, turbulent or transitional, depending on the velocity of flow and on the diameter and
configuration of the tube.
AIRWAY
The anatomical structures through which air passes on its way to or from the alveoli; the nasopharynx and
oropharynx, the larynx, the trachea, bronchi, and bronchioles.
ALVEOLAR HYPOVENTILATION
The inability to exchange sufficient amounts of air between the room and the lung to allow for gas exchange
that produces normal concentrations of oxygen and carbon dioxide in the blood. Also referred to as ventilatory
impairment.
ALVEOLAR PRESSURE
The pressure within the alveoli, conventionally given in cm H 20, with reference to an atmospheric pressure
of zero. Thus, a negative alveolar pressure indicates that the pressure is lower than atmospheric; a positive
alveolar pressure indicates that the pressure is above atmospheric.
ALVEOLI
The air sacs that act as the primary gas exchange units of the lung.
APNOEA
The cessation of ventilatory activity. Must persist for at least ten seconds.
ARDS
Acute Respiratory Distress Syndrome. Indicates respiratory failure with life threatening distress and
hypoxaemia, associated with acute pulmonary injuries.
30 | 31
ATELECTASIS
A shrunken and airless state of part or all of the lung; the disorder may be acute or chronic.
ASTHMA
A condition characterised by increased tone of the smooth muscle surrounding the bronchi and by bronchial
inflammation and excess mucous secretion. An individual with acute asthma will present with an obstructive
profile on respiratory function tests.
ATMOSPHERIC PRESSURE
Ambient air pressure averages 760 mm Hg at sea level. In pulmonary calculations, atmospheric pressure is
taken as the reference value, 0 cm H 20. Pressures higher than atmospheric pressure then are positive; those
lower than atmospheric pressure are negative.
BLOOD GASES
A term used to describe the assessment of arterial blood gas levels of oxygen (PaO2) and carbon dioxide
(PaCO2).
BRONCHITIS
A clinical condition marked by airway inflammation and excess mucus secretion, manifested by cough and
sputum production. It may cause narrowing of the airways and increase their resistance; this results in an
obstructive ventilatory defect.
CHEST WALL
The anatomical structures that border the parietal pleura, including the ribs with intercostal muscles,
and diaphragm; when the muscles of the chest wall are relaxed, the chest wall acts in an elastic fashion
comparable to the lung, responding passively to the pressure differences around it.
CHRONIC
Persisting for a long time.
COMPLIANCE
Comprises the distensability, or “stretchability”, and elastance of the lung. Defined as the relationship between
a given change in volume and the pressure required to achieve that change
COMPLIANCE CURVE
The pressure-volume curve for the lung or relaxed chest wall; plotting volume as a function of pressure inside
minus pressure outside. The slope of this curve is the compliance.
DEAD SPACE
The portion of each breath that does not participate in gas exchange. Anatomic dead space is the volume of the
conducting airways; physiologic dead space also includes the contribution of alveoli that are well-ventilated
but poorly perfused.
DIAPHRAGM
A thin, dome-shaped sheet of muscle that inserts into the lower ribs; it is the most important muscle of
inspiration – when it contracts, it lowers pleural pressure.
DISTENDING PRESSURE
The inside pressure minus the outside pressure of an elastic structure; for the lung, this is also referred to as
the transpulmonary pressure or the recoil pressure of the lung.
TELEFLEX Academy Ventilation Workshop Pre-Reading Package
DYSPNEA
Shortness of breath.
ELASTANCE
A component of lung compliance, it it’s the elastic recoil of the lungs after inspiration back to their original
shape. Can be measured by alveolar pressure minus pleural pressure (Palv-Ppl).
EMPHYSEMA
A condition characterised by dilation and destruction of alveolar walls; it produces airflow obstruction as
determined by pulmonary function testing.
ERV
Expiratory reserve volume. The difference between FRC and RV. This is the maximal amount of air that can be
expired starting at FRC.
ESOPHAGEAL BALLOON
A thin walled balloon positioned in the lower oesophagus and attached to a strain gauge for estimating pleural
pressure.
F i O2
The fraction of inspired oxygen. Can be expressed as a decimal or a percent. Room air has an FiO2 of 0.21 or
21%.
FORCED EXPIRATION
The recording of a maximal expiration from Total Lung Capacity (TLC). This permits the measure of forced
vital capacity (FVC) and various of air flow.
FUNCTIONAL RESIDUAL CAPACITY
Also known as FRC, this is the lung volume at the end of a normal expiration, when the muscles of respiration
are completely relaxed
FVC
Forced vital capacity; the total volume of air that can be exhaled from the lungs during a forced expiration
following a maximal inspiration.
GAS DILUTION
A method of ascertaining functional residual capacity (FRC) and residual volume (RV) by mixing the unknown
volume of gas in the lungs with a known volume of gas containing a known concentration of a poorly soluble
gas like helium.
GLOTTIS
The true vocal cords; when one closes the glottis, no air can escape from the lungs.
HYSTERESIS
The difference in the pressure-volume curves of the lung during inflation and deflation (the lung volume at any
given pressure during deflation is larger than during inflation).
HYPERCAPNIA
An elevated level of carbon dioxide in the blood. PaCO2 typically over 45mmHg.
32 | 33
HYPERVENTILATION
A situation where the patient’s breathe rate and/or tidal volume exceed their respiratory needs. PaCO2 is
reduced below normal levels.
HYPOXAEMIA
A reduced level of oxygen in the blood. PaO2 is 55mmHg or below.
IRV
Inspiratory reserve volume; the difference between VC and FRC. This is the maximal amount of air that can be
inspired starting at FRC.
LAMINAR FLOW
Air flow in the lungs which is streamlined, low velocity, and obeys Poiseuille’s Law; generally it is confined to
the small peripheral airways.
LAPLACE‘S LAW
Equation expressing the relationship between the surface tension of a sphere and the resultant pressure:
P=2T/r, where P=pressure, T=surface tension, and r=radius (for a soap bubble or sphere with two surfaces,
P=4T/r).
MINUTE VENTILATION
The volume of gas that moves out of the lungs (expressed in litres per minute). It is calculated by multiplying
the exhaled tidal volume by the respiratory rate.
MUSCLES OF RESPIRATION
During quiet inspiration: diaphragm and external intercostals. During active inspiration: the muscles of
quiet inspiration plus the scalenes and sternomastoids. During quiet expiration: passive active expiration:
abdominal muscles, internal intercostals.
OBSTRUCTIVE DISEASE
A respiratory abnormality characterised by delay in forced expiration of air from the lungs.
Palv
Alveolar pressure The pressure within the alveoli, conventionally given in cm H20, with reference to an
atmospheric pressure of zero. Thus, a negative alveolar pressure indicates that the pressure is lower than
atmospheric; a positive alveolar pressure indicates that the pressure is above atmospheric. Asthma, bronchitis,
and emphysema are all considered obstructive conditions.
PARIETAL PLEURA
The portion of the pleural membrane that lines the thoracic cavity.
PL
Transpulmonary pressure The pressure difference across the lung. Alveolar pressure minus pleural pressure
(Palv-Ppl), which is also known as the elastic recoil pressure of the lung.
PLEURAL EFFUSION
Collection of fluid within the pleural space. If the fluid is blood it may be referred to as a haemothorax, if there
is a collection of pus it is referred to as a empyema.
TELEFLEX Academy Ventilation Workshop Pre-Reading Package
PLEURAL PRESSURE PPL
The pressure within the pleural space. Its value is generally given with reference to an atmospheric pressure of
zero, and it is measured in cm H 2O. Its symbol is Ppl.
PLEURAL SPACE
The tiny fluid-filled ‘space’ between the visceral and parietal pleura; if air should enter this normally noncommunicating space, a pneumothorax will result.
PNEUMOTHORAX
The presence of air in the pleural cavity, which may occur spontaneously, as a result of trauma, overinflation of
the lungs, or a pathological process.
POISEUILLE‘S LAW
An equation which describes laminar flow in a straight tube. V=P¹r4/8nl, where V= flow P= driving pressure r=
radius of tube n= fluid viscosity l= length of tube
PULMONARY FIBROSIS
A condition characterised by deposition of fibrous tissue in the lung. It decreases lung compliance and results
in a restrictive ventilatory defect as seen on pulmonary function testing.
RESISTANCE
Refers to the opposition to gas flow through the airways. Affected predominantly by the diameter of the
airways.
RESPIRATORY FAILURE
Occurs when there is an impairment in the exchange of gases between the circulating blood and the room air.
Failure is seen when the PaO2 is reduced, but PaCO2 is normal, low or high.
RESPIRATORY INSUFFICIENCY
A broader class of respiratory impairment in which the patient is not capable of sustaining the work required
to maintain ventilation for a prolonged period.
RESTRICTIVE VENTILATORY DEFECT
A condition characterised by a reduction in total lung capacity and vital capacity. Restrictive disorders may be
caused by stiffening of the chest wall, stiffening of the lung itself, or by muscle weakness.
RESIDUAL VOLUME
Also known as RV, this is the volume of the lungs after a maximal expiration.
SPIROMETRY
A simple lung function test that measures lung volume as a function of time; it can be used to ascertain lung
volumes or to gain information about maximal expiratory flow rates..
SURFACE TENSION
The force of attraction between adjacent molecules of a liquid.
SURFACTANT
A phospholipid secreted by the Type II alveolar cells. It not only decreases surface tension, but decreases it
most at low volumes and least at high volumes, contributing to the overall stability of the alveolar units. The
lungs of neonates are often deficient in surfactant.
34 | 35
TIDAL VOLUME
Also known as V T, this is the volume of an individual breath during quiet breathing. It averages about 500 ml.
TOTAL LUNG CAPACITY
Also known as TLC, this is the volume of the lungs after a maximal voluntary inspiration.
TRANSITIONAL FLOW
An intermediate type of airflow which has characteristics of both laminar flow and of turbulent flow. See
Turbulent Flow.
TRANSPULMONARY PRESSURE
The pressure difference across the lung. Alveolar pressure minus pleural pressure (Palv-Ppl), which is also
known as the elastic recoil pressure of the lung.
TURBULENT FLOW
Air flow characterised by disorganised movement of gas molecules and/or eddy formation; it occurs when
there are high gas flow rates or the are irregularities in the lining of the airways. Turbulence can increase the
pressure within the airways for a given volume of gas.
VENTILATORY IMPAIRMENT
The inability to exchange sufficient amounts of air between the room and the lung to allow for gas exchange
that produces normal concentrations of oxygen and carbon dioxide in the blood. Also referred to as alveolar
hypoventilation.
VISCERAL PLEURA
The portion of the pleural membrane that covers the lung.
VITAL CAPACITY
Also known as VC, this is the difference between Total Lung Capacity (TLC) and Residual Volume (RV); i.e., it
is the maximum volume of air that can be exhaled starting at full lung inflation.
TELEFLEX Academy Ventilation Workshop Pre-Reading Package
References
Antonelli, et al.(1998). A Comparison of Non-Invasive Positive-Pressure Ventilation and Conventional
Mechanical Ventilation in Patients with Acute Respiratory Failure New England Journal of Medicine. 339:42935
Australian Institute of Health and Welfare (2001). Cancer in Australia, 2001[online] Available: http://www.aihw.
gov.au/publications/index.cfm/title/10083 [Accessed 24th January, 2006]
Ball, W.C. Jr (1996). Interactive Respiratory Physiology. [online] http://oac.med.jhmi.edu/res_phys/index.HTML
[Accessed 17th January 2006]
Bare, B.G. and O’Connell, S.C. (1992). Brunner & Suddarth’s Textbook of Medical-Surgical Nursing. (7th ed.).
Philadelphia: Lippincott
Bare, B.G. and O’Connell, S.C. (2004). Brunner & Suddarth’s Textbook of Medical-Surgical Nursing. (10th ed.).
Philadelphia: Lippincott [online] Available: http://connection.lww.com/Products/smeltzer10e/frc.asp [Accessed
9th January 2006]
Brochard, L. et al.(1995). Non-Invasive Ventilation for Acute Exacerbations of COPD. New England Journal of
Medicine. 333:817-822.
Burns, S.M. (1997). Understanding, applying and evaluating pressure modes of ventilation. American
Association of Critical Nurse 7(4): 495- 506.
Forrest, G. (1999) NSW College of Nursing. Critical Care Course Notes.
Grossan, M. (2003). Sinus Disease & Problems explained. [online] Available: http://www.ent-consult.com/sinus_
lay.html [Accessed 10th January, 2006]
Grossbach, I. (1986) Troubleshooting ventilator and patient related problems. Part 1. Critical Care Nurse. 6(4):
58-70.
Hillberg, et al.(1997). Non- Invasive Ventilation. New England Journal of Medicine 337: 746-1752
Huskey, R.J. (1999) Introductory Biology. [online] Available from The University of Virginia, website: http://
www.biologie.uni-hamburg.de/b-online/library/bio201/bio201.html [Accessed 23rd January, 2006]
Ingraham (P). The Respiration Connection: How the mechanics of respiration cause pain and upper body injuries.
[online] Available from MindBodyGuide.ca website: http://mindbodyguide.ca/articles/respiration-connection.
php [Accessed 7th November, 2005]
Ingraham, P. (2004). The Respiration Connection: How the mechanics of respiration cause pain and upper
body injuries [online] Available: http://mindbodyguide.ca/articles/respiration-connection.php [Accessed 7
November, 2005]
King, M. (1996). Oncology for GPs: Lung cancer. [online] Available: http://www.quitnow.info.au/oncology.html
[Accessed 24th January, 2006]
36 | 37
Kramer N. et al (1995). Randomized, prospective trial of non-invasive positive pressure ventilation in acute
respiratory failure. American Journal Respiratory Critical Care Medicine 151: 1799-1806.
Lin, M. et al. (1995). Reappraisal of CPAP therapy in acute pulmonary edema: short-term results and long-term
follow up. Chest 107:1379-86.
Marieb (2004). Human Anatomy & Physiology. (6th ed.). San Francisco: Benjamin Cummings [online] Available:
http://academic.pgcc.edu/~aimholtz/AandP/ANPmain.html [Accessed 7th November, 2005]
Mehta, S.. et al.(1997). Randomized, prospective trial of bi-level versus continuous positive airway pressure in
acute pulmonary edema. Critical Care Medicine. 25:620-628.
Moore, K.L. and Agur, A. (2003) Essential Clinical Anatomy (2nd ed.). Philadelphia: Lippincott [online]
Available: http://connection.lww.com/products/moore/frc.asp [Accessed 9th January 2006]
Morton, P.G.; Fontaine, D.K.; Hudak, C.M.; and Gallo, B.M. (2005). Critical Care Nursing: A Holistic Approach
(8th ed.) Philadelphia: Lippincott [online] Available: http://connection.lww.com/Products/morton/frc.asp
[Accessed 6th January 2006]
Paulev, P. (2000). Textbook in Medical Physiology and Pathophysiology: Essentials and clinical problems. [online]
Available: http://www.mfi.ku.dk/ppaulev/content.htm [Accessed 7th November, 2005]
Pocanic, D. (2004) Physics of the Human Body [online] Available from The University of Virginia, Faculty of
Physics website: http://www.people.virginia.edu/~dp5m/phys_304/pix.html [Accessed 6th July, 2005]
Poponick, J. et al. (1999). Use of a Ventilatory Support System (BIPAP) for Acute Respiratory Failure in the
Emergency Department. Chest 116:166-171
Porth, C.M. (2005). Pathophysiology: Concepts of Altered Health States. (7th ed.). Philadelphia: Lippincott
[online] Available: http://connection.lww.com/Products/porth7e/frc.asp [Accessed 9th January 2006]
Rappard, S. Use of CPAP and BiPAP in Acute Respiratory Failure. [online] Available: http://www.theberries.
ns.ca/Archives/CPAP
Stedman’s Medical Dictionary for the Health Professions and Nursing Illustrated (5th ed.). (2004). Philadelphia:
Lippincott [online] Available: http://connection.lww.com/Products/stedmansmedict/frc.asp [Accessed 9th
January 2006]
Tamarkin, D.A. (2004) Anatomy and Physiology I & II [online] Available: http://distance.stcc.edu/AandP/
[Accessed 7th November, 2005]
Taylor, L. and Stephens, D. (1990). Arterial blood gases: clinical application. Journal of Post Anaesthesia
Nursing. 5(4): 264-272.
U.S. National Cancer Institute’s Surveillance, Epidemiology and End Results (SEER). Introduction to the
Respiratory System. [online] Available: http://training.seer.cancer.gov/module_anatomy/unit9_4_resp_
passages4_bronchi.html [Accessed 12th January, 2006]
Whitfield, P., and D.M. Stoddard. (1984). Hearing, Taste, and Smell; Pathways of Perception. New York: Torstar
Books, Inc.
TELEFLEX Academy Ventilation Workshop Pre-Reading Package
Woronczuk, J.; Medwid, S.; Neumann, L. and Eshelman, S. The Olfactory System: Anatomy and Physiology
[online] Available http://www.macalester.edu/psychology/whathap/UBNRP/Smell/nasal.html [Accessed 10th
January, 2006]
TELEFLEX Academy
Clinical Support and Education Team
Level 4 Building B, 201 Coward Street, Mascot NSW 2020
Tel. +61 (0)409 533 759 e: [email protected]
www.teleflex.com/academyaustralia
TFXA-NIV-PREREADING - AP AU 01 ∙ REV B ∙MC/PDF ∙ 03 15 PDF