This document is posted to help you gain knowledge. Please leave a comment to let me know what you think about it! Share it to your friends and learn new things together.
Transcript
- -1
TABLE OF CONTENTS
1. INTRODUCTION1.1 Anatomy Of Respiratory System………………………….……….5
1.1.1 Function Of Respiratory System………………………….……….………..5
1.1.2 Components Of Respiratory System……………………………..…………5
1.2 Physiology Of the Respiratory System…………………………….7
1.2.1 Gas Exchange…………………………………………….…..…7
1.2.2 Pulmonary Ventilation………………………………….….…...9
1.2.3 Breathing Cycle……………………………………….……...…9
1.2.4 Change In Volume Of Thoracic Space To TheLungs……..….11
1.2.5 Difference Between Spontaneous and ArtificialRespiratory….12
1. INTRODUCTIONIn this chapter will talk about general information in respirator system ,which plays an
important role in other biological systems.
We will talk about anatomy, physiology and associated disease of this system.
1.1 Anatomy of Respiratory System
1.1.1 Function of Respiratory System The function of the respiratory system is rather simple in concept: to bring in oxygen
from the atmosphere and get rid of carbon dioxide from the blood. Since oxygen (O2) and
carbon dioxide (CO2)are gases, the process of bringing one in and excreting the other is called
gas exchange . Oxygen is necessary for normal metabolism; lack of it leads to death in a
few minutes. Carbon dioxide is a waste product of metabolism; if breathing stops, carbon
dioxide will quickly accumulate to a toxic level in the blood. Thus our lungs, the organs that
exchange O2 and CO2 with the atmosphere are vital since their total failure is quickly fatal.
Approximately 10 12 times a minute, the brain stem sends nerve impulses that tell the
diaphragms and thoracic cage muscles to contract. Contraction of these muscles expands the
rib cage, leading to the expansion of the lungs contained within. With each expansion of the
lungs we inhale a breath of fresh air containing 21% oxygen and almost no carbon dioxide.
After full expansion the brain command to inhale ceases and the thoracic cage passively
returns to its resting position, at the same time allowing the lungs to return to their resting
size. As the lungs return to their resting position we exhale a breath of stale air, containing
about 16% oxygen and 6% carbon dioxide. In health this breathing cycle is silent, automatic,
and effortless.
1.1.2 Components of Respiratory SystemNose /Nasal Cavity: Warms, moistens and filter air.
Pharynx “throat”: Passageway for air, lead to trachea.
Larynx: The voice box, where vocal chords are located.
Trachea: Tube from pharynx to bronchi rings windpipe of cartilage
provide structure,
keeps the windpipe open . Trachea is lined with fine hairs called cilia
which filter air
before it reaches the lungs.
- -6
Bronchi: 2 branches at the end of trachea, each lead to lung.
Bronchioles: Network of smaller branches leading from the bronchi into the lung tissue
and ultimately to air sacs.
Alveoli: The functional respiratory units in the lung where gases O2 & CO2 are
exchange enter and exit the blood stream. .
Diaphragm: The main muscle used for breathing; separate the chest cavity from
the abdominal cavity.
Intercostals muscles: Thin sheets of muscle between each rib that expand when
air inhaled and contract when air is exhaled . The chest bellows component of
the respiratory system includes the bony thoracic cage that contains the lungs; the
diaphragms, which air the major muscles of breathing; and pleural membranes,
thin tissues that line both the outside of the lungs and the inside of the thoracic cage.
The thoracic or chest cage consist of the ribs that protect the lungs from injury;
the muscles and connective tissues that tie the ribs together; and all the nerves
that lead into these muscles.
Figure1.1 anatomy of respiratory system
- -7
Anatomy of respiratory system
1.2 Physiology of the Respiratory System Respiration is defined as the gas exchange between the organism and its surroundings.
external respiration includes ventilation and gas exchange. Biologic oxidation (combustion)
of nutrients by means of oxygen (O2) to carbon dioxide (CO2) and water (H2O) is referred to
as internal respiration.
At rest the body of a healthy adult utilizes about 300 ml/min oxygen and simultaneously
produces about 250 ml/min carbon dioxide.
1.2.1 Gas Exchange The atmosphere contains approximately 21% oxygen and 78% nitrogen. There is
almost no CO2 in air (about 0.03%); the carbon dioxide humans and animals exhale is a
negligible part of the entire atmosphere. The nitrogen is inert and does not take part in gas
exchange.
To accomplish gas exchange the air, we inhale is delivered to tiny sacs (alveoli) which
are the terminal or end units of the airways. During breathing, a volume of air is inhaled
through the airways (mouth and/or nose, pharynx, larynx, trachea, and bronchial tree)
into millions of tiny gas exchange sacs (the alveoli) deep within the lungs. There it
mixes with the carbon dioxide-rich gas coming from the blood. It is then exhaled back
through the same airways to the atmosphere. Normally this cyclic pattern repeats at a
breathing rate, or frequency, of about 12 breaths a minute (breaths/min) when we are at
- -8
rest (a higher resting rate for infants and children). The breathing rate increases when
we exercise or become excited.
Gas exchange is the function of the lungs that is required to supply oxygen to the blood for
distribution to the cells of the body, and to remove carbon dioxide from the blood that
the blood has collected from the cells of the body. Gas exchange in the lungs occurs
only in the smallest airways and the alveoli as (figure 1.2). It does not take place in the
airways (conducting airways) that carry the gas from the atmosphere to these terminal
regions. The size (volume) of these conducting airways is called the anatomical "dead
space" because it does not participate directly in gas exchange between the gas space in
the lungs and the blood. Gas is carried through the conducting airways by a process
called "convection". Gas is exchanged between the pulmonary gas space and the blood
by a process called "diffusion".
Figure1.2 gas exchange through alveoli
One of the major factors determining whether breathing is producing enough gas exchange to
keep a person alive is the 'ventilation' the breathing is producing. Ventilation is
expressed as the volume of gas entering, or leaving, the lungs in a given amount of time.
It can be calculated by multiplying the volume of gas, either inhaled or exhaled during a
breath (called the tidal volume), times the breathing rate (e.g., 0.5 Liters x 12
breaths/min = 6 L/min).
- -9
Therefore, if we were to develop a machine to help a person breathe, or to take over his or her
breathing altogether, it would have to be able to produce a tidal volume and a breathing rate
which, when multiplied together, produce enough ventilation, but not too much ventilation, to
supply the gas exchange needs of the body. During normal breathing the body selects a
combination of a tidal volume that is large enough to clear the dead space and add fresh gas to
the alveoli, and a breathing rate that assures the correct amount of ventilation is produced.
This overview can be expanded by dividing gas exchange into:
1. The processes of alveolar ventilation (bringing air into the lungs for transfer of oxygen
and carbon dioxide).
2. Pulmonary circulation (bringing blood to the lungs to take up oxygen and excrete
carbon dioxide).
Air enters through the (mouth or nose) and then travels down the (larynx and trachea). Air
then enters the (lungs), which consist of multiple branching airways called (bronchi). These
bronchi end in clusters of air sacs the (alveoli). Each alveolus is surrounded by blood
capillaries, which take up the oxygen and give off carbon dioxide.
1.2.2 Pulmonary Ventilation• Describes the procedure of inspiration and expiration and thus the inflow and
outflow of the gases we breathe between the alveolus and the atmosphere.
• The physical basis of the mechanics of respiration is the Boyle-Mariotte Law
of the Gases :
P x V = constant
1.2.3 Breathing Cycle
• Breathing cycle consist of 2 phases : inspiration and expiration.
• The diaphragm is a dome-shaped muscular plate consisting of a central bean-
shaped tendon that is attached to the thoracic cage, the spine, the ribs and the
sternum.
• Contraction of the diaphragm pulls it down, causing it to flatten. The volume of
the thoracic cage increases and the pressure in the alveoli becomes negative
- -10
with respect to atmospheric pressure. A pressure gradient toward the alveoli
arises, causing inspiration.
• During normal quiet breathing this change in volume represents two thirds of
one breath. The remainder is produced by contraction of the external
intercostals muscles that function as inspiratory muscles by lifting the ribs.
During inspiration the elastic retraction forces (elastance) of the lungs must be
overcome, to be released again when the inspiratory muscles relax.
• Expiration can thus take place as a passive procedure requiring support by the
muscles of expiration. Only in case of deep (maximal) and/or accelerated
exhalation (Fig.1.3 and 1.4).
Fig. 1.3 Ventilation of the lungs
• After normal quiet expiration the retraction forces of the expanded lung equal
those of the thoracic wall, which work in the opposite direction. There also is
an equilibrium between the forces within the lung and in the thoracic wall .
The volume in the lung at this time is being called functional residual
capacity(FRC).
- -11
• The driving force for gas exchange between the alveoli and their surroundings,
that is for pulmonary ventilation, are the different pressures between the
alveoli at inspiration and expiration. During inspiration the pressure within the
alveoli must be lower than the atmospheric pressure of the surrounding air.
Conversely, the opposite pressure gradient must exist during expiration. If the
atmospheric pressure is assumed to be zero, the values of inspiration pressure
will be negative, whereas expiration will result in positive values (Fig. 1.4).
Fig. 1.4 Energy sources for inspiration and expiration and alveolar pressure changes
1.2.4 Change in volume of thoracic space to the lungs The lungs, which are completely surrounded by pleura, adhere closely to the inner walls
of the chest cavity. The only connection is a very thin liquid layer between the two pleural
membranes. This liquid layer prevents the two pleural membranes from being separated from
one another.
The pressure between both pleural membranes, the intrapleural pressure, is lower than
atmospheric pressure during normal quiet breathing varying from -4 to -8 mbr. During
inspiration the difference increases as breaths get larger and may reach -40 mbar. In forced
expiration the intrapleural pressure can reach positive values of up to +40 mbar.
- -12
1.2.5 Difference Between Spontaneous and Artificial Respiratory Pulmonary ventilation occurs both in spontaneous or artificial respiration. In both cases
ventilation of the alveoli results from cyclical changes in intrathoracic pressure.
In spontaneous breathing, inspiration is primarily elicited by expansion of the chest. A
negative pressure gradient arises in the pulmonary alveoli with respect to atmospheric
pressure, giving rise to air flow in direction of the alveoli. During inspiration the intrapleural
as well as the intrathoracic pressure are negative. This promotes venous blood flow to the
heart.
Artificial respiration usually involves applying positive pressure to the airways. This
also gives rise to a pressure gradient towards the alveoli. Due to the positive pressure the
intrapleural pressure as well as the intrathorcic pressure rise at the end of inspiration (Fig1.5)
reducing the venous return.
• The maximal midexpiratory flow rate can be altered in such a way, that a
positive end expiratory pressure is applied (PEEP). The functional residual
capacity is increased and in the case of reduced compliance may be brought
back to normal.
• Both in spontaneous breathing as well as artificial respiration expiration is
almost entirely a passive process elicited by the elastic recoil of the lung and
chest.
- -13
Fig1.5 Pressure-time-diagram in spontaneous and artificial respiration
1.3 Respiratory Failure
Definition and Clinical Signs
Respiratory failure is a state in which the pulmonary oxygen uptake is so severely
disturbed that O2-supply to and the CO2-elimination from the tissues are inadequate.
Metabolism at rest including the O2-demand arising from the work of breathing can no longer
be met.
Respiratory failure can usually be recognised clinically:
Clinical symptoms of impending respiratory failure:
ü tachypnea (respiratory rate > 35/ min CARDINAL SYMPTOM!)
ü dyspnea
ü paradoxical breathing
ü agitation, confusion
ü tachycardia, hypertension
ü possibly cyanosis
- -14
ü blood gas analysis
Only blood gas analysis allows precise evaluation of the extent and type of respiratory
failure, PaO2 and PaCO2 are essential parameters for initiation and administration of
ventilator support.
Hypoventilation is defined as inadequate clearance of CO2 a phenomenon that can only
be confirmed by arterial blood gas analysis (arterial hypercapnia PaCO2 > 6.0 kPa).
The cardinal symptom of acute respiratory failure is a drop of the PaO2 below 6.7 kPa
during spontaneous breathing of room air in combination with tachypnea > 35/ min.
The indication for respiratory support is therefore based on two pathophysiological
mechanisms:
1. Inadequate oxygenation
2. Reduced CO2-elimination
There are two types of acute respiratory failure:
Pulmonary ventilator failure with reduced alveolar ventilation and reduced
CO2elimination (PaCO2) and pulmonary parenchymal failure with reduced oxygenation
(PaO2) and an increased alveolarterial oxygen difference (A-aDO2).
ü Pulmonary ventilatory failure is characterized by insufficient elimination of CO2.
ü The hallmark of pulmonary parenchymal failure is inadequate oxygenation.
Table 1 summarizes the causes of parenchymal lung failure.
Table 2 gives an overview of the different causes of pulmonary ventilatory failure.
Table 1. Overview of the different causes of parenchymal lung failureCauses of parenchymal lung failureAll disorders of the alveolo-capillary membraneü pulmonary edemaü ARDSü pneumoniaü atelectasisü pulmonary fibrosis
- -15
Table 2. Overview of the different causes of pulmonary ventilatory failureCauses of ventilatory failure1. Central causesü Respiratory centre dysfunction (e.g. cranio-cerebral trauma, intoxication)ü Cervical or thoracic spinal cord injury (e.g. traumatic paralysis, tetanus)2. Peripheral causes
a) peripheral neuromuscular causes:ü neuromuscular transmission defect (e.g., myasthenia gravis, after effects of muscle
relaxants, botulism)ü polyneuritis (e.g., Guillain-Barre-syndrome, toxic, infectious)ü muscular weakness after long term mechanical respirationb) Disorders of breathing mechanics:ü obstructive and restrictive ventilation disordersü injury of the chest wall (e.g. multiple rib fractures after thoracic traumaü kyphoscoliosisü rupture and/ or herniation of the diaphragm
Pathomechanics of Postoperative and Posttraumatic Respiratory Failure
The main difference between both of the types of respiratory failure lies in the fact that
posttraumatic respiratory failure often involves acute lung failure with activation of
endogenous cascades and mediator systems, whereas postoperative respiratory failure is
usually caused by mechanical factors. The most important causes of postoperative respiratory
failure are listed in Table 3.
Table 3. Causes of postoperative respiratory failure
2.2.1 Alterations of Resistance during respiratory cycle During inspiration elongation of the elastic pulmonary fibers increases the elastic
retraction pressure. The bronchioles are stretched by the stronger radial pull; bronchial flow
resistance falls. With expiration the elastic recoil decreases, the bronchioles become narrower,
the flow resistance increases (Fig. 2.3).
Fig 2.3 Bronchial lumen variation with phase of respiration
These cyclical changes of flow resistance explain why the expiratory phase is always
slightly longer than the inspiratory phase. That is also why expiration always plays a larger
role in obstructive ventilation disorders than does inspiration.Accordingly expiration becomes
prolonged and more difficult and expiratory stenosis sounds such as wheezing or ronchi can
be auscultaled over the lungs.
Even during forced expiration an increase of intrapleural pressure to more than +40
mbar can cause dynamic compression of the small airways. This results in extreme narrowing
or even closure of the bronchioli and occurs when the intrapleural pressure is considerably
larger than the intraluminal pressure (Fig.2.4).
The alveolar pressure (Palv) is the sum of the intrapleural pressure (Pple) and the elastic
recoil pressure (elastance) of the lungs (Pelast).
Palv = Pple + Pelast
- -21
Fig. 2.4 Dynamic airway compression
2.3 Lung Compliance Compliance (C) is a measure of the expansibility of the lungs and describes the elastic
features of the breathing apparatus.
By definition it is the relationship of the volume change in the lungs for each unit
change in intra-alveolar pressure (Fig. 2.5 , 2.6).
Fig. 2.5 Model of lung compliance
- -22
Fig 2.6 Model of lung compliance under artificial ventilation
mbarp
VmlC =
If additional volume is pressed into an elastic body such as a ballon, that has a certain
volume and is under a certain pressure, the volume changes by the value ∆V and the pressure
increases by the value ∆p. The volume change involves complete filling of the lungs from the
beginning to the end of a taken breath.
The larger the compliance the less the pressure increases at a certain filling volume.
2.3.1 Static Compliance For clinical needs the static compliance can be calculated as follows:
(mbar)PEEP-pressurePlateau
(ml) volume tidalexpiratoryC =stat
The Cstat lies between 50 and 70 ml/mbar in the intubated patient without lung disease
A further requirement for correct measurement of the static compliance is a completely
relaxed respiratory musculature, that is a complete lack of muscular activity, which usually
can only be reached by deep sedation or relaxation.
- -23
2.3.2 Dynamic Compliance As artificial respiration methods without a plateau phase do not fulfil a static state,
namely Flow = 0, only the dynamic compliance Cdyn can be calculated.
(mbar)PEEP-pressurepeak
(ml) volume tidalexpiratoryCdyn =
Cdyn is of very little clinical use, as it measures resistive components in addition to the
elastic forces.
2.3.3 Effective Compliance If the pressure and volume are not measured close to the endotracheal tube for technical
reasons, but rather far away from the patient within the ventilator, the so-called effective
compliance is determined instead of the static compliance.
As the lungs fill, the chest expands simultaneously. The chest and the lungs represent
two elastic systems connected in parallel. The total compliance consists of the compliance of
the lungs and that of the chest. The compliance of the lung is 200 ml/mbar in the healthy
adult; the compliance of the chest equaling that.
thoraxc1
lungc1
totalc1
:ComplianceTotal +=
Normal values:
Newborn: 3 5 ml/mbar
Infants: 10 20 ml/mbar
Small children 20 40 ml/mbar
Adults 70 100 ml/mbar
The compliance of the lungs depends on the elasticity of the pulmonary fiber structure,
the intrapulmonary fluid content and the surfactant activity.
- -24
3. Mechanical Ventilator
A ventilator is an automatic mechanical device designed to provide all or part of the
work the body must produce to move gas into and out of the lungs. The act of moving air
into and out of the lungs is called breathing, or, more formally, ventilation.
3.1 Mechanical Ventilator Definition
A mechanical ventilator is a machine that generates a controlled flow of gas into a
patient's airways. Oxygen and air are received from cylinders or wall outlets, the gas is
pressure reduced and blended according to the prescribed inspired oxygen tension (FiO2),
accumulated in a receptacle within the machine, and delivered to the patient using one of
many available modes of ventilation.
The central premise of positive pressure ventilation is that gas flows along a pressure
gradient between the upper airway and the alveoli. The magnitude, rate and duration of flow
are determined by the operator. Flow is either volume targeted and pressure variable, or
pressure limited and volume variable. The pattern of flow may be either sinusoidal (which is
normal), decelerating or constant. Flow is controlled by an array of sensors and
microprocessor is passive (although modern ventilators has active exhalation valves).
There are two phases in the respiratory cycle, high lung volume and lower lung volume
(inhalation and exhalation). Gas exchange occurs in both phases. Inhalation serves to
replenish alveolar gas. Prolonging the duration of the higher volume cycle enhances oxygen
uptake, while increasing intrathoracic pressure and reducing time available for CO2 removal.
The rate pattern and duration of gas flow control the interplay between volume and
pressure. In volume controlled modes, a desired tidal volume is delivered at a specific flow
(peak flow) rate, using constant decelerating or sinusoidal flow. In pressure controlled
modes, flow occurs until a preset peak pressure is met over a specified inspiratory period, the
flow pattern is always decelerating.
Ventilator "cycling" refers to the mechanism by which the phase of the breath switches
from inspiration to expiration. Modes of ventilation are time cycled, volume cycled or flow
cycled. Time cycling refers to the application of a set "controlled" breath rate. In "controlled
ventilation" a number of mandatory breaths are delivered to the patient at a predetermined
interval.
- -25
Controlling rate and I/E ratio
I.E. ratio is an indication of the portioning of a breath into inspiration & expiration
Both a controlled rate and inspiratory time/ expiratory time ratio (I/E) are accomplished
by four basic procedures.
First, rate can be controlled either by adjusting a transmission-type gearing mechanism
or by changing motor speed. In this fashion rate is controlled directly, and the I/E ratio is
fixed at a certain value such as 1:1 or 1:2.
Second, with the rate set on a rate control I/E can be controlled by altering the
inspiratory time component of the ventilator's cycle. Flow and volume are the important
ingredients in controlling inspiratory time ,because flow is volume per unit of time, it controls
the time it will take to deliver a certain volume. In essence, the higher the flow is at a set
volume, the shorter the inspiratory time will be. Flow and tidal volume controls can be used
to control inspiratory time. Decreasing the tidal volume or increasing gas flow will decrease
inspiratory time and decrease the I/E ratio.
Third, inspiratory time and expiratory time can be controlled separately to acquire rate
and desired I/E ratio. This technique can be accomplished with a inspiratory and an
expiratory timer. Inspiratory time can also be controlled directly with a timer or flow
transducer that can control flow to maintain a set I/E ratio.
Fourth, tidal volume and flow controls can be used to establish inspiratory as just
described, and a timer can be used to control expiratory time; rate can be acquired from the
adjustment of the two (inspiratory and expiratory) time.
3.2 Classification of Mechanical Ventilator
The classification of ventilators refers to the following elements
1. Control: How the ventilator knows how much flow to deliver
a) Volume controlled (volume limited, volume targeted) and Pressure Variable.
b) Pressure Controlled (pressure limited, pressure targeted) and Volume Variable.
c) Dual Controlled (volume targeted pressure limited).
- -26
2. Cycling: how the ventilator switches from inspiration to expiration: the flow has been
delivered to the volume or pressure target how long does it stay there?
a) Time cycled such in pressure controlled ventilation
b) Flow cycled such as in pressure support
c) Volume cycled the ventilator cycles to expiration once a set tidal volume has
been delivered: this occurs in volume controlled ventilation. If an inspiratory
pause is added, then the breath is both volume and time cycled.
3. Triggering: what causes the ventilator to cycle to inspiration. Ventilators may be time
triggered, pressure triggered or flow triggered.
a) Time: the ventilator cycles at a set frequency as determined by the controlled rate.
b) Pressure: the ventilator senses the patient's inspiratory effort by way of a decrease
in the baseline pressure.
c) Flow: modern ventilators deliver a constant flow around the circuit throughout the
respiratory cycle. A deflection in this flow by patient inspiration, is monitored by the
ventilator and it delivers a breath. This mechanism requires less work by the patient
than pressure triggering.
4. Breaths are either: what causes the ventilator to cycle from inspiration.
a) Mandatory (controlled) which is determined by the respiratory rate.
b) Assisted (as in assist control, synchronized intermittent mandatory ventilation,
pressure support).
c) Spontaneous (no additional assistance in inspiration).
5. Flow pattern: constant, accelerating, decelerating or sinusoidal.
a) Sinusoidal = this is the flow pattern seen in spontaneous breathing and CPAP.
b) Decelerating = the flow pattern seen in pressure targeted ventilation: inspiration
slows down as alveolar pressure increases (there is a high initial flow). Most intensives
and respiratory therapists use this pattern in volume targeted ventilation also, as it
results in a lower peak airway pressure than constant and accelerating flow, and better
distribution characteristics.
c) Constant = flow continues at a constant rate until the set tidal volume is delivered.
- -27
d) Accelerating = flow increases progressively as the breath is delivered. This should
not be used in clinical practice.
6. Mode or Breath Pattern: there are only a few different modes of ventilation:
We will discuss it later in section 3.4 (ventilator mode).
3.3 Pressure, Volume, Flow and Time Diagrams
3.3.1 Pressure–Time Diagram
Figure 3.1 Pressure-Time diagram
3.3.2 Volume – Time Diagram
Figure 3.2 Volume-Time diagram
- -28
3.3.3 Flow-Time Diagram
Figure 3.3 Flow-Time Diagram
3.3.4 Pressure – Volume Diagram The pressure-volume-diagram in Fig. 3.4 describes the so-called static compliance of
the lung and chest. They are thus also referred to as the relaxation curve of the lung.
The curve takes a characteristic S-shaped course.
The curve can be divide into 3 parts:
1. Flat lower portion of the curve: If the end expiratory lung volume (L vendexp.)
is too low end expiratory closure of the small airways (airway closure) and
collapse of the distal alveoli will occur. During every inspiration the so-called
alveolar opening pressure must be applied to that these collapsed lung areas can
open.
Alveolar opening pressure = pressure necessary to open collapsed alveoli
(recruitment)
The alveolar opening pressure is always higher than the alveolar closing pressure,
that is the pressure at which the alveoli collapse.
2. Middle steep (linear) portion of the curve: In this portion of the curve the least
breathing work is necessary, the maximal steepness gives rise to the maximal
static compliance. The compliance thus varies with the lung volume. It is highest
in the area of the normal functional residual capacity (about 3 litres). A decrease
or an increase of the functional residual capacity from 2 or 5 litres respectively
- -29
lowers the compliance by half. This means that the application of the same
volumes of air requires twice the difference in pressure.
In clinical practice the ventilation parameters should be set such that the
endinspiratory and end expiratory volumes lie in the linear part of the pressure-
volume-curve.
Figure 3.4 Pressure-volume diagram
3. Flat upper portion of the curve: This part of the curve shows the maximal
alveolar elasticity. Further increase in pressure does not lead to any further
increase in volume. Overextension of the alveolar septa involve a loss of
elasticity. There is danger of structural damage to the alveoli and decrease in
perfusion due to capillary compression.
Both bending points of the curve are referred to as inflection points . The lower
inflection point lies in the area of the closing volume.
The force required for breathing is much less in the steep portion of the pressure-
volume-diagram than outside both of the inflection points .
3.4 Ventilator Modes
A ventilator mode can be defined:
1. As a set of operating characteristics that control how the ventilator functions. An
operating mode can be described by the way ventilator is triggered into inspiration and
cycled into exhalation.
- -30
2. What variables are limited during inspiration, and whether or not the mode allows only
mandatory breaths, spontaneous breaths, or both?
Many different functions are commonly available on modern ventilators regardless of
the mode. These functions include:
1.Control of the F1O2 (F1O2 is the oxygen fraction),
2.Control of the inspiratory flow rate.
3.Control of various alarms.
There are 13 essential ventilator modes available in different ventilators, two or more ofthese modes are often used together to achieve certain desired effect.
It is convenient here to refer that not all these operating modes are used to aid patient,
some of the these modes represent a stage that will be developed to generate another mode.
ensures that, within a trigger window, the mandatory breath can be activated by the patient
and is therefore synchronous with spontaneous breathing. The expectation window is 5
seconds long.
The mechanical breath is therefore triggered when the patient initiates an inspiratory
effort after the end of the spontaneous breathing phase and within the expectation window.
Apart from the number of mandatory breaths, with modern ventilators the ventilatory pattern
of the mandatory breath can also be varied via the adjustable variable VT, IPPV frequency,
inspiratory flow and I/E ratio, whereby IPPV frequency and I/E ratio determine the duration
of the mandatory breath
- -39
Figure 3.11 SIMV mode
The SIMV breaths can be volume or pressure-controlled (SIMV Volume-Controlled,
SIMV pressure-Controlled).
Because synchronization of the mandatory breath shortens the effective SIMV time and
would therefore undesirably increase the effective IMV frequency, modern ventilators
increase the following spontaneous breathing time by the missing time difference T. An
increase in the frequency of SIMV is therefore avoided. The other factor (apart from VT)
responsible for the minimum ventilation, F IMA remains constant.
If the patient has inhaled a significantly larger volume at the beginning of the trigger
window, the ventilator reduces the following mandatory breath by reducing the time for the
inspiratory flow phase and the inspiration time. Thus, the other factor responsible for the
minimum ventilation, the tidal volume, VT, remains constant.
SIMV has proved successful for weaning patients after long periods of mechanical
ventilation. During weaning, the SIMV frequency of the ventilator is gradually reduced, and
therefore the break times are prolonged, until the required minute volume is achieved by
spontaneous breathing.
During spontaneous breathing the patient can be pressure supported with ASB (SIMV +
Pressure Support).
SIMV can also be used for long-term ventilation, because, through is reduced average
ventilation pressure, it causes less stress on the circulation. Furthermore, the spontaneous
- -40
breathing rhythm of the patient remains largely intact, so that there is less risk of ventilator
dependency than with controlled ventilation. The basic idea of SIMV is that the patient
breathes largely spontaneously, and that the ventilator offers mechanical breaths with a very
low safety frequency, so that minimum ventilation is ensured.
* It trains the lung to go back to its original action.
How to Initiate SIMV
The use of SIMV is very similar to CMV. If implemented as SIMV (volume mode), an
appropriate mandatory tidal volume and a minimum mechanical ventilation rate must be
selected. This determines the minimum minute volume that the ventilator will provide.
When selecting the ventilator rate, the patient's spontaneous rate must be considered.
If the SIMV rate is set at a high rate, which lowers the PaCO2 below the patient resting
PaCO2, apnea will result, negating the benefit of SIMV. If the SIMV rate is set above the
patient's own respiratory rate, the result is complete mechanical ventilation or CMV. The
objective of SIMV is to provide a measure of ventilation back-up while permitting
spontaneous breathing to continue.
Unlike volume control ventilation, setting an I:E ratio is not required. In SIMV, the
inspiratory time is used to establish the timing of the breath. With spontaneously breathing
patients, the I:E ratios will be altered as the patient's respiratory rate and rhythm change.
Synchronization Window
The time interval just prior to time triggering in which the ventilator is responsive to the
patient's spontaneous inspiratory effort is commonly referred to as the "synchronization
window". Although the exact time interval of the synchronization window is slightly
different from manufacturer to manufacturer, 0.5 second is representative. For example,
given an SIMV mandatory rate of 10 breaths per minute, the ventilator would be expected to
time trigger every 6 seconds. If the synchronization window is 0.5 second, then at 5.5 seconds
from the beginning of the previous mandatory breath, the ventilator automatically becomes
sensitive to any spontaneous effort, i.e., the synchronization window becomes active. If the
patient makes a spontaneous inspiratory effort when the synchronization window is active, the
ventilator is patient triggered to deliver an assisted mandatory breath. Patient triggering may
be based either on pressure or flow. If however, no spontaneous inspiratory effort exists
while the synchronization window is active, the ventilator will time trigger when the full time
triggering interval elapses.
- -41
3.4.7 Different between CMV & SIMV
The most significant difference between CMV and SIMV is in the ability of SIMV to
both sense and respond rapidly to a patient's own breathing efforts. In conventional CMV,
historically employed as volume control ventilation, the ventilator initiates a time-cycled
ventilation, irrespective of any patient-initiated breath. If a patient's breath happens to
coincide with the mechanical ventilation, the impact may be minimal. On the other hand,
when the mechanical ventilation interrupts a patient's own exhalation, the resulting abrupt and
unexpected rise in airway pressure may produce conditions where the patient 'fights' the
ventilator. This may also occur as the patient attempts to terminate a mechanical ventilation.
Either condition may produce unacceptable ventilation, requiring additional intervention.
Synchronising the patient's efforts with those of the ventilator provides a clinically significant
advantage.
SIMV allows the ventilator to sense a patient's own breathing and permit spontaneous
breathing between mechanical ventilations while ensuring sufficient mandatory breaths
should the patient's own rate fall below a preset value. This combination can maintain a more
appropriate minimum minute ventilation. Because of the synchronization provided in SIMV
mode, the ventilator will assist a patient's own breath when that breath falls within the
synchronization window as specified by the operator. These synchronised ventilations
overcome difficulties experienced when patients attempt to compete with CMV mode
ventilations.
- -42
4. THEORY OF OPERATION4.1 Ventilator Block Diagram
Fig. 4.1 Functional Relationship of the operator, Patient, and the Ventilator
• This figure shows relationship between patient, operator and machine.
• Almost the ventilator consist of:
1. Gas Supply System:
2. Microprocessor Electronic
3. Keyboard display panel
4. Patient Service System
5. Pneumatic System.
4.1.1 Gas Supply System Tow gas supplies one providing O2 and other providing air gas supply
system (compressor may be used as alternate air source).Gas supply toventilators can utilise cylinders or pipeline gas supply. Gas cylinders andpipeline have to be colour coded to avoid confusion. The German DINStandard prescribes for:
• Oxygen: blue
• Nitrous oxide: grey
• Pressurised air: yellow, and
- -43
• Vacuum: white labelling.
In the UK
• Oxygen: white
• Nitrous oxide: blue
• Pressurised air: black
• Vacuum: yellow
The supply points of central gas supplies are secured with check valves, which can only
be opened with special couplings. To avoid confusion, these connectors are gas specific.
Gases from cylinders are under high pressure: maximum 147 bar for oxygen.
Regulating valves reduce the gas pressure to 4 bar. The pressures at the supply points of
central gas supplies are also at 4 bar. If the pressure in the oxygen pipeline drops below a
value specified by the manufacturer, e.g. 1.5 bar, an O2 gas deficiency alarm sounds, which
cannot be turned off . Because oxygen in cylinders exists in gas form, the reseve in litres can
be calculated using the Boyle-Mariotte gas law (volume x pressure = const.) by multiplying
the volume of the cylinder with the pressure shown at the pressure gauge .
Boyle-Mariotte gas law: volume x pressure = constant
Example: Cylinder volume: 2.51
Cylinder pressure: 200 bar (1 bar = 105 Pa)
⇒ available oxygen reserve: 2.5 x 200 = 500 litres
With the following equation one can easily calculate, how long a patient can be
ventilated with an O2 cylinder.
Duration = V x P : (MV + 1)
The 2.5 litre cylinders used in emergency medicine contain 500 L oxygen at 200 bar. If
the patient is ventilated with a volume of, for example, 9 1/min with 100% O2 ( No Air-
Mix ), the O2 supply will last 50 minutes. The equation allows for the gas demand of the
transport ventilator.
If the transport ventilator is switched over to the Air-Mix (60% oxygen) mode, the
supply duration is increased to about 100 minutes.
- -44
4.1.2 Microprocessor Electronic:• It is controlls and monitors the pneumatic system, keyboard display panel.
• Patient data such as breath type, pressure, volume, rate and I.E. rate are stored by
microprocessor and can be retrieved at any time.
The signals sent to the pneumatic system to control gas flow and pressure delivered to
the patient. Information sent to the displays indicates ventilator status and patient data.
The major components of the ventilator s microprocessor electronics are:
1. The microprocessor,
2. Memory,
3. Keyboard control
4. Display control
5. Conversion circuitry
6. Interface circuitry
The microprocessor receives information from keyboard, utility panel, DC power
supply, and memory as well as from pressure switches and temperature/flow sensors in the
pneumatic system.
4.1.3 Keyboard display panel• It is used to operation of pneumatic system, monitor patient and ventilator
performance and signal operator with alarm.
4.1.4 Patient Service System (Patient Circuit):It is mixed the gases to and from the patient
- -45
fig4.2 patient circuit
The patient service system consists of the:
1.Humidifier circuit, for warming and humidifying the inspiratory gases.
2.Patient service circuit, for transporting the from the pneumatic system to the patient
and back to the ventilator.
3.Nebulizer circuit, for adding medications to the gas; and exhalation flow circuit, for
monitoring and calculating the volume of exhaled gas.
4.Filters in its inspiratory and expiratory limbs that confine bacterial.
5.A check valve, that prevents retrograde gas flow and an exhalation valve that seals the
system during inspiration.
The internal exhalation valve is housed in the exhalation compartment, because
exhalation compartment components are the last elements in the pneumatic system.
4.1.5 Pneumatic System The pneumatic system, under control of the microprocessor in the electrical system,
supplies air and oxygen to the patient. The primary pneumatics system consists of two
parallel circuits one for oxygen and one for air. An important element of the pneumatic
- -46
system is the two proportional solenoid valves (PSOLS), which precisely control the flow
delivered to the patient.
Air and oxygen flow sensors provide feedback, which is used by the microprocessor to
control the PSOLS. As a result, the ventilator is able to supply air and oxygen to a patient
according to requirements pre-selected by an operator at the ventilator keyboard. The output
of mixed air and oxygen passes through a patient system external to the ventilator; this patient
system may be composed to tubing, filters, a nebulizer, water traps, and a humidifier
4.2 Pneumatic Block Diagram
The following pneumatic is general block and common for many ventilators
We will discuss it in details in section 5
- -47
- -48
5. APPLICATION - DRAEGER-EVITA45.1 IntroductionIn this chapter, we will discuss in detail one of the most used ventilator in most Ministry Of
Health hospitals in Kingdom of Saudi Arabia. This ventilator is the state of the art equipment
from draeger company. It is EVITA 4 ventilator.
The Evita 4 is a time-cycled, constant-volume long-term ventilator for adults and children.
The features and ventilation modes depend on the specific device and its optional features;
they are described in the instructions for use of the specific device. EVITA 4 has the
following characteristic :
§ Evita 4 First touch screen ventilator on the market.
§ First ventilator to have tube compensation.
§ Ventilator for all applications.
§ Improved monitoring functions.
5.2 Basic principle The Evita 4 consists of three components which communicate via a CAN as figure5.1
(fast serial interface).
1. Control unit
2. Electronics
3. Pneumatics
1. Control Unit
- -49
The control unit is the interface between the device and the operator. The control unit
serves to make adjustments, to display measured values and to generate alarms. In the control
unit the display, membrane keypad, touch screen and Graphics Controller PCB are
accommodated.
2. ElectronicsThe electronics is the central control unit of the Evita. It includes the CPU 68332
PCB, the CO2 Carrier PCB with the Processor Board PCB and Power Supply PCB and the
power Pack (Communication PCB, Paediatric Flow, IFCO PCB, and the optional SpO2 PCB).
3. PneumaticsThe pneumatics controls the pneumatic valves following preset ventilation parameters. It
includes an independent microprocessor system and the valve control. In the pneumatics the
Pneumatics Controller PCB, the HPSV Controller AIR/O2 PCB, the PEER valve, the mixer,
the pressure connection, the flow sensor and the O2 sensor are accommodated.
5.3 Block Diagram
This figure shows the block diagram of EVITA4 which consist of three systems:
5.3.2.1 Gas Connection Block§ The gas connection block comprises the O2 gas connection and the compressed
air connection.
§ The connections are fitted with filters F1.1 and F1.2 (metal fiber web).
- -55
§ The diodes or check valves D1.1 (AIR) and D1.2 (O2) prevent the gas from
flowing back into the central gas supply system.
§ The pressure regulators DR1.1 and DR1.2 are set to 2 bar. The control gas
flows past the DR1.1 to the 3/2-way valve Y1.1, from there to the emergency
valve Y1.3, to the PEEP/PIP valve Y4.1 and finally to the emergency valve
Y3.1.
§ The gas also flows to the expiratory prsessure sensor S6.2 (purge flow) via the
restrictor R1.1 (0.08 L/min).
§ Gas flows to the nebulizer via the 3/2-way valve Y1.4, if appropriately
adjusted.
§ In the event of AIR supply failure, the machine will switch over to O2 supply.
Switchover function .
Fig.5.5 Gas connection diagram
5.3.2.2 Parallel mixer or mixer blockThe parallel mixer is a fast, electrically controllable proportional valve for gas flows between
5 and 180 L/min at supply pressures of 3 to 6 bar. Partial flows of less than 5L/minare pulsed at a constant flow of 5 L/min. The supply gases compressed air (AIR) andoxygen (O2) available at the parallel mixer have a supply pressure of 2.7bar to6 barin the parallel mixer the two gases are mixed in accordance with the set parameters.The parallel mixer supplies the inspiratory gas to the patient.
- -56
The parallel mixer consist of the following components:
a) Mixer connection block.
b) 2 cartridge valves with displacement sensor system for compressed air
(AIR)and oxygen(O2).
c) 2 supply pressure sensors measuring the inlet pressure of the supply gases.
figure 5.6 mixer block
a) Mixer connection block.
The two cartridge valves are mounted to the mixer connection block. The inspiratory gases inthe mixer connection block are supplied to the respective cartridge valve. Therespiratory gas available at the outlet of the cartridge valves is mixed in the mixerconnection block and supplied to the inspiratory unit.
b) Cartridge valves with displacement sensor system for compressed air (AIR) andoxygen (O2).
The cartridge valve or HPS valve (HPS= high-pressure servo valve) supplies a definedamount of gas to the patient in accordance with the preset adjustment parameters forinspiration, trigger pressure, leak flow compensation.
c) 2 supply pressure sensors measuring the inlet pressure of the supply gases
1- Displacement sensor system.
2- Supply pressure sensor.
5.3.2.3 Pressure sensorThe Pressure sensor mount comprises the airway pressure sensors S6.1 for the inspiratory side
and S6.2 for the expiratory side. S6.1 monitors the inspiratory Paw high and Paw low.
Measuring range :140mbar.
- -57
Sensitivity: 36.5mV/mbar 0.3mV/mbar.
Offset voltage:1.74V 0.04V
Figure 5.7 Pressure sensor
5.3.2.4 PEEP/PIP valve The PEEP valve Y4.1 consists of a diaphragm valve acting as a flow-control device and
the linear drive whose plunger closes the diaphragm valve. A coil drives the PEEP valve
Y4.1. The values are set via the ventilation settings. These setting are a processed by a
computer program and the coil is driven by an appropriate current. The PEEP valve opens
and adjusts a pressure proportional to the adjusted electric current 0 mA will correspond to 1
mbar, 500 mA to 120 mbar.
The valve Y4.1 controls the expiratory valve Y5.1 in the patient system via a servo-line.
The solenoid valve Y1.3 and the restrictor R4.1 supplies the patient system with control gas.
The software compares the preset and measured airway pressures. This comparison is a
measure of the Pneumatic Controller PCB s control action on the PEEP/PIP valve. The
PEEP/PIP valve is calibrated to the electronics. The calibration data are stored on the
Pneumatic Controller PCB.
- -58
Figure5.8 PEEP/PIP valve diagram
5.3.2.5 Inspiration BlockThe safety valve D3.3 limits the pressure in the inspiratory line to 100 mbar max.
In the event of compressed air failure or power failure the pneumatically controlled
emergency air valve Y3.1 will open so that the patient can breathe ambient air passing the
filter F3.1. The check valve D3.1 prevents rebreathing of the air through the inspiratory line.
The spring-loaded check valve D3.2 allows pressure to drop if valve Y3.1 opens.
In the case of emergency air spontaneous breathing the patient can expire through the
expiratory valve Y5.1 on account of the spring loading (5 mbar) thus preventing rebreathing.
The inspiration block is provided with the plug-in connection for the oxygen sensor.
The restrictor R1.2 limits the medicament nebulizer flow to 9 L/min.
In the event of a gas or power supply failure, the patient can breath spontaneously via
filterF3.1. The emergency valve Y3.1 will in this case no longer be controlled. The patient
can breath spontaneously via filter F3.1,check valve D3.1 and the emergency air valve Y3.1
- -59
Fig.5.9: Inspiration Block diagram
5.3.2.6 Patient System The expiratory gas flows from the patient directly to the expiratory valve Y5.1. The
copper measuring line at the 8a connection has a germicidal effect and connects the expiratory
side to the pressure sensor S6.2.
The expiratory valve has a transmission ratio of approx. 1:1 The check valve D5.1
allows flow in one direction only and makes sure that gases do not travel backwards. The
expiratory flow is measured with flow sensor S5.1.
Fig. 5.10 Patient system diagram
The ratio between the control pressure at th 7a connection of the PEEP/PIP valve and
the resulting pressure at the expirartory port is linear of the following values.
Control pressure of 3 mbar = > expirarory pressure of 0 mbar
Control pressure of 33 mbar => expiratory pressure of 33 mbar.
5.3.2.7 AIR supply AIR flow through the filter F1.1 via the check valve D1.2 to the mixer and flow control
unit (pressure sensor S2.1 and HPSV Y2.1); at the same time, AIR flows to the 3/2-way
solenoid valve Y1.1 via the pressure regulator DR1.1 which is set to 2 bar. From here the gas
flows through the 3/2-way solenoid valve Y1.3 to the emergency air valve Y3.1 which closes.
Furthermore, AIR passes the restrictor R4.1 to reach the PEEP/PIP valve Y4.1 and from there
depending on the setting to the expiratory valve Y5.1. Finally, AIR passes the restrictor
R1.1 to flow to the expiratory pressure sensor S6.2 connecting line on the patient side. At this
point, expiratory humidity is prevented from reaching the pressure sensor S6.2.
- -60
Fig. 5.11 AIR supply diagram
5.3.2.8 O2 Supply
Compressed oxygen flows through the filter F1.2 via the check valve D1.2 to the mixer
and flow control unit (pressure sensor S2.2 and HPSV Y2.2). At the same time, O2 flows to
the 3/2-way solenoid valve Y1.1 via the pressure regulator which is set to 2 bar.
Fig 5.12 O2 supply diagram
- -61
5.3.2.9 Inspiration Depending on the setting (O2 concentration, inspiratory volume, frequency, T1,
inspiratory flow, inspiratory pressure) the HPSVs Y2.1 and Y2.2 open. The gas flows via the
inspiratory connector to the patient. At the same time, gas flows to the O2 sensor S3.1 and to
the safety valve D3.3; from there, it flows through the 3/2-way solenoid valve Y6.1 to the
inspiratory pressure sensor S6.1.
The safety valve D3.3 is fixed to 100 mbar and serve as an additional safety device in
the event of a complete failure of the electronic control.
When calibrating the O2 sensor S3.1 the sensor will be disconnected with valve Y3.3
from the inspiratory gas. The O2 sensor S3.1 is purged with calibration gas via the valve
Y1.2, the restrictor R1.3, the restrictor R3.1, and the valve Y3.2. The O2 concentration and
the inspiratory gas flow are not affected.
The pressure sensors S6.1 and S6.2 monitor the inspiratory pressure. During the entire
inspiratory time the PEEP/PIP valve Y4.1 provides pressure to the expiratory valve Y5.1.
Fig5.13 Inspiration Function Diagram
- -62
5.3.2.10 Expiration
At the start of expiration, the HPSV Y2.1 and Y2.2 are closed. No gas will be supplied to the
patient. The PEEP/PIP valve Y4.1 is switched to the set PEEP value. The expiration valve
Y5.1 will also be relieved and the patient can exhale via check valve D5.1 and the flow
sensor S5.1. The flow sensor S5.1 measures the expiratory volume.
Fig5.14 Expiration Diagram
5.3.2.11 Nebulizer
After pressing the button the medicament nebulizer is switched on for 30 minutes. At the
same time the solenoid valve Y1.4 is switched through in the flow active inspiratory phase.
The medicament nebulizer is supplied with drive gas by the restrictor R1.2. After
completion of the inspiratory gas supply phase the solenoid valve Y1.4 is also switched back.
The minute volume remains constant while the flow setting is being corrected. after
termination of the medicament nebulization the flow sensor S5.1 is automatically glowed
clean.
Note: the minimum inspiratory flow required by the medicament nebulizer is 16l/min.
- -63
Fig5.14 Nebulizer Diagram
- -64
6. TYPES AND PROBLEMS6.1 Intensive Care 6.1.1 Purpose
It provide temporary ventilatory support or respiratory assistance to patients who cannot
breathe on their own or who require assistance to maintain adequate ventilation because of
illness,trauma, congenital defects, or drugs .
Figure 6.1
6.1.2 problems
The most common problem with intensive care ventilators is the risk of a patient
Acquiring ventilator associated pneumonia (VAP). It is generally accepted that prolonged
ventilation periods greatly increase a patient s risk of acquiring VAP. The link between
prolonged ventilation and VAP is unclear, but following proper infection control procedures
in maintaining the ventilator, the breathing circuit, and all associated
equipment can minimize patient risk.
Leaks, including those of the ventilator breathing circuit, are another problem that can
affect the ventilator s ability to maintain the PEEP level. This in turn may affect oxygen
saturation and can result in autocycling.
- -65
Leaks may also prevent the ventilator from delivering a preset tidal volume or accurately
sensing flow and terminating a pressure-supported breath.
The friction-fit connector that attaches a ventilator to a patient s artificial airway can be
accidentally disconnected if it is not attached securely by the clinician.
Patient-ventilator dyssynchrony refers to the situation in which a mechanically ventilated
patient fails to trigger the ventilator, or the ventilator erroneously senses a patient s effort and
delivers breaths. The result is amachine breath rate that is inappropriate to the rate of the
patient s inspiratory efforts. This is also called trigger failure or desynchronization,
mismatching, and fighting the ventilator. One cause for patient-ventilator dyssynchrony is
improper setting of trigger sensitivity.
Clinical observation is highly specific in identifying patient-ventilator dyssynchrony,
since observation of thoracoabdominal movement has been the standard method of
determining respiratory rate, and patients with patient-ventilator dyssynchrony often have
heightened and prominent accessory muscle activity associated with inspiratory efforts.When
gas delivery is not synchronized with the patient s efforts to initiate a breath, increased patient
discomfort and work of breathing can result. This can also lead to respiratory distress, can
inhibit pulmonary gas exchange, and can make weaning the patient from mechanical
ventilation more difficult.
6.2 Portable
6.2.1 Purpose
Portable ventilators provide long-term ventilatory support for patients who do not require
complex critical care ventilators. These portable units are commonly used in special extended
care facilities, in step-down respiratory care units, or in the home. They can also be used for
short-term transport or in emergencies.
- -66
Figure 6.2
6.2.2 Problems
Most of the reported problems involving portable ventilators arise from user error, poorly
maintained exhalation valve assemblies, or the use of poor-quality
breathing circuits. Disconnection of the breathing circuit from the device is one of the most
commonly reported problems.
Caring for a patient receiving mechanically assisted ventilation in the home is potentially
dangerous due to the possibility of equipment failure, resulting in hypoxic brain damage or
death. Ventilator failures can be caused by improper equipment care, damage, tampering, or
incorrect use by caregivers.
Many reported incidents of a patient s inability to exhale are suspected to be caused
by jammed mushroom valves in the exhalation-valve.
6.3 Transport 6.3.1 Purpose
Transport ventilators are designed to take the place of manual bagging in emergency or
transport situations.Hand ventilation, even by nurses, respiratory therapists, emergency
medical technicians, and other trained professionals, tends to be at too fast a rate and at an
unstable tidal volume when performed for extended periods and can produce unintended acute
respiratory alkalosis and its sequelae (e.g., acute electrolyte imbalances and coronary
- -67
vasoconstriction,which can lead to arrhythmias).Transport ventilators are well suited for both
prehospital and emergency department applications.
6.3.2 problems
Inherent in the use of transport ventilators are problems associated with both general
patient transport (e.g., disconnection of the breathing circuit, accidental extubation) and
emergency transport (e.g.,emergency vehicle noise interfering with monitors).Other problems
are associated with user error, poorly maintained units, and use of poor-quality breathing
circuits.
- -68
7. History and Development of Ventilator
7.1 History of Ventilator
There really is only two ways to ventilate a patient, using (conventional) positive
pressure or negative pressure. Some of the earliest ventilators were negative pressure
chambers (iron lungs).
A severe poliomyelitis epidemic broke out in Northern Europe in the mid 1950s.
Patients suffering with this virus die from asphyxia respiratory muscle paralysis and failure
to ventilate. Medical students were assigned to manually ventilate paralysis victims until
restoration of neuromuscular activity occurred. Iron lungs mimicked the chest cage's activity
in generating minute ventilation, but were of little value in diseases characterized by failure to
oxygenate. The machines were bulky, expensive and somewhat unhygienic.
The first positive pressure ventilators were pressure controlled. This made sense as the
chest is a negative pressure ventilator. Volume controlled ventilators became ubiquitous in
the 1960s as this mechanism was perceived to be more reliable at delivering minute
ventilation, and thus normalizing blood gases.
During the 1970s and 1980s ventilators were developed which allowed patients breathe
spontaneously, initially with assisted breaths (assist control ventilation) and subsequently with