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1.1 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 The Lungs...11 1.2.5 Difference Between Spontaneous and Artificial Respiratory.12

1.3 Respiratory Failure..13


2.1 Static Lung Volume.17 2.2 Lung Resistance...19 2.2.1 Alterations of Resistance during respiratory cycle20 2.3 Lung Compliance.21 2.3.1 Static Compliance..22 2.3.2 Dynamic Compliance....23 2.3.3 Effective Compliance....23


3.1 Mechanical Ventilator Definition...24 3.2 Mechanical Ventilator Classification..25 3.3 Pressure , Volume , Flow And Time Diagram...27 3.3.1 Pressure Time Diagram....27 3.3.2 Volume Time Diagram.27 3.3.3 Flow Time Diagram.28 3.3.4 Pressure Volume Diagram...28 3.4 Ventilator Mode ...29 3.4.1 Spontaneous....31 3.4.2 Positive End Expiratory Pressure (PEEP)...31 3.4.3 Continuous Positive Airway Pressure (CPAP)...34 3.4.4 Different Between PEEP and CPAP ..36 3.4.5 Controlled Mechanical Ventilation (CMV)36 3.4.6 Synchronized Intermittent Mandatory Ventilation (SIMV)38 3.4.7 Different Between CMV and SIMV41

4.1 Ventilator Block Diagram42 4.1.1 Gas Supply System..42 4.1.2 Microprocessor Electronic...44 4.1.3 Keyboard display panel...44 4.1.4 Patient Service System (Patient Circuit).44 4.1.5 Pneumatic System..45

4.2 Pneumatic Block Diagram..46


5.1 Introduction48 5.2 Basic principle.48 5.3 Block Diagram.49 5.3.1 Electronics System...50 5.3.2 Pneumatics System..52 Gas Connection Block....54 Parallel mixer or mixer block.55 Pressure sensor ....56 PEEP/PIP valve57 Inspiration block...58 patient system59 Air supply..59 O2 supply...60 Inspiration.61 Expiration62 Neubilizer62


6.1 Intensive care ventilator...64 6.1.1 purpose64 6.1.2 problems..64

6.2 Portable ventilator.65

6.2.1 purpose...65 6.2.2 problems 66

6.3 Transport ventilator..66


6.3.1 purpose...66 6.3.2 problems.67


7.1 History of Ventilator68 7.2 Development Of Ventilator....69
7.2.1 Absolute...69 Negative-pressure ventilation..69 Iron Lung.69 Chest Cuirass /Chest Shell...71 7.2.2 Positive-pressure ventilation.74 7.2.3 State of the art75 High Frequency Ventilation (HFV)..75 Independent lung ventilation (ILV).78 Applictions.79 7.2.4 Emerging.84 7.2.5 visoniary..88



In 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 System

Nose /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.


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


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


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).


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 beanshaped 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


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).

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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.

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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.

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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: tachypnea (respiratory rate > 35/ min CARDINAL SYMPTOM!) dyspnea paradoxical breathing agitation, confusion tachycardia, hypertension possibly cyanosis

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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. 2. Inadequate oxygenation 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). Pulmonary ventilatory failure is characterized by insufficient elimination of CO2. 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 failure Causes of parenchymal lung failure All disorders of the alveolo-capillary membrane pulmonary edema ARDS pneumonia atelectasis pulmonary fibrosis

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Table 2. Overview of the different causes of pulmonary ventilatory failure Causes of ventilatory failure 1. 2. Central causes Respiratory centre dysfunction (e.g. cranio-cerebral trauma, intoxication) Cervical or thoracic spinal cord injury (e.g. traumatic paralysis, tetanus) Peripheral causes a) b) peripheral neuromuscular causes: neuromuscular transmission defect (e.g., myasthenia gravis, after effects of muscle relaxants, botulism) polyneuritis (e.g., Guillain-Barre-syndrome, toxic, infectious) muscular weakness after long term mechanical respiration Disorders of breathing mechanics: obstructive and restrictive ventilation disorders injury of the chest wall (e.g. multiple rib fractures after thoracic trauma kyphoscoliosis 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 Reduced lung volume due to elevated diaphragm abdominal distension (intestinal paralysis, ileus) atelectasis retention of secretions pulmonary oedema

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pleural effusion pneumothorax Reduced movement of the diaphragm and chest wall due to pain central suppression abdominal distension Impediment of coughing pain central suppression (e.g. sedation!) abdominal distension tenacious bronchial secretions Diseases:

Acute Obstructive Disease (e.g., acute severe asthma, airway mucosal edema) Altered Ventilatory Drive (e.g., hypothyroidism, idiopathic central alveolar hypoventilation, hemorrhage) dyspnea-related anxiety, apnea of prematurity, intracranial

Cardiopulmonary Problems (e.g., congestive heart failure; in neonates: persistent bradycardia, massive pulmonary hemorrhage)

Chest Wall Deformities (e.g., kyphoscoliosis, severe obesity, rheumatoid spondylitis; in neonates: hyper compliant rib cage [prematurely], large diaphragmatic hernia)

Chronic Obstructive Pulmonary Disease (e.g., emphysema, chronic bronchitis, asthma, bronchiectasis, cystic fibrosis)

Chronic Restrictive Pulmonary Disease (e.g., pulmonary fibrosis) Neuromuscular Disease (e.g., polio militias, Duchene muscular dystrophy, amyotrophic lateral sclerosis, Guillain-Barre syndrome, peripheral neuropathies, malnutrition, cancer, infections)

Atelectatic Disease (e.g., ARDS, neonatal RDS, hyaline membrane disease, pneumonia).

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2.1 Static Lung Volume
The following static lung volumes are differentiated from one another (Fig 2.1): The normal values refer to an adult weighing about 70 kg. 1.Tidal Volume (VT): the volume inhaled and exhaled during quiet breathing. Normal value: about 0.5 L 0.6 L.

2.Inspiratory Reserve Volume (IRV): the volume that can be inhaled further after quiet inhalation, that is, the difference between normal and maximal ventilation. Normal value: about 2.5 L about 2/3 of the VC.

3.Expiratory Reserve Volume (ERV): the volume, that can be further exhaled after quiet expiration, that is the difference between normal and maximal expiration. Normal value: about 1.5 L about 1/3 of the VC.

4.Residual Volume (RV): the volume remaining after maximal expiration in the lungs. Normal value: about 1.5 to 2 L. 5.Functional Residual Capacity (FRC): the volume left in the lungs at the end of quiet expiration. Normal value: 3 to 3.5 L. FRC = RV + ERV

The FRC is by definition the gas volume remaining in the lungs during quiet breathing. It can be considered a measure for the gas exchange area. It results from the balance between the opposite elastic forces exerted by the lungs and chest.

The FRC falls by 20% within a few minutes after initiation of anaesthesia.

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Obstructive ventilation disorders lead to an increased FRC, restrictive ventilation disorders to a decreased FRC.


Vital Capacity (VC): the volume difference between maximum inspiration and maximum expiration. It is therefore a measure for the largest possible breathing excursion. Normal value: 3.5 5.5 L


Total Lung Capacity (TLC): Maximal air capacity of the lung. It is calculated from the sum of the VC and RV. Normal value: approximately 6 L. TLC = VC + RV

Fig. 2.1: Static lung volumes

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2.2 Lung Resistance

Resistance (R) is a measure of airway resistance (airflow resistance). It is defined by the pressure difference between the beginning and end of a tube and the flow of gas volume per time unit. In the case of the pulmonary airways it would be the difference between atmospheric pressure at the mouth minus the alveolar pressure (Fig2.2).

Fig. 2.2 Obstructive ventilation disorder Resistance is measured in mbar/l/sec. R = p/V In healthy adults normal values of airway resistance lie between 2 4 mbar/l/sec. 6

In intubated patients with healthy lungs the inspiratory resistance lies between 4 mbar/l/sec.

In children, both the anatomical as well as the physiological features of the respiratory organs cause considerably higher airflow resistance: Normal values: Newborn Infants Small children Adults 30 20 50 mbar/l/sec 30 mbar/l/sec

20 mbar/l/sec 2 4 mbar/l/sec

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Determination of an effective resistance: Resistance effective =(maximum pressure-plateau pressure)/ flow.

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

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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

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Fig 2.6 Model of lung compliance under artificial ventilation

Vml p mbar


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:
expiratory tidal volume (ml) Plateau pressure - PEEP (mbar)

Cstat =

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.

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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.
expiratory tidal volume (ml) peak pressure - PEEP (mbar)

Cdyn =

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.
1 c total 1 c lung 1 c thorax

Total Compliance :

Normal values: Newborn: Infants: Small children Adults 3 10 20 70 5 ml/mbar 20 ml/mbar 40 ml/mbar 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.

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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.

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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. expiratory timer. This technique can be accomplished with a inspiratory and an

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) b) c) Volume controlled (volume limited, volume targeted) and Pressure Variable. Pressure Controlled (pressure limited, pressure targeted) and Volume Variable. Dual Controlled (volume targeted pressure limited).

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Cycling: how the ventilator switches from inspiration to expiration: the flow has been delivered to the volume or pressure target a) b) c) Time cycled Flow cycled how long does it stay there?

such in pressure controlled ventilation such as in pressure support the ventilator cycles to expiration once a set tidal volume has If an inspiratory

Volume cycled

been delivered: this occurs in volume controlled ventilation. 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) b) Time: the ventilator cycles at a set frequency as determined by the controlled rate. Pressure: the ventilator senses the patient's inspiratory effort by way of a decrease in the baseline pressure.


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.


Breaths are either: what causes the ventilator to cycle from inspiration. a) b) Mandatory (controlled) which is determined by the respiratory rate.

Assisted (as in assist control, synchronized intermittent mandatory ventilation, pressure support).

c) 5.

Spontaneous (no additional assistance in inspiration).

Flow pattern: constant, accelerating, decelerating or sinusoidal. a) b) Sinusoidal = this is the flow pattern seen in spontaneous breathing and CPAP. 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.

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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 PressureTime Diagram

Figure 3.1 Pressure-Time diagram

3.3.2 Volume Time Diagram

Figure 3.2 Volume-Time diagram

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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

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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 pressurevolume-curve.

Figure 3.4 Pressure-volume diagram 3. Flat upper portion of the curve: This part of the curve shows the maximal alveolar elasticity. increase in volume. Further increase in pressure does not lead to any further 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 pressurevolume-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.

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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 of these 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. 1. 2. 3. 4. 5. 6. 7. 8. 9. Spontaneous. Positive End-Expiratory Pressure (PEEP), Continuous Positive Airway Pressure (CPAP), Bi-level Positive Airway Pressure (BIPAP), Controlled Mandatory Ventilation (CMV), Assist Control (AC), Intermittent Mandatory Ventilation (IMV), Synchronized Intermittent Mandatory Ventilation (SIMV), Mandatory Minute Ventilation (MMV),

10. Pressure Support Ventilation (MMV), 11. Pressure Control Ventilation (PCV), 12. Airway Pressure Release Ventilation (APRV). 13. Inverse Ration Ventilation (IRV). We will concentrate mainly on only five modes which are the most important in ventilation and are common on all ventilator equipments, which are: 1. 2. Spontaneous. Positive End-Expiratory(PEEP)

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3. 4. 5.

Continuous Positive Airway Pressure (CPAP), Controlled Mandatory Ventilation (CMV). Synchronized Intermittent Mandatory Ventilation (SIMV).

3.4.1 Spontaneous mode

Essential where the patient control breathing. Patient can breath normally but he has a problem with gas exchange. The machine supply O2 and air and take away CO2 at rate which determined. It is very simple mode and available in every types of ventilators. Breathing rate (Br) and Tidal Volume (TV) are controlled by the patient.

figure 3.5 Spontaneous Mode

3.4.2 Positive End-Expiratory Pressure (PEEP)

Positive end-expiratory pressure (PEEP) increases the end-expiratory or baseline airway pressure to a value greater than atmospheric. It is often used to improve the patient's

oxygenation status, especially in hypoxemia that is refractory to increasing FIO2. The term PEEP is usually used only in context with mechanical ventilation. Spontaneous ventilation with continuously increased positive airway pressure is referred to as CPAP (continuous positive airway pressure). The level of PEEP can be pre-set in the ventilator. In practice PEEP levels between 5 and 15 cm H2O are generally used. The useful effect of PEEP is exhaust at about 15 cm H2O. At pressure exceeding 15 cm H2O the alveolar diameter does not increase with increasing PEEP levels. The alveolar tissue cannot be stretched further by higher pressure so there is a danger of "over distension" and alveolar rupture, Barotrauma may be the result. The effect begins at PEEP levels of cm H2O. 15 20

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figure 3.6 PEEP mode

Indications for PEEP Two major indications for PEEP are: 1. 2. 1. Intrapulmonary shunt and refractory hypoxemia. Decreased functional residual capacity (FRC) and lung compliance. Intrapulmonary Shunt and Refractory Hypoxemia The primary indication for PEEP is refractory hypoxemia induced by intrapulmonary shunting. This condition may be caused by a reduction of the functional residual capacity (FRC), atelectasis, or low Ventilation to Perfusion (V/Q) mismatch. Refractory hypoxemia is defined as hypoxemia that responds poorly. To moderate to high levels of oxygen. A helpful

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clinical guideline for refractory hypoxemia is when the patient's PaO2 is 60 mm Hg or less at an FIO2 of 50% or more. 2. Decreased FRC and Lung Compliance A severely diminished FRC and reduced lung compliance greatly increase the alveolar opening pressure. If the patient is breathing spontaneously, a decreased lung compliance always increases the work of breathing and if severe enough can lead to fatigue of the respiratory muscles and ventilatory failure. Since PEEP increases the FRC, this pulmonary impairment may be prevented or improved by early application of PEEP therapy. Advantage of PEEP PEEP produces an increase in PaO2 by increasing the functional residual capacity (FRC) (increasing the gas-exchange area) reopening atelectatic lung areas ("alveolar recruitment") reducing the right-to-left shunt avoiding end-expiratory alveolar collapse improving the ventilation/ perfusion ration

PEEP opens up the alveoli and keeps those alveoli open. Side-Effect 1. 2. 3. 3. Decreased venous return and cardiac output. Barotrauma. Increased intracranial pressure, and ICP increases due to impedance of venous return. Alterations of renal functions and water "metabolism".

When ventilating with PEEP considerations must be given to venous return cardiac output blood pressure organ perfusion

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PEEP should therefore only be reduced when there is adequate pulmonary gas exchange at an FIO2 < 0.5. Abrupt termination of PEEP therapy can result in pleural effusions.

3.4.3 Continuous Positive Airway Pressure (CPAP)

By this we mean spontaneous breathing with a continuous positive respiratory tract pressure in all phases of the respiratory cycle. The patient breathes spontaneously with an increased level of respiratory tract pressure (Figure 3.7)

Figure 3.7 Continuous Positive Airway Pressure(CPAP)

CPAP can be applied with an endotracheal tube or via a tight fitting face or nose mask. CPAP breathing requires the patient to be awake and co-operative, to have adequate spontaneous breathing, i.e. sufficient pulmonary pumping function.

CPAP improves gas exchanges, particularly in lung diseases.

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The combination of intra-operative ventilation with PEEP and post-operative CPAP therapy has proved particularly successful in the prophylaxis of atelectasis.

CPAP is now part of every ventilator.

Advantage of CPAP Improved oxygenation (rise in PaO2) through increasing the functional residual capacity.

PaO2 FRC with CPAP the breathing effort is reduced, because the inspiratory gas flow makes breathing in easier Reduced likelihood of small airway collapse because of the continuous positive respiratory tract pressure Re-opening of atelectatic areas of the lung ("alveolar recruitment") Reduction of the intra-pulmonary right-left shunt Improvement of the ventilation/ perfusion ration

Indications Post-traumatic (lung contusion) and post-operative (atelectasis particularly after upper abdominal surgery) gas exchange disturbances Pulmonary oedema Pneumonias Weaning from mechanical ventilation RDS-Syndrome of new-borns Failure to oxygenate is caused by reduced diffusing capacity and ventilation perfusion mismatch. This can often be overcome by restoring FRC by increasing baseline airway

pressure using CPAP. If the problem is atelectasis due, for example, to mucus plugging or diaphragmatic splinting following abdominal surgery, or moderated amounts of pulmonary edema, CPAP, as delivered by facemask or endotracheal tube, may sufficiently restore pulmonary mechanics to avoid addition inspiratory support. CPAP is easy to apply: all that is required is a PEEP valve and a flow generator.

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Side-Effects Are similar to PEEP ventilation because of the increased intra-thoracic pressure.

3.4.4 Different between PEEP & CPAP

1. PEEP mode is not stand alone in ventilator machine. It comes as assistance mode in big and complex ventilators. 2. PEEP is a part of the CPAP. CPAP = PEEP + spontaneous breath. 3- A. PEEP indicates: a) b) Intra pulmonary shut and refractory hypoxemia. Decrease lung compliance and functional residual capacity.

B. CPAP indicates: 1) 2) 3) 4) 5) Post-traumatic and post-operative Pulmonary odema. Pneumonias Weaning RDS-syndrome of new born.

3.4.5 Controlled Mandatory Ventilation (CMV)

In this mode, it introduce automatically and independently from any possibly existent spontaneous breathing, that is no synchronization. It is a control mode. Why? Because the ventilator controls both respiratory rate and tidal volume and triggered breaths are allowed. This mode is used when the patient in operation room or after operation when he still unconscious, because all his muscles are in hebted (do not work). It used for paralyzed or apneic patient.

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This figure shows the controlled mandatory ventilation wave:

Figure 3.8 CMV mode

If PEEP = O, the type of ventilation is called IPPV (intermittent positive pressure ventilation). (figure 3.9)


PEEP is grater than O, the type of ventilation is called CPPV (CPPV =

continuous positive pressure ventilation). (figure 3.10)

Figure3.9 CPAP without PEEP(IPPV)

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3.4.6 Synchronized Intermittent Mandatory Ventilation (SIMV)

SIMV ventilation is a mixture between spontaneous breathing and mechanical ventilation. The mandatory breaths ensure a certain minimum ventilation of the patient. This minimum minute volume is determined by setting tidal volume and IMV frequency. Minimum minute volume = VT x f lMV SIMV differs from IMV because mandatory breaths are synchronized with the breathing of the patient. In order to prevent the mechanical breath being applied in the expiratory spontaneous breathing phase, a finely adjusted trigger mechanisms (variable flow trigger) ensures that, within a trigger window, the mandatory breath can be activated by the patient and is therefore synchronous with spontaneous breathing. 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 The expectation window is 5

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Figure 3.11 SIMV mode

The SIMV breaths can be volume SIMV pressure-Controlled).

or pressure-controlled (SIMV Volume-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

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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.

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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.

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4.1 Ventilator Block Diagram

Fig. 4.1 Functional Relationship of the operator, Patient, and the Ventilator 1. 2. 3. 4. 5. This figure shows relationship between patient, operator and machine. Almost the ventilator consist of: Gas Supply System: Microprocessor Electronic Keyboard display panel Patient Service System 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 to ventilators can utilise cylinders or pipeline gas supply. Gas cylinders and pipeline have to be colour coded to avoid confusion. The German DIN Standard prescribes for: Oxygen: blue Nitrous oxide: grey Pressurised air: yellow, and

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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 = 10 5 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 AirMix ), 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.

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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. 2. 3. 4. 5. 6. The microprocessor, Memory, Keyboard control Display control Conversion circuitry 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

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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

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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

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5.1 Introduction
In 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

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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. Electronics The 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. Pneumatics The 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: 1. Control unit. 2. Electronics.






Supply voltages

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Rotary knob including acknowledgement (by pressing knob) Touchscreen TFT display 640 x 480


Power switch

3 4

15 16

Second inspiratory Paw Reset pneumatics processor and venting Electronics processor reset and second loudspeaker alarm Inspiratory Paw O2 sensor FiO2 (HPSV mixer) AIR (HPSV mixer) Flow sensor Expiratory valve with PEEP

Information LEDs and Alarm LEDs


6 7 8 9 10 11

CAN bus Graphics processor reset Not applicable Loudspeaker with sound chip Second loudspeaker (piezo) Voltage monitoring (activates reset of the processors and the piezo) Rechargeable battery (Goldcap capacitor)

18 19 20 21 22 23



Expiratory Paw

5.3.1 Electronics System

The CPU 68332 PCB is integrated in the electronic unit of the Evita. The board includes an independent processor system, two external interfaces, three internal interfaces, the loudspeaker control and a serial EEPROM.

The EEPROM is connected to the synchronized, serial interface 68832. The EEPROm characterizes the Evita (enabled options, serial number, etc). When replacing the CPU 68332 PCB the EEPROM has to be transferred to the new printed circuit board.

2. Processor System

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The processor system comprises a 68332 CPU, a 512 kBytes RAM and a 1 Mbyte flash EPROM (electrically programmable and erasable read-only memory). The RAM has a

battery back-up. When the battery is being replaced a Goldcap capacitor ensures voltages voltage supply of the RAMs. Programming of the flash EPROMS is only possible if the system identified the SERVICE-Q signal.

3. RS232 interface
The CPU 68332 PCB provides an RS232 interface in the Evita. The interface is labeled COM1. The interface is elecrtrically isolated from the Evita. Electrical isolation is made by means of optocouplers.

4. ILV interface
The ILV interface is required for independent-lung ventilation with two Evita units. The ILV interface is not electrically isolated. Pin 3 of the ILV interface is provided with a filler plug. This filler plug prevents confusion with the RS232 interface.

5. Driver
The driver adjusts the access times between the 68332, the clock and the DUART.

6. Clock
The clock gives the current time. It has a battery back-up and continues to operate even after the Evita has been switched off.

The DUART (Dual Universal Asynchronous Receiver / Transmitter) has two serial interfaces and digital inputs and outputs. The serial interfaces are intended for connection of the SpO2 and the CO2 module.

8. DC/DC converter
The DC/DC converter provides the voltage supply (+5 V ISO) required for the interface. The input voltage of the DC/DC converter is +5 V.

9. CAN
The CAN interface is a fast, serial interface (Controller Area Network). The control unit, the electronics and the pneumatics communicate via a CAN interface. The transmission rate is 800 kbit/s.

10. Bus Driver

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The address bus, the data bus and the check-back signals are transferred by the bus driver to the motherboard. The 68332 CPU communicates with the optional printed circuit boards located on the motherboard via the bus driver. Currently, it is only the Pediatric Flow PCB (Neoflow option).

11. Sound generator

The sound genrator controls the loudspeaker in the control unit. The sound generator incorporates the vlume control and sound generation for the loundspeaker. The volume is controlled by the DUART.

12. Reset logic

The CPU 68332 can reset the control unit and the pneumatics. A reset is also triggered if there is an undervoltage or overvoltage of the +5 Vvoltage.The pneumatics can also reset the CPU 68332 PCB. The reset logic controls and displays the resets.


5.3.2 Pneumatics System

Compressed air(AIR) and compressed oxygen(O2) must be available at a supply pressure of 2.7 to 6 bar to drive the machine. The pneumatics consist of the following components:

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1. Gas connection block 2. Parallel mixer or mixer block 3. Pressure sensors 4. PEEP/PIP valve 5. Inspiration Block 6. Patient system

Figure 5.4 pneumatic diagram


Compressed air connection Compressed oxygen connection

Y3.1 Y3.3 Y4.1

Emergency air valve Inspiratory valve PEEP/PIP valve Expiratory valve




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F1.2 F3.2

Filter Filter

Y6.1 Y6.2

3/2-way solenoid valve, insp. 3/2-way solenoid valve, exp.

D1.1 D1.2 D3.1 D3.2 D3.3 D5.1

Non-return valve Non-return valve Non-return valve Non-return valve 10 mbar Non-return valve 100 mbar Non-return valve

S2.1 S2.2 S6.1 S6.2 S3.1 S5.1 R1.1 R1.2 R1.3 R3.1

AIR pressure sensor (HPSV) O2 pressure sensor (HPSV) Inspiratory pressure sensor Expiratory pressure sensor O2 Sensor Flow sensor Restrictor 0.08 L/min/2 bar Restrictor 9 L/min/2 bar Restrictor 0.4 L/min/2 bar Restrictor (hole in the diaphragm in Y3.3) 0.25 L/min/1.4 bar Restrictor 3.5 L/min/2 bar

DR1.1 AIR pressure regulator DR1.2 O2 pressure regulator

R4.1 Y1.1 Y1.2 Y1.3 Y1.4 3/2-way solenoid valve, O2/AIR 3/2-way solenoid valve calibration O2 sensor 3/2-way solenoid valve, venting 3/2-way solenoid valve, nebulizer

Y2.1 Y2.2

HPSV AIR (high-pressure servo-valve) parallel mixer HPSV O2 (high-pressure servo-valve) parallel mixer 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).

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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 Parallel mixer or mixer block

The 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/min are pulsed at a constant flow of 5 L/min. The supply gases compressed air (AIR) and oxygen (O2) available at the parallel mixer have a supply pressure of 2.7bar to6 bar in the parallel mixer the two gases are mixed in accordance with the set parameters. The parallel mixer supplies the inspiratory gas to the patient.

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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 in the mixer connection block are supplied to the respective cartridge valve. The respiratory gas available at the outlet of the cartridge valves is mixed in the mixer connection block and supplied to the inspiratory unit. b) Cartridge valves with displacement sensor system for compressed air (AIR) and oxygen (O2). The cartridge valve or HPS valve (HPS= high-pressure servo valve) supplies a defined amount of gas to the patient in accordance with the preset adjustment parameters for inspiration, 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. Pressure sensor

The 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.

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Sensitivity: 36.5mV/mbar Offset voltage:1.74V



Figure 5.7 Pressure sensor 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. Pneumatic Controller PCB. The calibration data are stored on the

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Figure5.8 PEEP/PIP valve diagram Inspiration Block

The 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

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Fig.5.9: Inspiration Block diagram 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. 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.

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Fig. 5.11 AIR supply diagram 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

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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

- 61 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 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.

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Fig5.14 Nebulizer Diagram

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6.1 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.

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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.

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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

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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.

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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. 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 Some of the earliest ventilators were negative pressure

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 spontaneous breathing limbs (synchronized) intermittent mandatory ventilation (SIMV).

The latter was the first mode to allow partial ventilatory support and thus gradual liberation from the ventilator. Pressure support was initially developed as a method of lending partial support to the patient's spontaneous breaths, and interactivity became a function of microprocessor driven ventilators. Physicians rapidly discovered that this could be used as a primary ventilation mode, with full patient interaction. Using the ventilator as an interactive weaning device emerged at this time. During the 1990s widespread concern developed about ventilator induced lung injury. Accumulating evidence revealed that larger tidal volume, low PEEP, ventilation strategies were damaging the lungs. This has led to the development of lung protective ventilator strategies, using PEEP to maintain alveolar recruitment (the "open lung" approach), and lower tidal volumes, leading to reduced end inspiratory volumes, to prevent stretch injury. There was renewed interest in plateau pressure limitation and increasing mean airway pressures. Various strategies have been developed to achieve this goal. Pressure controlled ventilation has emerged as a viable alternative, although all strategies involve tidal volume targeting.

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Technology has played a large part in the development of modern ventilators. However, the introduction of a multitude of new modes has not been accompanied by good quality outcomes research. Dual modes, combing pressure limitation with tidal volume, have been developed. Physicians are now demanding more control over gas flow than before hence

the development of active exhalation valves, dynamic inspiration valves, rise time control, automatic tube compensation and, of course, waveform analysis. Modern ventilators deliver enhanced patients interactivity using better triggering sensors, and more comfortable spontaneous breathing even in inverse ratio ventilation. AN exciting prospect is the gradual

arrival of high frequency oscillation into adult critical care units. Using this technique, the physician sets the mean airway pressure, and there is minimal tidal gas movement.

7.2 Development of Ventilator

7.2.1 Absolute Negative-pressure ventilation The use of negative pressure to expand the lungs dates back to the start of the nineteenth century. There are basically two types of negative-pressure ventilators employed in respiratory therapy: (1) the body tank respirator (commonly called the iron lung) (Figure 825) and (2) the cuirass, which is a chest shell piece. Iron Lung The first iron lung to have widespread use was invented by Drinker and Shaw in 1928 and was produced commercially by J.H. Emerson Company. It consisted of an airtight

cylinder that enclosed the patient up to his neck. A seal was formed with foam rubber around the neck so that there was no leak. The cylinder made isolation of the patient's body unavoidable, and even ports on the side made it difficult to provide adequate patient care. In addition, the units had no assist mode, nor was there any means of regulating I/E ratios or respiratory flow rates. The units were reasonably effective on patients who had relatively normal airways, such as polio victims, but they inadequately ventilated patients with significant respiratory disorders. Also, negative pressure exerted on the abdomen often

caused abdominal pooling of blood called tank shock. Because the abdominal wall is flaccid and thus extremely subject to the negative pressure,1 abdominal pooling of blood can occur, decreasing venous return and cardiac output. These units were difficult or impossible to sterilize and were often noisy as well. Tracheotomy or intubation of the patient was usually not necessary for long-term ventilation because maintaining an airway was not a crucial

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problem affecting volume delivery. This aspect reduced the chance of incurring pulmonary infection or other problems associated with artificial airway. Iron lungs were also rugged and dependable, with little maintenance or down time, and were easy to operate by personnel. The newer isolate negative-pressure ventilators for newborns works basically as an iron. Lung.

Figure 7.1 * Iron lung. All but the head is enclosed in a sealed chamber. Slowly revolving wheel

imparts reciprocal motion to bellows assembly connected to chamber. When bellows expand, subatmospheric pressure generated within chamber causes chest to rise and inspiration to begin. During upward motion of bellow a one-way valve opens and returns pressure within chamber to atmospheric. Chest recoils to normal position and exhalation begins. Amount of positive and negative pressure can be controlled independently.

- 70 Chest Cuirass of Chest Shell Drinker and Collins collaborated in 1939 to produce a cuirass or shell unit in hopes that they would eliminate the abdominal pooling. Basically, the unit consisted of a rigid shell that came in varying sizes. It confined the thorax so that subatmospheric pressure could be exerted within the shell and only around the chest

Figure 7.2 Position of chest shell used for negative-pressure ventilation. Inspiration is initiated when pump unit generates subatmospheric pressure in airtight shell. When subatmospheric pressure is released, exhalation begins.

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Figure7.3 Cuirass shell used for negative pressure ventilation. Patient's is placed in supine position and cuirass is stabilized with the use of straps and posts. Method of ventilation is identical to chest shell unit. An electric pump, similar in design to a vacuum cleaner, was used to generate negative extrathoracic pressure. Units a pump (Fig 7.4) reduce the pressure within the chamber to below atmospheric level. This reduction causes the pressure surrounding the chest to drop below the pressure within the lungs, and the chest rises. As the chest rises, the lungs expand and the pressure within them becomes less than atmospheric. Atmospheric gases are thus drawn into the lungs until equilibrium between lung pressure and surrounding pressure is reached. At that moment inspiration ends. To allow exhalation the subatmospheric pressure surrounding the chest is released. The natural elastic recoil of the lungs and thoracic cage causes lung pressure to exceed atmospheric pressure, and gas leaves the lungs until lung pressure and atmospheric pressure are again equal. Maximum pressure was less than that attainable with an iron lung and was dependent on the tightness of the fit of the shell.

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Figure7.4 Schematic representation of pump unit used to provide negative pressure ventilation to shell or garments. Pump unit consists of piston connected off center to a slowly revolving wheel. The downward stroke of the piston releases the subatmospheric pressure and allows chest to recoil to normal resting position and allow exhalation. pressure generated can be controlled independently. Cuirass-type units also fell into disuse for some of the same reasons as did body-tank Amount of negative or positive

respirators: (1) they were excessively noisy; (2) providing patient care was still hampered, although improved over the body-respirator type; (3) regulation of I/E ratios was difficult, and there was no consideration for the regulation of inspiratory flow rates; (4) the seal around the chest was difficult to achieve, which often made the unit periodically undependable; and (5) the negative pressure was not as great as in the iron lung, so it was impossible to totally ventilate a patient who has no respiratory drive.1 These units, however, were used to augment patients with weakened respiratory muscles to ventilate adequately through the night. Because the negative pressure was primarily extrathoracic only, these devices provided for an increased venous return compared with the tank units. In addition, the modification of adding a flow sensor at the patient's nose for a triggering mechanism during an assist mode provided easier synchronization of the ventilator and the patient than could be achieved with the iron lung.

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7.2.2 Positive-pressure ventilation The process of lung inflation by use of positive pressure is similar in principle to mouthto-mouth artificial ventilation. In this approach the rescuer exhales into the victim's airway and directs positive pressure into the victim's lungs. When the victim's chest has expanded to a suitable level the rescuer stops exhaling and releases the pressure, and the victim's lungs are allowed to empty. The procedure is then repeated at a frequency appropriate to the victim's size. When a device is used to inflate the lungs, the device is called a ventilator. Principles of operation A ventilator in general consists of a flexible breathing circuit, a control system a gas supply, plus monitors and alarms. Heating and humidification devices are available as add-on components. Most ventilators are microprocessor controlled, and they regulate the pressure, volume, or flow of the delivered positive-pressure breath, as well as the fraction of inspired oxygen (FiO2), based on control settings. Communications interfaces are also typically

included so that information on control settings, monitored variables, and alarm status can be transferred to a bedside monitor, an information system, or some other interfaced device. Power is supplied from either an electrical wall outlet or a battery; battery power is used for short-term ventilation, such as during intra-hospital patient transport. Some intensive care ventilators can receive gas (both air and oxygen) from a wall outlet that generally provides gas at a pressure of approximately 50 pounds per square inch (psi) The flow of gas to the patient can be regulated by a flow-control valve on the ventilator. Alternately, some models regulate the 50 psi pressure source to a lower pressure and then control the breath to the patient through venture or bellows components. To obtain the desired FiO2 for delivery to the patient, most ventilators mix air and oxygen internally, although some models require an external gas blender. During inspiratory gas delivery, an exhalation valve is closed to maintain pressure in the breathing circuit and lungs. The gas is delivered to the patient through the flexible breathing circuit. Most intensive care ventilators use a double-limb breathing circuit made of corrugated plastic tubing to transport the gas from the ventilator to the patient and return the exhaled gas to the ventilator through one of the limbs (referred to as the expiratory limb). During inspiratory gas delivery,

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an external exhalation valve or one within the ventilator is closed to maintain pressure in the breathing circuit and lungs. After the inspiratory phase, the gas is released to ambient air through this valve. The breathing circuit also provides sites where the delivered gas may be heated, humidified, monitored for proximal airway pressure, and conditioned with nebulized medications and where condensation may be collected. Many model have sensors within the ventilator or flow and provide feedback to the ventilator to automatically adjust its output. The controls system are used to select breathing mode and ventilation pattern parameters (e.g., tidal volume, breathing rate). For the ventilator to produce a prescribed breathing pattern, several parameters can be independently set, such as length of the inspiratory or expiratory phase, rate of mechanical breaths, ratio of inspiratory time to expiratory time (I:E ratio), wave-form shape, tidal volume, minute volume (the volume inhaled during a minute), peak inspiratory flow, peak pressure, and positive end-expiratory pressure (PEEP). 7.2.3 State of the art High Frequency Ventilation (HFV) High Frequency Ventilation is a collective description of all high frequency ventilation techniques. Applied tidal volumes are some times smaller than anatomical dead space (= 2ml/kg). Three high frequency ventilatory modes depend on applied Ventilatory.

1. High Frequency Positive Pressure Ventilation (HFPPV)

This is basically positive pressure ventilation with ventilatory frequencies of I-2Hz. Inspiratory gas is supplied at a frequency of 1-2 Hz into the endotracheal tube via one arm of a Y-piece. Tidal volumes are in the range 2-4 ml/kg. During inspiration, a pneumatic valve occludes the expiratory limb. During expiration, this valve opens and exhalation occurs passively .figure 7.5

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Fig7.5 High frequency positive pressure ventilation

Because the valve is closed during inspiration, there is no air entrainment. This technique can be used with some conventional ventilators.

2. High Frequency Jet Ventilation (HFJV)

This ventilatory technique is applied via a cannula (injector cannula) introduced directly into an endotracheal tube or integrated wall of a special tube.The jet gas is applied via the injector cannula into the open endotracheal tube with a ventilatory frequency between 2 and 10Hz (Fig.7.6)

Fig 7.6 High Frequency Jet Ventilation The tidal volume is also between 2-4 ml/kg .

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The lack of an expiratory valve in this technique (open system) allows Venturi effect to occur which enhances inspiration. Gas volumes are enhanced through entrainment .

Exhalation is passive between jet gas impulses, because of this there is a danger of "air trapping" with consequent over-stretching and , barotrauma if expiratory times are too short. HFJV can be combined with conventional ventilators modes (IPPV or IMV) with low tidal volume.(Fig7.7)

Fig 7.7 Combined high frequency ventilation

3.High Frequency Oscillation (HFO)

This ventilatory technique differs from other methods in having active expiration. High frequency (sine wave) oscillations up to 50 Hz are produced by a piston pump, which is connected to the endotracheal tube via an adapter and a T piece, which cause the gas column in the tube to oscillate (Fig7.8)

Fig (7.8 ) High Frequency Oscillation

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These sine pressure waves propagate down the bronchial system into the lungs. The active expiratory flow avoids "air trapping". Fresh gas is supplied via a T piece lateral to the direction of oscillation. This lateral respiratory gas flow is called "bias flow". The exhaust arm of this lateral flow has a resistive tube ("impedance tube") to avoid excess oscillatory volume loss at the "bias flow . Inspiratory and expiratory times are equal and not adjustable. Finally, High Frequency ventilatory techniques are not widely used clinically. Independent lung ventilation (ILV) Separate ventilation of the lungs is called independent lung ventilation. Separation is achieved with a double lumen tube, ventilation with two ventilators (Master, Slave). Synchronization of the ventilators may appear physiologically correct but ventilation without synchronization does not appear to have any negative effects. Indications for independent lung ventilation in the intensive care unit are single sided lung diseases, or lung diseases with emphasis on one side, which cannot be treated adequately with conventional ventilation techniques. The crucial criterion is lateralisation, whilst the type of disease be it pneumonia, lung contusion, septic lung failure, bronchopleural fistula or following a single sided lung transplant is of secondary importance.

Principle of Operation Because of the differing mechanical properties of the lung, tidal volumes are distributed according to compliance. With conventional ventilation, PEEP in the healthy lung with the better compliance results in a greater increase in lung volume than in the damaged lung with lower compliance. This results in reduced ventilation of the diseased lung, and over-stretching of the healthy lung with increased ventilation perfusion disturbance. The mechanical effect of PEEP leads to compression of lung capillaries, with an increase in pulmonary vascular resistance in the healthy parts of the lung. This results in increased circulation in the damaged lung, with deteriorating oxygenation and increasing right-left shunt. Furthermore, ILV offers the opportunity to adjust the I: E ratios according ted to the different compliance of each lung. If the lungs are ventilated with different I:E ratios, the term asynchronous independent lung ventilation is used. If the I:E ratio is the same, synchronous independent lung ventilation is used .

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The term inverse I:E ratio is used when the inspiration of the slave machine begins with the expiration of the master machine and vice versa . Usually, both lungs are ventilated with identical but reduced, tidal volumes. This ensures that, in the event of inadvertent separation of the machines, the lungs are not ventilated at different frequencies (safety measure). With asymmetric lung diseases, independent lung ventilation offers the opportunity to specifically treat ventilation/perfusion mismatches with SPEEP, and to improve pulmonary gas exchange. Furthermore, general haemodynamics are less affected, and oxygen availability is optimised for metabolic demand. Applications we will consider some models of draeger ventilators. 1.Savina

Fig 7.9 Savina ventilator Savina is a Critical Care Ventilator for advanced long term ventilation. For adult and paediatric application with tidal volumes in volume controlled ventilation starting from 50ml. For use in recovery rooms, intensive care units, sub-acute care facilities, intra- and inter-hospital transport. Ventilation modes for volume controlled ventilation, augmented spontaneous breathing. Pressure controlled ventilation with Option (BIPAP). Volume oriented ventilation with automatic adjustment of the flow rate: Option (Auto Flow) In case of failing electricity supply, Savina continues to work without any interruption for one hour with internal battery (smart power management).

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up to seven hours with internal and external batteries (smart power management). For inner clinical transport , you do not have to disconnect the patient from Savina just take it along. With Option AutoFlow Savina offers automatic adjustment of the flow rate to deliver the set volume with the least possible pressure Benefits: 1. Peak pressures are reduced. 2. The patient can breathe spontaneously during all phases of the ventilatory cycle. 3. No nuisance alarms if patient coughs. 4. Improved gas distribution esp. in inhomogeneous lungs. 5. Flow rise can be adjusted to the patient by Flow Acceleration.

Autoclavable Parts (steam sterilisation 134C): 1. Expiration Valve. 2. Autoclavable Hose sets (incl. Y-piece, water traps).

Trigger indicator

Display with real-time curves

Alarm LEDs


Standby key

Flow sensor

Exhalation valve

O2 inlet on the right side of the device

Fig 7.10 Front view of the savina ventilator.

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AC inlet DC inlet

Main switch

Nurse call (option)

Side rail (option)

Serial port Inlet for breathing air Fig 7.11 Back phase of the savina ventila


Mode Mode

Alarm Alarm message message

Real-time Real-time curve curve
30 20 10 0

Assist Paw





Measured Measured values values

V Te





Advice Advice

Fig 7.12

Display showing different parameters

2. EVITA 2 dura.
This device have and will do the following function s Select-Adjust-Confirm . Start-up settings.

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Standby function. Advisory Information. Guided checklist. Intelligent alarm management. Automated calibration . Optimised Mask Ventilation (optional). Remote Control for Routine functions (optional). Nurse Call (optional). Expiratory Valve easy to sterilise. no filters needed. exchange in seconds. low exhalatory Resistance.

Fig 7.13 Expiratory Valve With Option (Auto Flow) Evita 2 dura offers automatic adjustment of the flow rate to deliver the set volume with the least possible pressure Peak pressures are reduced. The patient can breathe spontaneously during all phases of the ventilatory cycle. No nuisance alarms if patient coughs. Improved gas distribution esp. in inhomogeneous lungs. Intelligent Alarm management: Volume Strategy: Paw high alarm. Pressure Strategy: Tidal Volume high alarm. Alarms with priorities and clear messages

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! !!

Advisor y Caution



Evita 2 dura offers exactly the right parameters for clinical routine. In addition, options such as Ventilation Plus or Monitoring Plus are available to extend the range of functions. Evita 2 dura is your tailor-made solution all times and in all situations.

3. Draeger- EVITA 4. (newest)

EVITA 4 Is the same as Evita 2 dura but it has additional characteristic : Evita 4 First touch screen ventilator on the market. First ventilator to have tube compensation. Ventilator for all applications. Improved monitoring functions.

Additional functions : Power Back Up. external flow source. open communication interface. Software Updates with PC-Download.

With AutoFlow in Evita 4 offers automatic adjustment of the flow rate to deliver the set volume with the least possible pressure:
Peak pressures are reduced. The patient can breathe spontaneously during all phases of the ventilatory cycle. No nuisance alarms if patient coughs. Improved gas distribution esp. in inhomogeneous lungs.

Nurse Call (Multifunction board (required for Evita Remote). Evita Remote (Remote pad for routine functions).

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7.2.4 Emerging
Evita XL from draeger.

Fig 7.14 Evita XL Venilator This ventilator is different from other ventilators, because it has some new technology, which it is not available in others. The difference in some characteristic, which is: 1. Operation Panel 15 colour Touch screen. Swivel mounted. Easy to move. Central rotary knob. Easy to clean and disinfect. Rail connector for standard rail. Sealed unit, no openings. Easy to clean and disinfect.

2. User Interface Up to 12 values shown on the screen. Only displays essential settings for easier readability.

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Additional settings, alarms or diagnostic data readily available in the background and easily configurable to the screen. Intelligent logbook and trends. Measured values configurable to clinical standards.

3. User Interface Screen displays three curves Every curve can be replaced by two loops or one trend Loop can be zoomed to the size of two curves

Fig 7.15 Screen displaying three curves 4. Special Functions Inspiration hold Expiration hold Maximum time for both functions (15 seconds) Nebulizer activation and deactivation Nebulization time 30 minutes Suction Procedure 3 min pre-oxygenation, up to 2 min time for suction procedure, 2 min postoxygenation The most important function is to control weaning process (SMART CARE) 30, March, 2004 Protocol based weaning defines and organizes a process for ventilator adjustments, expected outcomes, patient monitoring and patient care during weaning. Several studies have shown

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that implementation of protocols to aid the weaning process results in a significant reduction in ventilation days. Due to shortened ventilation, possible complications may be reduced, which could lead to a significant decrease in costs. Smart Care, knowledge based weaning system, contains automated clinical guidelines based on recognized medical expertise. by this ventilator; we are freeing the clinician for the "art of medicine . The complete weaning process is continuously monitored by the EvitaXL, provided that the patient is hemodynamically stabile, tracheotomized or intubated and has an adequate oxygenation. SmartCare divides the control process into three steps: Step 1: Stabilizing the patient within a respiratory comfort zone by regulating the level of pressure support based on the three parameters breathing rate, tidal volume and end tidal CO2. Step 2: Reducing invasiveness by testing if the patient can tolerate a lower pressure support level without leaving the comfort zone. Step 3: Testing readiness for extubation by maintaining the patient at the lowest limit of support. Smart Care continuously takes data and uses the mean parameter values to take decisions in two- or five-minute intervals on whether to adapt pressure support. A knowledge-based system has clear advantages over one based on a preset minute ventilation (MV). Infections or fever may induce a higher metabolic rate, which has to be counterbalanced by an increase in MV, and temporary situations such as increased secretion or suction stress may lead to a higher MV demand. Preset MV systems cannot automatically adjust to such changes. A knowledge-based approach to therapy can. Smarter device EvitaXL has been designed to follow the path of innovation as an integrative

platform. Consequently, it is equipped for: Powerful monitoring: Respiratory mechanics, display space, configuration. Improved modes: Ready for the challenges of today s and tomorrow s ICU. SmartCare Pressure Support is based on a clinical protocol for weaning. In order to wean successfully, rapidly and with few or no complications, certain settings and patient information are required for operation. Settings: Patient range: body weight (BW) between 35 and 100 kg CPAP/ASB in adult mode Apnoea ventilation activated

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Automatic tube compensation (ATC) deactivated CO2 and flow monitoring activated

Patient Information Patient weight Type of intubation Type of humidification Medical history of neurologic disorder or COPD SmartStim mounting 1) Place the SmartStim at the device side rail. (see # 1) 2) Connect SmartStim to the power supply. 3) Connect with the provided hose (see # 2) the SmartStim with the Filter (see # 3). 4) Regulate the desire virtual frequency using the rotary knob on the SmartStim. (see # 4) 5) Place the CO2 sensor on the reference cell (provided with the CO2 Sensor) (see # 5)

Fig 7.16 SmartStim

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Fig 7.16 CO2 sensor

7.2.5 Visionary
1.Future ventilators will use fresh air and do not need to O2 and air containers. 2.It will be portable and very small in size (hand size) , flexible tube is connected to it and it uses regular battery. 3. When connected to a patient, it will be very smart and sensitive to detect diseases and lung damage, it will directly select the appropriate mode. 4.some models will use solar cells to provide power instead of electricity .

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1. Breathing and mechanical support (version1993)

2. Respiratory therapy equipment(version 1985)

3. Ventilators Theory and clinical Application (version 1991)


5. Service manual of Draeger-EVITA4 (version2002)

6. Course 335 BMT prepared by Dr. Bassim Odah

7. Lectures with Eng. Mohmmad Shaban

8. National guard hospital

9. Draeger medical company (Riyadh, Germany) 10. www.ventworld.com/education/wiav-part1.asp 11. www.ccmtutorials.com/rs/mv/page2.htm 12. www.corexcel.com/courses/body.vent6.htm 13. www.stemnet.nf.ca/~dpower/resp/exchange.htm#Cellular


This report talk about one of the most important life support medical device which can be used in many area as(e.g. critical care units, patient room, emergency and house). It talk 3 months of hard work and we face many complication, but we pass it. Successfully by god mercy and insist to finish it. More than 12 references used to get information. Most benefit reference are:

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1- National guard hospital. 2- Draeger company (RIYADH-GERMANY)

With, thanks to eng.Mohammod Shaban who helped and instruct us. Thank to other people we did not mention This report prepared by ventilator group 1- Ali Mohmmad Al Hawwas 2- Abdulaziz Ahmad AL Somali 3- Mohmmad Ahmad Maghrbi 4- Muhannad Nasser Alshiban

We ask god to benefit all student and Muslims from this report

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