SSM Mechanical Ventilation 29 JAN 2011

NURSING SERVICES, KING ABDULAZIZ MEDICAL CITY
_____________________________________________________________________
NURSING SERVICES - EDUCATION DEPARTMENT
SELF STUDY MODULE
MECHANICAL VENTILATION
CONTACT HOURS: 4
Developed by A. Morrow, RN, RM, B.Ed., 2001
Edited by Bill Burgess, RRT, 2001
Revised by A. Morrow, RN, RM, B.Ed., M.P.E.T., Certs IC & CC Nsg, 2003, 2011
Reviewed by Karen Amihan, RN, CRN
Reviewed by Rani Tharumalingam, RN, BN, EMBA, Cert Crit Care
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SSM Mechanical Ventilation
z-riysvfss-001/gen/ed/AM/SSM/2010
January 2011
SELF STUDY MODULE INSTRUCTIONS
1. Read Module objectives.
2. When available complete pre-test questions.
3. Study content.
4. Complete post- test questions, using answer sheets provided.
5. Please complete legibly answer sheets with the following information: (CAPITAL
Letters and Pen)
a) title of SSM
b) name
c) badge number
d) ward / unit
e) date
6. Complete evaluation provided in the library.
7. Submit the following to the Nursing Education Department- (Mail Code 1212):
a) post test answer sheet

b) EVALUATION FORM
8. Please return the Self Study Module to the Medical Library.
9. Contact Nursing Education at nursingservices-ed@ngha.med.sa , as necessary,

for assistance.
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TABLE OF CONTENTS
No Description Page
1 Table of Contents 3
2 Introduction and Objectives 4
3 Respiratory Terminology 5-8
4 Indications for Mechanical Ventilation 9 - 12
5 Goals of Mechanical Ventilation 12
6 PEEP and CPAP 13 - 14
7 Non-Invasive Positive Pressure Ventilation (NIPPV) 15 - 18
8 Mechanical Ventilation 19 - 20
9 Modes of Ventilation 20
- Pressure-Control Ventilation (PCV) 20 - 21
- Controlled Mandatory Ventilation (CMV) 21
- Assist-Control (AC) 22
- Synchronized Intermittent Mandatory Ventilation (SIMV) 22 - 23
- Pressure Support Ventilation (PSV) 23 - 24
- High Frequency Ventilation (HFV) 26 - 26
10 Ventilator Gauges and Alarms 26 - 28
11 Work of Breathing 28 - 29
12 Trouble-shooting Alarms 29
13 End-Tidal CO2 Montoring 30
14 Nursing Considerations in the Care of the Ventilated Patient 31 - 39
15 Complications of Mechanical Ventilation 39 - 44
16 Adjuncts to Mechanical Ventilation 44 - 46
17 Weaning from Mechanical Ventilation 46 - 50
18 Summary 51
19 Addendum: Formula for calculating A-a Gradients 51
20 References 52 - 53
21 Post Test 54 - 60
22 Test Answer Sheet (please print for your use) 61
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Positive pressure ventilation has been used in Critical Care settings for many years, and has
had a tremendous impact upon patient survival. In more recent years, new and innovative
approaches to ventilation have continued to be developed. These advances result from
important new gains in the understanding of pulmonary dynamics and related
cardiopulmonary interactions.
Your role as a critical care nurse caring for the ventilated patient means you need to
continue to evolve to keep pace with these changing approaches to mechanical
ventilation.
Your nursing management of the ventilated patient should incorporate patient advocacy,
coordination of interactions between the various health professionals involved in patient
care, and provision of continuity of safe and competent care.
The aim of this Self-Study Module is to help you become more familiar with all aspects of
ventilation. These include the indications and complications of mechanical ventilation, the
different modes of ventilation, and the various considerations for safe patient care.
NB: It is assumed that you have completed the Self-Study Module – Arterial Blood Gas
Interpretation – prior to commencing this module.
OBJECTIVES
On completion of this Self-Study Module, the learner will be able to:
1. Differentiate between Type I and Type II Respiratory Failure.
2. List the subjective and objective indications for mechanical ventilation.
3. Discuss the different modes of ventilation.
4. Describe the nursing considerations for care of the ventilated patient.
5. Outline the adjuncts to ventilation.
6. Describe various techniques for weaning patients from mechanical ventilation.
7. Outline the complications of mechanical ventilation.
Before proceeding with this Self-Study Module, take some time to review terms related to
respiratory physiology and function, as appearing on the following pages. If further
explanation of any of these terms is required, please refer to the Respiratory section in
any medical physiology textbook.
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RESPIRATORY TERMINOLOGY
_______________________________________________________________________________
a. Airway resistance: this is the pressure difference between the alveoli and the mouth
necessary to produce a unit of flow. Airway resistance is the major physiological
component of the total resistance to breathing in the respiratory system.
b. Alveolus: is the smallest and most

distal structure in the terminal
respiratory unit where gas exchange
takes place in the lung (see diagram
opposite).
c. Compliance: relates to distensibility of

the lungs, chest wall, or both. Lung
compliance is increased in
emphysema and decreased in
interstitial fibrosis.
d. Carina: is the site where the trachea divides into left and
right main stem bronchi.
e. Hypoxaemia: means insufficient amount of oxygen in arterial

blood, i.e., less than about 80mmHg in a normal adult.
f. Humidification: is the saturation of dry air with water vapor.
g. Tidal Volume (VT): is the volume of gas exhaled per breath, during normal quiet
breathing (normally measured in milliliters).
h. Minute Ventilation (VE): is the total amount of gas exhaled per minute (i.e., VT x RR).
i. Vital Capacity (VC): is the largest amount of air exhaled after maximal inspiration,
without using force or effort.
j. Functional Residual Capacity (FRC): is the amount of gas remaining in the lungs at
the end of expiration. FRC is important for maintaining normal ventilation-perfusion
matching.
facstaff.bloomu.edu/gwassmer/.../respphysiology.ppt
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k. Negative Inspiratory Force (NIF): is the amount of negative pressure the patient is
able to generate on inspiration, and is an indicator of inspiratory muscle force.
l. Maximal Voluntary Ventilation (MMV): is the maximum amount of air that can be
inhaled and exhaled as rapidly as possible over a period of one minute.
m. Respiration: is the exchange of oxygen for carbon dioxide at the alveolar level in the
lungs (external respiration), or at the tissue or cellular level (internal respiration).
n. Ventilation: is the movement of gas in and out of the lungs.
o. Dead space: is the volume of inspired

air that does not participate in gas
exchange (see diagram opposite) – there is
ventilation, but no perfusion. There are 4
types of dead space: anatomic,
alveolar, physiologic and mechanical.
Anatomic dead space is the amount of

air filling the airways but not involved in
gas exchange. In most adults this is
estimated at 2ml/kg body weight.
Alveolar dead space is the amount of gas filling the alveoli that does not contribute
to gas exchange. Mechanical dead space is caused by the addition of the
ventilator circuit to the patient’s dead space. Physiologic, or total, dead space is the
sum of the anatomic and alveolar dead space.
As the amount of dead space increases, the amount of gas that contributes to
gaseous exchange decreases.
p. Shunt: A form of ventilation-perfusion

mismatch in which alveoli which are not
ventilated (e.g., due to collapse or oedema
fluid) but are still perfused. As a result, blood
passing these alveoli is not oxygenated.
www.nda.ox.ac.uk/wfsa/html/u12/u1211_02.htm
This form of respiratory failure is relatively resistant to oxygen therapy. Increasing the
inspired oxygen concentration has little effect because it can not reach alveoli
where shunting is occurring and blood leaving normal alveoli is already 100%
saturated. Shunting is the commonest cause of hypoxaemic respiratory failure in
critically ill patients. Hypoxic pulmonary vasoconstriction, the body’s normal
response to alveolar hypoventilation, reduces the blood flow to non-ventilated
alveoli and reduces the severity of the hypoxaemia. Causes of shunting may include:
intracardiac
any cause of a right to left cardiac shunt eg Fallot's Tetralogy, Eisenmenger's
Syndrome
pneumonia
pulmonary oedema
atelectasis / collapse
pulmonary haemorrhage
pulmonary contusion
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q. V/Q Ratio: Ventilation / perfusion ratio –
a major determinant of oxygenation in
the body - should roughly approximate
1:1.
A high V/Q ratio is characteristic of dead

space-producing disorders (e.g.
pulmonary embolus), whereas a low V/Q
ratio is indicative of shunt-producing
disorders (e.g. sputum plug (see diagrams
opposite)
r. Transthoracic pressure: is the pressure

difference between the pleural space
and the external surface of the chest. It
is considered to be a measure of the
elastic recoil of the chest wall.
s. Work of breathing: relates to the effort expended for the breathing process – normal
work of breathing is 0.3-0.6J/L. The workload of breathing is determined by:
The effort to expand the elastic tissues of the chest wall and lungs (related to
lung compliance)
The effort required to expand the inelastic tissues of the chest wall and lungs
(represents tissue resistance).
The effort required to move air against the resistance of the airways (resistance
work).
A further discussion on factors which increase work of breathing can be found on p. 28-29 of this
module.
t. Partial Pressure: relates to the pressure, or tension, of a gas, whether it is alone, or in a

mixture with other gases. Clinically, we are interested in the partial pressures of
oxygen (PaO2) and carbon dioxide (PaCO2) in arterial blood. The PaO2 relates to the
partial pressure of oxygen in the alveoli.
u. Oxygen Saturation Percentage (SaO2%): refers to the amount of hemoglobin actually

combined with oxygen. It may be measured clinically via arterial blood gases by co-
oximetry, or by non-invasive pulse oximetry.
v. Alveolar-arterial Gradient (A-a Gradient or AaDO2) is the difference between the

partial pressure of oxygen in the alveolar gas and in the systemic blood. The normal
gradient in young adults is < 10mmHg (on room air), and may increase up to
20mmHg in the elderly.
“During ideal gas exchange, blood flow and ventilation would perfectly match each
other, resulting in no alveolar-arterial PO2 difference. However, even in normal lungs,
not all alveoli are ventilated and perfused perfectly. For a given perfusion, some
alveoli are under-ventilated while others are over-ventilated. Similarly, for known
alveolar ventilation, some units are under-perfused while others are over-perfused.
The optimally ventilated alveoli that are not perfused well are called high V/Q units
(acting like dead space), and alveoli that are optimally perfused but not adequately
ventilated are called low V/Q units (acting like a shunt)” (Kaynar & Sharma, 2010).
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The A-a gradient provides an index of how efficient the lung is in equilibrating
pulmonary capillary oxygen with alveolar oxygen – it indicates whether gas transfer is
normal. A large A-a gradient generally indicates that the lung is the site of
dysfunction (except when cardiac left-to-right shunting is present).
w. Oxygen-Hemoglobin Dissociation Curve: is a

graphical representation of the relationship
between the PO2 and O2 saturation.
The normal oxyhemoglobin dissocation

curve shows that the normal arterial blood
has a PO2 of about 97mmHg and an O2
saturation of 97% (see diagram opposite, downloaded
from www.frca.co.uk/article.aspx?articleid=100345).
Please refer to the Arterial Blood Gas

Interpretation Self Study Module for more
information regarding the Oxygen-Hemoglobin
Dissociation Curve.
The diagram below shows the abnormalities in ventilation and perfusion mentioned on
the previous page.
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January 2011
INDICATIONS FOR MECHANICAL VENTILATION
_____________________________________________________________________________
Probably the most frequent indication for initiating mechanical ventilation is as supportive
therapy in the setting of respiratory failure, which can be classified as either acute or
chronic. Respiratory failure may be due to inadequate oxygenation, inadequate
ventilation, or a combination of the two entities.
Acute or chronic severe malfunction in gas exchange between the lungs and the blood
can cause hypoxia with or without hypercapnoea.
The pathophysiology and clinical determination of the type of respiratory failure, and the
need to intubate and ventilate, are determined from the pattern of blood gas and
metabolic abnormalities, as well as the clinical condition of the patient.
Inadequate ventilation causes an increased carbon dioxide tension (PaCO2) and
respiratory acidosis.
Inadequate oxygenation means a decreasing arterial oxygen tension (PaO2), (less than
60mmHg, with an oxygen saturation of less than 90%), despite increasing inspired oxygen
concentrations.
Hypoxic respiratory failure (type 1 respiratory failure) is hypoxia without hypercapnoea

and with an arterial partial pressure of oxygen (PaO2) of less than 60 mmHg (8 kPa) on
room air at sea level.
Hypercapnoeic respiratory failure (type 2 respiratory failure) is hypoxia with an arterial

partial pressure of carbon dioxide (PaCO2) of more than 50 mmHg (6.5 kPa) on room air
at sea level.
OBJECTIVE CRITERIA:
Because virtually any disease process is capable of contributing to or actually causing

respiratory failure, specific criteria have been developed which can be applied to all
clinical situations. Nursing staff, while not responsible for performing the direct
measurements required for determining this objective criteria, need to be aware of their
significance in relation to the patient’s overall clinical condition.
Acute respiratory acidosis, with an arterial pH of 7.25 or less, a PaO2 of 60mmHg or less,
and a PaCO2 greater than 60mmHg, in combination with worsening arrhythmias and
haemodynamic instability, generally indicates the need for mechanical ventilation in
order to prevent further clinical deterioration. Additionally, development of respiratory
distress in a patient who has relatively normal blood gases, if associated with a
respiratory rate of greater than 30 / minute, tidal volumes below 3 - 5 ml/kg, and a vital
capacity of less than 12 - 15 ml/kg, with an inspiratory effort of less than –20cm H2O may
also indicate the need for mechanical ventilation.
A further objective decisive factor is an A-aDO2 (alveolar-arterial oxygen difference /

gradient) of more than 450. As mentioned earlier in this module, the A-a gradient
represents the difference between alveolar and arterial oxygen concentration, and is
normally between 5 to 20mmHg (the difference is due to the normal small anatomical
shunt which exists within the lungs). A value over 20mmHg indicates increased shunting,
and may be due to venous admixture, uneven ventilation in relation to perfusion, alveolar
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hypoventilation or impaired diffusion. Serial measurements provide a rough index of the
amount of acute, potentially reversible lung disease.
Please see Addendum # 1 (pg. 50) for the formula for calculating the A-a Gradient.
Remember, however, that the overall clinical status of your patient needs to be
considered before deciding whether or not mechanical ventilation should be
commenced. For example, a person who has a chronic obstructive lung disorder may
be quite comfortable with a PaO2 in the 50’s and a PCO2 in the 70’s – his / her body has
made the necessary compensatory metabolic changes to accommodate the state of
chronic respiratory acidosis and hypoxaemia. Therefore, certain subjective criteria also
need consideration in order to establish the need for mechanical ventilation.
SUBJECTIVE CRITERIA:
1. Is the patient awake, co-operative and alert?
2. Can the patient cough and deep breathe effectively?
3. What are the secretions like, and is there any bronchospasm?
4. Can the patient swallow?
5. Is there ventilatory dis-coordination, e.g., flail chest, paradoxical movement?
6. What is the work of breathing?
7. Is there adequate muscle tone, e.g., can the patient lift his/her head and arms
off the bed for more than 5 seconds?
8. Is the patient haemodynamically stable?
The flow diagram above, downloaded from www-archive.thoracic.org/.../index.html outlines the end results of airway
problems which impact ventilation. These points will be covered later in this module.
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Classification of Acute Respiratory Failure
Failure of oxygenation (Hypoxaemia):-

- Acute respiratory distress syndrome
- Pneumonia
- Hydrostatic pulmonary oedema
- Exacerbation of asthma
- Pulmonary embolus
Failure of Ventilation (Hypercapnoea):-

a. Hypoventilation:
- Reduced respiratory drive:
- Drug intoxication
- Head trauma, cerebral vascular accident
- Impaired respiratory pump function:
- Respiratory muscle fatigue
- Neuromuscular disease
- Chest wall deformity / trauma
b. Increased dead space:
- Emphysema
- Pulmonary embolus
- Cystic fibrosis
c. Increased CO2 production:
- Increased work of breathing any cause)
- Fever
- Excessive carbohydrate intake.
Diagram 1: Delicate balance between the loads imposed on the respiratory system and its capacity. The inability to tolerate
spontaneous unassisted breathing is the result of an excessive demand, a failing respiratory system, or a combination of the two. From
Lessard , M. & Brochard, L. (1996) “Weaning from Ventilatory Support” in Clinics in Chest Medicine: Recent Advances in Ventilation;
Vol. 17; No.3.
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Table 1: Summary of Clinical Parameters Associated With Respiratory Failure
Respiratory Parameter Usual Range Respiratory Failure
Respiratory rate (breaths/min) 12 – 25 > 30
Vital capacity (ml/kg) 30 – 70 < 15
Tidal volume (ml/kg) 5- 8 <3–5
Oxygenation – PaO2 (mmHg) 75 – 100 < 60
Ventilation – PaCO2 (mmHg) 35 – 45 > 55
Adapted from: Tung, A., Indications for Mechanical Ventilation, in International Anesthesiology Clinics: Mechanical
Ventilation; Vol. 35, No. 1, 1997.
GOALS OF MECHANICAL VENTILATION:

The goals of mechanical ventilation include the following:-
1. To adjust alveolar ventilation to an individualized “normal” level for each patient, in

order to meet metabolic demands.
2. To improve ventilation / perfusion relationships and oxygenation.
3. To decrease the work of breathing.
4. To provide prophylactic ventilation for 12-24 hours post-operatively for high risk
surgical patients
5. To control PaCO2 levels in selected neurological conditions.
In the modern Critical Care setting, mechanical ventilation is accomplished by positive
pressure ventilation. A positive pressure ventilator forces gas into the lungs, and the
positive intra-thoracic pressure created expands the lungs and chest wall. It is important
to remember that this is the exact reverse of the normal pressure changes of
spontaneous inspiration, which we will now briefly examine.
At the end of expiration, the pressure within the pleural space is approximately –2cm
H2O, that is, it is negative with respect to atmospheric pressure. During normal
spontaneous inspiration, contraction of the inspiratory muscles causes the chest cage to
enlarge and the pleural pressure becomes even more subatmospheric (see diagram below).
As pleural pressure is transmitted across the lung, alveolar pressure also becomes
subatmospheric (about –1 to –2 cmH2O). This negative intrathoracic pressure “sucks” air
into the lungs until alveolar pressure again reaches zero, and cessation of gas flow
occurs. During expiration, the elastic recoil of the lung creates positive alveolar pressure
(+1 to + 2cmH2O). This produces a driving pressure that results in airflow out of the lung.
-2cm H2O -2cm H2O
Diagrams above from Butcher & Boyle, 1997, p. 7

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PEEP & CPAP
_________________________________________________________________________________
Positive End Expiratory Pressure (PEEP) and Continuous Positive Airway Pressure (CPAP) are
not ventilation, but are used in spontaneous breathing and with other modes of ventilation
to improve oxygenation. The term PEEP is used for mechanically ventilated patients,
whereas CPAP is the term used when the patient is spontaneously breathing.
Positive End Expiratory Pressure (PEEP)

The concept of PEEP is that a pressure is applied at the
end of expiration to maintain alveolar recruitment (i.e.,
to keep alveoli from collapsing at the end of
expiration).
The diagram opposite shows how, in Acute Lung Injury
(ALI) and Acute Respiratory Distress Syndrome (ARDS),
alveoli collapse due to interstitial oedema. Such
collapse interferes with gaseous transfer, particularly
oxygen diffusion, resulting in hypoxaemia.
Increasing the FiO2 won’t have any significant effect
upon the PaO2 in patients who have refractory
hypoxaemia as a result of significant atelectasis. In this
type of patient, however, the application of PEEP will
recruit collapsed alveoli and help prevent further loss of
lung volume, thus improving oxygenation.
When PEEP is applied, airway pressure is maintained at positive levels and is never allowed
to return to atmospheric. This has the result of forcing alveoli to remain open, thus aiding
oxygen diffusion into the bloodstream.
With PEEP, when inspiration commences, it does so on top of the pressure remaining in the
airway at the end of expiration. This is the baseline airway pressure and it lasts for the
duration of the respiratory cycle, regardless of the inspiratory mode of ventilation.
Application of PEEP is achieved on most modern ventilators by turning the PEEP/CPAP dial
until the end-expiratory pressure on the pressure gauge matches the prescribed level of
PEEP. The dial regulates an expiratory resistance valve that effectively keeps airway
pressure above atmospheric pressure at end of expiration. PEEP is indicated when a high
inspired oxygen concentrations fail to maintain a satisfactory SaO2.
Optimal PEEP is the level of PEEP that recruits most alveoli without causing over-distension
and adversely affecting overall oxygen delivery to the tissues (i.e., by decreasing venous
return and cardiac output).
The diagram opposite (from Pierce, 2002, p. 58), shows
the effects of application of PEEP on the alveoli.
A: Atelectatic alveoli before the application of PEEP
B: Application of optimal PEEP has reinfalted alveoli to
normal volume.
C: Application of excessive PEEP over-distends the
alveoli and compresses adjacent pulmonary capillaries,
creating dead space with subsequent hypercapnoea,
pulmonary stress fractures and lung rupture.
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Continuous Positive Airway Pressure (CPAP) is achieved by the addition of a fixed amount
of positive airway pressure to spontaneous respirations. CPAP does not require the use of a
mechanical ventilator as it can also be applied to a non-intubated patient via a face /
nasal mask and appropriate respiratory circuit (please refer to the following page). This results in
an increase in Functional Residual Capacity (FRC), with associated improvement in
oxygenation and lung compliance in non-intubated patients.
When CPAP is used for a patient on a ventilator, it usually described a mode of ventilation
without additional inspiratory support. So if you put somebody on CPAP of 5cmH2O on a
mechanical ventilator, this is 5cm of positive pressure applied to the airway in both
inspiration and expiration. Any level of Pressure Support set on a ventilator is above CPAP:
5cmH20 of PEEP (CPAP) and 5cmH20 pressure support provides a peak inspiratory airway
pressure of 10cmH2O: Pressure Support is always described as a pressure above
PEEP/CPAP.
CPAP may be used as an adjunct to spontaneous ventilation to assist in re-expanding

atelectactic lung tissue, or as a method of weaning from ventilatory support. For the
intubated patient, institution of CPAP usually requires the same ventilator circuitry as the
SIMV mode. Airway pressures of between about +5 to +15cm H20 are maintained by a
continuous or demand flow system. The usual range of PEEP or CPAP is 5 to 15cm. H2O.
Benefits of PEEP & CPAP: With the addition of PEEP / CPAP, previously inflated alveoli
are further inflated, and previously collapsed alveoli may be recruited. This increases
overall gas volume and redistributes lung water away from the alveoli to the interstitial
space. The net effect of addition of PEEP / CPAP is an improvement in oxygenation, and so
a reduction in inspired oxygen concentration may be possible. PEEP and CPAP also
decrease the work of breathing by reducing airway resistance and improving lung
compliance.
Disadvantages of PEEP include increased mean intrathoracic pressure, which may interfere
with venous return to the heart, resulting in a decreased cardiac output. However, these
effects upon cardiac output can be minimized by ensuring an adequate circulating
volume.
Excessive alveolar pressure may be distributed to more compliant lung segments in acute
lung injury, with the potential for causing over-distension and damage of normal alveoli.
Patients who have a decrease in lung compliance may be at increased risk for
development of pneumothorax with the addition of high levels of PEEP.
When spontaneous and mechanical breaths are superimposed upon on PEEP or CPAP,
various terms may be used, depending on the ventilatory mode (e.g., SIMV with CPAP / AC
with PEEP, etc).
REQUIREMENTS FOR VENTILATORS:
1. Patient size: The ideal ventilator should be able to ventilate all sizes of patient from
the neonate to the adult. However, most hospitals have dedicated ventilators for
paediatric and neonatal use. Ventilators that have the capability of ventilating both
neonates and adults have only recently been developed.
2. Versatility of operation: This should include delivery of an accurate fractional inspired
oxygen concentration (FiO2), ability to function in a variety of ventilatory modes, with
a range of ventilatory settings.
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3. Minimal work of breathing: The circuit should provide minimal resistance to
spontaneous and assisted breathing.
4. Monitoring and alarm functions: Continuous monitoring of airway pressures, expired
volumes, cycle timing, apnoea alarms, circuit leaks / occlusions alarms, power failure
and a disconnect alarm are essential features in the modern ventilator. Individual
ventilators will exhibit different alarm features.
5. Humidification / nebulization options.
6. Maintenance and reliability.
The level of ventilatory support needed to achieve the above goals depends upon
the physiological and clinical state of the patient. The method of ventilation is chosen
according to the level of ventilatory support required to maintain a normal PaCO2
and adequate oxygenation.
NONINVASIVE POSITIVE PRESSURE VENTILATION (NIPPV)
Non-invasive positive pressure ventilation involves
the delivery of mechanical ventilation without an
invasive artificial airway (such as endotracheal /
trachesotomy tube). It has been proven to be a
safe and effective way to improve gas
exchange in patients with acute respiratory
failure.
With NIPPV, the patient wears a tightly-fitting
nasal or full facial mask (see photos opposite), which
can be connected to a standard mechanical
ventilator, or, more commonly, to a continuous
positive airway pressure (CPAP) or bi-level airway
pressure unit (BiPap). Use of CPAP & BiPap for
NIPPV will be discussed on the following page.
The nasal mask is usually well tolerated because
it causes less claustrophobia and discomfort,
and permits the patient to eat, drink and
expectorate. On the other hand, a facial mask
is preferable in severe respiratory failure, as
dyspneoic patients mouth-breathe in order to
bypass resistance of the nasal passages – and
mouth-opening during nasal mask ventilation www.aic.cuhk.edu.hk/web8/Nasal%20BiPAP.htm
results in air leakage and decreased effectiveness of the system.
NIPPV aids the patient’s breathing by:
Decreasing the work of breathing
Increasing the tidal volume
Increasing oxygenation
Criteria for selection of patients for NIPPV

Conscious & cooperative patient (COPD patients may be an exception)
No need for urgent endotracheal intubation to protect the airways or to remove copious secretions
No acute facial / head trauma
No recent gastro-oesophageal surgery / bleeding
No pneumothorax
Adequate gag & cough reflexes
Haemodynamic and rhythm stability
Face mask adequately fitted
Table above modified from Antonelli & Conti, 2000, p. 16.
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NIPPV has been successfully used (reduced mortality and morbidity) in a number of conditions,
such as COPD exacerbations, acute cardiogenic pulmonary oedema, hypoxaemic
respiratory failure, and weaning from mechanical ventilation. NIPPV can be applied
continuously or intermittently, allows speech and swallowing, and is generally well
accepted by patients.
The patient needs to be alert and cooperative for initiation of NPPV or mask continuous
CPAP. The patient must be able to synchronize his / her respiratory efforts with those of the
ventilator, although COPD patients with hypercapnoea are the exception – and their level
of alertness generally improves within15-30 minutes of NIPPV. Patients can achieve a
degree of control and independence quite different from when they are intubated, and
sedation is not usually required.
CPAP is indicated for Type I respiratory failure, where CO2 elimination is not an issue,
whereas BiPap is used to augment CO2 removal, as well as for improving oxygenation
(Type II respiratory failure).
BiPAP (Bilevel Positive Airway Pressure) is a form of non-invasive ventilation designed to

increase the patient’s tidal volume while reducing inspiratory effort. This form of
noninvasive ventilation has been used for many years in patients with chronic respiratory
failure due to neuromuscular problems or chest wall abnormalities. Many research studies
have shown that BiPAP reduces the need for endotracheal intubation and may impact
subsequent mortality in patients with COPD.
The BiPap machine is attached to the patient via a breathing circuit (see photo below).
This tubing delivers the inspiratory gas and also allows sensors to detect the patient’s
respiratory effort. An important part of the circuit is the mandatory expiratory valve, which
allows exhaled gases to escape. If this valve becomes blocked for any reason, the high
flow gas being delivered to the patient will have no means of escape – with potentially
disastrous consequences – so you need to make sure that the valve is clear at all times.
BiPap works by providing assistance during inspiration, and by preventing airway closure
during expiration. As the patient breathes in, the machine generates positive pressure, at
a preset level. This positive pressure increases the patient’s tidal volume and minute
ventilation, and therefore, alveolar ventilation. In turn, this results in a decrease the PaCO2,
an improvement in dyspnoea, and a reduction in the use of accessory muscles.
The pressure support stops at the end of inspiration, but a

continuous positive airway pressure (CPAP) is maintained in
the airways. This helps to inflate collapsed alveoli, and to keep
them open, thus increasing the surface area for gaseous
exchange. In summary, BiPap ventilation results in:
Decreased respiratory muscle effort due to assisted inspiration
Increased tidal volumes due to the reduction in inspiratory

effort
Decreased respiratory rate as breathing efficiency increases
Decreased PaCO2 as alveolar ventilation improves.
Increased PaO2 due to the improvement in functional residual

capacity.
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BiPap has three available modes:
Spontaneous, in which the machine will sense and support spontaneous breaths in
patients who have good respiratory drive (similar to pressure support ventilation).
Timed – the machine will provide mandatory breaths at a set rate in patients with
inadequate spontaneous respirations (similar to controlled mandatory ventilation).
Spontaneous / timed – the machine will support spontaneous breaths, but if the patient
does not breathe for a set time, the machine will deliver a mandatory breath (similar to
Simultaneous Intermittent mandatory Ventilation with Pressure Support).
In patients with respiratory failure, a common technique is to begin with the expiratory
level at 5cm H20 and the inspiratory level at 10 to15 cm H20. The levels are adjusted based
on patient comfort, the tidal volume achieved, and blood gas results.
The inspired oxygen concentration should be slightly higher than what the patient was
receiving prior to receiving NIPPV, and should be adjusted to achieve an SaO2 that is
considered suitable for the underlying disease process.
Nursing considerations in the care of patients receiving NIPPV
_________________________________________________________________________________
Remember that dyspnoeic patients are often anxious and agitated as a result of
hypoxaemia. It is absolutely essential that a full explanation of the aims of the
treatment is given, and that the patient is made familiar with the equipment before
therapy is commenced, which may help minimize his / her anxiety, and increase the
likelihood of tolerance of the treatment. Involving patients in the process empowers
them and gives them some control over what is happening to them.
Your explanation should include the ventilator and the noise level associated with the
high-flow gases, the importance of wearing the mask continuously, and the level of
monitoring required throughout.
Correct placement, position and size of the full-face or nasal mask is a key factor in
the success of BiPap ventilation. Before securing the mask, get your patient to hold
the mask over his / her face and ask him / her to breathe with the machine at the
pressures that have been set. If this is successful the mask can then be secured.
The mask is held in position

by straps to ensure a tight
seal. If the mask is fitted
too tightly, pressure
ulceration may occur,
especially over the bridge
of the nose. As well, a too-
tight mask may make the
patient uncomfortable,
while a loose mask will
result in air leakage,
reducing the efficiency of
the system. Be aware that
there is a tendency for the
straps of the headgear to
gradually work loose at
high pressure, resulting in
gas leakage.
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January 2011
Frequent inspection of the mask, straps and nasal bridge should be part of your
nursing assessment. A comfortable mask and tolerable pressure settings are the key
to success – so taking time to get them right is very important.
Skin protection, especially for full-face masks is essential. It is suggested that a
hydrocolloid dressing is used on the bridge of the nose and forehead to prevent
pressure necrosis.
The mask must have a quick-release strap, which the patient must be shown how to
use in case he/she vomits or needs to expectorate.
Close monitoring of vital signs is required, including continuous SaO2 monitoring.
Check with your unit protocol regarding the frequency of assessment, although 15
minutely assessment of level of consciousness, respiratory rate, blood pressure
measurement and continuous ECG monitoring are recommended during the initial
part of the treatment.
Frequent assessment of the abdomen for gastric distension should be carried out, and
a nasogastric tube inserted if needed to release the swallowed air. In this case, the
patient should be nursed with the head of the bed elevated to at least 30˚.
Arterial blood gases (ABGs) should be taken 30 – 60 minutes after commencement of
treatment, and settings adjusted as necessary, followed by further checking of ABGs.
Check that the tubing does not become kinked, and that the mandatory expiratory
valve is not blocked. As well, make sure that the exhaust valve does not open
towards the patient’s face, as the continuous flow of cold air is uncomfortable, and
might cause drying of the eyes and conjunctivitis.
Nutrition: Most patients have no desire to eat during the first few hours of NIPPV, but
when they are ready to do so, they may remove the mask briefly, preferably with
intranasal oxygen supplementation. Alternatively, consider using a nasal mask rather
than a full face mask while the patient is eating. Adequate fluid intake is important to
prevent development of thickened and tenacious secretions. For patients unable to
tolerate oral fluids, regular mouth care and lubrication of the lips is advised.
NIPPV can cause an excess loss of water vapour, leading to thickened secretions, as
well as drying of the nose and mouth. Therefore, humidification of the inspired gas is
recommended.
HOW DO YOU KNOW IF YOUR PATIENT IS RESPONDING TO NIPPV?
This is fairly simple – the patient will look and feel better! As well, ABGs should be used to
assess changes in oxygenation and CO2 clearance.
If your patient is getting progressively more tired, or his / her ABGs are deteriorating despite
optimal settings, then he / she may need endotracheal intubation and mechanical
ventilation. It is essential that you recognize these signs before your patient’s condition
deteriorates significantly.
Criteria for discontinuation of NIPPV & endotracheal intubation

Mask intolerance due to pain, discomfort or claustrophobia
Inability to improve gas exchange and / or dyspnoea
Haemodynamic instability or evidence of cardiac ischaemia or ventricular arrhythmias
Need for urgent endotracheal intubation to manage secretions or protect the airways
Inability to improve mental status, within 30 minutes after the application of NIPPV; in hypercapnoeic, lethargic COPD patients
or agitated hypoxaemic patients.
Table above taken from Antonelli & Conti, 2000, p. 16.
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January 2011
VENTILATION: TYPES / MODES
_________________________________________________________________
Positive pressure ventilation can basically be classified into two groups: volume-targeted or
pressure-targeted. This classification relates to the limit variable, or the target value, which
is set for inspiration.
“The limit variable is the variable that the ventilator maintains at a preset value during
inspiration, but reaching the limit variable does not cause inspiration to end. In volume-
targeted ventilation, the limit variable during inspiration is the preset tidal volume” (Pierce,
2002, p. 56). In pressure-targeted ventilation, the target is pressure, and it is maintained at a
constant preset level throughout inspiration.
Volume and pressure targeted ventilation can be integrated, for instance, as in SIMV + PS,
“in which the mandatory (SIMV) breaths are delivered with a target volume during
inspiration and the patient’s spontaneous breaths are supported with a target pressure”
((Pierce, 2002, p. 56).
The table below (Pierce, 2002, p. 57), shows the variable parameters monitored during
pressure and volume targeted ventilation.
MODE SET PARAMETER VARIABLE PARAMETER MONITORED
Pressure-targeted Peak Inspiratory Pressure Tidal Volume. The volume delivered to the patient varies because it
depends on the compliance ans resistance factors of the patient’s
pulmonary system and the ventilator circuitry.
Volume-targeted Tidal volume Peak Inspiratory Pressure. The amount of pressure required to
deliver the breath depends on the compliance and resistance factors of
the patient-ventilator system.
Volume targeted modes include Continuous Mandatory Ventilation (CMV), Assist-Control

(AC) and Synchronized Intermittent Mandatory ventilation (SIMV). Pressure-targeted
modes include Pressure-Support (PS), Pressure-Control, Pressure Assist-Control, and Airway
Pressure-Release Ventilation (APRV).
Each of these modes will be discussed later in this module. We will now examine in more
detail, both pressure and volume targeted ventilation approaches.
Pressure-targeted ventilation (also called pressure-limited): This type of ventilatory
cycling will deliver a flow of gas, until a certain preset pressure has been reached. At this
time the inspiratory valve closes, the expiratory valve opens, and passive exhalation takes
place.
The flow and volume of gas delivered may change due to:
Alterations in airway resistance
Alterations in resistance from the ventilator circuit
Thus, a specific tidal volume cannot be guaranteed. If the patient’s lung compliance
alters, for whatever reason, the tidal volume will also change. Because this type of
ventilator has a limited pressure capability, the patient who has very high airway pressures
(such as may occur with severe bronchospasm) may not receive an adequate tidal
volume. It is important to monitor expired tidal volumes in this type of ventilator to ensure
that the patient receives an adequate minute ventilation.
Pressure-limited ventilation can be delivered via several ventilation modes, such as
controlled mechanical ventilation (CMV), assist control (AC), and synchronized
intermittent manadatory ventilation (SIMV) – which will be discussed later in this module.
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January 2011
Volume-targeted ventilation (also called volume-limited or volume-cycled ventilation)
delivers a:
set volume of gas
with a variable pressure - determined by resistance, compliance, inspiratory effort
set flow, and an
inspiratory time that is determined by the inspiratory pause (if activated), flow rate,
and tidal volume.
This means that the ventilator will deliver a constant tidal volume, regardless of alterations in
lung compliance and airway resistance. Because pressure is the variable parameter in
volume cycled ventilation it is critical to observe the patient's inspiratory pressures and act
appropriately if they become elevated.
In volume cycled ventilation, airway pressures (peak, mean, plateau) depend on:
the size of the breath delivered to the patient
gas flow rate
the resistance of the endotracheal / tracheostomy tube
the resistance of the upper airways
the patient’s lung compliance, and
inspiratory effort.
By monitoring the peak and plateau pressures in volume cycled ventilation it is possible to
get an estimate of the patient's airway resistance and lung compliance. Peak and
plateau pressures will be discussed on pages 26-28 of this module.
Volume-cycled ventilation can be delivered via several ventilation modes, such as
controlled mechanical ventilation (CMV), assist control (AC), and synchronized
intermittent manadatory ventilation (SIMV) – which will be discussed on the following
pages.
MODES OF VENTILATION:
________________________________________________________________________________
The various techniques used in mechanical ventilation to help patients breathe are called
ventilation modes. Generally, ventilation modes are either controlled or assisted, and the
choice of which mode will depend on the patient’s clinical situation and the goals of
treatment. There are many modes of ventilation available, although not all ventilators
provide each type.
In controlled ventilation, the ventilator initiates all of the breaths and does all the work of
breathing. In assisted ventilation, the patient initiates and terminates some or all of the
breaths, with the ventilator giving various amounts of support throughout the respiratory
cycle. Hence, the modes of ventilation vary in the degree of the patient’s effort versus
ventilator support. (Adapted from Pierce, L., [2000] in Critical Care Nurse, P. 81)
Pressure Control Ventilation (PCV) is actually generally considered a type of ventilation,
rather than a mode, and differs from pressure-targeted ventilation because the rate of
gas flow is variable, while the inspiratory time is set.
“PCV does much more than limit or control pressure; it gives a variable flow at a constant
preset pressure for a fixed set inspiratory time” (Shortall & Oakes, 2005, p.1). The patient is
ventilated to a specific airway pressure, which is not exceeded, even if this leads to low
tidal volumes and hypercarbia (high PaCO2 levels).
20
January 2011
Pressure is the controlled parameter and time is the signal
that ends inspiration, and the delivered tidal volume is
determined by these parameters. The highest flow is
provided at the beginning of inspiration, allowing more time
for pressures to equilibrate. Gas flow slows down as the
pressure rises, and the preset inspiratory pressure is
maintained for the duration of the operator-set inspiratory
time (see diagram opposite, taken from Butcher & Boyle, 2009,
p.110).
PCV results in a more even distribution of ventilation in the lungs, allowing alveoli to
potentially be kept open for the entire inspiratory time, thus optimizing oxygenation. The
resultant tidal volume will depend on airway resistance, chest wall and lung compliance
and the amount of auto-PEEP (see p. 44). The greatest disadvantage of PCV is, as
mentioned above, that the tidal volume cannot be guaranteed – and so it becomes very
important that the low volume alarms are set appropriately by the Respiratory Therapist –
and monitored closely at the bedside by the nurse.
PCV is usually used in either assist/control mode, where every breath, whether machine
initiated or patient initiated, receives the set tidal volume, or SIMV mode, where the
minimum set pressure is delivered at the rate set for mandatory machine-delivered
breaths. These ventilatory modes will be discussed in more detail on pages 22-25 of this
module.
Controlled Mandatory Ventilation (CMV) involves delivery of a set respiratory rate and tidal
volume. CMV does not require any patient effort. The patient does not initiate any
breaths, and any effort to do so will result in competition between the ventilator and the
patient. CMV is the most basic pattern of positive-pressure ventilation. It provides full
ventilatory support in situations where there is a complete lack of patient-initiated breaths
(such as total neuromuscular blockade, during anaesthesia, etc.).
In this type of ventilation, the operator must select a suitable tidal volume (around 6 -
8ml/kg), to a predetermined pressure, volume or time limit, an inspired oxygen
concentration, and a ventilation rate sufficient to maintain blood gases within the desired
limit. Subsequent adjustments to ventilation may be made dependent upon serial blood
gas analysis. Also, PEEP may be added if considered necessary, to augment oxygenation
(please refer to section on PEEP later in this Module). Patients receiving this type of
ventilatory support should be sedated and possibly muscle-relaxed, to suppress their
respiratory drive. This avoids potential ventilator-patient competition and minimizes possible
patient distress. For example if the patient is on a rate of 10, then he/she will receive a
breath every 6 seconds, regardless of his/her inspiratory effort (see diagram below, from
Butcher & Boyle, 1997, p.43). In this mode there are no spontaneous or assisted breaths.
21
January 2011
A WORD ABOUT TIDAL VOLUME…
The most suitable initial tidal volume selected depends on many factors, particularly the
disease for which the patient needs mechanical ventilation. Studies have shown that tidal
volumes of ≤ 6mL per kg of ideal body weight (IBW) improved mortality in patients with
acute lung injury (ALI) or acute respiratory distress syndrome (ARDS), although the optimal
TV for patients who are mechanically ventilated for reasons other than ALI/ARDS is
unknown.
Assist Control Ventilation is available in both pressure control and volume cycled
ventilation.
In this form of ventilation a fixed number of breaths, with a set tidal volume or time limit, will
be delivered to the patient whether he/she is breathing spontaneously or not. If the
patient makes any inspiratory effort above this preset number of breaths, he/she will
receive extra breaths with that same fixed pressure or volume. i.e., all breaths will either be
controlled (ventilator initiated) or assisted (patient initiated) with the same tidal volume
(eg 500mls in volume cycled) or pressure limit and inspiratory time (eg. 30 cmsH2O, 1.2
seconds in pressure controlled ventilation).
For example, the ventilator is set to deliver 20 breaths per minute, at a tidal
volume of 500mL, so the lowest possible minute ventilation is 10L/minute (20
breaths per minute times 500mL per breath). If the patient then takes an
additional 5 breaths above the 20/minute delivered by the ventilator, the
ventilator will deliver 500mL for each patient-triggered breath, and the minute
ventilation will then rise to 12.5L/minute (25 breaths per minute time 500mL per
breath).
The triggering mechanism for the assisted mechanical breath is set to a sensitivity level that
is similar to the patient’s own inspiratory effort, to make it as easy as possible for the patient
to trigger the ventilator. An appropriate tidal volume for assisted breaths, and a backup
rate of controlled breaths must also be set to guarantee a minimum minute ventilation.
PEEP may also be added to facilitate oxygen delivery.
This mode allows the patient to exercise his / her respiratory muscles to trigger each
inspiration, with the ventilator performing the majority of the work of breathing. Increasing
or maintaining strength of the respiratory muscles is essential if the patient to be weaned
from mechanical ventilation.
http://img.medscape.com/pi/emed/ckb/clinical_procedures/295571-1347017-304068-1544011.jpg
Synchronized Intermittent Mandatory Ventilation (SIMV) is a commonly used mode of

ventilation, in which each mechanical breath is synchronized with spontaneous efforts to
reduce the likelihood of breath stacking. This mode is often used for weaning the patient
from mechanical ventilation. Ventilatory support in the SIMV mode can range from full
support (the set respiratory rate is high enough that the patient does not over-breathe) to
no ventilatory support (the set respiratory rate is zero).
22
January 2011
Theoretically (although not actually proven in clinical trials), SIMV mode provides “resting
breaths”, and the patient hardly needs to alter his / her inspiratory effort throughout the
cycle. In fact, however, the patient’s work of breathing may actually increase during
spontaneous breaths, due to the increased resistance provided by the endotracheal tube,
ventilator tubing, humidifier, and the ventilator demand valve. This added work of
breathing may be counteracted to a degree by the addition of a low level of inspiratory
Pressure Support (see section below).
Diagram above, showing ventilator pressure waveforms from www.medscape.com
Pressure-Support Ventilation (PSV) is a spontaneous mode of assisted mechanical

ventilation in which each breath is initiated and determined by the patient’s respiratory
drive – the patient must trigger each breath as there is no set respiratory rate. Pressure
support only applies to spontaneous breaths. The ventilator gives a "boost" to the patient
by providing a small amount of inspiratory pressure - usually about 5 to 10 cm H20. This low
level of inspiratory pressure contrasts with the much higher inspiratory pressures seen during
CMV or ACV modes of ventilation.
Pressure support has a:

set pressure (pressure support added to the CPAP/PEEP)
variable volume - determined by the resistance, compliance, inspiratory effort and
level of pressure support
variable flow rate determined by the resistance, compliance, inspiratory effort and
level of pressure support
variable inspiratory time
is cycled off when the patient's inspiratory flow declines to a value determined by
the manufacturer of the ventilator.
As a flow-cycled mode, the patient has considerable control over the depth and duration
of the inspiratory phase, and each of his / her inspiratory efforts is assisted by a preset level
of pressure generated by the ventilator. The patient’s tidal volume is determined by the
sum of the patient’s inspiratory effort and the ventilator’s inspiratory pressure.
Pressure support usually reduces the inspiratory work of each breath and increases the tidal
volume, thereby improving the overall efficiency of spontaneous breathing. PSV can also
compensate for the additional work of breathing imposed by the endotracheal tube,
ventilator tubing, and ventilator demand valve. As the patient’s respiratory compliance
improves, and the respiratory muscles strengthen, the level of pressure support can be
gradually decreased, allowing a subsequent increase in the patient’s total work of
breathing.
The commencement level of PSV should be determined by clinical observation of the
patient’s breathing pattern after setting an empiric starting level (for example, 15cm. H2O).
A tidal volume of 8 to 10ml/kg, a respiratory rate of around 25 per minute, and the patient’s
comfort are the usual objectives of PSV. Because PSV is a spontaneous mode of
ventilation, there is no preset guaranteed tidal volume or backup respiratory rate.
Therefore, the patient must have an adequate respiratory rate and must be capable of a
23
January 2011
suitable inspiratory effort. Therefore, ventilator alarms need to be appropriately set and
carefully monitored, and the overall clinical condition of the patient closely observed.
The inspiratory pressures in the pressure supported breath are set by the operator. The
peak pressure is determined by the addition of the level of pressure support to the level of
CPAP/PEEP, ie peak pressure = pressure support + CPAP/PEEP. There is no plateau
pressure in pressure supported breaths as it is impossible to achieve an inspiratory pause.
As mentioned previously, PSV may be used as a method of assisting the spontaneous
breaths in the SIMV mode. The ventilator delivers the set respiratory rate using SIMV, but
the patient-initiated breaths beyond the set respiratory rate are delivered using PSV.
The purpose for adding PSV to patient-initiated breaths is to overcome the increased work
of breathing due to the resistance of the endotracheal tube and the ventilator circuit. It is
important to be aware that the smaller the endotracheal tube, the greater the resistance:
for example, with small endotracheal tubes (e.g. < 7mm.), a pressure-support level of ≥
10cm H2O may be needed to overcome the resistance.
The disadvantages of PSV are that:

every breath must be patient-initiated. Apnoea may occur if the respiratory drive is
depressed secondary to sedatives, critical illness, or hypocapnoea due to excessive
ventilation.
an adequate minute ventilation cannot be guaranteed because both tidal volume
and respiratory rate are variable.
PSV has been shown to upset patient sleep patterns more than AC.
relatively high levels of pressure support (e.g. >20 cm H2O) are necessary during full
ventilator support to prevent alveolar collapse and subsequent atelectasis and
ventilator-associated lung injury, and to ensure a stable breathing pattern. These
high levels of support are not very comfortable for the patient. PSV thus is
considered unsuitable if the patient requires full ventilatory support.
High Frequency Ventilation (HFV): In this type of ventilation, relatively small tidal volumes (1
to 3 ml/kg) are administered at very high respiratory rates (100 to 300 per minute).
Ventilation and oxygenation are achieved by gas diffusion and convection rather than
bulk gas flow, as occurs in conventional ventilation.
Delivery of gas at these high frequencies is almost impossible for conventional ventilators,
and consequently a system using jets or oscillators has been developed. The goal of HFV is
to achieve oxygenation and ventilation at relatively low peak airway pressures, thus
minimizing trauma secondary to high inspiratory pressures and volumes.
For many years, HFV was predominantly used for infants and children with acute lung injury
(ALI), but in more recent times, HFOV has been utilized in adult patients at risk of lung
trauma due to high airway pressures and volumes. Patients with Acute Respiratory Distress
Syndrome (ARDS), who have either decreased lung compliance and / or increased lung
resistance may benefit from HFOV.
There are three types of HFV:
i. High Frequency Positive Pressure Ventilation (HFPPV) most closely resembles conventional
ventilation. Flow is delivered through a pneumatic valve at the airway opening, and
exhalation occurs due to passive recoil of the lung. Respiratory rates of 60-100/minute,
inspiratory times of 20% - 33%, and tidal volumes of 3-6 ml/kg are usually used. This form
of HFV is least commonly used clinically – and generally for anaesthesia.
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January 2011
ii. High Frequency Jet Ventilation (HFJV) generally utilizes a high pressure gas source
connected to a small cannula built into the wall of an endotracheal tube. Respiratory
rates of up to 360 / minute, with variable inspiratory times, and tidal volumes of 200-
400ml. are used. Use of this form of HFV is limited clinically by the need for specialized
endotracheal tubes, as well as by the increased risk of tracheal injury. It is generally used
for anaesthesia and in some ICU situations.
iii. High Frequency Oscillation

Ventilation (HFOV) utilizes a high
frequency pulse generator to
create oscillations during both
inspiration and expiration at rates
of 900-3000 per minute, with
exceptionally small tidal volumes
of 50-150ml.
ccforum.com/content/figures/cc4968-2.gif
HFOV has been associated with a decreased incidence of secondary chronic lung
disease in pre-term infants with hyaline membrane disease, compared with conventional
ventilation techniques. In the adult population, HFOV is used to minimize ventilator-
related lung injuries in ALI / ARDS, and it is thought that the earlier it is commenced the
better the outcome.
“HFOV provides small tidal volumes (not really a tidal volume but an Amplitude, usually
referred to as Delta P:P), usually equal to, or less than, the dead space; 150 millilitres, at a
very fast rate (Hertz-Hz) of between 4 – 5 breaths per second. The delivery of tidal
volumes of dead space or less at very high frequencies enables the maintenance of a
minute volume. Lungs are kept open to a constant airway pressure via a mean pressure
adjust system. Further, HFOV allows for the decoupling of oxygenation from ventilation: it
allows the clinician to separately adjust either oxygenation or ventilation” (Higginson, 2003,
p. 6).
The mean airway pressure can be adjusted, keeping the lungs and alveoli open at a
constant pressure, which avoids the cycle of lung expansion and collapse which has
been shown to damage alveoli and to further complicate lung disease. It is thought that
HFOV may also facilitate gas mixing and improve ventilation / perfusion (V/Q) matching.
NURSING CONSIDERATIONS IN THE CARE OF PATIENTS ON HFOV
There are a number of important nursing considerations in the care of patients receiving
HFOV:
Patients on HFOV must have 1:1 nursing care.
Patient bed placement in the ICU is a consideration, as HFOV is noisy and may disturb
other critically ill patients.
The appearance of the patient being ‘oscillated” can be disturbing to family, so make
sure that they receive adequate explanation regarding their loved one’s situation.
Only gentle turning is recommended – with the Respiratory Therapist on hand to assist
with monitoring the oscillator.
Head movement may cause the HFOV to alarm and stop, so be very careful when
repositioning the patient’s head.
Head elevation of 30˚ is recommended.
Observation of the patient for equal and continuous chest vibrations (known as chest
‘wiggle’) should be performed upon commencement of HFOV, after re-positioning the
patient, and as per unit protocol thereafter. Chest wiggle should be present from
25
January 2011
clavicular region to mid-thigh bilaterally. If chest wiggle decreases, it may indicate that
the ETT has moved or is obstructed. Unilateral chest wiggle may indicate that the
patient has developed a pneumothorax.
Because of the movement of gases throughout the lung-fields is different during HFOV,
lung auscultation is almost impossible to interpret. As well, heart and bowel sounds will
not be able to be heard over the noise of the HFOV.
Ideally, the patient should have his / her airway thoroughly suctioned prior to
commencement of HFOV, and further suctioning is regarded as unnecessary,
particularly for the first 12 – 24 hours, to encourage lung recruitment. Closed system
suction should be utilized to prevent potential de-recruitment of lung volumes.
Endotracheal tube position should be regularly checked.
A small intentional ETT cuff leak will be present to assist with ventilation (CO2 elimination)
during HFOV. It is essential to monitor mean airway pressure to ensure it is maintained.
Invasive line placement should occur prior to initiation of HFOV as the body vibrations
caused may make placement difficult and potentially dangerous.
The patient should be well sedated – and may need muscle relaxants as well.
Obtain both CXR and arterial blood gases within the first hour of commencement of
HFOV, and thereafter as indicated by patient clinical condition.
Humidification of gases before they reach the patient is essential to prevent
Necrotizing Tracheo-bronchitis.
Ensure the patient has an adequate circulating volume prior to commencement of
HFOV so that blood pressure is maintained. It is recommended that CVP is measured
prior to commencement, as waveform interpretation can be difficult during HFOV.
It is recommended to use personal protective equipment (PPE) - face shield – when
within one metre of the patient on HFOV.
VENTILATOR GAUGES / ALARMS

_________________________________________________________________________________
Modern ventilators may have gauges, digital readouts, or LCD graphics, to monitor various
ventilator functions, and / or to advise the clinician when certain preset limits have been
reached.
The Peak Inspiratory Airway Pressure (PIP) gauge shows the highest level of airway
pressure (in cm H2O) reached on inspiration. Patient initiation of a breath (in the absence
of PEEP and CPAP) will be shown as a brief negative pressure reading at the onset of
inspiration.
The PIP is the maximum pressure achieved during the inspiratory part of the cycle, usually
at or near the end of inspiration. It represents the total pressure needed to push a volume
of gas into the lung and is composed of pressures resulting from inspiratory flow resistance
(resistive pressure), the elastic recoil of the lung and chest wall (elastic pressure), and the
alveolar pressure present at the beginning of the breath (positive end-expiratory pressure
[PEEP] (Please refer to the diagram on the following page).
Increased PIP usually reflects increased airway resistance, secondary to narrowed airways
due to bronchospasm or secretions, or to kinking of the endotracheal tube, or decreased
airway compliance (e.g. stiff lungs, such as seen in ARDS or pulmonary oedema, tension
pneumothorax, or stiff chest wall due to chest wall deformities). Increased PIP may also
occur when high inspiratory flow rates are used.
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January 2011
Plateau pressure: If volume is kept constant at the
end of inspiratory flow, the peak inspiratory
pressure will fall to a pressure level called the
plateau pressure. The plateau pressure reflects
lung and chest wall compliance. It is measured
during an inspiratory pause on the ventilator.
Without lung disease, the peak inspiratory pressure
(PIP) is only slightly above the plateau pressure,
whereas in cases of increased tidal volume or
decreased pulmonary compliance, the PIP and
plateau pressure rise together proportionately.
Diagram above shows the components of airway
The plateau pressure is the pressure when there is pressure. Downloaded from
no flow within the circuit and patient airways, and http://www.merck.com/mmpe/sec06/ch065/ch06
so it most closely represents the alveolar pressure.
Therefore, plateau pressure is very important to
monitor, as ideally, the pressure that the alveoli are
subjected to should be limited, to prevent
extrapulmonary air (e.g. pneumothorax) and acute
lung injury (Butcher & Boyle, 2009, p. 83). To prevent
barotrauma, i.e., lung injury secondary to over-
distension of alveoli, the goal plateau pressure should
be <30 cm H2O.
If the peak pressure rises with no change in the
plateau pressure, either increased airway resistance or
high inspiratory gas flow rates should be suspected.
A large difference between the peak and plateau pressures indicates an increased
airway resistance, whereas an elevated plateau pressure indicates a decreased
pulmonary compliance.
NB: it is possible to have both an increased resistance and decreased compliance, in which case there may be a
large difference between the peak and the plateau pressures as well as elevated plateau pressures.
Resistive pressure is the product of circuit resistance and airflow. In the mechanically
ventilated patient, resistance to airflow occurs in the ventilator circuit, the endotracheal
tube, and, most importantly, in the patient's airways.
A high pressure alarm, usually set about 10 to 20cm H2O above the peak inspiratory
pressure, will sound whenever this pressure level is reached or exceeded. Airway pressures
may increase due to worsening lung compliance, occlusion of any part of the ventilator
circuit (e.g., kinking of the tubing or water condensation), endotracheal tube obstruction,
or the patient developing a cough, hiccoughs, increased lung secretions or
bronchospasm.
A low pressure alarm is usually set at a point below the patient’s peak inspiratory pressure,
and will sound if the preset low-pressure level is not reached. Failure to reach the preset
lower pressure limit may be due to improved lung compliance, hypoventilation, or, more
commonly, an airway leak, which may occur at certain points throughout the ventilator
circuit.
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January 2011
Loss of Power Alarms: These may be triggered when the power source (electricity, battery
or gas) fails. Should this occur, your first response must be to disconnect the patient from
the ventilator, and manually ventilate him / her via a bag/valve device until the problem
has been resolved.
The Sensitivity dial determines the amount of patient effort required to initiate an assisted
breath.
The lower the number, the easier it is for the patient to initiate inspiration. If the sensitivity is
set too high, the ventilator may inappropriately self-cycle. If it is set too low, the increased
work of breathing may make it difficult for the patient to achieve a satisfactory minute
ventilation.
The Inspiratory Flow Rate is the volume of gas flow from
the ventilator in the inspiratory phase, and may be
adjusted to meet certain clinical requirements. The
usual inspiratory flow rate is roughly 40 to 60 litres per
minute. When adjusting the flow rate, the most
important factor to consider is the relationship of flow
to inspiratory time. The higher the flow rate, the shorter
the inspiratory time, and vice versa. Remember also
that the higher the inspiratory flow rate, the greater
the peak inspiratory pressure will be, whereas a lower
inspiratory flow will result in a lower peak inspiratory
pressure.
The Inspiratory / expiratory ratio (I:E Ratio): During
normal respiration the expiratory phase (expiration plus
the pause between breaths) is approximately twice as
long as the inspiratory phase, to allow optimal passive
emptying of the lungs.
This provides an I:E ratio of 1:2. Ventilators can be programmed to maintain this ratio by
controlling the flow of gas being pushed into the lungs during inspiration.
In certain clinical conditions, (e.g. C.O.P.D.), a greater expiratory time may be needed to
achieve optimal alveolar emptying on expiration to prevent gas trapping. I:E ratios of up
to 1:3 to 1:5 may be needed. On occasion, in the critically ill patient, the I:E ratio may
even be inversed, which is termed inverse ratio ventilation (IRV).
Work of breathing
Work of breathing (WOB) is accomplished during inspiration in three phases: the energy
required to expand the lungs against its elastic forces (lung compliance work), that required
to overcome the viscosity of the lung and chest wall structures (tissue resistance work), and
that required to overcome airway resistance during the movement of air into the lungs
(airway resistance work).
Work of breathing does not refer to expiration, which is entirely a passive process caused by
elastic recoil of the lung and chest cage. WOB accounts for 5% of total body oxygen
consumption in a normal resting state, but can increase dramatically during acute illness.
Factors that increase the work of breathing:
Increased tidal volume – increases work needed to overcome elastic resistance
Increased respiratory rate – increases work needed to overcome airflow resistance
Reduced lung compliance (stiff lungs):
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January 2011
o Restrictive lung disease (pulmonary fibrosis). With stiff lungs patients tend to take
rapid small breaths, to minimize the elastic workload. Decreased compliance is
seen with pulmonary oedema, haemorrhage or contusions.
Increased airway resistance:
o Obstructive lung disease. With high airway resistance patients take large slow
breaths. Increased airway resistance is seen with bronchoconstriction such as
asthma, emphysema and airway collapse.
Troubleshooting Ventilator Alarms
When a ventilator alarm sounds, your primary concern is to maintain the patient’s respiratory
status. Therefore, both the first and last thing you should do when you respond to a
ventilator alarm is to assess the patient. In between, here’s what to do to troubleshoot some
of the common problems that can cause an alarm to sound.
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January 2011
End-Tidal CO2 Monitoring (EtCO2)
End-tidal CO2 (EtCO2) monitoring (Capnography) is a non-invasive method of measuring
exhaled Carbon Dioxide levels in intubated and non-intubated patients.
EtCO2 is the partial pressure of carbon dioxide
(CO2) at the end of exhalation, and is
expressed as a percentage of CO2 or mmHg.
Normal values are 5% to 6% of CO2 – which

equates to 35 – 45mmHg. CO2 provides a
reflection of cardiac output and pulmonary
blood flow, as gas is transported by the
venous system to the right side of the heart
and then pumped to the lungs by the right
ventricle.
Diagram above from St. John, 2003, p. 84.
When CO2 diffuses out of the lungs into the exhaled air, a device called a capnometer
measures its partial pressure at the end of expiration (Hudson, 2009).
Why monitor EtCO2?
Because excretion of CO2 is the final common pathway of metabolism, it provides a useful
global indication that all is well. It indicates:
That patient ventilation is sufficient to inhale oxygen into the lungs.
That oxygen is being transported to the tissues to support metabolic processes.
That aerobic metabolism is then utilizing the oxygen and producing carbon dioxide.
That ventilation is sufficient to produce a level of CO2 in the exhaled air.
EtCO2 is considered a better tool than pulse oximetry to evaluate the patient’s ventilation
status as it provides breath-to-breath information, whereas there is a slight delay before
oximetry reflects hypoxaemia. The higher the metabolic rate, the more CO2 will be
produced. An increasing EtCO2 may help warn of development of such dangerous hyper-
metabolic conditions as malignant hyperthermia, severe sepsis or thyrotoxicosis. It is also a
useful indicator that the endotracheal tube is in the lungs.
intensivecare.hsnet.nsw.gov.au/five/.../EtCO2_Marquette_V_am_stgeorge.pdf
Above: Hypoventilation Above: Hyperventilation Bronchospasm

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January 2011
NURSING CONSIDERATIONS FOR CARE OF THE VENTILATED PATIENT
_________________________________________________________________________________
Providing the best possible care for a seriously ill ventilated patient can be a Critical Care
nurse’s greatest challenge, but it may also provide the greatest satisfaction and rewards.
You, as the bedside nurse, are the one member of the multidisciplinary health care team
who is with the patient for long periods of time, and so you are responsible for regulating
and coordinating care for a patient who is totally dependant (both physically and
emotionally) upon health care personnel.
To do this effectively, you must have a solid understanding of the physiologic processes
involved in ventilation, and must be competent in the monitoring of clinical parameters in
order to promptly detect complications. You must be skilled in care of the artificial airway,
and be capable of prompt intervention if problems arise.
An outline of the main nursing care considerations follows.
a. Maintenance of airway:
The major things considered necessary to provide a safe level of care for the patient
with an endotracheal/tracheostomy tube may be categorized under the following
headings:
Securing the tube - Part of your nursing assessment should include ensuring that the
tube (ETT or tracheostomy) is securely attached to the patient. There are a number
of ways to safely secure tubes - check your unit protocol to establish which method is
being used in your unit.
Cuff management - The main function of the ET /
tracheostomy tube cuff is to ensure a proper seal
between the patient’s trachea and the cuff itself
(see diagram opposite). This will ensure that there is
minimal leakage around it during positive
pressure ventilation. Another important function
of the cuff is to centre the tube correctly in the
trachea, and to inflate evenly so that the tip of
the tube is unlikely to damage the tracheal
mucosa.
Cuff pressure should be high enough to seal the
trachea to prevent aspiration of oropharyngeal
secretions and to avoid gas leak.
http://img.tfd.com/dorland/tube_orotracheal.jpg
At the same time, it must be low enough to allow adequate perfusion of the tracheal
mucosa. Excessive cuff pressure has been associated with post-extubation pain,
tissue necrosis and/or rupture, bleeding, and trans-oesophageal fistula development.
Pressure-limiting valves are a feature on the proximal end of the inflation tube, and
they generally act as a reservoir for excessive pressure within the cuff, to keep the
pressure within a preset range – usually around 25cm H2O.
While a cuff pressure of about 20 cm H2O is generally sufficient to seal the trachea,
the recommendation for maximum cuff pressure using traditional PVC cuffed ET
tubes is between 25 – 35 cm H2O in adults.
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January 2011
However, because the volume needed to achieve a
cuff pressure of 20 to 30 cm H2O varies significantly
between patients, regardless of both tube and patient
size, actual measurement of pressures is essential.
The anaeroid manometer (see opposite) is the most
commonly used device for monitoring cuff pressure.
When first inflating the cuff, it is recommended to use
a maximum of 10mL, and then measure the cuff
pressure. Pressures should be checked post tube
insertion and at least every 8 hours (check with your unit
Policy re this).
Suctioning of secretions:
The intubated patient has an ineffective cough reflex due to the interference of the
tube with glottic closure, and so he / she will require assistance to clear lung
secretions. Endotracheal suctioning is not without significant risks, and the critical
care nurse must be aware of possible complications in order to take the necessary
precautions to ensure patient safety.
Aspiration of secretions should be performed only when secretions are present and
never as a routine procedure, as unnecessary suctioning may cause tracheal
irritation and increase the risk of infection. Frequent suctioning is associated with
complications such as hypoxaemia, cardiac arrhythmias, and elevated mean
arterial and intracranial pressures.
Clinical indications for endotracheal suctioning include:
i. secretions in the endotracheal / tracheostomy tube;
ii. frequent or sustained coughing;
iii. adventitious breath sounds on lung auscultation;
iv. desaturation related to airway secretions;
v. increased peak airway pressures;
vi. sudden onset of respiratory distress whenever airway patency is questioned.
Clinical contra-indications for suctioning include:

i. Raised intracranial pressure
ii. Bleeding disorders
iii. bronchospasm
Pre-oxygenation, with or without hyper-inflation, before and after suctioning is
indicated to decrease the occurrence of arterial desaturation associated with
suctioning. This may be achieved either by use of a manual resuscitation bag with
supplemental oxygen, or via the ventilator by increasing the inspired oxygen
concentration to 100% for 30 – 60 seconds before and for at least one minute after
suctioning. An increase in oxygenation to 10% above baseline is recommended in
neonates.
Research has failed to demonstrate any significant reduction in the incidence of
ventilator-associated pneumonia (VAP), mortality, or length of ICU stay with use of
closed-system suctioning versus open systems, although closed systems are reported
to minimize the incidence of hypoxaemia and contamination while maintaining
PEEP. Closed suction systems are indicated in patients such as neonates, who are
considered to be at higher risk for desaturation, and also for patients requiring high
FiO2 and PEEP (e.g. patients with Acute Lung Injury).
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January 2011
The suction catheter should be soft and have an external diameter no greater than
one half of the internal diameter of the endotracheal or tracheostomy tube (adults)
and less than 70% of tube lumen in neonates. In most adult patients, a 14 or 16
French gauge catheter is generally adequate. Larger catheters may cause a high
degree of negative intrapulmonary pressure, which in turn may produce dramatic
deterioration in both cardiac and pulmonary performance.
Current recommendations for the amount of suction pressure that should be applied
are less than 150mmHg in adults, and between 80 – 100mmHg in neonates. Higher
pressures have been associated with tracheal damage.
There are two schools of thought regarding how deep to insert the suction catheter.
The “deep” suctioning technique recommends that the suction catheter is inserted
to the depth of the carina and then withdrawn by 1cm before commencing
suctioning. The “shallow” technique involves insertion of the catheter to a
predetermined length – usually the length of the artificial airway plus the adaptor.
Prolonged contact with the carina can cause mucosal ulceration, and may induce
haemodynamic changes secondary to stimulation of coughing and vagal
responses, so it is essential that you monitor your patient’s cardiovascular and
respiratory status throughout the suctioning procedure.
The number of passes of the catheter in a single suctioning episode should be limited
to three or less to minimize occurrence of complications. The duration of suctioning
should be limited to less than 15 seconds (AARC Guidelines 2010).
The application of suction during suction catheter withdrawal may be with either a
continuous or intermittent technique – but remember that both techniques are
capable of damaging the tracheal mucosa.
The Centre for Disease Control in the United States recommends that Standard
Precautions are followed. Sterile technique is recommended to prevent airway
contamination. Remember to suction the oropharynx as well to remove potentially
infected secretions.
Instillation of normal saline into the trachea has long been used to aid in the
removal of secretions, but is a controversial intervention in view of the fact that
mucus does not actually readily mix with saline. Current thought is that instillation of
saline produces a lavage rather than a dilutional and thinning effect upon
secretions. Also, it has been associated with decreases in oxygen saturation and
may contribute to airway contamination secondary to bacterial contamination. For
these reasons, instillation of saline is not recommended as a routine measure.
Humidification – During mechanical ventilation with an artificial airway in place, the
normal “air-conditioning” functions of the upper airway are bypassed. To ensure
that the water content and temperature of the inspired gas reaching the airways is
adequate, some form of humidification is essential. Humidification of inspired gases
will prevent hypothermia, thickening of airway secretions, destruction of airway
epithelium, and atelectasis. Humidification may be accomplished using either a
heated humidifier or a heat and moisture exchanger (HME). (HMEs are also known as
hygroscopic condenser humidifiers, or artificial noses).
Heated humidifiers operate actively to increase the heat and water vapor content
of inspired gas, while HMEs operate passively by storing heat and moisture from the
patient's exhaled gas and releasing it to the inhaled gas.
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January 2011
HMEs contain a fibrous insert that repels water and traps heat and moisture on the
patient side of the insert. They are cheaper and easier to use than heated
humidifiers, but are considered more suitable for short-term ventilation (48 to 72
hours) only, as several clinical studies have found an increased incidence of tracheal
tube obstruction, caused by thickened secretions, thought to be related to
inadequate humidification.
As well, because HMEs are placed between the ETT and the ventilator Y-piece, they
can affect ventilation. Firstly, they may increase resistance to gas flow, increasing
the work of breathing and making them a potential obstacle for the difficult-to-wean
patient. Secondly, HMEs increase the amount of dead space considerably, which
has implications to patients with very small tidal volumes.
Heated humidifiers work by heating a large surface area of water in a reservoir and
passing a large volume of gas over it. Water vapour is produced by heating the
reservoir water, and the chamber outlet temperature is regulated by the chamber
control, resulting in fully saturated gas. The temeprature and humidity of the gas are
maintained within the breathing circuit by a heated wire, thus preventing formation
of condensation.
It is important to be aware that water collecting in the tubing can be a source of
nosocomial infection, as well as increasing the work of breathing. Additionally,
accidental lavage of the patient’s airway could occur if the water in the tubing ends
up in the patient’s airway. For these reasons any water collecting in patient circuit
must be drained – but not back into the reservoir, as it is contaminated.
The inspired gas temperature should not exceed 37˚C.
b. Physiologic Observations:
Close monitoring of the clinical condition of the ventilated patient is essential. A thorough
assessment includes:
i. evaluation of neurological status, including level of consciousness, mental status, level
of anxiety, presence of pain, and the patient’s ability to communicate non-verbally;
ii. vital signs (heart rate, blood pressure, peripheral perfusion, temperature) should be
taken and recorded as frequently as the patient’s condition mandates. This may
mean every 5 minutes, or hourly, according to your Unit policy. Haemodynamic
waveforms (eg. ECG / arterial pressure / pulmonary artery pressures) should be
continuously monitored, and documented according to Unit policy;
iii. respiratory status evaluation includes respiratory rate and effort, use of accessory
muscles, lung auscultation, assessment of airway patency, ventilator settings, and
nature and quantity of aspirated sputum. Cuff inflation pressure should be checked
routinely (check your Unit policy). Precise values vary from patient to patient, and
may also change depending upon the type of cuff pressure measurement utilized
(i.e., minimum leak technique vs. minimal occlusion volume technique). Peripheral
haemoglobin saturation (SaO2) should be continuously monitored, and arterial blood
gas sampling and analysis should be attempted as frequently as the patient’s clinical
condition demands (for example, 15-30 minutes after changes to ventilator settings).
iv. renal function assessment involves accurate measurement of intake and output, daily
weight, and examination of electrolyte status as dictated by the patient’s condition;
v. gastrointestinal status includes evaluation of nutritional state, including assessing the
patency of the gastric / feeding tube, and the patient’s tolerance of enteral feeds.
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January 2011
Abdominal girth measurement, auscultation of bowel sounds, and monitoring of
bowel movements should also be detailed, according to Unit policy;
vi. monitoring of all ventilatory settings, according to Unit policy;
vii. laboratory studies, such as haematology profile and blood chemistry, should be
monitored at least daily;
viii.
A Chest X-Ray should be taken at least CARINA
daily, (more frequently if patient condition
ETT Tip
changes dramatically).
ETT and tracheostomy tubes have a radio-

opaque line running their length – so that
they can be easily seen on CXR.
Assessment of the CXR should include the

location of the ETT tip (should be just
above (between 3 to 7cm) the carina – see x-
ray opposite), and the overall lung
condition, including assessment for
pneumothorax.
c. Adequate body repositioning:
Frequent repositioning of the dependent patient is one of the most important but often
neglected measures for both prevention and treatment of respiratory problems.
Maintenance of the same body position for long periods results in poor distribution of
alveolar ventilation, and may lead to atelectasis and development of pneumonia. It is
also very uncomfortable for the patient to remain in the same position for long periods
of time. Ventilation and perfusion can both be preferentially delivered to particular
lung segments via positioning maneuvers that promote drainage of some segments
and ventilation of others.
Research has shown that the semi-recumbent position for ventilated patients, with the
head of the bed elevated between 30˚ - 45˚ reduces the incidence of ventilator-
acquired pneumonia (VAP). Patient positioning should take into account
haemodynamic stability and the underlying lung pathology, as positioning can assist in
matching ventilation to perfusion, given that blood flow is gravity-dependant.
Placing the patient in a sitting position, where tolerated, aids gravity drainage of the
upper lobes, decreases the pressure of abdominal contents on the diaphragm, and
allows the patient better visual orientation to his / her surroundings. Regardless of
patient position, it is important that he / she be as comfortable as possible. This may be
achieved by using pillows for support and ensuring that limbs are in correct alignment.
This is especially important for patients who have received muscle-relaxant drugs.
It is generally accepted that patients should be turned every 2 – 4 hours, and nursed on
a pressure-relieving mattress where possible, although there are no actual studies to
confirm this practice.
d. Exercise:
Exercise is crucial to maintain muscle strength and tone as well as joint mobility. Passive
or active range-of-motion exercises should be attended on a routine basis, as
indicated by the Unit physiotherapist.
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January 2011
e. Psychological Aspects:
Any type of illness limits the ability of the patient to adapt to his /her surroundings, and
a person who finds himself dependant will respond in characteristic ways. Early
researchers defined four specific psychological features which occur secondary to
dependency and which may be easily related to the majority of Intensive Care
patients:
i. The patient becomes self-centred, and perceives all events in relation to
himself and his own benefit. (The reality may actually be quite different). He
does not appear to understand why his immediate concerns and
requirements are not being met.
ii. His interest is limited and he focuses on the present moment only.
iii. His emotional dependence on those around him is overriding and he
interprets their behaviour in terms of rejection or acceptance of him.
iv. Bodily function is his main preoccupation.
It is important that you, as the bedside nurse, understand the emotional and
psychological implications of total dependency in order to successfully meet your
patient’s needs. Sensory overload and sleep deprivation contribute to the patient’s
sense of anxiety and isolation, and may lead to patient-ventilator dyssynchrony (further
discussed on p.43 of this module).
Effective two-way communication is essential. The ventilated patient is unable to

communicate verbally, and thus may be frustrated or frightened. His / her frustration
may present as uncooperative or antagonistic behaviour or as total listlessness and
apathy.
If the patient is able, provide him / her with a clipboard, paper and pencil, so that he /
she can write. Sometimes you may be able to understand a patient’s wishes by asking
him / her specific questions that require a simple “yes” or “no” answer – nodding or
shaking the head suffices.
If you do not speak the same language as your patient, request translator assistance to
make a set of bilingual cards with commonly used phrases. This will allow you to
continue to communicate with the patient if the translator is not available.
Alternatively, suggest that one of his visitors who speaks both languages fulfill this role.
Be aware, however, that untrained translators, especially if family members, may
choose not to interpret your words accurately if they are thought to be culturally
sensitive or to contain bad news. If you are unable to find anyone who is able to
interpret, remember that intonation, gestures and facial expressions may convey more
than we realize to the patient, and may be relatively effective modes of
communication.
Try to establish a rapport with the patient’s family and remember to keep them well
informed of the situation. Where possible, involve them in planning patient care, and
take time to listen and to answer their questions. Respect your patient’s privacy and
dignity at all times and be mindful that a sedated, muscle-relaxed, ventilated patient
may still be able to hear what you are saying, and, because of various factors, may
misinterpret your words.
f. Nutritional and metabolic requirements:
Meeting the nutritional and metabolic needs of the ventilated patient is crucial to
patient recovery. Many patients who have respiratory failure, especially the elderly,
may be debilitated, and without adequate nutrition, will become even more so.
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January 2011
Critical illness and associated increase in stress results in a hyper-metabolic state. This is
known as stress hyper-metabolism and is characterized by dramatic increases in
metabolic rate, oxygen consumption, and production of CO2 and heat. Energy
requirements may increase by up to 50%. This occurs at the expense of lean body
mass. The catabolic, malnourished patient has a diminished respiratory drive and
effort, which may compromise the ability to wean from ventilation. Additionally,
patients in this group will be predisposed to opportunistic infection, which may further
compromise their condition.
A collaborative approach is required to set nutritional goals that will not only meet the
patient’s increased metabolic and caloric requirements, but which will assist in
replenishing muscle tissue and protein levels. Feeding regimes may involve enteral or
parenteral routes of administration.
g. Eye care:
Strict eye care is essential for all patients who are sedated and / or muscle-relaxed, as
the normal blink reflex may be lost and the cornea may not be adequately covered by
the eyelid. This may potentially lead to drying, abrasion and superimposed infection.
Stringent eye toilet and instillation of suitable eye-drops / ointments are necessary.
h. Oral Hygiene
Meticulous oral hygiene is vital for the intubated patient who is at increased risk for
development of stomatitis and infection. This is due to a number of factors including
tissue trauma secondary to the endotracheal and suction tubes, increased oral
secretions, which provide a medium for bacterial overgrowth, poor nutritional status,
and possible immunodeficiency. Mouth care should be attended frequently,
according to the condition of the patient’s mouth and Unit policy.
i. Rest and sleep periods:
Prolonged periods without adequate sleep may cause disturbances in mental function
- the patient may become irritable, disoriented, or even psychotic. Additionally, sleep
deprivation has been shown to suppress the immune system, resulting in a decreased
ability to deal with infection, delayed wound healing, weakened respiratory muscles
and delayed weaning from mechanical ventilation. Common causes of sleep
deprivation include environmental noise (such as alarms, equipment noise, telephones
and talking).
As the bedside nurse, you are in a unique position to coordinate and cluster most
patient-related activities, such as general nursing care, physical examinations and
tests, so that some time can be allocated for the patient to rest undisturbed and to
sleep. Attempt to provide some sort of day / night pattern, by turning off unnecessary
lights and minimizing noise.
j. Hygiene and Skin care:
Maintenance of personal hygiene for any patient is a fundamental aspect of nursing
care, and promotes patient comfort and psychological well-being. Critically ill,
debilitated and bed-ridden patients are prone to skin breakdown and decubitus
ulcers, especially over bony prominences. Pressure-ulcer prevention includes frequent
(2 – 4 hourly) turns from side-to-side, taking care to lift, rather than drag, the patient
across the bed. Also, ensure that bed linen is not wrinkled, and that the skin is clean
and dry. Cleansing agents used may range from soap to emollient-based lotions,
depending upon patient and nurse preference, and availability, however remember
that frequent washing with soap-based products is considered to have a drying effect
on the skin.
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January 2011
The Pressure Ulcer Prevention team will be able to assist you in formulating a nursing
care plan to prevent skin breakdown (or one to optimally treat decubitus ulcers once
they have occurred). Ensuring an adequate nutritional status is essential to promote
skin integrity and to aid in wound healing.
k. Pain Assessment
Accurate assessment of the ventilated patient’s pain status can be difficult. The
intubated and ventilated patient is unable to verbalize, and his / her non-verbal
communication ability may be impaired due to sedation and the underlying critical
illness. While several tools have been specifically developed for evaluation of pain
status in ventilated patients, they have not been sufficiently validated clinically.
Both physiological and behavioural indicators may help in the assessment of pain in the
ventilated patient, although it is important to be aware that changes in these
parameters may not be apparent, even when the patient has significant pain. The
table below, modified from Coyer et al (2006, p. 76) outlines behavioural and
physiological indicators of pain which may help you in evaluating your patient’s pain
status.
Behavioural indicators: Physiological indicators:
Facial expression – grimacing, frowning, wincing, tear Heart rate, blood pressure, respiratory rate – elevated or
development reduced (altered to previous readings)
Movements – restless, tentative, withdrawing, rocking / Dilated pupils (but take into account possible drug effects
rhythmic on pupil size)
Posture – rigidity, guarding, stiffness Pallor
Non-compliance with ventilation – coughing, gagging, Diaphoresis
“fighting” the ventilator
l. Sedation Assessment
It is quite common for ventilated patients to experience fear, pain, agitation or delirium.
Agitation is a behavioural response to complex stimuli – either internal stimuli or
environmental. Delirium is charactized by a fluctuating mental status, poor attention,
disorganized thinking, and an altered level of consciousness. To manage agitation or
delirium in the ventilated patient requires careful consideration of the patient’s overall
clinical condition and the treatment modalities being used, as well as other possible
stressors.
The agitated patient is at increased risk for self-extubation, removal of lines and
catheters, and “fighting” with the ventilator. As well, there is a potential for long-term
psychiatric problems, such as post-traumatic stress disorder. On a more immediate
level, prolonged and excessive sedation may interfere with the patient’s ability to
wean successfully, leading increased risk for nosocomial pneumonia, prolongation of
ICU stay, and increased morbidity.
To accurately assess the ventilated patient’s
sedation level, it is essential that pain and other
correctable causes of distress have been
eliminated. There are numerous tools to
determine the patient’s level of anxiety and
agitation (and therefore, their sedation
requirements). At KAMC-R, the Ramsey
Sedation Scale (opposite), which is based upon
the depth of sedation, is used.
This scale, although widely used in ICU settings, is probably not the ideal tool, as it has a
limited ability to discriminate between the quality and degree of sedation.
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January 2011
The table below (taken from Agkun & Siegel, 2007), outlines possible causes of agitation in the
ventilated patient.
LIFE THREATENING NOT (or less) LIFE THREATENING
Respiratory failure: Patient-ventilator dyssynchrony:
Hypoxaemia Inadequate flow rates
Hypercarbia Excessive tidal volumes
Hypoglycaemia Uncomfortable position in bed
Acidosis Fear, inability to communicate
Tension pneumothorax Sleep-wake cycle disturbances
Malposition of endotracheal tube Full bladder / need to defaecate
Sepsis / CNC infection Nausea
Intoxication / withdrawal Nicotine withdrawal
Ischaemia: Drug side-effects:
Myocardial Anticholinergic
Intestinal Paradoxical response to benzodiazepines
Cerebral
COMPLICATIONS OF MECHANICAL VENTILATION

________________________________________________________________________________
Although mechanical ventilation can save the lives of critically patients, it is also
associated with numerous complications, most of which can be eliminated completely or
at least minimized by good nursing care, combined with a solid understanding of the
physiologic effects of artificial ventilation. Complications may relate to either tracheal
intubation, or to ventilator-related issues.
a. Ventilator-Induced Lung Injury (VILI) was initially thought to be related to high peak
airway pressures, but recent studies have indicated that it is more likely to be the result
of high tidal volumes (with or without high airway pressures). Thus, the term
“volutrauma”, rather than “barotrauma” is now used. Volutrauma results from alveolar
over-distension and rupture, producing changes in pulmonary membrane permeability,
with development of pulmonary oedema,
accumulation of neutrophils and proteins,
disruption of surfactant production,
development of hyaline membranes and an
overall decrease in compliance of the
respiratory system. NB: All of these acute
pathophysiological changes are also seen in
A.R.D.S
Opposite: Potential mechanisms of ventilator-induced lung injury.
Downloaded from ccforum.com/content/7/3/233/figure/F1
Clinically, volutrauma may present as

pneumomediastinum, pneumothorax,
subcutaneous emphysema, pneumo-
peritoneum, or gas embolus. At particular risk
are patients with chronic obstructive lung
disease, acute respiratory distress syndrome,
chest trauma, or chest surgery.
The ventilated patient will be at increased risk for

development of a tension pneumothorax (see
opposite), which is the most dramatic
presentation of ventilator-induced lung trauma.
39
January 2011
The points below outline situations when you should be suspicious of the development
of a pneumothorax.
Clinical change in the patient’s condition:
- sudden or progressive increase in peak airway pressure
- hypotension or cardiovascular collapse
- sudden onset of agitation – patient “fighting the ventilator”
- sudden decrease in arterial saturation
Chest X-Ray findings:
- general increase in volume of one hemithorax
- downward displacement of the costophrenic angle or hemidiaphragm
- increase in relative radiolucency of one lung or part of one lung
- loss of vascular markings in affected portion of lung
Clinical settings suggesting high risk for pneumothorax:
- use of large tidal volumes (e.g.,> 12ml/kg) in patients with acute lung injury or underlying chronic
pulmonary disease
- use of high levels of PEEP (e.g. > 15cm H2O)
- high peak airway pressure (e.g.,>50-60cm H2O), esp. if increasing on same inspiratory flow rate settings.
- A.R.D.S., especially late in the clinical course (e.g., 2-3 weeks)
- severe underlying obstructive lung disease (e.g., C.O.P.D. or asthma)
- pulmonary infection complicating A.R.D.S.
c. Atelectasis may develop during mechanical ventilation if the preset tidal volume is
insufficient to maintain alveolar expansion or if secretions or foreign bodies cause
airway obstruction. Atelectasis may be avoided by ensuring that an adequate tidal
volume is delivered, as well as by position changes, frequent chest physiotherapy, and
appropriate suctioning of secretions.
d. Pulmonary infection. Since artificial airways (endotracheal and tracheostomy tubes)

bypass the normal upper airway defense mechanisms, intubated patients are at
increased risk of airway contamination. Patients may be unable to spontaneously
increase their tidal volume to re-expand alveoli, and they may not be able to
adequately clear their secretions.
Prevention of pulmonary infection is dependant upon aseptic technique for suctioning

of airways, scrupulous hand-washing before patient care is attended, and frequent
ventilator tubing changes (as per hospital policy). Appropriate isolation techniques,
and an effective routine for cleaning and sterilizing all respiratory equipment between
use are mandatory.
Additional considerations for the prevention of infection include ensuring an adequate

nutritional status, and proper oral hygiene. Sputum culture is usually ordered every
three days (or as per Unit policy), and may also be indicated if the patient becomes
febrile, or the sputum alters in amount, consistency or appearance.
e. Positive Water Balance: Patients who are mechanically ventilated lose little or no water
via their airways, particularly if the inspired gas is saturated with water vapor or at near
body temperature. Humidifiers help to eliminate water loss from the airways, while some
nebulizers may actually increase water intake, (up to 300-500mls/24 hours). Some of this
water may then be partially stored in the lungs.
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The actual mechanism underlying fluid retention is poorly understood, but may relate to
any or all of the following :
- low serum albumin in nutritionally deficient patients
- elevation of mean airway and intrathoracic venous pressures
- decreased renal perfusion
- reduced lymphatic flow
- subclinical cardiac failure
- inappropriate secretion of ADH, resulting in failure to excrete the excess water
Physiologic changes associated with a positive water balance in mechanically

ventilated patients may include any or all of the following:
- increased A-a gradient

- decreased vital capacity
- weight gain
- fluid intake exceeding output
- reduced effective compliance
- hemodilution: low hematocrit / low serum sodium
- pulmonary oedema on CXR
- lung crackles or decreased breath sounds
- peripheral oedema
Treatment of water retention includes fluid restriction and diuretic therapy.
e. Gastrointestinal complications may include:

Gastric distention and ileus may be easily prevented by placement of a nasogastric
tube. This may be used to decompress the stomach, and / or to feed the patient. The
gradual introduction of nutrients to the GI tract promotes tolerance of feeds, and may
help prevent such complications as malabsorption, which in turn results in diarrhoea and
electrolyte disturbances. Monitoring bowel sounds and abdominal girth, and careful
measurement of intake and output may permit early recognition of this problem
Gastrointestinal bleeding is a relatively frequent occurrence in patients who receive
prolonged mechanical ventilation. At increased risk are those patients on steroids,
antibiotic therapy. Those who have hypoxaemia, hypercarbia, a low platelet count or
clotting disorders are also subject to this disorder. Early commencement of tube feeding
reduces the risk of GI bleeding from stress ulcerations, as does the early administration of
histamine antagonists, such as Ranitidine.
f. Pulmonary Oxygen Toxicity is a potentially life-threatening complication associated with
impaired surfactant activity, progressive capillary congestion, fibrosis, oedema, and
thickening of the alveolar membranes. Pulmonary oxygen toxicity is more likely to occur
in those elderly patients with pre-existing lung disease who have prolonged (>24-48
hours) administration of a high inspired oxygen concentrations (usually > 50%), and who
have abnormalities in their metabolic and nutritional status. General measures for
prevention of this very serious complication include reduction of FiO2 to as low a level as
possible in order to maintain an adequate PaO2. Also, limiting exposure to high oxygen
concentrations to 24 hours or less, where possible, may minimize the occurrence of this
complication.
g. The potential for Malnutrition has been discussed previously in this Module.
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January 2011
h. Cardiovascular compromise frequently occurs with commencement of mechanical
ventilation in patients who have underlying cardiac impairment. This is due to the
increase in intrathoracic pressure associated with positive pressure ventilation, which
impedes venous return, decreasing preload, and therefore, cardiac output. While this
effect may be magnified in patients with cardiac disease, it also has the potential to
cause problems with patients who are relatively hypovolaemic or who have high mean
intrathoracic pressures. The addition of as little as 5cm of PEEP in a susceptible patient
may result in a significant reduction in cardiac output.
Factors which influence the degree of cardiac depression include the following:
- a peak inspiratory pressure > 30cm H2O;

- the mode of ventilation: for example, CMV causes the greatest degree of cardiac
impairment, while IMV with PEEP causes less problems;
- lung and chest wall compliance: the healthier and more compliant the lungs, the
greater the degree of cardiac depression. This is because diseased, non-compliant
lungs buffer the transmission of airway pressure to the pleural space;
- right ventricular preload, which is mainly determined by systemic venous return;
- pulmonary vascular resistance, when high, increases RV afterload, making it more
difficult for the RV to maintain its stroke volume;
- hypoxaemia, acidosis, hypovolaemia, negative inotropic drugs, and vasoactive
therapy, may all increase the speed, or extent, of cardiovascular depression.
The flow chart below, from Butcher & Boyle, 2009, p. 86, shows the complex
cardiovascular and renal interactions resulting from mechanical ventilation.
Close monitoring of the patient’s overall clinical status, particularly following any
alteration in ventilation pattern, is essential in order to prevent cardiovascular collapse.
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January 2011
i. “Fighting the ventilator” – otherwise known as patient-ventilator dyssynchrony (PVD) - is
frequently seen in the ICU, and, while often blamed on inadequate sedation, may
also indicate a number of potentially dangerous clinical situations. Physical signs may
provide clues for an early diagnosis, therefore prompting management of the problem.
The table below, from Mellott et al, 2009, (p. 48), outlines both biological and
behavioural signs that may suggest patient-ventilator dyssynchrony. Importantly, it also
provides subjective (actual patients) comments about coping with mechanical
ventilation and PVD.
The following table outlines a suggested protocol for assessment of respiratory distress that may develop during
mechanical ventilation.
MANAGEMENT RATIONALE
Provide reassurance to the conscious patient. Anxiety and agitation may increase bronchial constriction, airway
resistance and alveolar pressure.
Remove the patient from the ventilator and manually If the patient improves rapidly following removal from the
ventilate with 100% oxygen. ventilator, the problem must exist within the ventilator / circuit. If the
patient does not improve with manual ventilation, the problem must
be with either the endotracheal tube, or the patient.
Perform a rapid physical examination, with emphasis on Note results of monitored physical parameters:
cardiopulmonary aspects. - absolute values
- trends during past few hours.
Assess the airway for patency. Suction airway; auscultate lungs for bilateral air entry.
If death appears imminent, treat likely causes of Emergency procedures instituted as necessary:
deterioration: - re-intubation
- airway obstruction - needle decompression
- tension pneumothorax. - cardiopulmonary resuscitation.
Once the patient is supported adequately, perform more CXR to examine tube placement and lungfields
time-consuming diagnostic and therapeutic strategies as ABG analysis
indicated by clinical status. Review of ventilator parameters and mode of ventilation – may
need alteration
Review adequacy of sedation / analgesia.
As the bedside nurse, it is important that you are aware that simply increasing your
patient’s sedation level, or asking the Respiratory Therapist to adjust the ventilator
settings, without identifying the underlying cause of the PVD, may unnecessarily
prolong the time your patient receives mechanical ventilation.
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m. Dynamic Hyperinflation: Auto PEEP is the name used to describe increased alveolar
pressure caused by gas trapping during mechanical ventilation when there is
inadequate time to exhale the mechanical tidal volume. It may also be called
intrinsic PEEP, or gas trapping. It is seen most frequently in patients with COPD or
asthma, who normally require longer expiration times. Auto-PEEP causes an increase
in intrathoracic pressure, decreased venous return, cardiac output and blood
pressure. It also falsely elevates the pulmonary capillary wedge pressure. Auto-PEEP
results in an increase in dead-space ventilation and increases the work-of-breathing.
You should suspect development of auto-PEEP if the patient’s respiratory rate is much
greater than the ventilator rate (or when the expiratory pattern given below is
present on the ventilator console).
Diagram opposite:
Auto-PEEP.
In (A), the patient has received a breath and
passively exhales. The expiratory wave on the
ventilator console returns to baseline before another
breath is triggered.
In (B), the expiratory wave does not return to

baseline, indicating the presence of auto-PEEP.
(From Thies, R, et al, 1999; P. 36)
ADJUNCTS TO MECHANICAL VENTILATION
Various strategies have been developed to assist in the improvement of oxygenation and
removal of carbon dioxide during mechanical ventilation of critically ill patients. These
techniques allow ventilatory goals to be achieved with lower levels of ventilatory support.
a. Body Position
Prone positioning:
It has been shown that lying face down results in recruitment of atelectatic, but
previously well-perfused lung tissue. This results in better matching of ventilation and
perfusion, thus improving oxygenation.
Further possible explanations for the benefits of prone positioning include changes in
diaphragmatic motion, changes in chest wall compliance, shifting of water and
exudates from dependant to non-dependant regions, and drainage of bronchial
secretions. Additionally, the respiratory status of the premature infant may improve
dramatically due to this maneuver. Unfortunately, individual patient response to this
type of positioning cannot be predicted, with some patients showing improvement
while others may actually deteriorate.
Despite these physiological effects, however, a recent systematic review and meta-
analysis of the literature has shown that, although prone positioning does improve
oxygenation and reduce the risk of pneumonia, it does not reduce overall mortality or
the length of ventilation.
The patient’s haemodynamic status must be stable before prone positioning is
attempted, and his / her response to positioning carefully monitored. Expected
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January 2011
responses are an increase in PaO2 and SaO2, and a return to baseline values of heart
rate and blood pressure within 5 minutes of the turn. As well, the respiratory rate (in the
adult) should stabilize, with no increase in PaCO2.
The use of lateral decubitus positioning in the patient with unilateral lung disease, (with
the healthy lung down), can improve oxygenation by increasing the perfusion and
ventilation to the dependant lung.
b. Pharmacologic Agents:
The aims of medication usage in the management of ventilated patients are: to
improve lung compliance, to decrease oxygen demand and consumption, and to
alleviate pain, fear and anxiety. The clinical diagnosis and overall condition of the
patient will influence the type of drug used, as well as its dosage.
i. Narcotics / Benzodiazepines / Sedatives / Hypnotics (e.g. Morphine / Midazolam /
Propofol ) are generally the first-line drugs chosen to reduce pain and anxiety,
and to provide sedation for the ventilated patient. They have the additional
physiological effects of decreasing respiratory rate and airway resistance,
improving chest wall compliance, tidal volume and oxygen utilization.
ii. Neuromuscular-blocking agents (e.g. Pancuronium / Atracurium) are used to
optimize ventilation patterns by eliminating competition between the patient and
the ventilator. This will result in decreased oxygen consumption, decreased airway
pressures, and an improvement in tidal volumes and gas exchange. It is very
important when using muscle-relaxants to remember that they have no sedative
or analgesic effects, and while your patient may appear to be clinically “relaxed”,
he / she may be fully aware of his / her surroundings, and may in reality be
experiencing pain or fear. This situation should be suspected when unexplained
tachycardia, hypertension and decreased oxygen saturation develop in an
otherwise stable patient. Additionally, the muscle-relaxed ventilated patient
should never be left unattended as accidental disconnection from the ventilator
would result in respiratory arrest and possible death.
iii. Bronchodilators: Any diffuse lung injury can result in airway hyper-reactivity, with
subsequent increased airflow resistance. Bronchodilating drugs are useful in
reversing a proportion of this increased airway resistance and also have actions on
improving mucociliary clearance of secretions. Agents generally used in this
institution are the anticholinergics (e.g. Ipratropium Bromide), and the ß2 agonists
(e.g. Salbutamol, Terbutaline). A third agent (not used at this institution), is
Theophylline, a phosphodiesterase inhibitor, which has an anti-inflammatory effect
and also increases diaphragmatic contractility.
iv. Corticosteroids: Steroids are potent anti-inflammatory agents and may increase
the sensitivity of ß-adrenergic receptors. In this manner, they accentuate the
actions of ß-agonists such as Salbutamol. Steroids are also thought to speed up
the resolution of airflow obstruction and to decrease mucus production.
v. Nitric Oxide (NO):
NO is a highly lipid-soluble molecule that rapidly penetrates into airway and
vascular smooth muscle cells. It is a powerful vasodilator and modifies interactions
between inflammatory cells and vascular endothelium. Inhaled NO enters the
pulmonary vascular smooth muscle cells via diffusion from the alveolar spaces and
causes vascular relaxation.
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The benefit for patients with Acute Respiratory Distress Syndrome is that NO
produces vasodilation mainly in ventilated lung areas, rather than in collapsed or
fluid-filled alveoli. The localized vasodilation produced in the well-ventilated
alveoli diverts pulmonary blood flow to these areas, improving the match of
ventilation to perfusion. Several studies have suggested, however, that in order to
optimize the effects of inhaled NO in the management of ARDS, it is also important
to optimize the level of PEEP for alveolar recruitment. Additionally, individual
patient response to NO must be closely monitored as it has a very narrow
therapeutic range. Undesirable by-products include methaemoglobin and
nitrogen dioxide production, both of which have toxic effects at high
concentrations.
In some post-surgical cardiac patients, and also in patients who have persistent
pulmonary hypertension, NO has been used successfully to lower pulmonary
vascular resistance. This is a short-term strategy, however.
v. Surfactant Replacement Therapy: The major function of naturally-occurring
pulmonary surfactant is to reduce surface tension in the alveoli and small airways, thus
improving lung compliance. The effectiveness of surfactant therapy for very
premature babies as prophylaxis for Newborn Respiratory Distress Syndrome is well
established. Experimental studies indicate that replacement of surfactant may also be
beneficial in the treatment of A.R.D.S. Surfactant replacement therapy may be via
endotracheal instillation or aerosol nebulization.
WEANING FROM MECHANICAL VENTILATION

________________________________________________________________________________
Weaning involves a transition from

ventilatory support to a situation where the
patient resumes spontaneous, unassisted
breathing. This may occur relatively
quickly (in a few hours), or more gradually
(hours / days / weeks), depending upon
such factors as overall length of
ventilation, underlying disease processes,
and hemodynamic stability.
Some patients may initially be able to

meet the objective criteria for weaning,
but may tire before the weaning process is
completed, necessitating continued ventilation. This group of patients will need a very
gradual withdrawal of ventilatory assistance, as well as a high level of psychological
support. It is very important that your patient understands what is involved in the weaning
process, so that he / she is able to cooperate fully.
Weaning should be considered when the underlying disease process has been either fully
or at least partially resolved, the patient is able to resume the work of breathing, and is
able to maintain adequate gas exchange.
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The table below outlines certain clinical conditions which should be met before a trial of
weaning is commenced:
1. Significant resolution of the disease process which caused the respiratory failure.
2. Cessation of sedative and neuromuscular-blocking drugs.
3. Normal level of consciousness and ability to cooperate.
4. Absence of sepsis or marked hyperthermia.
5. Stable cardiovascular state.
6. Correction of fluid and electrolyte / metabolic imbalances.
7. Correction of anaemia.
8. Adequate nutritional state.
9. No expected need for general anaesthesia.
10. Adequate gas exchange:
- PaO2 ≥ 60mmHg, with FiO2 ≤ 0.4, with PEEP ≤ 5cm H2O
- PaO2 / PAO2 ratio ≥ 0.35
- Alveolar-arterial gradient < 350mmHg
- PaO2 / FiO2 ratio ≥ 200
11. Adequate respiratory pump capacity.
12. Patient able to cough / protect own airway
The Spontaneous Breathing Trial (SBT) is considered the strongest predictor of readiness to
wean for a wide range of patients across a variety of settings. Implementation of the SBT is
recommended as follows:
A brief (less than 30 minutes) screening of SBT to assess if the patient is able to progress
to a formal trial of weaning.
If the patient tolerates the SBT, then a longer trial (e.g., 120 minutes) can then
commence.
There are several ways in which a patient may be weaned from mechanical ventilation:
T-Piece trial: this is probably the simplest method

of weaning and is one in which the patient’s
endotracheal / tracheostomy tube is
connected to a T-tube system, through which
there is a continuous flow of humidified gas at a
known FiO2 (see photo opposite). The patient
assumes the total work-of-breathing. The T-Piece
trial may last for 5-10 minutes, following which
the patient is returned to the ventilator, usually
on assist-control mode, for the remainder of the
hour or day. The cycle is then repeated,
gradually increasing the T-Piece time, taking
care that the patient does not become
fatigued.
CPAP may be included in the T-Piece trial to help prevent micro-atelectasis and to preserve
functional residual capacity, as well as to improve oxygenation. Weaning may proceed
fairly rapidly (over a few hours), or more slowly (over several days / weeks), up to the point
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January 2011
of extubation. Alternatively, the short-term ventilated patient may be connected to the T-
Piece and if all parameters are satisfactory after a period of 1-2 hours, can be extubated.
SIMV: By gradually and progressively reducing the number of ventilator breaths per minute,
the patient must increase his / her spontaneous inspiratory efforts concurrently. When the
SIMV frequency has been reduced to roughly 2 to 4 breaths per minute with no signs of
patient respiratory distress and no deterioration in gas exchange, weaning is generally
considered complete, and the patient ready for extubation.
The usefulness of the SIMV mode for weaning is controversial, however, as some SIMV
systems require generation of a significant amount of negative pressure to open a demand
valve. This may increase the work of breathing for the patient. The increased airway
resistance associated with breathing through a high-resistance circuit has been shown to
cause increased work of breathing and oxygen consumption, and may result in chronic
respiratory muscle fatigue. Addition of a low level of Pressure Support to the SIMV mode
when weaning may help to overcome the increased work of breathing, while at the same
time maintaining an adequate tidal volume and minute ventilation.
Weaning from Pressure Support Ventilation occurs via gradual reduction of PSV by 2 to 4
cm. H2O at a time, according to patient tolerance. When the patient shows no sign of
respiratory distress, with a PSV level of less than or equal to 8 to 10cm. H2O (which
approximately compensates for circuit resistance), the patient may be considered weaned
and ready for extubation.
Nursing Responsibilities during weaning procedure (regardless of method used)
1. Try to start weaning in the morning, when your patient is rested and able to cope with
the increased work and stress associated with the process. An exception to this rule is
the patient who has been ventilated for only a short time post-operatively.
2. Withhold any medications which may cause respiratory depression. It is important,

however, to ensure that the patient is pain-free – the patient in pain will not be able to
take deep breaths, which could then result in atelectasis, poor gas exchange, and
failure to wean. Recent research has shown that a daily “sedation vacation” can
reduce the length of time that a patient needs ventilation. This is thought to be
because the awake, alert patient is far more likely to undergo daily evaluation of his /
her readiness to wean.
3. Explain the weaning process to your patient, ensuring that he / she understands what is
expected of him / her. Points to emphasize include:
i. a degree of dyspnoea, general discomfort and fatigue are to be expected;
ii. a nurse or respiratory therapist will be close by at all times, closely monitoring
progress;
iii. the call-bell will be within reach, and the patient should ring for assistance should
he / she become distressed. He / she will be returned to the ventilator if necessary.
4. Set realistic, achievable goals. The weaning process for the long-term ventilated
patient may take weeks, and your patient may experience many ups and downs – so
it is important that he / she understands what may happen.
5. Ensure that your patient is in an upright position for optimal lung expansion and is
comfortable. If it is possible, organize some diversional activity for him / her (such as
watching television, or listening to the radio), to help minimize anxiety.
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6. Take baseline vital signs: heart rate and rhythm, blood pressure, respiratory rate,
peripheral perfusion, arterial O2 saturation, lung auscultation. Additional parameters to
be monitored include VC, VT and NIF.
7. Suction the endotracheal tube if secretions are present.
8. Re-check all parameters every 5 minutes (or according to your Unit Protocol). Notify
the respiratory therapist or physician if your patient develops respiratory distress, or
exhibits signs of haemodynamic deterioration.
NB: It is quite normal for the weaning patient to develop a slight increase in heart rate,
blood pressure and respiratory rate, while tidal volume may decrease, and a mild
diaphoresis may occur. However, should the respiratory rate increase by more than 10
per minute, or the heart rate increase by more than 20 beats per minute, hypoxia,
hypercarbia, or both, should be suspected.
Elevation of systolic blood pressure by more than 20mmHg may indicate re-
mobilization of fluid into the circulatory system, extreme patient anxiety or distress, or
hypoxaemia.
A fall in systolic blood pressure may be due to arrhythmias or to development of heart

failure following the decrease in positive intrathoracic pressure once spontaneous
respirations have resumed.
Pulmonary oedema may also develop if the heart is unable to adequately pump the
increased venous return which occurs following cessation of positive pressure
ventilation, especially if PEEP is being used.
9. Arterial blood gases are usually taken 30–60 minutes after weaning is commenced.
Depending upon the results and patient condition, the weaning process may continue
or the patient may be extubated.
Weaning parameters are specific, measurable indices, which show patient readiness for
extubation and resumption of spontaneous breathing, following a period of weaning. A
general outline is as follows:
awake and alert

PEEP < 5cm H2O
PaO2 > 60 mmHg on FiO2 < 0.40
PaCO2 acceptable, with normal pH
Respiratory rate < 25 / minute
Tidal Volume 4-5ml/kg
Vital capacity > 10-15ml/kg
Minute Ventilation 5-10 L/min.
Maximum Voluntary Ventilation 10-20 L/min.
Negative Inspiratory Force > -20cm H2O
FAILURE TO WEAN
Failure to wean usually has an underlying pathophysiological basis, although

psychological (e.g. excessive fear or anxiety) and iatrogenic (e.g. increased work-of-
breathing due to ventilator tubing) factors may also be involved.
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January 2011
Outlined below are various clinical situations which may be responsible for a patient failing
to wean from mechanical ventilation.
Inadequate respiratory centre output, due to:
⇒ Residual effect of sedative drugs
⇒ CNS damage
⇒ Severe metabolic alkalosis
Increased respiratory workload, related to:
⇒ increased minute ventilation, which in turn may be caused by:
hyperventilation (pain, anxiety, restlessness)
increased metabolic rate (excessive feeding, sepsis)
increased physiologic dead space
⇒ increased elastic workload, due to:
low thoracic or lung compliance
⇒ increased resistive workload, due to:
lower airway obstruction
thick or copious airway secretions
artificial airway (endotracheal tube)
ventilator circuitry and/or demand valve obstruction/malfunction
post-extubation upper airway obstruction
Respiratory pump failure:
⇒ thoracic wall abnormality or disease
⇒ peripheral neurologic disorder:
phrenic nerve injury
cervical spine damage
Guillain-Barré syndrome
⇒ muscular dysfunction, caused by:
malnutrition, muscular catabolism
pulmonary hyperinflation
severe electrolyte & metabolic disorders
prolonged post-neuromuscular blockade
Left ventricular failure, caused by:
⇒ left ventricular dysfunction
⇒ coronary artery disease (mechanisms discussed on next page)
The diagram opposite (from Lessard, et al,

1996, P. 481) illustrates the mechanisms
underlying development of cardiovascular
compromise following resumption of
spontaneous breathing. There is an increase
in O2 consumption (VO2), in catecholamine
release, and in left ventricular afterload. This
results in a tachycardia and a decrease in
myocardial O2 supply (MVO2). Any increase
in respiratory workload, such as occurs with
C.O.P.D. or auto-PEEP, will lead to a critical
situation. In a patient with pre-existing
coronary artery disease or left ventricular
dysfunction, the increased workload may be
too great, and left ventricular failure may
follow.
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January 2011
SUMMARY
________________________________________________________________________________
Caring for a critically ill ventilated patient means that you, as the bedside nurse, assume
responsibility for integrating and coordinating all aspects of care. With this in mind, your
aims should be to ensure that all interventions (those of nursing and other health care
team members) are necessary, safe and effective, and that complications are either
avoided completely or their effects minimized, and that you provide optimal nursing care
at all times. To effectively achieve these aims you need to possess advanced skills in
patient assessment, an understanding of the significance of your clinical findings, and the
ability to act appropriately on those findings.
Addendum # 1
Formula for calculating the A-a Gradient:
A-a gradient = PAO2 - PaO2

PAO2 = PiO2 - (PaCO2 ÷ 0.8)
PiO2 = (PB– 47) x FiO2
Where
47mmHg = water vapor pressure at 37°C

PB = atmospheric pressure
PiO2 = pressure of inspired oxygen (i.e., PB – 47) (FiO2)
0.8 = assumed respiratory quotient (ratio of CO2 produced to O2 consumed per unit time)
FiO2 = fraction (percent) of inspired oxygen
Therefore:
FiO2 (PB – 47) – PaCO2 ÷ 0.8) – PaO2 = A-a gradient (also called A-aDO2)
Example of calculation:
0.21(760-47) - (40 ÷ 0.8) - 90 = 10
i. Normally, values for A-a gradient increase with age and with increased FiO2
ii. Pathologic conditions causing increased A-a gradient:
i. ventilation-perfusion (V/Q) mis-matching

ii. shunting
iii. diffusion abnormalities.
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January 2011
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http://emedicine.medscape.com/article/167981-print
**Martin, W. 1999, Pulmonary Physiology in Clinical Practice, Chapter 10: Mechanical Ventilation.
Mellott, K., Grap, M., Munro, C., Sessler, C. & Wetzel, P., 2009, “Patient-Ventilator Dyssynchrony:
Clinical Significance and Implications for Practice”, Critical Care Nurse, vol. 29, no. 6, pp. 41-55.
Naqvi, S., n.d., “Ventilation Modes – New and Not So New”, downloaded 27th October 2010 from
http://www.datex-ohmeda.com /…/Shahab%20Naqvi%20VENTILATION%20MODES.pdf
Newmarch, C., 2006, “Caring for the Mechanically Ventilated Patient: Part One”, Nursing Standard,
vol. 20, no. 17, pp. 55-66.
**Parsons, P. & Heffron, J., 2002, Pulmonary Respiratory Therapy Secrets, 2nd Ed., Hanley & Belfus Inc.,
Philadelphia.
**Pierce, L., 2002, “Traditional and Nontraditional Modes of Mechanical Ventilation”, Critical Care
Nurse, vol. 22, no. 4, pp. 56-59.
** Post, M., 1998, “Pressure-Controlled Ventilation”, downloaded 26th October 2010 from
http://www.rtmagazine.com/issues/articles/1998-04_08.asp?mode=print
**Preston, R., 2001, “Introducing Non-Invasive Positive Pressure Ventilation”, Nursing Standard, vol.
15, no. 26, pp. 42-45.
Pruitt, B., 2006, “Weaning Patients from Mechanical Ventilation”, Nursing2006, September, pp. 37-41.
Rappard, S., n.d., “Use of CPAP and BiPAP in Acute Respiratory Failure”, downloaded 31st October
2010 from http://www.theberries.ca/Archives/CPAP.html
Rose, L., 2007, “Decisions Made by Critical Care Nurses During Mechanical Ventilation and Weaning
in an Australian Intensive Care Unit”, American Journal of Critical Care, vol. 16, no. 5, pp. 434-444.
**Sawkins, D., 2001, “Non-Invasive Positive Pressure Ventilation”, Nursing Times, vol. 97, no. 26, pp. 52-
54.
Shortall, S. & Oakes, D., 2005, “Practical Uses of Pressure-Controlled Ventilation”,

RespiratoryBooks.com
Souliere, G., 2010, “Nursing Tip Sheet for Patients on HFOV (High Frequency Oscillatory Ventilation)”,
downloaded 23 October 2010 from www.lhsc.on.ca/Health.../NursingTipSheetforPatientson HFOV.pdf
St. John, R., 2010, “End-tidal Carbon Dioxide Monitoring”, Critical Care Nurse, vol. 23, no. 4, pp. 83-88.
Sud, S., Sud, M., Friedrich, J., & Adhikari, N., 2008, « Effect of Mechanical Ventilation in the Prone Position
on Clinical Outcomes in Patients with Acute Hypoxemic Respiratory Failure : A Systematic Review and
Meta-Analysis”, Canadian Medical Association Journal, vol, 178, no. 9, pp. 1153-1161.
**Tung, A., Indications for Mechanical Ventilation, in International Anesthesiology Clinics: Mechanical
Ventilation; vol. 35, no. 1, 1997.
Urden, L., Stacey, K. & Lough, M., 2010, Critical Care Nursing, 6th Ed., Chapters 23-25, Mosby Elsevier, St.
Louis.
** Reference remains current
53
January 2011
Self-Study Module
POST TEST
Please use the answer sheet provided. Do not write on the test.
Indicate the most correct answer. One mark per question.
1. In the normal, spontaneously breathing person:
a. intrapleural pressure rises on inspiration

b. intrapleural pressure falls on inspiration
c. intrathoracic pressure increases on inspiration
d. intrapleural pressure does not change but alveolar pressure becomes sub-
atmospheric.
2. Dead space refers to:
a. the exchanges of gases that occurs in the alveoli

b. the amount of air filling the airways that contributes to gas exchange
c. the amount of gas filling the airways that does not contribute to gas
exchange
d. the volume of gas remaining in the lung at the end of expiration
3. Tidal Volume relates to:
a. the maximum amount of air exhaled after normal inspiration

b. the maximum amount of air exhaled after maximal inspiration
c. the amount of air exhaled per breath, in normal breathing
d. the total amount of gas exhaled per minute.
4. A shunt refers to
a. alveoli which are perfused but not ventilated

b. alveoli which are ventilated but not perfused
c. over-expanded alveoli
d. the combination of anatomic and physiologic dead space
5. The alveolar-arterial gradient:
a. represents the relationship between PaO2 and saturation

b. indicates whether gas transfer in the lungs is normal
c. is normally > 30mmHg in young adults
d. reflects the amount of oxygen combined with hemoglobin.
54
January 2011
6. Mrs Jones, admitted to ER with acute dyspnoea and hypotension, has the
following arterial blood gases: pH 7.28; PaCO2 52; PaO2 58; Bic. 28.
These gases show that Mrs Jones is in:
a. type 1 respiratory failure

b. type 2 respiratory failure
c. chronic respiratory failure
d. metabolic alkalosis.
7. Subjective criteria for initiating mechanical ventilation may include:
i. inadequate cough reflex

ii. thick secretions
iii. awake, alert & cooperative patient
iv. flail chest
Answer:
a. if i), ii), & iii) are correct
b. if i), iii), & iv) are correct
c. if all are correct
d. if i), ii), & iv) are correct.
8. Criteria for initiating non-invasive positive pressure ventilation (NIPPV) includes:
a. patients with acute facial trauma

b. patients with adequate cough and gag reflexes
c. haemodynamic and rhythm stability
d. b) and c)
9. Benefits of NIPPV include:
a. decreased work of breathing

b. improved oxygenation
c. larger tidal volumes
d. all of the above
10. Clinical conditions which may result in hypoventilation may include:
a. chest wall trauma

b. drug intoxication
c. neuromuscular disease
d. all of the above.
11. The FiO2 setting on the mechanical ventilator gives you information about:
a. tidal volume
b. inspired O2
c. mode of ventilation
d. SaO2
55
January 2011
12. Benefits of BiPap non-invasive ventilation include:
i. improved oxygenation and tidal volumes

ii. decreased respiratory rate
iii. decreased work of breathing
iv. increased alveolar ventilation and decreased PaCO2
Answer:
a. if i), ii), & iii) are correct
b. if i), iii), & iv) are correct
d. if i), ii), & iv) are correct.
13. Pressure cycled ventilation:
a. permits gas flow into the lungs until a preset volume has been reached
b. may not ensure an adequate tidal volume if lung compliance changes
c. provides a constant tidal volume, regardless of lung compliance
d. none of the above.
14. Controlled Mandatory Ventilation (CMV) is used when:
a. there may be patient-ventilation competition

b. intermittent ventilatory support is required
c. full ventilatory support is required
d. the patient is ready to wean.
15. The ventilation mode in which the patient breathes spontaneously, with the
ventilator supplying a preset number of breaths, coordinated with the patient’s
own breaths is called:
a. assist-control ventilation
b. pressure support ventilation
c. synchronized intermittent mandatory ventilation
d. continuous positive airway pressure.
16. The greatest disadvantage of Pressure Control Ventilation (PCV) is that:
a. pressure may spontaneously increase

b. tidal volume cannot be guaranteed if lung compliance changes
c. respiratory rate will change as pressure changes
d. the patient must be muscle-relaxed and sedated
17. Adding Positive End Expiratory Pressure (PEEP) to a ventilation mode:
a. optimizes alveolar expansion and gas exchange

b. increases the respiratory rate
c. decreases peak airway pressures
d. promotes venous return to the heart.
56
January 2011
18. A daily “sedation vacation” may result in:
a. a prolonged ICU stay

b. lengthening of the duration of mechanical ventilation
c. resting of the patient’s respiratory muscles
d. an accurate assessment of the patient’s readiness to wean
19. A patient who is ready to wean should be able to tolerate a spontaneous

breathing trial of:
a. 4 hours
b. 2 to 5 minutes
c. 30 to 120 minutes
d. 15 to 20 minutes
20. Which of the following conditions is not a prerequisite to commence weaning?
a. haemodynamic stability
b. normal level of consciousness
c. normal renal function
d. adequate gas exchange.
21. Nursing responsibilities during weaning include all of the following except:
a. administering routine narcotic analgesia

b. ensuring that the patient is well rested, alert and cooperative
c. positioning the patient to ensure optimum lung expansion
d. checking all hemodynamic parameters as per unit protocol.
22. Failure to wean the patient from mechanical ventilation may be due to:
i. CNS depression, malnutrition and copious secretions

ii. thoracic wall defects, cardiac failure and sepsis
iii. increased work of breathing due to ventilator tubing
iv. pain, anxiety, and fear.
Answer:
a. if i), iii) and iv) are correct
b. if all are correct
c. if iii) only is correct
d. if ii), iii) and iv) are correct.
23. Suctioning of the endotracheal tube should be attended:
i. routinely every 2 hours

ii. when airway pressures increase
iii. when secretions are present
iv. for frequent or prolonged episodes of coughing
Answer:
a. if ii), iii) and iv) are correct
b. if i), and iii) are correct
c. if i), ii) and iv) are correct
d. if all are correct.
57
January 2011
24. Which of the following responses may a ventilated, critically ill patient exhibit?
a. frustration, fear and anger

b. apathy and withdrawal
c. combative and aggressive behaviour
25. Prevention of decubitus ulcers involves:
i. frequent, vigorous massage of dependent areas

ii. two-hourly turns
iii. ensuring an adequate nutritional intake
iv. keeping the skin clean and dry
Answer:
a. if i) and ii) are correct
b. if ii) and iv) are correct
c. if ii), iii) and iv) are correct
d. if all are correct.
26. Ventilator-Induced Lung Injury (VILI) may be manifested by:
a. subcutaneous emphysema
b. pneumothorax
c. pneumomediastinum
27. Prevention of atelectasis in the ventilated patient involves:
i. ensuring an adequate minute volume is delivered

ii. frequent position changes
iii. sedating the patient to ensure adequate rest
iv. suctioning and physiotherapy as needed
Answer:
a. if i), ii) and iv) are correct
b. if ii), iii) and iv) are correct
c. if ii) and iv) are correct
d. if i) and iv) are correct.
28. Clinical features suggestive of development of a pneumothorax may include:
i. sudden dramatic haemodynamic deterioration

ii. sudden onset of copious sputum
iii. absence of breath sounds unilaterally
iv. acute arterial desaturation.
Answer:
a. if i), ii) and iv) are correct
b. if i), iii) and iv) are correct
c. if ii), iii) and iv) are correct
d. if all are correct
58
January 2011
29. Complications of mechanical ventilation may include:
a. infection, atelectasis, water overload and malnutrition

b. bowel obstruction, renal failure and sepsis
c. diabetes, pulmonary oxygen toxicity and heart failure
30. Nursing considerations in the care of the patient receiving NIPPV include:
a. a comprehensive explanation of the procedure

b. abdominal assessment for gastric distension
c. close monitoring of vital signs
d. all of the above
31. Nitric Oxide therapy may be indicated in which of the following clinical situations?
a. acute respiratory distress syndrome

b. acute exacerbation of asthma
c. burns patients who are in renal failure
d. all premature babies
32. What might be the underlying cause for a muscle-relaxed, sedated patient to
suddenly develop tachycardia, hypertension, desaturation and high airway
pressures?
a. pneumothorax
b. inadequate sedation
c. obstruction to endotracheal tube
33. Causes of a low-pressure alarm sounding include:
a. kinked ventilator tubing

b. loss of power or gas
c. a leak in the circuit
d. water condensation.
34. Nursing considerations in the care of the patient receiving high-frequency

oscillatory ventilation (HFOV) include:
a. extreme caution when turning the patient’s head

b. ensure patient is well sedated
c. close observation for “chest wiggle”
d. all of the above
35. Monitoring of End-tidal CO2 provides information about:
a. oxygen levels and carbon dioxide use

b. oxygen utilization and carbon dioxide production
c. both of the above
d. neither of the above
59
January 2011
36. Unequal chest expansion in an intubated, ventilated patient may indicate:
i. water in ventilator circuit

ii. endotracehal tube cuff leak
iii. endotracheal tube displacement
iv. pneumothorax
Answer:
a. if i)and iii) are correct
b. iii) and iv) are correct.
d. if iii) only is correct
37. Which of the following may be responsible for patient-ventilator dyssynchrony?
a. sensitivity dial set too high – patient unable to trigger inspiration

b. weakened respiratory muscles due to malnutrition
c. excessive water in ventilator circuit
d. all of the above
38. Immediate nursing management for a loss of power to the ventilator is to:
a. call Biomedical services for assistance

b. check all ventilator tubing for disconnection
c. disconnect patient from ventilator and manually ventilate
d. increase the oxygen level to 100%.
39. Which of the following may indicate an increased risk for development of
pneumothorax?
i. high levels of PEEP and high peak airway pressures

ii. decreased venous return
iii. use of high tidal volumes in patients with acute lung injury
iv. A.R.D.S.
Answer:
a. if i)and iii) are correct
b. iii) and iv) are correct.
d. if i), iii) and iv) are correct
40. Which of the following drugs would be indicated for first-line management of
pain and agitation in the ventilated patient?
a. sedatives and narcotics

b. neuromuscular-blocking agents
c. narcotics and inotropes
d. bronchodilators and neuromuscular-blocking agents
60
January 2011
Kingdom Of Saudi Arabia
National Guard, KAMC-R
NURSING SERVICES - EDUCATION
Mail Code 1212
SELF-STUDY MODULE
ANSWER SHEET
_____________________________MECHANICAL VENTILATION__________________________
Module Title
(Name & Family Name):_____________________________ WARD/UNIT: _____________________
BADGE NO: _______________ TITLE: ____________________ DATE: ______________________
Please circle the correct answer.
1) a b c d e 26) a b c d e
2) a b c d e 27) a b c d e
3) a b c d e 28) a b c d e
4) a b c d e 29) a b c d e
5) a b c d e 30) a b c d e
6) a b c d e 31) a b c d e
7) a b c d e 32) a b c d e
8) a b c d e 33) a b c d e
9) a b c d e 34) a b c d e
10) a b c d e 35) a b c d e
11) a b c d e 36) a b c d e
12) a b c d e 37) a b c d e
13) a b c d e 38) a b c d e
14) a b c d e 39) a b c d e
15) a b c d e 40) a b c d e
16) a b c d e 41) a b c d e
17) a b c d e 42) a b c d e
18) a b c d e 43) a b c d e
19) a b c d e 44) a b c d e
20) a b c d e 45) a b c d e
21) a b c d e 46) a b c d e
22) a b c d e 47) a b c d e
23) a b c d e 48) a b c d e
24) a b c d e 49) a b c d e
25) a b c d e 50) a b c d e
* Some of the tests contain fewer than 50 questions. Please answer the correct number of questions as indicated
on each module test. Thank you/
SSM Revised Answer Sheet
March 2010
61
January 2011

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NURSING SERVICES, KING ABDULAZIZ MEDICAL CITY

NURSING SERVICES - EDUCATION DEPARTMENT

SELF STUDY MODULE

1. Read Module objectives.

2. When available complete pre-test questions.

4. Complete post- test questions, using answer sheets provided.

6. Complete evaluation provided in the library.

a) post test answer sheet

8. Please return the Self Study Module to the Medical Library.

9. Contact Nursing Education at nursingservices-ed@ngha.med.sa , as necessary,

On completion of this Self-Study Module, the learner will be able to:

1. Differentiate between Type I and Type II Respiratory Failure.

2. List the subjective and objective indications for mechanical ventilation.

3. Discuss the different modes of ventilation.

4. Describe the nursing considerations for care of the ventilated patient.

5. Outline the adjuncts to ventilation.

6. Describe various techniques for weaning patients from mechanical ventilation.

7. Outline the complications of mechanical ventilation.

b. Alveolus: is the smallest and most

c. Compliance: relates to distensibility of

e. Hypoxaemia: means insufficient amount of oxygen in arterial

f. Humidification: is the saturation of dry air with water vapor.

n. Ventilation: is the movement of gas in and out of the lungs.

o. Dead space: is the volume of inspired

Anatomic dead space is the amount of

p. Shunt: A form of ventilation-perfusion

A high V/Q ratio is characteristic of dead

r. Transthoracic pressure: is the pressure

t. Partial Pressure: relates to the pressure, or tension, of a gas, whether it is alone, or in a

u. Oxygen Saturation Percentage (SaO2%): refers to the amount of hemoglobin actually

v. Alveolar-arterial Gradient (A-a Gradient or AaDO2) is the difference between the

w. Oxygen-Hemoglobin Dissociation Curve: is a

The normal oxyhemoglobin dissocation

Please refer to the Arterial Blood Gas

Hypoxic respiratory failure (type 1 respiratory failure) is hypoxia without hypercapnoea

Hypercapnoeic respiratory failure (type 2 respiratory failure) is hypoxia with an arterial

Because virtually any disease process is capable of contributing to or actually causing

A further objective decisive factor is an A-aDO2 (alveolar-arterial oxygen difference /

1. Is the patient awake, co-operative and alert?

2. Can the patient cough and deep breathe effectively?

3. What are the secretions like, and is there any bronchospasm?

4. Can the patient swallow?

5. Is there ventilatory dis-coordination, e.g., flail chest, paradoxical movement?

6. What is the work of breathing?

8. Is the patient haemodynamically stable?

Failure of oxygenation (Hypoxaemia):-

Failure of Ventilation (Hypercapnoea):-

GOALS OF MECHANICAL VENTILATION:

1. To adjust alveolar ventilation to an individualized “normal” level for each patient, in

-2cm H2O -2cm H2O

Diagrams above from Butcher & Boyle, 1997, p. 7

Positive End Expiratory Pressure (PEEP)

CPAP may be used as an adjunct to spontaneous ventilation to assist in re-expanding

Criteria for selection of patients for NIPPV

BiPAP (Bilevel Positive Airway Pressure) is a form of non-invasive ventilation designed to

The pressure support stops at the end of inspiration, but a

 Decreased respiratory muscle effort due to assisted inspiration

 Increased tidal volumes due to the reduction in inspiratory

 Decreased respiratory rate as breathing efficiency increases

 Decreased PaCO2 as alveolar ventilation improves.

 Increased PaO2 due to the improvement in functional residual

The mask is held in position

Criteria for discontinuation of NIPPV & endotracheal intubation

Decreased respiratory muscle effort due to assisted inspiration

Increased tidal volumes due to the reduction in inspiratory

Decreased respiratory rate as breathing efficiency increases

Decreased PaCO2 as alveolar ventilation improves.

Increased PaO2 due to the improvement in functional residual

awake and alert