Critical Care Practice

Nursing Care of Clients with Life

Threatening Conditions. Acutely
Ill/Multi-Organ problems, High
Acuity and Emergency situation.
 Critical
• Crucial
• Crisis
• Emergency
• Serious
• Requiring immediate action
• Thorough and constant observation
• Total dependent
 Critical Care
• Term used to describe as the care of patients
who are extremely ill and whose clinical
conditions is unstable or potentially
unstable.
 Critical Care Unit
• Unit in which comprehensive care of
a critically ill patient which is deemed
to recoverable stage is carried out.
 Critical Care Nursing
• Refers to those comprehensive, specialized
and individualized nursing care services
which are rendered to patients with life
threatening conditions and their families.
 Critical care nursing is defined by the World
Federation
of Critical Care Nurses as:

• Specialized nursing care of critically ill patients who

have manifest or potential disturbances of vital
organ functions. Critical care nursing means
assisting, supporting and restoring the patient
towards health, or to ease the patient’s pain and to
prepare them for a dignified death. The aim of
critical care nursing is to establish a therapeutic
relationship with patients and their relatives and to
empower the individuals’ physical, psychological,
sociological, cultural and spiritual capabilities by
preventive, curative and rehabilitative interventions.
 DEVELOPMENT OF CRITICAL CARE
NURSING
• Critical care as a specialty emerged in the 1950s and
1960s in Australasia, North America, Europe and South
Africa.
• During these early stages, critical care consisted
primarily of coronary care units for the care of
cardiology patients, cardiothoracic units for the care of
postoperative patients, and general intensive care
units for the care of patients with respiratory
compromise.
• Later developments in renal, metabolic and
neurological management led to the principles and
context of critical care that exist today.
 Development of critical care nursing was
characterized by a number of features,
including:
• the development of a new, comprehensive partnership between
nursing and medical clinicians
• the collective experience of a steep learning curve for nursing and
medical staff
• the courage to work in an unfamiliar setting, caring for patients
who were extremely sick – a role that required development of
higher levels of competence and practice
• a high demand for education specific to critical care practice,
which was initially difficult to meet owing to the absence of
experienced nurses in the specialty.
• the development of technology such as mechanical ventilators,
cardiac monitors, pacemakers defibrillators, dialyzers, intra-aortic
balloon pumps and cardiac assist devices, which prompted
development of additional knowledge and skills.
 CRITICAL CARE NURSING IN THE
PHILIPPINES
• In 1970, the health care system in the
Philippines was greatly affected by
advancements in care and technology and the
changing nature of care. These factors
influenced the development of speciality
practice, particularly in critical care.
• Critical care practice is a collaborative process
and nurses play a vital part in it.
• Critical care nurses assume the role of
direct caregivers to the patient.
• They are expected to possess the competency
necessary to work in complex critical care areas
or the intensive care unit (ICU) environment.
• The patient to nurse ratio in the ICU of most
Metro Manila tertiary hospitals is usually
1:2.
 CRITICAL CARE NURSING EDUCATION
• Appropriate preparation of specialist critical
care nurses is a vital component in providing
quality care to patients and their families.
• A central tenet within this framework of
preparation is the formalized education of
nurses to practice in critical care areas.
• Formal education – in conjunction with
experiential learning, continuing professional
development and training, and reflective
clinical practice – is required to develop
competence in critical care nursing.
 SPECIALIST CRITICAL CARE
COMPETENCIES
• Critical care nursing involves a range of skills, classified
as psychomotor (or technical), cognitive or
interpersonal.
• Performance of specific skills requires special training
and practice to enable proficiency.
• Clinical competence is a combination of skills,
behaviors and knowledge, demonstrated by
performance within a practice situation and specific to
the context in which it is demonstrated.
• A nurse who learns a skill and is assessed as
performing that skill within the clinical environment is
deemed competent.
 CRITICAL CARE NURSING
PROFESSIONAL ORGANISATIONS
• Professional organizations representing
critical care nurses were formed as early as
the 1960s in the USA with the formation of
the American Association of Critical Care
Nurses (AACN).
• Other organizations have developed around
the world, with critical care nursing bodies
now operating in countries from Australasia,
Asia, North America, South America, Africa
and Europe.
CRITICAL CARE NURSES ASSOCIATION
OF THE PHILIPPINES, INC.(CCNAPI)
• Is the national organization of nurses
interested in the field of critical care nursing.
• It was founded in February 1977 with
approved SEC registration (CN 200813601), a
founding member of the World Federation of
Critical Care Nurses (2001) and accredited as a
Provider of Continuing Professional Education
by the Professional Regulation Commission
(Provider Number 2009-019).
• The framework of critical care nursing is a complex, challenging
area of nursing practice.
• It utilizes the nursing process applying assessment, diagnosis,
outcome identification, planning, implementation, and evaluation.
• The critical care nursing practice is based on a scientific body of
knowledge and incorporates the professional competencies
specific to critical care nursing practice and is focused on
restorative, curative, rehabilitative, maintainable, or palliative
care, based on identified patient’s nee.
• It upholds multi and interdisciplinary collaboration in initiating
interventions to restore stability, prevent complications, achieve
and maintain optimal patient responses.
• The critical care nursing profession requires a clear description of
the attributes guidelines and nursing practice standards in guiding
the critical care nursing practice to fulfill this purpose.
 PHILOSOPHY OF CRITICAL CARE
NURSING
• Critical Care Nursing reflects a holistic approach in
caring of patients. It places great emphasis on the
caring of the bio-psycho-social-spiritual nature of
human beings and their responses to illnesses
rather than salary on the disease process. It helps
maintain the individual patient’s identity and
dignity. The focus of caring includes preventive
care, risk factor modification and education to
decrease future patient admissions to acute care
facilities.
• The Critical Care Nurses of the Philippines, Inc.
(CCNAPI) is responsible for the promotion of man’s
health and welfare for national development. It
desires to support the professional and personal
growth and development of initial core nurses.
CCNAPI has organized itself into a national
association committed to the ideals of service to the
people, equality, justice and social progress.
• In the Critical Care Units, each patient is viewed as a unique
individual with dignity and worth. The critically ill patient
should receive comfort and provided privacy in a highly
technological environment.
• In collaboration with other health care team members,
critical care nurses provide high level of patient care which
includes patient and family education, health promotion
and rehabilitation.
• To achieve this holistic care process, participation by the
patient and his/her family is always emphasized. At the
forefront of critical care science and technology, critical care
nurses maintain professional competence based on a broad
base of knowledge and experience through continuous
education and evidence-based research.
 THE RIGHT OF THE CRITICALLY ILL
PATIENT
• The International Council of nurses (ICN) views
health care as the rights of every individual
regardless of financial political, geographical,
racial and religious consideration.
• This right includes the right to choose or decline
care, including the right to accept or refuse
treatment or nourishment; informed consent;
confidentiality and dignity, including the right to
die with dignity. It involves both the right of those
seeking care and the providers
 GOALS OF CRITICAL CARE NURSING
• To promote optimal delivery of safe and quality care to the critically ill
patients and their families by providing highly individualized care so that
the physiological dysfunction as well as the psychological stress in the ICU
are under control;

• To care for the critically ill patients with a holistic approach, considering
the patient’s biological, psychological, cultural and spiritual dimensions
regardless of diagnosis or clinical setting;

• To use relevant and up-to-date knowledge, caring attitude and clinical

skills, supported by appropriate technology for the prevention, early
detection and treatment of complications to facilitate recovery.

• To provide palliative care to the critically ill patients in situations where

their health status is progressing to unavoidable death, and to help the
patients and families go through their painful sufferings.
 LEVELS & CATEGORIES OF CRITICAL CARE
PROVISIONS WITHIN PHILIPPINES
• With respect to the physical set-up and supporting facilities of
critical care units in the Philippines, the Department of Health
(DOH) Standards requires the critical care units / intensive
care unit to be a self-contained area, with the provisions for
resources that will support critical care practice.
 Levels of Care Provision
• The role of a particular critical care unit will
vary, depending on the staffing, facilities
and support services as well as the type and
number of patients it has to manage.
• Level 1
• Should be capable of providing immediate resuscitation for
the critically ill and short term cardio-respiratory support
because the patients are at risk of deterioration;
• Has a major role in monitoring and preventing
complications in “at risk” medical and surgical patients;
• Must be capable of providing mechanical ventilation and
simple invasive cardiovascular monitoring;
• Has a formal organization of medical staff and at least one
registered nurse.
• A certain number of nurses including the nurse in-charge of
the unit should possess post-registration qualification in
critical care or in the related clinical specialties; and
• Has a nurse: patient ratio of 1:1 for all critically ill patients.
• Level 2
• Should be capable of providing a high standard of general critical
care for patients who are stepping down from higher levels of care
or requiring single organ support/support post-operatively;
• Capable of providing sustainable support for mechanical
ventilation, renal replacement therapy, invasive hemodynamic
monitoring and equipment for critically ill patients of various
specialties such as medicine, surgery, trauma, neurosurgery,
vascular surgery;
• Has a designated medical director with appropriate intensive care
qualification and a duty specialist available exclusively to the unit
at all times;
• The nurse in-charge and a significant number of nursing staff in
the unit have critical care certification; and
• A nurse: patient ratio is 1:1 for all critically ill patients.
• Level 3
• Is a tertiary referral unit, capable of managing all aspects of
critical care medicine (This does not only include the
management of patients requiring advanced respiratory
support but also patients with multi-organ failure);
• Has a medical director with specialist critical / intensive care
qualification and a duty specialist available exclusively to the
unit and medical staff with an appropriate level of
experience present in the unit at all times;
• A nurse in-charge and the majority of nursing staff have
intensive care certification; and
• A nurse: patient ratio is at least 1:1 for all patients at all
times.
 SCOPE OF CRITICAL CARE NURSING
• The scope of critical care nursing is defined by
the dynamic interactions of the critically ill
patient/family , the critical care nurse and the
critical care environment to bring about
optimal patient outcomes through nursing
proficiency in an environment conducive to
the provision of this highly specialized care
• Constant intensive assessment, timely critical
care interventions and continuous evaluation
of management through multidisciplinary
efforts are required to restore stability,
prevent complications and achieve optimal
health. Palliative care should be instituted to
alleviate pain and sufferings of the patient and
family in situations where death is imminent.
CRITICAL CARE NURSE QUALIFICATION
• A critical care nurse is a licensed
professional nurse who is responsible for
ensuring that all critically ill patients and
their families receive optimal care.
ROLES OF THE CRITICAL CARE NURSES
• 1. Care Provider
• A. Direct patient care
• Detects and interprets indicators that signify the varying conditions of
the critically ill with the assistance of advanced technology and
knowledge;
• Plans and initiates nursing process to its full capacity in a need driven
and proactive manner;
• Acts promptly and judiciously to prevent or halt deterioration of
patients’ condition when conditions warrant, and
• Co-ordinates with other healthcare providers in the provision of
optimal care to achieve the best possible outcomes.
• B. Indirect patient care – Care of the Family
• Understands family needs and provide information to allay fears
and anxieties and
• Assists family to cope with the life-threatening situation and/or
patient’s impending death.
• 2. Extended roles as critical care nurses
• Critical care nurses have roles beyond their professional boundary. With
proper training and in accordance with established guidelines,
algorithms, and protocols that are continuously reviewed and updated,
critical care nurses also perform procedures and therapies that are
otherwise done by doctors. Such procedures and therapies are:
• a. Sampling and analyzing arterial blood gases;
• b. Weaning patients off ventilators;
• c. Adjusting intravenous analgesia / sedations;
• d. Performing and interpreting ECGs;
• e. Titrating intravenous and central line medicated infusion and
nutrition support;
• f. Initiating defibrillation to patient with ventricular fibrillation or
lethal ventricular tachycardia;
• g. Removal of pacer wire, femoral sheaths and chest tubes,and
• h. Other procedures deemed necessary in their respective
institutions under a clinical protocol.
• 3. Educator
• As an educator, the critical care nurse must
be able to:
• Provides health education to patient and family
to promote understanding and acceptance of the
disease process thus facilitate recovery and
• Participates in the training and coaching of
novice healthcare team members to achieve
cohesiveness in the delivery of patient care.
• 4. Patient Advocate
• The critical care nurses’ role includes being an advocate –
someone who acts or intercedes on behalf or another. Typically,
the critical care nurse may be in the best position to act as the
liaison between patient and family and other team members and
departments because they are the healthcare professionals with
the most interpersonal contact with the patients. To perform this
function adequately, the nurse must be knowledgeable about the
involved in all aspects of the patient’s care and have a positive
working relationship with other team members. The critical care
nurses are expected to:
• Acts in the best interests of the patient and
• Monitors and safeguards the quality of care which the patient
receives.
•
Assessment Of Critically Ill Patients
• 1. Subjective Data
– Health history
• 2. Objective Data
– Physical assessment
– Diagnostic procedures/Studies
• Analysis/ Nursing Diagnosis
• Planning
– 1. Planning for Health Promotion
– 2. Planning for Health Restoration and Maintenance
• Implementation of Care of Clients
– 1. independent nursing care
– 2. interdependent Care

• Client education
• Evaluation of the outcome of care
• Reporting and Documentation of Care
• Thank you….
 Respiratory Assessment and
Monitoring
• The respiratory system ensures adequate
tissue and cellular oxygenation for the body.
• It is responsible for gas exchange through the
uptake of oxygen and excretion of carbon
dioxide; assists in optimal organ function;
contributes to acid–base balance; and
therefore plays a large role in maintaining
homeostasis.
RELATED ANATOMY AND PHYSIOLOGY
• The thorax cavity contains the trachea
and bronchial tree, the two lungs, pleura
and diaphragm.
• The mediastinum, located between the lungs,
houses and protects the heart, great vessels
and the esophagus.
• Twelve pairs of ribs cover the lungs, ten of which
are connected to the spine posteriorly, and to the
sternum or to the cartilage of the rib above
anteriorly (ribs 8–10). The 11th and 12th ribs
have no anterior attachment.
The respiratory system is divided into
upper and lower respiratory tracts:
• Upper airways consist of the nose, nasal
conchae, sinus and pharynx
• The lower respiratory tract includes the
larynx, trachea, bronchi and lungs.
• Larger airways are lined with stratified epithelial
tissue, which have a relatively high cellular
turnover rate; these cells protect and clear
these large airways.
• Extensive distribution of mucus/goblet cells
and cilia, which facilitate the mucociliary
clearance system and aid airway clearance.
 Upper Respiratory Tract
• The nasal cavities contain an extremely
vascular and mucoid environment for warming
and humidifying inhaled gases.
• Cilia at the top of the epithelial cells and mucus
provide filtration and cleaning of the inhaled
air.
• Mucus is moved by the cilia lining the conducting
airways towards the pharynx at a rate of 1–2 cm
per minute. One litre of mucus is produced every
day with only a small part not reabsorbed by the
body.
• The pharynx is a muscular tube that transports food and air to the
esophagus and larynx, respectively.
• Inferior to the pharynx, the larynx consists mostly of cartilage
attached to other cartilage and surrounding structures, and houses
the vestibular (false) vocal folds and the true vocal cords .
• An important pair of cartilages within the larynx is the pyramid-
shaped arytenoids, which act as attachment points for the vocal
cords.
– This area is easily damaged by pressure from endotracheal tubes; the
most significant independent risk factor for injury to the arytenoids is
the length of intubation time.
• The thyroid cartilage (‘Adam’s apple’) and the cricoid cartilage
protect the glottis and the entrance to the trachea.
• Another cartilage in the larynx is the triangular shaped elastic
epiglottis which protects the lower airways from aspiration of food
and fluids into the lungs.
• The epiglottis usually occludes the inlet to the larynx during
swallowing. The primitive cough, swallow and gag reflexes further
protect the airway.
 LOWER RESPIRATORY TRACT
• The trachea is a hollow tube approximately 11 cm long and 2.5 cm
in diameter, and marks the beginning of the lower respiratory
tract.
• The trachea is supported by 16–20 C-shaped cartilages, and is
another area at risk of pressure damage from artificial airways.
• The trachea divides at the carina into the left and right main
bronchi.
• The bronchial tree has two main stem bronchi that are structurally
different.
• The right bronchus is wider and angles slightly where it divides
further into the three lobes of the right lung. The most common
site of aspiration of foreign objects is the right bronchus because
of its anatomical position.
• The acutely angled left main bronchus divides further into the two
main lobes of the left lung.
 THORAX/LUNGS
• The lungs and heart are protected within the thoracic cage. Expansion of
the thorax enables the lungs to fill with air during inspiration when
respiration is triggered, and to passively compress to expel air from the
lungs during expiration.
• The diaphragm separates the thorax from the abdomen and actively
participates in the ventilation process. The diaphragm is the most important
inspiratory muscle, performing approximately 80% of the work of breathing.
Inspiration is initiated from the medulla, sending impulses through the
phrenic nerve to stimulate the diaphragm to contract and flatten.
• The phrenic nerve originates in the cervical plexus and involves the third to
fifth cervical nerves. It splits into two parts, passing to the left and right side
of the heart before it reaches the diaphragm. For this reason, patients can
have ventilation difficulties if phrenic nerve damage is due to C3–C5 trauma.
• The conducting airways move inspired air towards the respiratory unit,
ending in the terminal bronchioles.
• The respiratory bronchioles, the alveolar ducts and alveolar sacs form the
respiratory unit where the diffusion of gas molecules, or gas exchange,
occurs. The respiratory unit makes up most of the lung with a volume of 2.5–
3 L during rest.
 Surfactant
• Of particular importance to the structure and function of
the respiratory system are the type I and II alveolar
epithelial cells.
• Type I cells provide support of the wall within the alveolar
unit.
• Type II cells produce an important lipoprotein, surfactant,
that lines the inner alveolar surface, and lowers surface
tension of the alveoli, stabilizing the alveoli to optimize lung
compliance and facilitate expansion during inspiration.

• If surfactant synthesis is reduced due to pulmonary disease,

lung compliance decreases and the work of breathing
increases.
 Pleura
• Each lung is contained within a continuous thin membrane called
the pleura, and thus each lung is surrounded by a pleural sac.
• The parietal pleura lines the inner surface of the chest wall and is in
close contact with the visceral pleura, which covers the lungs.
• The pleural space, between these two layers, contains a small amount
of serous fluid, which normally limits friction during lung expansion.
• The intra-pleural pressure in the pleural space under normal
circumstances is always negative with a range of −4 to −10 cmH2O; this
negative pressure keeps the lungs inflated.
• During inhalation the pressure becomes more negative as both the lungs
and the chest wall are elastic structures. These elastic fibres of the lung
pull the visceral pleura inwards while the chest wall pulls the parietal
pleura outward. The pressure difference between the alveolar pressure (0
cmH2O pressure in the lungs) and the intra-pleural pressure (−4 cmH2O)
across the lung wall is termed the trans-pulmonary pressure (+4 cmH2O
[0
– (−4) = +4]), and is the force that hold the lungs open.
During inhalation the pressure becomes more
negative as both the lungs and the chest wall
are elastic structures. These elastic fibres of the
lung pull the visceral pleura inwards while the
chest wall pulls the parietal pleura outward.
The pressure difference between the alveolar
pressure (0 cmH2O pressure in the lungs) and
the intra-pleural pressure (−4 cmH2O) across
the lung wall is termed the trans-pulmonary
pressure (+4 cmH2O [0 − (−4) = +4]), and is the
force that hold the lungs open.
 Pulmonary Circulation
• The circulatory system of the lung receives the entire cardiac output but
operates as a low pressure system, as it only directs blood back to the left
side of the heart (unlike the systemic circulation which pumps blood to
different regions of the entire body).

• The pulmonary circulation involves oxygen-depleted blood being pumped

by the right ventricle to the lungs via the pulmonary artery, with oxygen-
rich blood returning to the left atrium via the pulmonary veins.

• Pulmonary blood vessels follow the path of the bronchioles, with the
capillaries forming a dense network in the walls of the alveoli.
As illustrated in Figure 13.5, 5 the
entire surface area of the alveolar
wall is covered by these capillaries,
where gas exchange occurs as the
capillaries are just large enough for
a red blood cell to pass through.
• Pulmonary vessels are short, thin and have
relatively little smooth muscle.
• The pressure inside the vessels is remarkably
low (normal pulmonary artery pressure is only
25/8 mmHg; mean 15 mmHg).
This low pressure system ensures that the work of the right heart is as
small as feasible, while promoting efficient gas exchange in the lungs.
 Bronchial Circulation
• The bronchial circulation, part of the systemic
circulation, supplies oxygenated blood, nutrients
and heat to the conducting airways (to the level of
the terminal bronchioles) and to the pleura.
• Drainage of this deoxygenated blood is
predominantly through the bronchial network,
although some capillaries drain into the
pulmonary arterial circulation, contributing to
venous admixture or right-to-left shunt.
 CONTROL OF VENTILATION
• Normal breathing occurs automatically and is
a complex function not fully understood.
• It is coordinated by the respiratory center,
regulated by controllers in the brain, effectors
in the muscles and sensors including
chemoreceptors and mechanoreceptors.
• There are also protective reflexes that
respond to irritation of the respiratory tract
such as coughing and sneezing
• CONTROLLERS:

• In the brainstem, the medulla oblongata and the pons regulate automatic
ventilation while the cerebral cortex regulates voluntary ventilation .
• The inspiratory center (or dorsal respiratory group) triggers inspiration.
• The expiratory center (or ventral respiratory group) only functions during
forced respiration and active expiration.
• The pneumotaxic and apneustic center in the pons adjusts the rate and
pattern of breathing.
• The cerebral cortex provides conscious voluntary control over the respiratory
muscles. This voluntary control cannot be maintained when PCO2 and
hydrogen ion (H+ ) concentration become markedly elevated; an example is
the inability to hold your breath for very long.
• Emotional and autonomic activities also often affect the pace and depth of
breathing.
• EFFECTORS
• The diaphragm is the major muscle of inspiration.
• The accessory muscles of inspiration (scalenes,
sternocleidomasteoid muscles and the pectoralis minor of the
thorax) are active only during exercise or strenuous breathing.
• Expiration is a passive act and only the internal intercostal muscles
are involved at rest.
• During exercise, the abdominal muscles also contribute to
expiration.
• Inspiration is triggered by stimulus from the medulla, causing the
diaphragm to contract downwards, and the external intercostal
muscles to contract, lifting the thorax up and out.
• This action lowers pressure within the alveoli (intra-alveolar
pressure) relative to atmospheric pressure. Air rushes into the
lungs to equalize the pressure gradient.
• After contraction has ceased, the ribs and diaphragm relax, the
pressure gradient reverses, and air is passively expelled from the
lungs and return to their resting state due to elastic recoil.
 Sensors
• A chemoreceptor is a sensor that responds to a change
in the chemical composition of the blood; there are
two types: central and peripheral.
• Central chemoreceptors account for 70% of the
feedback controlling ventilation, and respond quickly
to changes in the pH of cerebral spinal fluid (CSF)
(increase of PCO2 in arterial blood).If the PCO2 in
arterial blood remains high for a prolonged period, as
in chronic obstructive pulmonary disease (COPD), a
compensatory change in HCO3 occurs and the pH in
CSF returns to its near normal value.
• Peripheral chemoreceptors respond to low partial pressure of oxygen
in arterial blood (PaO2) and contribute to maintaining ventilation,
functioning optimally when oxygen levels fall below 70 mmHg.
• Central chemoreceptors located in the medulla respond to changes in
hydrogen ion concentration in the CSF that surrounds these
receptors.
• Note also that hyperventilation may reduce the level of PaCO2 to a level
that could cause accidental unconsciousness if the breath is held after
hyperventilation. This phenomenon is well known amongst divers and is
due to increasing levels of CO2 as the primary trigger of breathing. If the
CO2 level is too low due to hyperventilation, the breathing reflex is not
triggered until the level of oxygen has dropped below what is necessary
to maintain consciousness.
 PULMONARY VOLUMES AND
CAPACITIES
• In healthy individuals, the lungs are readily distensible or
compliant; when exposed to high expanding pressures or in
disease states, compliance is increased or decreased.
• Tidal volume (TV) is the volume of air entering the lungs
during a single inspiration and is normally equal to the
volume leaving the lungs on expiration (around 500 mL).
During inspiration, the TV of inspired air is added to the
2400 mL of air already in the lungs.
• This volume of air that remains in the lungs after a normal
expiration is the functional residual capacity (FRC), which
has an important role in keeping small alveoli open and
avoiding atelectasis.
• Alveolar Ventilation Minute volume (MV), often
referred to during mechanical ventilation, is TV
multiplied by respiratory frequency (e.g. 500 mL ×
12 breaths per minute = 6000 mL MV).
• Importantly, only the first 350 mL of inhaled air in
each breath reaches the alveolar exchange
surface, with 150 mL remaining in the conducting
airways (called the ‘anatomic dead space’).
• Alveolar ventilation is the amount of inhaled air
that reaches the alveoli each minute (e.g. 350 mL
× 12 = 4200 mL of alveolar ventilation).8
 WORK OF BREATHING
• In a resting state, energy requirements to breathe is minimal (less than 5% of total O2
consumption).However, changes in airway resistance and lung compliance affect the work of
breathing (WOB), resulting in increased oxygen consumption (VO2).
• As noted earlier, the lungs are very distensible and expand during inspiration. This expansion
is called the elastic or compliance work and refers to the ease by which lungs expand under
pressure.
• Lung compliance is often monitored when patients are mechanically ventilated, and is
calculated by dividing the change in lung volume by the change in transpulmonary pressure.
• For the lung to expand, it must overcome lung viscosity and chest wall tissue (called ‘tissue
resistance work’).
• Finally, there is airway resistance work – movement of air into the lungs via the airways. The
work associated with resistance and compliance is easily overcome in healthy individuals but
in pulmonary disease, both resistance and compliance work is increased.
• During exertion, when increased muscle function heightens metabolic rate, oxygen demand
rises to match consumption and avoid anaerobic metabolism, and work of breathing is
increased. The term ‘work of breathing’ is often used in those who are critically ill, when
basic respiratory processes are challenged and breathing consumes a far greater proportion
of total energy.
 PRINCIPLES OF GAS TRANSPORT AND
EXCHANGE IN ALVEOLI AND TISSUES
• Oxygen and carbon dioxide is transported in the bloodstream between
the alveoli and the tissue cells by the cardiac output.
• Delivery of oxygen to tissues and transfer of carbon dioxide from the
tissues to the capillary occurs by diffusion and is therefore dependent
on the pressure gradient between the capillary and the cell.
• Diffusion involves molecules moving from areas of high concentration
to low concentration.
• Other determinants of the rate of diffusion include the thickness of
the alveolar membrane, the amount of surface area of the membrane
available for gas transfer and the inherent solubility of the gas.
• Carbon dioxide diffuses about 20 times more rapidly than oxygen
because of the much higher solubility of carbon dioxide in blood.
• Gas exchange occurs through the exceptionally thin alveolar membranes.
Oxygen uptake takes place from the external environment via the lungs
through to the blood in the adjacent alveolar capillary networks.
Similarly, carbon dioxide diffuses from capillaries to the alveoli and is
then expired
 ACID–BASE CONTROL: RESPIRATORY
MECHANISMS
• The respiratory system plays a vital role in acid–base balance.
• Changes in respiratory rate and depth can produce changes in
body pH by altering the amount of carbonic acid (H2CO3) in the
blood.
• When dissolved, CO2 forms bicarbonate ion (HCO3 − ), carbonic
acid (H2CO3) and carbonate ion (CO3 2− ); these concentrations
affect the acid–base balance.
• Carbonic acid partially dissociates when in solution, to form CO2
and water or bicarbonate and hydrogen ion: CO H O H CO HCO H 2
2+↔↔+233+.
• The strength of the dissociation is defined by the Henderson–
Hasselbach equation that describes the relationship between
bicarbonate, CO2 and pH, and explains why an increase in
dissolved CO2 causes an increase in the acidity of the plasma,
while an increase in HCO3 − causes the pH to rise (i.e. acidity falls)
• Respiratory acidosis is caused by CO2 retention and
increases the denominator in the Henderson–
Hasselbach equation resulting in a decreased pH
level.
• This condition occurs when a patient takes small
breaths at a low respiratory rate (hypoventilation).
In the acute state the body cannot compensate. If
the patient develops chronic CO2 retention over a
long period, there will be a renal response to the
increase in CO2. The renal system retains
bicarbonate to return the pH to normal (i.e.
respiratory acidosis is compensated).
• Respiratory alkalosis occurs when a patient
hyperventilates with large, frequent breaths;
CO2 decreases in arterial blood and pH rises.
• If this condition is maintained (e.g. walking at
high altitude), the kidney excrete bicarbonate
and pH returns to normal (i.e. the respiratory
alkalosis is compensated).11
 PATHOPHYSIOLOGY
• Three common pathophysiological concepts
that influence respiratory function in
critically ill patients are hypoxemia,
inflammation and edema.
 HYPOXEMIA
• A decrease in the partial pressure of oxygen in arterial blood
(PaO2) of less than 60 mmHg.
• This state leads to less efficient anaerobic metabolism at the
tissue and end-organ level, and resulting compromised
cellular function.
• Hypoxia is abnormally low PO2 in the tissues, and can be due
to: l
– ‘hypoxic’ hypoxia: low PaO2 in arterial blood due to pulmonary disease
– circulatory’ hypoxia: reduction of tissue blood flow due to shock or local obstruction
– ‘anemic’ hypoxia: reduced ability of the blood to carry oxygen due to anemia or carbon
monoxide poisoning l
– ‘histotoxic’ hypoxia: a cellular environment that does not support oxygen utilization due
to tissue poisoning (e.g. cyanide poisoning).
–
• A hypoxic patient can show symptoms of fatigue and
shortness of breath if the hypoxia has developed gradually. If
the patient has severe hypoxia with rapid onset, they will
have ashen skin and blue discoloration (cyanosis) of the oral
mucosa, lips, and nail beds. Confusion, disorientation and
anxiety are other symptoms. In later stages, unconsciousness,
coma and death occur.
• Acute respiratory failure is a common patient presentation in
ICU that is characterized by decreased gas exchange with
resultant hypoxemia.
• Two different mechanisms cause acute respiratory failure:
• Type I presents with low PO2 and normal PCO2
• Type II presents with low PO2 and high
• In general, impaired gas exchange results from alveolar
hypoventilation, ventilation/perfusion mismatching and
intrapulmonary shunting, each resulting in hypoxemia.
• Hypercapnia may also be present depending on the underlying
pathophysiology.
• Alveolar hypoventilation occurs when the metabolic needs of the
body are not met by the amount of oxygen in the alveoli. Hypoxemia
due to alveolar hypoventilation is usually extra pulmonary (e.g.
altered metabolism, interruption to neuromuscular control of
breathing/ ventilation) and associated with hypercapnia.
• Ventilation/perfusion (V/Q) mismatch results when areas of lung that
are perfused are not ventilated (no participation in gas exchange)
because alveoli are collapsed or infiltrated with fluid from
inflammation or infection (e.g. pulmonary edema, pneumonia).
 Compensatory Mechanisms to
Optimise Oxygenation
• When PO2 in the alveolus is reduced, hypoxic
pulmonary vasoconstriction occurs, with contraction of
smooth muscles in the small arterioles in the hypoxic
region, directing blood flow away from the hypoxic
area of the lung.
• Peripheral chemoreceptors also detect hypoxemia and
initiate compensatory mechanisms to optimize cellular
oxygen delivery. Initial responses are increased
respiratory rate and depth of breathing, resulting in
increased minute ventilation, and raised heart rate
with possible vasoconstriction as the body attempts to
maintain oxygen delivery and uptake.
 INFLAMMATION
• Inflammatory processes can occur at a local level
(e.g. as a result of inhalation injuries, aspiration or
respiratory infections) or are secondary to
systemic events (e.g. sepsis, trauma).
• Inflammation results in platelet aggregation and
complement release. Platelet aggregation
attracts neutrophils, which release inflammatory
mediators (e.g. proteolytic enzymes, oxygen free
radicals, leukotrienes, prostaglandins,
platelet-activating factor [PAF]).
 EDEMA
• Alters gas exchange, and results from abnormal
accumulation of extravascular fluid in the lung.
• The two main reasons for this are:
• 1. ‘increased pressure’, where there is an increase in
hydrostatic or osmotic forces (e.g. left heart ventricular
dysfunction or volume overload)
• 2. ‘increased permeability’ edema, that results from increased
membrane permeability of the epithelium or endothelium in
the lung, allowing accumulation of fluid (also called
‘noncardiogenic).
 Changes to Respiratory Function
• During the early exudative phase of ALI/ARDS, tachypnea, signs of
hypoxemia (apprehension, restlessness) and an increase in the use
of accessory muscles are usually evident as a result of infiltration
of fluids into the alveoli.
• With impaired production of surfactant during the proliferative
phase, respiratory function deteriorates, and dyspnea, agitation,
fatigue and the emergence of fine crackles on auscultation are
common.

• Airway resistance is increased when edema affects larger airways.

• Lung compliance is reduced as interstitial edema interferes with
the elastic properties of the lungs, and patients may be quite a
challenge to adequately ventilate.
• Infiltration of type II alveolar cells into the epithelium may lead to
interstitial fibrosis on healing, causing chronic lung dysfunction.
 Respiratory Dysfunction: Changes to
Work of Breathing
• Clinical manifestations include tachypnea,
tachycardia, dyspnoea, low tidal volumes and
diaphoresis. Hypercapnea will ensue, which
further compromises respiratory muscle function
and precipitates diaphragmatic fatigue. Oxygen
consumption during breathing can be so great
that reserve capacity is reduced. If patients with
preexisting COPD (who may breathe close to the
fatigue work level) experience an acute
exacerbation, this can easily tip them into a
fatigued state.
 ASSESSMENT
• Assessment is a systematic process
comprising history taking of a patient’s
present and previous illnesses, and physical
examination of their thorax, lungs and related
systems.
• PATIENT HISTORY
• History-taking determines a patient’s baseline
respiratory status on admission to ICU.
• If the patient is in distress only a few questions may
be asked but, if the patient is able, a more
comprehensive interview can be performed,
focusing on four areas: the current problem,
previous problems, symptoms and personal and
family history.
• Current Respiratory Problems
• Begin by asking why the patient is seeking care.
• If possible, let the patient describe the respiratory
problem in his or her own words.
• Be focused and listen actively.
• Ask for location, onset and duration of the respiratory
symptoms.
• Previous Respiratory Problems
• Respiratory disorders can be chronic and pulmonary
diseases may recur (e.g. tuberculosis), and new
diseases can complicate old ones.
• Ask about problems with breathing and their chest,
number of hospitalizations, treatments, and childhood
respiratory diseases.
• Symptoms
• Assess any presenting symptoms in relation to: onset
and duration, pattern, severity, and episodic or
continuous.
• Ask about the patient’s perception of their respiratory
problem, their opinion about its cause and if the
symptoms cause fatigue, anxiety or stress.
• Ask the patient specifically about: dyspnea, cough,
sputum production, hemoptysis, wheezing, chest pain
or other pain, sleep disturbances and snoring.
 Personal and Family History
• The focus of this questioning is on: tobacco use, allergies,
recent travel, type of occupation, home situation and family
history.

• Ask the patient to quantify the amount of cigarette packs per week
and how many years they have smoked.
• Exposure to secondhand smoke may also be of interest.
• A history of recent travel increases the possibility of exposure to
infectious diseases affecting the respiratory system.
• Recent long flights are also responsible for the possibility of deep
venous thrombosis which can lead to pulmonary embolism.
• An occupation with exposure to allergens and toxins in the work place
is important information to collect because this can be associated with a
decline in lung function.
• Ask about the patient’s home situation and whether they live with
someone with an infection or disease such as influenza or
tuberculosis.
• Check also whether there is a family history of cancer, heart or
respiratory diseases.
• PHYSICAL EXAMINATION
• The four activities of physical examination
are inspection, palpation, percussion and
auscultation.
 Inspection

• Inspection involves carefully observing the

patient for signs of respiratory problems.
Focus on: patient position, chest wall
inspection, respiratory rate and rhythm,
respiratory effort, central or peripheral
cyanosis and clubbing.
 Palpation
• Palpate the patient’s chest with warm hands,
focusing on: areas of tenderness, tracheal
position, presence of subcutaneous
emphysema and tactile fremitus.
• Assess for symmetry (left compared to right)
and anterior and posterior surfaces.
Palpate cervical lymph nodes and supraclavicular nodes as wells as the
salivary glands.
 Auscultation
• Careful interpretation of breath sounds and
integration of this assessment data with other
findings can provide important information
about lung disorders.
• Use the diaphragm of the stethoscope and
ensure full contact with the skin for optimal
listening.
 Documentation and Charting
• Document the findings of your respiratory
assessment in the patient’s chart; if this is the
first respiratory assessment, describe the
patient’s respiratory history carefully.
• Any abnormal findings including abnormal
sounds and their characteristics should be
described to enable subsequent re-
assessment.
 RESPIRATORY MONITORING
• PULSE OXIMETRY
• A pulse oximeter is a non-invasive device that measures
• the arterial oxygen saturation of haemoglobin in a
• patient’s blood flow. The technology is commonly standard
• in critical care units and other acute care areas.
• It is important to note that the device does not provide
• information on the patient’s ventilatory state, but it can
• determine their oxygen saturation and detect hypoxaemia.
• This prompt non-invasive detection of hypoxaemia
• enables identification of clinical deterioration and more
• rapid treatment to avoid associated complications
 Limitations of Pulse Oximetry
• Pulse oximetry in isolation does not provide all the
necessary information on ventilation status and acid–
base balance.
• Pulse oximeters are relatively reliable when the SaO2
is 90% or above, however accuracy deteriorates when
the SaO2 falls to 80% or less.33 When SpO2 appear
abnormal, assess the ABGs.
• As satisfactory arterial perfusion of the monitoring
area is required, low cardiac output states,
vasoconstriction, peripheral vascular disease and
hypothermia can cause inaccurate pulse signals and
falsely low oxygen saturation readings.
• As cardiac arrhythmias can impair perfusion and
flow, signal quality may be compromised.
• Motion artifact caused by patient movement or
shivering, is a significant cause of erroneously low
readings and false alarms.
• There is conflicting evidence as to whether nail
varnish or acrylic nails interfere with SpO2
readings. Blue, green and black nail varnishes may
affect accuracy of readings. To ensure accuracy, it
is recommended that nail varnish and acrylic nails
be removed if possible.
• Dark skin pigmentation can lead to falsely elevated
SpO2 values especially at low saturation levels.
• External light, especially fluorescent light and heat
lamps, can lead to an over- or under-estimation of
SpO2.
• Dyshaemoglobins, particularly carboxyhaemoglobin
and methaemoglobin render SpO2 monitoring
unreliable.
• Injection of intravenous dyes may lead to a false
underestimation of SpO2 for up to 20 minutes after
their administration (methylene blue, indocyanine
green, indigo carmine).
• CAPNOGRAPHY
• Capnography monitors expired CO2 during
the respiratory cycle (also termed end-tidal
CO2 [PetCO2] monitoring) by infrared
spectrometry.
• it is the best method of confirming correct ETT
placement and maintaining correct positioning of the
ETT, ensuring tube patency and detecting leaks or
disconnection of the circuit.
• monitoring ventilation status during weaning from
mechanical ventilation and after extubation.
• assessing the effectiveness of cardiopulmonary
resuscitation compressions and detecting return of
spontaneous circulation.
• monitoring ventilation continuously during sedation
and anaesthesia
• assessing ventilation/perfusion status
 VENTILATION MONITORING
• Mechanical ventilation is a common
intervention in ICU for patients with
respiratory failure or who require respiratory
support.
• ARTERIAL BLOOD GASES
• Arterial blood gases (ABGs) are one of the most commonly
performed laboratory tests in critical care, and accurate
interpretation of ABG analysis is therefore an important
clinical skill.
• ABG measurements enable rapid assessment of
oxygenation and ventilation and all ICUs are recommended
to have a blood gas analyzer as a minimum standard.
• Blood for ABG analysis is sampled by arterial puncture, or
more commonly in critically ill patients, from an arterial
catheter usually sited in the radial or femoral artery.
• Arterial Blood Gas Analysis
• ABG analysis includes the measurement of the
partial pressure of oxygen in arterial blood
(PaO2), the partial pressure of carbon dioxide
in arterial blood (PaCO2), the hydrogen ion
concentration of the blood (pH), and the
chemical buffer, bicarbonate (HCO3–).
• When assessing PaO2, hypoxaemia (<60 mmHg)
will be the most common abnormality, and
supplemental oxygen will be required to maintain
adequate tissue oxygenation.
• Hyperoxia rarely occurs unless a patient is
receiving supplemental oxygen therapy. Oxygen
can be toxic to cells if delivered at high
concentrations for a prolonged period.
• The pH level is assessed to determine if it falls on
the acidic or alkaline side of 7.4.
• On the pH scale of 1–14 (1 = the strongest acid, 14
= the strongest alkali), a pH of 7.4 is the middle of
the normal range.
• pH measures the acid–base balance of the blood
sample, where Hydrogen (H+) ions are the acid
and HCO3− is the base or buffer.
• The body’s acid–base balance is affected by both
the respiratory and metabolic systems.
• Acidaemia is present with a pH of <7.36;
alkalaemia is present with a pH of >7.44.
• PaCO2 is an indicator of the effectiveness of ventilation in
removing CO2.
• CO2 is a potential acid as it combines with H2O in the blood to
form carbonic acid (H2CO3). Retention of CO2 (through
hypoventilation) leads to increased H+ resulting in a lower pH, and
similarly a loss of CO2 (through hyperventilation) results in a
higher pH.49
• A PaCO2 of >45 mmHg (6 kPa) indicates alveolar hypoventilation,
due to chronic obstructive pulmonary disease, asthma, pulmonary
edema, airway obstruction, over sedation, narcosis, drug
overdose, pain, neurological deficit or permissive hypercapnea in
mechanically ventilated patients.
• Conversely, a PaCO2 of <35 mmHg (4.7 kPa) reflects alveolar
hyperventilation, and can be due to hypoxia, pain, anxiety,
pregnancy, permissive hypocapnia in mechanically ventilated
patients or as a compensatory mechanism for metabolic acidosis.
• Bicarbonate (HCO3−) is regulated by the renal
system and indicates metabolic functioning.
• A HCO3− of < 22 mmol/L can be caused by renal
failure, ketoacidosis, lactic acidosis, diarrhoea, or
cardiac arrest.
A HCO3− of >32 can be caused by severe
vomiting, continuous nasogastric suction,
diuretics, corticosteroids, or excessive citrate
administration from stored blood or renal
replacement therapy.
• Base excess is an additional parameter measured as part of
the ABG report and it reflects the excess (or deficit) of base
to acid in the blood.
• A positive figure indicates a base excess (more base than
acid; i.e. alkalosis if >+3); a negative figure indicates a base
deficit (more acid than base i.e. acidosis if >−3).
• If the base excess is +2 mmol/L, then removal of 2 mmol of
base per litre of blood is required to return the pH to 7.4.
• If the base excess is −2 mmol/L (i.e. a base deficit), then 2
mmol ofbase per litre of blood needs to be added to have a
pH of 7.4.
To assess compensation, pH, CO2 and HCO3 − are examined in the context
of a patient’s clinical presentation:

• In a fully compensated state, the pH is returned to within

normal limits, but the other two parameters will be outside
normal limits as the body has successfully manipulated CO2
and HCO3 − levels to restore pH,
• l in a partially compensated state, the pH is not within normal
limits, and the other parameters will also be back to within
normal limits
• l in a non-compensated state, the pH will be outside normal
limits, and the primary disruption (either CO2 or HCO3−) will
also be outside normal limits while the remaining parameter
has not compensated for this derangement and has stayed
within normal limits.
• BLOOD TESTS
• Investigation of hematology and biochemistry values for a patient with
respiratory dysfunction can aid their overall treatment.
• Full blood count (FBC), including a leukocyte differential count, can track a
patient’s white cell count (WCC) if they have a confirmed or suspected
infective process.
• When infections are severe, the FBC will show a dramatic rise in the
number of immature neutrophils.
• Blood cultures can also be drawn to assist in diagnosis of bacterial or
yeast infections and isolation of the causative organism. Viral studies may
be conducted to aid diagnosis for respiratory infections of unknown
origin.
• If the patient is suspected of having a pulmonary embolism, a D-dimer
test can determine the presence of a thrombus.
• Urea and electrolytes will also be routinely measured to monitor a
patient’s renal function and acid–base status
• SPUTUM, TRACHEAL ASPIRATES AND
NASOPHARYNGEAL ASPIRATES
• Colour, consistency and volume of sputum
provides useful information in determining
changes in a patient’s respiratory status and
progress. Regular cultures of tracheal sputum
facilitates tracking of colonisation by
opportunistic organisms, or the identification of
the cause of an acute chest infection or sepsis.
 DIAGNOSTIC PROCEDURES
• Chest X-ray
• Chest X-ray (CXR) is a common diagnostic tool
used for respiratory examination of critically
ill patients. Chest radiography allows basic
information regarding abnormalities in the
chest to be obtained relatively quickly. The
image provides information about lung fields
and other thoracic structures as well as the
placement of various invasive lines and tubes
 Common abnormalities that can be detected by CXR
include:
• Lobar collapse or atelectasis: The image reveals all or some of the following features:
loss of lung volume, displacement of fissures and vascular markings, and
diaphragmatic elevation on the affected side.
• l Pneumothorax: Check for lack of pulmonary vascular markings on the affected side
so the lung field appears black; there will be mediastinal and possibly tracheal shift
away from the affected side in a tension pneumothorax.
• l Pleural effusion: Visualised in the dependent areas of the pleural spaces;
costophrenic angles are blunted by fluid and there may be a shift of the mediastinum
away from a large effusion; best visualised with the patient upright, and will only be
evident on an AP image with 200–400 mL of fluid in the pleural space.
• l Pulmonary edema: Lung fields, particularly central and perihilar areas, appear
white; Kerley B lines (small horizontal lines no more than 2 cm long) may be present
in the lung periphery near the costophrenic angles.
• l Pulmonary embolism: Although not the optimal diagnostic tool, areas of infarction
may be visualised although these can be mistaken for collapse or consolidation.
• l Pneumoperitonium: Free air under the diaphragm elevates the diaphragm.
• Ultrasound
• Ultrasound imaging (sonography) is a useful
bedside diagnostic tool for a select group of
critically ill patients and can add to the diagnostic
information provided by chest X-rays and
computerized tomography (CT) scanning.
• The technique uses high-frequency sound waves
which when probed on the body, reflect and
scatter.
• Computed Tomography
• Computed tomography (CT) is a diagnostic
investigation that provides greater specificity
in chest anatomy and pathophysiology than a
plain CXR, as it uses multiple beams in a circle
around the body. These beams are directed to
a specific area of the body and provide
detailed, consecutive cross-sectional slices of
the scanned regions
• Magnetic Resonance Imaging
• Magnetic resonance imaging (MRI) uses radiofrequency waves and
a strong magnetic field rather than X-rays to provide clear and
detailed pictures of internal organs and soft tissues.
• These high-contrast images of soft tissue are clearer than those
generated by X-ray or CT scans.
• The strong magnetic field around the scanner means that
ferromagnetic objects (metallic objects containing material that
can be attracted by magnets, such as iron or steel) can become
potentially fatal projectiles.
• MRI scans may therefore be unsuitable for patients with implanted
pacemakers, defibrillators or neurostimulation devices; some
types of intracranial aneurysm clips; and loose dental fillings.
• Ventilation/Perfusion Scan
• The ventilation/perfusion (V/Q) scan is indicated
when a mismatch of lung ventilation and
perfusion is suspected; the most common
indication is for pulmonary embolism.
• The ventilation scan is performed with the patient
inhaling a radio isotopic gas to demonstrate
ventilation of the lung, while the perfusion scan is
performed using an intravenous radioisotope that
reveals distribution of blood flow in the blood
vessels of the lungs.
• BRONCHOSCOPY
• Bronchoscopy is a bedside technique used for both diagnostic and
therapeutic purposes.
• The bronchoscope can be either rigid or flexible; the most widely used
type in critical care is the flexible fibrotic bronchoscope. A flexible fibre
optic bronchoscope allows direct visualisation of respiratory mucosa and
thorough examination of the upper airways and tracheobronchial tree.
• The scope is passed into the trachea via the oropharynx or nares. In
mechanically-ventilated patients, the scope can be passed quickly and
easily down the endotracheal (ETT) or tracheostomy tube (TT) allowing
rapid access to the airways.
• Supplemental oxygen can be administered during the bronchoscopy in
non-intubated patients and FiO2 can be increased in intubated patients.
• Accurate continuous monitoring during the procedure includes
continuous pulse oximetry, electrocardiography, respiratory rate, heart
rate and blood pressure.
 Respiratory Alterations
and Management
• The most common reason that patients
require admission to an intensive care unit
(ICU) is for support of their respiratory
system.
 RESPIRATORY FAILURE
• Respiratory failure occurs when there is a
reduction in the body’s ability to maintain either
oxygenation or ventilation, or both.
• It may occur acutely, as observed in pneumonia
and ARDS or it may exist in chronic form, as
observed in asthma and COPD.
• Respiratory failure, and the disorders that cause
it, are responsible for a high proportion of death
and disability throughout the world.
 ETIOLOGY OF RESPIRATORY FAILURE
• For the respiratory system to function
effectively, the rate and depth of breathing is
controlled by the brain, the chest wall must
expand adequately, air needs to flow easily
through the airways and effective exchange of
gases needs to occur at the alveolar level.
Conditions that impact on one or more aspects of the normal
physiological functioning of the respiratory system can cause
respiratory failure:
• decreased respiratory drive may be caused by brain trauma, drug
overdose or anaesthesia/sedation
• decreased respiratory muscle strength may be caused by Guillain–
Barré syndrome, poliomyelitis, myasthenia gravis or spinal cord
injury
• decreased chest wall expansion may be caused by postoperative
pain, rib fractures or a pneumothorax
• increased airway resistance may be caused by asthma or COPD.
• increased metabolic oxygen requirements may be caused by
severe sepsis
• decreased capacity for gas exchange may be caused by
impairment in either ventilation (e.g. pulmonary edema,
pneumonia, acute lung injury, COPD) or pulmonary perfusion (e.g.
pulmonary embolism), or a combination of the two.
 PATHOPHYSIOLOGY

• Respiratory failure occurs when the

respiratory system fails to achieve one or both
of its essential gas exchange functions:
oxygenation or elimination of carbon dioxide,
and can be described either as type I
(primarily a failure of oxygenation) or type II
(primarily a failure of ventilation).
 Type I Respiratory Failure
• A patient with type I (‘hypoxaemic’) respiratory
failure presents with a low PaO2 and a normal or
low PaCO2.
• Hypoxaemic respiratory failure may be caused by
a reduction in inspired oxygen pressure (e.g. such
as extreme altitude), hypoventilation, impaired
diffusion or ventilation-perfusion mismatch.
• Most major respiratory alterations cause this type
of failure, usually as a result of hypoventilation
due to alveolar collapse or consolidation, or a
perfusion abnormality.
 Type II Respiratory Failure
• A patient with Type II respiratory
(‘hypercapnoeic/hypoxaemic’) failure presents
with a high PaCO2 as well as a low PaO2.
• This failure is caused by alveolar hypoventilation,
where the respiratory effort (or minute
ventilation) is insufficient to allow adequate
exchange of oxygen and carbon dioxide.
• This may be caused by conditions that affect
respiratory drive such as neuromuscular diseases,
chest wall abnormalities or severe airways disease
(e.g. asthma or COPD).
 CLINICAL MANIFESTATIONS
• Dyspnea is the most common symptom
associated with ARF; this is often
accompanied by an increased rate and
reduced depth of breathing and the use of
accessory muscles.
• Patients may also present with cyanosis,
anxiety, confusion and/or sleepiness
• INDEPENDENT NURSING PRACTICE
• The primary survey (airway, breathing and circulation) and
immediate management form initial routine practice.
• Frequent assessment and monitoring of respiratory
function, including a patient’s response to supplemental
oxygen and/or ventilatory support, is the focus.
• Patient comfort and compliance with the ventilation mode,
ABG analysis and pulse oximetry guide any titration of
ventilation.
• The key goals of management are to treat the primary cause
of respiratory failure, maintain adequate oxygenation and
ventilation and prevent or minimise the potential
complications of positive pressure mechanical ventilation.
 Maintaining Oxygenation and
Ventilation
• The therapeutic aim is to titrate the
fraction/percentage of inspired oxygen (FiO2) to
achieve a PaO2 of 65–70 mmHg and to maintain
minute ventilation to achieve PaCO2 within
normal limits where possible.
• Nursing staff in ICU are therefore commonly
responsible for titration of oxygen therapy to
maintain a specific PaO2 or SpO2, and the
alteration of respiratory rate and/or tidal volume
to maintain a specified PaCO2.
• COLLABORATIVE PRACTICE
• A patient with ARF requires extensive
multidisciplinary collaboration between nurses,
physiotherapists, specialist medical staff, speech
and occupational therapists, dietitians, social
workers, radiologists and radiographers.
• Chest physiotherapy is a routine activity for
managing patients with ARF. This involves
positioning, manual hyperinflation, percussion
and vibration and suctioning
• Medications
• Medications commonly prescribed in
respiratory failure include inhalation steroids
and bronchodilators, intravenous steroids and
bronchodilators, antibiotic therapy, analgesia
and sedation to maintain patient–ventilator
synchrony, but may also involve nitric oxide,
glucocorticoid or surfactant administration.
• SPECIAL CONSIDERATIONS
• Respiratory failure in patients who are
pregnant, elderly or have comorbidities
require specific attention to avoid
clinical deterioration.
• Post-anaesthesia Respiratory Support
• Short-term respiratory support may be required after major
surgery, in cases of extended anaesthesia, preexisting
comorbidities and/or diminished physical reserve(e.g.
elderly, patients with obstructive sleep apnea).
• Preoperative assessment and management is a key factor in
preventing respiratory complications.
• This involves optimising physical condition and nutritional
status, planning the timing of surgery to reduce the
likelihood of preexisting respiratory infection and patient
education regarding the importance of respiratory support,
including postoperative mobilisation and physiotherapy.
• The key focus in management of postoperative
ventilation is to limit ventilation time, as
prolonged ventilation time is associated with poor
outcome.
• Once a patient has reached normothermia, is
hemodynamically stable, responsive and has
adequate analgesia, weaning of ventilation is
commenced.
• Rapid and/or nurse-led weaning protocols are
often implemented to minimize delays in the
weaning process.
 PNEUMONIA
• Pneumonia is infection of the lung.
• Pneumonia can be caused by most types
of microorganisms, but is most commonly
a result of bacterial or viral infection.
 Two types:
• community-acquired pneumonia (CAP)
• ventilator-associated pneumonia (VAP)
 PATHOPHYSIOLOGY
An invading pathogen provokes an immune response in the
lungs, resulting in the following pathophysiological processes:
• Alteration in alveolar capillary permeability that leads to an
increase in protein-rich fluid in the alveoli; this impacts on gas
exchange and causes the patient to breathe faster in an effort
to increase oxygen uptake and remove CO2
• mucous production increases and mucous plugs may develop
which block off areas of the lung, further reducing capacity
for gas exchange
• consolidation occurs in the alveoli, filling with fluid and
debris; this occurs particularly with bacterial pneumonia
where debris accumulates from the large number of white
blood cells involved in the immune response.
 ETIOLOGY
• Pneumonia is caused by a variety of
microorganisms, including bacteria, viruses, fungi
and parasites.
• Viral pneumonias, especially influenza, are most
common in young children, while adults are more
likely to have pneumonia caused by bacteria such
as Streptococcus pneumoniae and Haemophilus
influenzae.
• Pneumonia is a particular concern among elderly
adults as they experience an increase in the
frequency and severity of pneumonia.
Community-acquired Pneumonia
• Clinical assessment, especially patient history, is
important in distinguishing the etiology and likely
causative organism in patients with community-
acquired pneumonia (CAP).
• Specific information regarding exposure to
animals, travel history, nursing home residency
and any occupational or unusual exposure may
provide the key to diagnosis.
• Personal habits such as smoking and alcohol
consumption increase the risk of developing
pneumonia and should be explored.
• Etiology was identified in 46% of episodes,
with the most frequent causes being
Streptococcus pneumoniae (14%),
Mycoplasma pneumoniae (9%) and
respiratory viruses (15%). Mechanical
ventilationor vasopressor support was
required in 11% of cases.
 Diagnosis of CAP
• Routine screening of patients with suspected
pneumonia continues to rely on microscopy
and culture of lower respiratory tract
specimens, blood cultures, detection of
antigens in urine and serology.
 Hospital-acquired and
Ventilator-associated Pneumonia
• Hospital-acquired or nosocomial pneumonia is defined
as pneumonia occurring more than 48 hours after
hospital admission.
• It is the second-most common nosocomial infection
and the leading cause of death from infection acquired
in-hospital.
• Ventilator-associated pneumonia (VAP) is a
nosocomial pneumonia in patients who are
mechanically ventilated.
• The incidence of VAP is reported at 10–30% among
patients who require mechanical ventilation for
greater than 48 hours
• Most cases (58%) of VAP are associated with
infection involving gram-negative bacilli such
as Pseudomonas aeruginosa and
Acinetobacter spp.
• A high number of cases (20%) are associated
with gram-positive Staphylococcus aureus.
Many cases of VAP are associated with
multiple organisms
 Diagnosis and treatment of VAP
• VAP can be difficult to diagnose, as clinical features can
be non-specific and other conditions may cause
infiltrates on chest X-ray (CXR).
• There are new infiltrates observed on CXR or when
clinical signs of infection begin to develop, e.g. new
onset of pyrexia, raised white blood cell counts,
purulent sputum and a difficulty in maintaining
adequate oxygenation.
• The most widely-recognized risk factor is the provision
of appropriate antibiotic treatment, which has reduced
mortality and the rate of complications.
 CLINICAL MANIFESTATIONS
• Common characteristics include fever, sweats,
• rigours, cough, sputum production, pleuritic
chest pain, dyspnea, tachypnea, pleural rub,
inspiratory crackles on auscultation, plus
radiological evidence of infiltrates or
consolidation.
• Cough is the most common finding and is
present in up to 80% of all patients with CAP
 COLLABORATIVE PRACTICE
• Early recognition of pneumonia and timely
administration of antibiotic therapy are
key aspects for patient management.
• The most important aspect of management in
VAP is prevention and this is a key emphasis in the
care of all mechanically-ventilated patients.
• Ventilator Care Bundle: elevating the head of
bed to 30–45 degrees, daily sedation vacation
and assessment of readiness to extubate, peptic
ulcer disease (PUD) prophylaxis and deep vein
thrombosis (DVT) prophylaxis.
 RESPIRATORY PANDEMICS
• Serious outbreaks of respiratory infections that spread
rapidly on a global scale are termed pandemics.
• Their spread is so rapid because the infection is usually
associated with emergence of a new virus where the
majority of the population has no immunity.
• These infections are characterized by extremely rapid
‘transmission with concurrent outbreaks throughout the
globe; the occurrence of disease outside the usual
seasonality, including during the summer months; high
attack rates in all age groups, with high levels of mortality
particularly in healthy young adults; and multiple waves of
disease immediately before and after the main outbreak.
 SEVERE ACUTE RESPIRATORY
SYNDROME
• In 2002–03 an outbreak of a novel Coronavirus
occurred in China and rapidly spread throughout the
world. The infection was highly virulent with over 8000
cases reported and a mortality rate of 11%.
• The infection was called Severe Acute Respiratory
Syndrome (SARS) due to the severity of the disease,
characterised by diffuse alveolar infiltrates, resulting in
about 20% of patients requiring respiratory support. ‘
• The SARS outbreak provoked a rapid and intense
public health response coordinated by the World
Health Organization (WHO), resulting in a cessation of
disease transmission within ten months.
• Coronavirus disease (COVID-19) is an infectious
disease caused by the SARS-CoV-2 virus.
• Most people infected with the virus will experience
mild to moderate respiratory illness and recover
without requiring special treatment. However, some
will become seriously ill and require medical attention.
Older people and those with underlying medical
conditions like cardiovascular disease, diabetes,
chronic respiratory disease, or cancer are more likely
to develop serious illness. Anyone can get sick with
COVID-19 and become seriously ill or die at any age.
• The virus can spread from an infected
person’s mouth or nose in small liquid
particles when they cough, sneeze, speak, sing
or breathe. These particles range from larger
respiratory droplets to smaller aerosols. It is
important to practice respiratory etiquette,
for example by coughing into a flexed elbow,
and to stay home and self-isolate until you
recover if you feel unwell.
• COVID-19 affects different people in different ways. Most infected
people will develop mild to moderate illness and recover without
hospitalization.
Most common symptoms:
• fever
• cough
• tiredness
• loss of taste or smell.
Less common symptoms:
• sore throat
• headache
• aches and pains
• diarrhoea
• a rash on skin, or discolouration of fingers or toes
• red or irritated eyes.
Serious symptoms:
• difficulty breathing or shortness of breath
• loss of speech or mobility, or confusion
• chest pain.

• Seek immediate medical attention if you have serious

symptoms. Always call before visiting your doctor or health
facility.
• People with mild symptoms who are otherwise healthy
should manage their symptoms at home.
• On average it takes 5–6 days from when someone is
infected with the virus for symptoms to show, however it
can take up to 14 days.
To prevent infection and to slow transmission of COVID-19, do the
following:

• Get vaccinated when a vaccine is available to you.

• Stay at least 1 metre apart from others, even if they don’t appear
to be sick.
• Wear a properly fitted mask when physical distancing is not
possible or when in poorly ventilated settings.
• Choose open, well-ventilated spaces over closed ones. Open a
window if indoors.
• Wash your hands regularly with soap and water or clean them
with alcohol-based hand rub.
• Cover your mouth and nose when coughing or sneezing.
• If you feel unwell, stay home and self-isolate until you recover.
 INFLUENZA PANDEMICS
• Epidemics of influenza occur regularly and are
associated with high morbidity and mortality.
Incidence is usually highest in the young,
while mortality is highest in the elderly
population.
• A feature of the influenza virus that
explains why it continues to be associated
with epidemic and pandemic disease is its
high frequency of antigenic variation.
• ISOLATION PRECAUTIONS AND PERSONAL PROTECTIVE
EQUIPMENT
• Key aspects of infection control in an epidemic or pandemic
situation focus on limiting opportunities for nosocomial
spread and the protection of health care workers.
• Guidelines for institutional management of these infections
involve designing and implementing appropriate isolation
procedures and recommending appropriate personal
protective equipment (PPE).
• The importance of adequate PPE was highlighted
particularly in the SARS epidemic where there was over
representation of health care workers who became patients
infectedwith the virus.
 PNEUMOTHORAX
• Pneumothorax describes air that has escaped from a
defect in the pulmonary tree and is trapped in the
potential space between the two pleura.
• A pneumothoraxnormally resolves with treatment.
• A pneumothorax is termed persistent if the air leak
lasts for more than five days,while one reappearing on
the same side after seven days is termed reoccurring.
• A pneumothorax can arise spontaneously, from
disease or from traumatic injury and can be life-
threatening.
• A tension pneumothorax involves significant
and progressive respiratory or hemodynamic
compromise that is quickly offset by
decompression.
• A patient with a tension pneumothorax can
present with symptoms similar to asthma, i.e.
‘respiratory distress, wheeze, tachycardia,
tachypnea, desaturation, hyper-expansion,
agitation and decreased air entry.’
• PATHOPHYSIOLOGY
• If the pleural defect functions as a one-way valve,
air enters the pleural cavity on inspiration but is
unable to exit on expiration, leading to increasing
ipsilateral intrapleural pressure.
• This causes further lung collapse, diaphragmatic
depression, and (dependent on mediastinal
distensibility) contralateral lung compression.
• CLINICAL MANIFESTATIONS
• Severe presentations are identified by history
and clinical examination (respiratory distress,
cyanosis, tachycardia, tracheal shift and
unilateral movement of the chest).
• They are also detected on CXR with a
translucent appearance of the air and absence
of lung markings.
• COLLABORATIVE PRACTICE
• Insertion of a thoracic underwater seal drain
allows the collapsed lung to re-expand. This
is facilitated with mechanical ventilation if
required.
• If a hemothorax is present,suction on the
underwater seal drain (20–60 mmHg) will
expedite drainage and re-expansion of
the lung.
• Pain management and facilitation of
respiratory care with oxygen therapy, non-
invasive or invasive ventilation, positioning
and deep-breathing and coughing, and the
monitoring of the chest tube and drainage for
presence of air-leak and serous drainage, are
key to recovery without development of
further complications.
 Ventilation and Oxygenation
Management
• Supporting oxygenation and ventilation
are two of the most common
interventions in intensive care.
 OXYGEN THERAPY
• Oxygen is required for aerobic cellular
metabolism and ultimately for human
survival, with some cells, such as those in the
brain, being more sensitive to hypoxia than
others.
• Oxygen therapy should be considered for
patients with a significant reduction in arterial
oxygen levels, irrespective of diagnosis and
especially if the patient is drowsy or
unconscious.
• Indications for oxygen therapy include:
• l cardiac and respiratory arrest
• l type I respiratory failure
• l type II respiratory failure
• l chest pain, cardiac failure, myocardial infarction
• l low blood pressure, cardiac output
• l increased metabolic demands
• l carbon monoxide poisoning
• COMPLICATIONS
• Administration of oxygen, regardless of the
delivery device, has potential adverse
effects. High concentrations of oxygen cause
nitrogen washout, resulting in absorption
atelectasis.
• Hypoventilation and CO2 Narcosis
• High-dose oxygen therapy may lead to
hypoventilation, worsening hypercapnia and
CO2 narcosis due to inhibition of the
hypoxic drive in a small proportion of
patientswith chronic obstructive pulmonary
disease (COPD).
• Oxygen Toxicity
• Administration of high concentrations of oxygen
may lead to oxygen toxicity; symptoms include
non-productive cough, substernal pain, reduced
lung compliance, interstitial edema, and
pulmonary capillary hemorrhage.
• The concentration and duration of oxygen
exposure that induces oxygen toxicity varies
between patients;4 the lowest possible FiO2
should therefore be used to achieve the target
PaO2 or SpO2.
Signs and symptoms of oxygen toxicity
Central nervous system:
• l nausea and vomiting
• l anxiety
• l visual changes
• l hallucinations
• l tinnitus
• l vertigo
• l hiccups
• l seizures
Pulmonary:
• l dry cough
• l substernal chest pain
• l shortness of breath
• l pulmonary oedema
• l pulmonary fibrosis
 OXYGEN ADMINISTRATION DEVICES
• Initial management of hypoxia in a
spontaneously-breathing patient with an
intact airway is low-flow oxygen via nasal
cannulae (up to 6 L/min) or face mask (up to
15 L/min).
• Oxygen devices have traditionally had FiO2
ascribed to specific flow rates, the FiO2
delivered to the alveoli is influenced by:
– patient factors: inspiratory flow rate, respiratory
rate, tidal volume, respiratory pause
– oxygen device factors: oxygen flow rate, volume
of mask/reservoir, air vent size, tightness of fit
• Normal inspiratory flow in a healthy adult ranges
between 25 and 35 L/min. Patients with
respiratory failure tend to increase their flow
demand from 50 up to 300 L/min.

• All oxygen delivery devices use some type of

reservoir to support oxygen delivery and prevent
CO2 rebreathing. In the case of a face mask, the
reservoir is the mask; for nasal cannulae it is the
patient’s pharynx.
 VARIABLE FLOW DEVICES
• Low-flow Nasal Cannulae
• Traditional low-flow nasal cannulae sit at the
external nares and deliver 3–4 L/min of oxygen.
Higher flows may cause discomfort and damage
from the drying effect on respiratory mucosa.
• They are generally well-tolerated by the patient.
Increased flow demand with respiratory distress
dilutes the oxygen, reducing the FiO2 to the
alveoli. Mouth-breathing and talking can also
render nasal cannula ineffective.
• High-flow Nasal Cannula
• High-flow nasal cannula (HFNC) have slightly
larger prongs that facilitate oxygen flow of up to
60 L/min leading to less air entrainment effect
than with other oxygen delivery systems.
• HFNC generate low levels of end-expiratory
pressure and can therefore reduce tachypnea and
work of breathing.
• The high gas flow may flush CO2 from the
anatomical dead space preventing CO2
rebreathing and thereby decreasing PaCO2
• Oxygen Masks
• Loose-fitting oxygen masks include simple
(Hudson) face masks, aerosol masks used in
combination with heated humidification and
nebulizer treatments, tracheostomy masks and
face tents.
• All are considered low-flow or variable-flow
devices, with the delivered FiO2 varying with
patient demand.
• Flow rates ≥5 L/min minimize CO2 rebreathing.
 AIRWAY SUPPORT
• The most common cause of partial airway obstruction
in an unconscious patient is loss of oropharyngeal
muscle tone, particularly of the tongue.
• Tilting their head slightly back and lifting the chin, or
thrusting the jaw forward.
• The head-tilt/chin-lift maneuver is not used if cervical
spine injury is suspected.
• The jaw-thrust maneuver may require two hands to
maintain.
• If more prolonged support is required, an oro- or
nasopharyngeal airway can be used that may also
facilitate bag–mask ventilation
• ORO- AND NASOPHARYNGEAL AIRWAYS
• The Guedel oropharyngeal airway is available in
various sizes (a medium-sized adult requires a size 4).
• The airway is inserted into the patient’s mouth past
the teeth, with the end facing up into the hard palate,
then rotated 180 degrees, taking care to bring the
tongue forward and not push it back.
• Oropharyngeal airways are poorly tolerated in
conscious patients and may cause gagging and
vomiting.
• A nasopharyngeal airway is inserted through the
nares into the oropharynx; it can be difficult to
insert and require generous lubrication to
minimize trauma.
• This type of airway should not be used for
patients with a suspected head injury.
• As well as opening the airway, suction catheters
can be passed to facilitate secretion clearance.
Once inserted these airways are better tolerated
than an oropharyngeal airway.
• INTUBATION
• Endotracheal intubation is the ‘gold standard’
for airway support, providing airway
protection in the presence of an airway
edema, absent gag, cough or swallow reflex.
Intubation facilitates delivery of mechanical
ventilation and pulmonary secretion clearance
• ENDOTRACHEAL TUBES
• Endotracheal tubes (ETT) are available with
internal diameters ranging from 2–10 mm
(common adult sizes are 7–9 mm), and are
up to 30 cm long.
• PREPARATION FOR INTUBATION
• Adequate preparation of the patient, equipment
and environment, as well as strong knowledge of
emergency procedures is important to ensure
safe and efficient intubation.
• Up to 50% of patients undergoing endotracheal
intubation in ICU will experience a complication;
28% will have a serious complication, including
hypoxemia, circulatory collapse, cardiac
arrhythmia, cardiac arrest, esophageal intubation,
aspiration and death
 • Patient Preparation
If appropriate, and time permits, explain the procedure to
the patient and family. Prepare the patient with:
• l reliable intravenous access established to allow rapid
fluid and drug administration
• l accurate blood pressure monitoring (preferably
intra-arterial)
• l continuous oxygen saturation and ECG monitoring
• l nasogastric tube (if in situ) should be aspirated and
placed on free drainage
• l positioned supine in the ‘sniff’ position
• Equipment and Drugs
All equipment should be checked immediately prior to intubation, including
• l oxygen supply
• l suction supply, with a range of Yankaeur and Y-suction catheters
• l laryngoscope blades and holder are compatible, with a functioning light
• l appropriately-sized face mask
• l manual ventilation (ambubag™) available and attached to oxygen supply
• l ETT cuff inflated in sterile water to ensure no leaks and even inflation
• l water-based lubricant of tube and cuff (while maintaining sterility)
• l capnography (chemical CO2 detectors are often used in
emergency situations)
• l ventilator and circuit
• l emergency/resuscitation trolley at bedside
• l gloves, eye protection
• l drugs (sedative and muscle relaxant)
• PROCEDURE
• The patient is preoxygenated to minimize
desaturation during apnea and laryngoscopy,
commonly via bag and mask, although other
methods such as non-invasive ventilation have
been suggested.
• Intubation in ICU is usually performed via
laryngoscopy with insertion of an oral ETT.
• Intubation may be performed using a fibreoptic
bronchoscope when difficulty is encountered, or
for nasal intubation.
• Endotracheal Tube Fixation
• The purpose of ETT fixation is to maintain the tube
in the correct position, prevent unintended
extubation and facilitate mechanical ventilation
while maintaining skin integrity and oral hygiene.
• ETT fixation methods include:
– l tying cotton tape around the tube, then around the
patient’s neck
– l taping the tube to the patient’s face using medical
adhesive tape
– l commercial tubeholders of varying designs.
• Confirmation of Tube Position
• The correct position of the ETT distal end is 3–5
cm above the carina. A lip level of 20 cm for
women and 22 cm for men should prevent
endobronchial intubation, with the proximal end
fixed at either the center or the side of the mouth.
• Confirmation of the ETT position is required
immediately following intubation and at regular
intervals thereafter as movement of the tube can
occur.
• TRACHEOSTOMY
• Tracheostomy may be required for upper airway
obstruction, although it is most commonly performed
for ICU patients who require prolonged mechanical
ventilation. The advantages of tracheostomy over
endotracheal intubation include decreased risk of
laryngeal damage and subglottic stenosis, reduced
airway resistance and deadspace which decreases the
work of breathing and therefore supports weaning,
and improved patient tolerance enabling reduction of
sedation.
• PROCEDURE
• Tracheostomy can be performed using a surgical
technique (ST) or percutaneous dilatational
technique (PDT).
• PDT is contraindicated in patients with anatomical
anomalies of the neck and serious bleeding
disorders, and should be undertaken with caution
in patients who are obese, have a cervical spine
injury, coagulopathy, difficult airway or require
high levels of ventilatory support.
• TRACHEOSTOMY CARE
• The aim of tracheostomy care is to keep the site free of infection,
and prevent tube blockage or dislodgement.
• The site is cleaned with normal saline and fixation devices changed
at least 12-hourly with two nurses to safely perform tape changes.
Velcro tapes are easier to change and more comfortable than
cotton tape.
• Lint-free or superabsorbent foam dressings may be placed under
the flange to absorb secretions.
• Adequate humidification and suctioning will usually prevent tube
obstruction
• . The use of inner cannula has obviated the need for frequent
tracheostomy tube changes.
• Single lumen (no inner cannula) tracheostomy tubes should be
changed every 7–10 days.
 COMPLICATIONS OF ENDOTRACHEAL
INTUBATION AND TRACHEOSTOMY
• Tube blockage, tube dislodgement and aspiration are
major complications.
• Complications during and immediately after
endotracheal intubation and tracheostomy include
cardiovascular compromise, bleeding, injury to the
tracheal wall, damage to the vocal cords,
pneumothorax, pneumomediastinum and
subcutaneous emphysema.
• Late complications of tracheostomy include tracheal
stenosis, tracheomalacia and tracheo-oesophageal
fistula and infection. As noted earlier, damage to the
trachea is exacerbated by high cuff pressures.
• TRACHEAL SUCTION
• Patients with an ETT or tracheostomy tube
require tracheal suction to remove pulmonary
secretions that can lead to atelectasis or airway
obstruction and impair gas exchange.
• Suction should be performed as clinically
indicated, with assessment of visible or audible
secretions, rising inspiratory pressure, decreasing
VT or increased work of breathing.
• A sawtooth pattern on the flow-volume
waveform may also indicate the need for suction.
• Preoxygenation using a FiO2 of 1 for 60
seconds prior to performing suction minimizes
hypoxia and the potential for cardiac
arrhythmias.
• Manual hyperinflation is discouraged due to
the risk of barotrauma and lack of benefit.
• Installation of saline is not supported due to
increased risk of flushing pathogens into distal
lung regions.
METHODS
• The three methods of suctioning are:
• Open suction: a suction catheter is passed under aseptic technique
directly into the ETT/tracheostomy after disconnection from the
ventilator circuit. Disadvantages include loss of PEEP resulting in
loss of alveolar recruitment and increased risk of transmission of
infective organisms. A surgical mask and protective eyewear
should be worn.

• Semi-closed suction: a suction catheter is passed through a swivel

connector with a self-sealing rubber flange.

• Closed suction: in-line system is attached between the

ETT/tracheostomy tube and the ventilator circuit where the
suction catheter is contained in an integrated plastic sleeve.
Alveolar derecruitment occurs toa lesser degree than with open
suction.
• ADVERSE EFFECTS
• Adverse effects of suction can include
hypoxemia, introduction of infective
organisms, tracheal trauma, bradycardia,
hypertension and increased intracranial
pressure.
• EXTUBATION
• Following successful weaning from mechanical
ventilation , assessment of the patient prior to
extubation should include adequate gas exchange,
respiratory rate and work of breathing on minimal
support for prolonged periods, respiratory muscle
strength, the ability to cough and clear secretions
spontaneously and a stable hemodynamic status
and mental status.
• PRINCIPLES OF MECHANICAL VENTILATION
• Mechanical ventilation describes the
application of positive or negative pressure
breaths using non-invasive or invasive
techniques
• INVASIVE MECHANICALVENTILATION
• Critically ill patients with persistent
respiratory insufficiency
(hypoxaemia and/or
hypercapnia), due to drugs, disease or other
conditions, may require intubation and
mechanical ventilation to support oxygenation
and ventilatory demands.
• INDICATIONS
• Indications for intubation and mechanical ventilation include:
– apnoea
– inability to protect airway; e.g. loss of gag/cough reflex; decreased
Glasgow Coma Scale (GCS) score
– clinical signs indicating respiratory distress; e.g. tachypnoea,117
activation of accessory and expiratory muscles, abnormal chest wall
movements,118 tachycardia and hypertension
– inability to sustain adequate oxygenation for metabolic demands;
e.g. cyanosis, SpO2 <88%, with supplemental FiO2 ≥0.5
– respiratory acidosis (e.g. acute decrease in pH <7.25)
– postoperative respiratory failure
– shock.
• The goals of mechanical ventilation are to
achieve and maintain adequate pulmonary
gas exchange, minimize the risk of lung injury,
reduce patient work of breathing and
optimize patient comfort.
• WEANING FROM THE VENTILATOR
• Weaning traditionally occurs via clinician-
directed adjustments to the level of support
provided by the ventilator, culminating in a
spontaneous breathing trial comprising either
low level pressure support or a T piece trial.