CRITICAL CARE NURSING • Provide education and support help to the
patient or patient’s designated surrogate to
Module 1: Introduction to Critical Care
A. Scope of critical care practice:
B. Critical care body of knowledge,
competencies
SOURCES:
1. S.M. Burns, S.A. Delgado. American Association of
Critical Care Nurses: Essentials of Critical Care
Nursing. McGraw-Hill Education. 4th Ed. (2019).
2. K.O. Perrin, C.E. McLeod. Understanding the
Essentials of Critical Care Nursing. Pearson Education
Inc. NY. 3rd Ed. (2018).
3. P.G. Morton, D.K. Fontaine. Critical Care Nursing: A
Holistic Approach. Lippincott Williams Inc. 11 th Ed.
(2017).
4. L.D. Urden, K.M. Stacy, M.E. Lough. Critical Care
Nursing: Diagnosis and Management. Elsevier
Publishing. 7th Ed. (2014).
CRITICAL CARE
To be considered critical, an illness or injury must
acutely impair one or more vital organ systems
to such a degree that there is a high probability
of life threatening deterioration (Department of
Health and Human Services, 2008)
Critically ill patients - high risk for actual or
potential life threatening health problems.
The more critically ill the patient is, the
more likely he or she is to be highly
vulnerable, unstable, and complex,
thereby requiring intense and vigilant
nursing care.” (ACCN)
DEVELOPMENT OF CRITICAL CARE NURSING
The innovation of creating a separate area
proximal to the nursing station for battle-injured
British soldiers during the Crimean War of the
1850s, especially for watchful nursing care after
major battle injuries and surgical interventions,
is attributed to Florence Nightingale. This is most
often cited as a beginning of Intensive Care.
In the 1800s, Florence Nightingale described the
advantages of placing patients recovering from
surgery in a separate area of the hospital. A
three-bed postoperative neurosurgical intensive
care unit was opened in the early 1900s at Johns
Hopkins Hospital in Baltimore. This was soon
followed by a premature infant unit in Chicago.
Major societal issues have affected the
development of intensive care as a specialty.
During World War II, shock wards were
established to care for critically injured patients.
The nursing shortage after the war forced the
grouping of postoperative patients into
designated recovery areas so that appropriate
monitoring and care could be provided.
The technologies and combat experiences of
health care providers during the wars of the 20th
century also provided an impetus for specialized
medical and nursing care in the civilian setting.
The 1950s brought the new technology of
mechanical ventilation and the need to group
patients receiving this new therapy in one
location.
AACN CRITICAL CARE NURSE ROLE
RESPONSIBILITIES
(From American Association of Critical-Care Nurses. Fact
sheet: about critical care nursing (press room).
http://www.aacn.org. Accessed. December 2008.)
• Respect and support the right of the patient or
patient’s designated surrogate to autonomy
and informed decision making.
• Intervene when the best interest of the patient
is in question.
• Help the patient obtain necessary care.
• Respect the values, beliefs, and rights of the
patient.
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make decisions.
• Represent the patient in accordance with the
patient’s choices.
• Support the decisions of the patient or
patient’s designated surrogate or transfer care
to an equally qualified critical care nurse.
• Intercede for patients who cannot speak for
themselves in situations that require
immediate attention.
• Monitor and safeguard the quality of care that
the patient receives.
• Act as a liaison between the patient and the
patient’s family and other
health care professionals.
CRITICAL CARE NURSING ROLES:
The most prevalent role for the professional
registered nurse is that of direct care provider.
• Expanded-nursing role positions:
o interact with critical care patients,
families, and the health care team
o nurse case managers work closely with
the care providers to ensure appropriate,
timely care and services and to promote
continuity of care from one setting to
another.
o specific types of expanded-role nursing
positions are determined by patient
needs and individual organizational
resources
• Advanced practice nurses:
o have met educational and clinical
requirements beyond the basic nursing
educational requirements for all nurses
o have a broad depth of knowledge and
expertise in their specialty area and
manage complex clinical and systems
issues.
o most commonly seen APNs in the critical
care areas are the clinical nurse
specialist (CNS) and the nurse
practitioner (NP) or acute care nurse
practitioner (ACNP)
o CNS are instrumental in ensuring that
care is evidence-based and that safety
programs are in place
o may be designated as case managers for
specific patient population
CATEGORIES OF CRITICAL CARE NURSING
THOUGHT, ACTION, AND PRACTICE
Thought and Action
• Clinical grasp and clinical inquiry: problem
identification and clinical problem solving
• Clinical forethought: anticipating and
preventing potential problems
• Practice diagnosing and managing life-
Sustaining physiologic functions in unstable
patients
• Managing a crisis by using skilled know-how
• Providing comfort measures for the critically ill
• Caring for patients’ families
• Preventing hazards in a technologic
environment
• Facing death: end-of-life care and decision
making
• Communicating and negotiating multiple
perspectives
• Monitoring quality and managing breakdown
• Exhibiting the skilled know-how of clinical
leadership and the coaching and
mentoring of others
CORE COMPETENCIES FOR INTERPROFESSIONAL
COLLABORATIVE PRACTICE
1. Values/Ethics for Interprofessional Practice
• Work with individuals of other professions to
maintain a climate of mutual respect and shared
values.
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1 Compiled by BJ SORRILLA, R.N., M.D.
2. Roles/Responsibilities for Collaborative
Practice
• Use the knowledge of one’s own role and the role
of other professions to appropriately assess and
address the health care needs of the patients and
populations served.
3. Interprofessional Communication
• Communicate with patients, families,
communities, and other health professionals in a
responsive and responsible manner that
supports a team approach to maintaining health
and treatment of disease.
4. Interprofessional Teamwork and Team-Based
Care
• Apply relationship-building values and principles
of team dynamics to perform effectively in
different team roles to plan and deliver patient/
population-centered care that is safe, timely,
efficient, effective, and equitable.
GUIDELINES FOR CRITICAL CARE SERVICES BASED
ON THREE LEVELS (Haupt et al., 2003)
LEVEL I:
Comprehensive care for a wide variety of
disorders. Sophisticated equipment,
specialized nurses, and physicians with
specialized preparation (intensivists) are
continuously available.
Comprehensive support services from
pharmacy, nutrition, respiratory, pastoral
care, and social work are nearby. Most of
these units are located in teaching hospitals.
LEVEL II
Comprehensive critical care for most
disorders but the unit may not be able to
care for specific types of patients (e.g.,
cardiothoracic surgical patients).
Transfer arrangements to Level I facilities
must be in place for patients with the specific
disorders for which the unit does not provide
care.
LEVEL III
Initial stabilization of critically ill patients
provided but limited ability to provide
comprehensive critical care.
A limited number of patients who require
routine care may remain in the facility, but
written policies should be in place
determining which patients require transfer
and where they ought to be transferred.
CARE MANAGEMENT TOOLS
1. ALGORITHM
a stepwise decision-making flowchart for a
specific care process or processes.
guide the clinician through the “if, then”
decision-making process, addressing
patient responses to particular treatments.
Well-known examples of algorithms are the
advanced cardiac life support (ACLS)
algorithms published by the American Heart
Association.
2. PRACTICE GUIDELINES
usually created by an expert panel and
developed by a professional organization
(e.g., AACN, Society of Critical Care
Medicine, American College of Cardiology,
government agencies such as the Agency for
Health Care Research and Quality [AHRQ])
text prose style rather than in the flowchart
format of algorithms
3. PROTOCOL
are more directive and rigid than guidelines,
and providers are not supposed to vary from
a protocol. Patients are screened carefully
for specific entry criteria before being
started on a protocol.
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are helpful when built-in alerts signal the
provider to potentially serious problems.
4. ORDER SET
consists of preprinted provider orders that are
used to expedite the order process after a
standard has been validated through analytic
review of practice and research.
Order sets complement and increase
compliance with existing practice standards.
also be used to represent the algorithm or
protocol in order format.
CHARACTERISTICS OF CRITICAL CARE
ENVIRONMENT
1. Critical care is provided by multi-professional teams
of highly experienced and professional physicians,
nurses, and others.
• Healthcare professionals use their expertise
to interpret information and provide care
utilizing technologically advanced equipment
that leads to the best outcomes for their
patients.
2. Critically ill patients require complex, carefully
coordinated care. When a care pattern is complex,
failure in one part of the system can unexpectedly
affect another. In addition, the care provided to
critically ill patients is often coupled, meaning there
is little or no buffer between events.
• In addition, when things are tightly coupled,
even when an error is identified, it can be
difficult to prevent the situation from
deteriorating. In part, this is because of the
complexity and high degree of coupling of
care in critical care areas, specifically
emergency departments (EDs), ICUs, and
operating rooms (ORs), where healthcare
errors most commonly occur.
3. Not only do the critically ill patients receive highly
complex care, but the care they receive is also highly
technological.
• In a foundational study, Leape and Brennan
(1991) found that 44% of healthcare errors
were related to technology, and that all
errors were more likely to occur in
technologically advanced fields such as
vascular, cardiac, and neurosurgery.
The Institute of Medicine (Kohn, Corrigan, & Donaldson,
2000) postulates that technology increases errors for
several reasons, including the following:
1. Technology changes the tasks people do by shifting
the workload and eliminating human decision-
making.
2. Although technology may decrease human workload
during nonpeak hours, it often increases the
workload during peak hours or when the system fails
or is inadequate (e.g., when medication-scanning
devices fail without warning and nurses are required
to utilize paper systems to dispense medications
then must back- track and re-document when the
scanner is working).
3. When the system becomes opaque, users no longer
know how to perform a function without it (e.g.,
when intravenous [IV] pumps are constantly used to
calculate doses of continuous medication infusions,
nurses can no longer calculate the rate to infuse a
drug at a specific dose of mcg/kg/min by hand).
Therefore, errors may occur when the system fails.
4. When devices are not standardized and demand
precision to use (e.g., an ICU uses multiple brands
of IV pumps or ventilators), problems can result.
SAFETY
Mattox (2010) confirmed that the most vulnerable of
unstable ICU patients are at highest risk for medical
error (e.g., patients in isolation, patients with limited
English proficiency or health literacy, and patients at
end of life).
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 Valentin et al. (2006) examined errors that occurred
in 205 ICUs worldwide during one 24-hour period.
Only about a quarter of the ICUs reported no errors.
The remaining units reported the following types of
errors:
1. Dislodgment of lines, catheters, and drains
2. Medication errors (such as wrong dose,
wrong drug, or wrong route)
3. Failure of infusion devices
4. Failure or dysfunction of a ventilator
5. Unplanned extubation while ventilator
alarms were turned off
This concern about the frequency of errors and the
need to develop preventive strategies is also
apparent in a study by Garrouste-Orgeas et al.
(2010), who measured the incidence and rates of
adverse events in critical care. Twenty-six percent of
the patients they followed experienced at least one
adverse event.
Garrouste-Orgeas et al. (2010) concluded that
serious errors were common in critical care settings
and translated to a rate of 2.1/1,000 patient days.
These preventable errors were often associated with
a combination of human factors and system- wide
problems that caused errors or near misses
(Garrouste-Orgeas et al., 2012).
They concluded that it is important to find ways to
develop work conditions (systems) that engineer out
slips and lapses so that treatment is delivered as
intended. In a system-based approach, the focus is
not on who committed the error but rather
determination of how the error occurred.
Since the release of the Institute of Medicine’s (IOM)
report, To Err Is Human (Kohn et al., 2000), there
has been a focus on uncovering system-wide
problems and diminishing the potential for errors in
hospitals in the United States. To decrease the
potential for errors, the report recommends the
following:
1. Utilizing constraints: An example of a
constraint is when the height, weight, and
allergies of the patient must be on file to obtain
medication for the patient.
2. Installing forcing functions or system-level
firewalls: An example of a forcing function is
that concentrated (undiluted) potassium chloride
(KCl) is no longer available on hospital units.
3. Avoiding reliance on vigilance: Because
humans can- not remain vigilant for a protracted
amount of time, checklists, protocols, and
rechecking with another professional should be
required before major procedures and before
potentially dangerous medication administration.
Examples are timeouts before surgery or double-
checking doses on intensive insulin protocols.
4. Simplifying key processes.
5. Standardizing key processes.
MULTIDISCIPLINARY APPROACH TO CARE
Evidence suggests that care should be delivered
by a multidisciplinary team headed by a full-time
critical care–trained physician and consisting of
at least an ICU nurse, a respiratory therapist,
and a pharmacist (Kim, Barnato, Angus, Fleisher,
& Kahn, 2010).
Daily rounding by such a multidisciplinary team
has been associated with fewer adverse drug
effects, reduced duration of mechanical
ventilation, and shorter ICU stay.
Strategies that encourage teamwork and
communication among staff members caring for
critically ill patients can further improve patient
outcomes (Whelan, Burchill, & Tilin, 2003).
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INSTITUTING A CULTURE OF SAFETY
Culture of safety - “practice responsibility of all health-
care team members working together in the moment to
provide good healthcare” (Benner, 2001)
Sammer, Lykens, Singh, Mains, and Lackan (2010)
considered how healthcare leaders might be able to
determine if a “culture of safety” exists within their
institutions. They determined that there were seven
essential properties of a culture of safety:
1. teamwork
2. evidenced-based practice
3. communication
4. patient-centered care
5. leadership
6. learning
7. justice
ENSURING ADEQUATE STAFFING
Tarnow-Mordi, Hau, Warden, and Shearer (2000)
demonstrated that “patients exposed to high ICU
workload were more likely to die than those exposed to
lower ICU workload”
The three measures of ICU workload most
closely tied to mortality in their study were:
1. peak occupancy of the ICU
2. average nursing requirement/ occupied
bed per shift
3. ratio of occupied to appropriately staffed
beds.
*This study remains significant because it is the only
published study that has related total nursing
requirement, not just nurse/patient ratio, to patient
outcome (Kiekkas et al., 2008)
LIMITING HOURS OF WORK
IOM recommended that nurses work no more than 60
hours each week or 12 hours in a 24-hour period (Page,
2004).
In 2006, Scott, Rogers, Hwang, and Shang
determined that when critical care nurses
worked longer than 12 hours, the likelihood of
errors and near errors increased and the nurses’
vigilance decreased. Unfortunately, in their study
of 502 nurses, only one critical care nurse left
work on time every day. Most nurses rarely left
work on time, even those who were working 12-
hour shifts.
Scott et al. found that two-thirds of the nurses
struggled to stay awake at least once during the
28-day study period and that 20% fell asleep.
Allen et al. (2014) determined that this pattern
of sleepiness and sleep deprivation was
especially apparent in nurses who worked
consecutive 12 hour shifts, especially
consecutive night shifts. Such sleep and fatigue
leads to faulty decisions and decision regret
(Scott, Arslanian-Engoren and Engoren, 2014).
Nurses are aware of the number of hours they
have worked in a day or week. They need to limit
their work hours to 12 hours per shift and 60
hours per week to enhance patient safety.
CRITICAL CARE NURSING
Specialty that deals specifically with human responses to
life- threatening problems
A critical care nurse is a licensed professional
nurse who is responsible for ensuring that
acutely and critically ill patients and their families
receive optimal care. (AACN)
AACN believes that critical care nursing should
be defined more by the needs of the patients and
those of their families than by the environment
in which care is delivered or the diagnoses of the
patients.
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COMPETENCIES OF A CRITICAL CARE NURSE AS
DEFINED BY THE AACN IN THE SYNERGY MODEL
AACN Synergy Model for Patient Care
Model describes each of the competencies of the critical
care nurse on a continuum of expertise from 1 to 5,
ranging from competent to expert
1. CLINICAL INQUIRY
CCN should be engaged in the “ongoing
process of questioning and evaluating
practice and providing informed practice.”
provide care based on the best available
evidence rather than on tradition.
expert critical care nurse might be able to
evaluate research and develop evidence-
based protocols for nursing practice in her
agency, whereas a competent nurse might
follow evidence based agency policies and
protocols.
Critical care nurses (both novice and expert)
can develop the mindset that questioning
practice is an issue of safety.
A safe practitioner is one who wonders, “Why
do we do things this way?” or “Why am I
being asked to provide this specific type of
care to this patient at this moment?
2. CLINICAL JUDGMENT
CCN should engage in “clinical reasoning
which includes clinical decision-making,
critical thinking, and a global grasp of the
situation, coupled with nursing skills acquired
through a process of integrating formal and
experiential knowledge.”
competent critical care nurse is able to collect
and interpret basic data and then follow path-
ways and algorithms when providing care.
expert nurse is able to use past experience,
recognize patterns of patient problems, and
“see the big picture.” Her previous experience
coupled with the ability to see the “big
picture” often allows her to anticipate possible
untoward events and develop interventions to
prevent them.
3. CARING PRACTICES
AACN defines caring behaviors as “nursing
activities that create a com- passionate,
supportive, and therapeutic environment for
patients and staff, with the aim of promoting
comfort and preventing unnecessary
suffering.”
a competent nurse might focus on the basic
and routine needs of the patient, an expert
nurse is able to anticipate patient/ family
changes and needs, varying caring approach
to meet their needs.
4. ADVOCACY AND MORAL AGENCY
AACN states that “Foremost, the critical care
nurse is a patient advocate and defines
advocacy as ‘respecting and supporting the
basic rights and beliefs of the critically ill
patient.’ ”
a competent nurse assesses her personal
values and patient rights, represents the
patient if the patient’s needs and desires are
consistent with her framework, and
acknowledges death as a possible outcome.
an expert nurse advocates from the
family/patient perspective, whether it is
similar to or different from her own;
empowers the patient and family to speak for
or represent themselves; and achieves
mutuality in relationships.
5. SYSTEMS THINKING
Synergy Model defines systems thinking as
managing the existing environmental and
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system resources for the benefit of patients
and their families.
A competent nurse might see himself as a
resource for the patient on the specific unit
where the patient is receiving care, whereas
an expert nurse might know how to
negotiate and navigate for the patient
throughout the healthcare system to obtain
the necessary or desired care.
6. FACILITATOR OF LEARNING
nurses should be able to facilitate both
informal and formal learning for patients,
families, and members of the healthcare
team.
A competent nurse might follow planned
educational programs using standardized
materials or see the patient and family as
passive recipients of educational materials.
An expert nurse would be able to “creatively
modify or develop patient/family
educational programs and integrate
family/patient education throughout the
delivery of care.”
7. RESPONSE TO DIVERSITY
response to diversity as “sensitivity to
recognize, appreciate, and incorporate
diversity into the provision of care.”
A competent nurse might recognize the
values of the patient but still provide care
based on a standardized format.
An expert nurse would anticipate the needs
of the patient and family based on their
cultural, spiritual, or personal values, and
would tailor the delivery of care to
incorporate these values.
8. COLLABORATION
collaboration in its Synergy Model as
“working with others in a way that promotes
each person’s contributions toward
achieving optimal and realistic
patient/family goals.”
A competent nurse might participate in
multidisciplinary meetings and listen to the
opinions of various team members.
An expert nurse might facilitate the active
involvement and contributions of others in
meetings and role model leadership and
accountability during the meetings.
HEALTHY WORK ENVIRONMENT STANDARDS
Standard I: Skilled Communication
Nurses must be as proficient in communication
skills as they are in clinical skills.
Standard II: True Collaboration
Nurses must be relentless in pursuing and
fostering true collaboration.
Standard III: Effective Decision Making
Nurses must be valued and committed partners
in making policy, directing and evaluating clinical
care, and leading organizational operations.
Standard IV: Appropriate Staffing
Staffing must ensure the effective match
between patient needs and nurse competencies.
Standard V: Meaningful Recognition
Nurses must be recognized and must recognize
others for the value each brings to the work of
the organization.
Standard VI: Authentic Leadership
Nurse leaders must fully embrace the imperative
of a healthy work environment, authentically live
it, and engage others in its achievement.
QUALITY AND SAFETY EDUCATION FOR NURSES
(QSEN) COMPETENCIES
Patient-Centered Care
Recognize the patient or designee as the source
of control and full partner in providing
compassionate and coordinated care based on
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4 Compiled by BJ SORRILLA, R.N., M.D.
 respect for patient’s preferences, values, and
needs.
Teamwork and Collaboration
Function effectively within nursing and
interprofessional teams, fostering open
communication, mutual respect, and shared
decision-making to achieve quality patient care.
Evidence-Based Practice
Integrate best current evidence with clinical
expertise and patient/family preferences and
values for delivery of optimal health care.
Quality Improvement
Use data to monitor the outcomes of care
processes and use improvement methods to
design and test changes to continuously improve
the quality and safety of health care systems.
Safety
Minimizes risk of harm to patients and providers
through both system effectiveness and individual
performance.
Informatics
Use information and technology to communicate,
manage knowledge, mitigate error, and support
decision making.
COMMON STRESSORS FOR PATIENTS IN CRITICAL
CARE UNITS
Threat of death
Uncertainty about future and fear of permanent
residual health deficits
Pain, discomfort, and physical restrictions
Lack of sleep
Loss of autonomy and control over one’s body,
environment, privacy, and daily activities
Unfamiliar environments with excessive light,
noises, alarms, and distressing events
Worry about finances, potential job loss, and
stress on loved ones
Separation from family, friends, and meaningful
social roles and work
Loss of dignity, embarrassing exposures, and a
sense of vulnerability
Boredom broken only by brief visits, threatening
stimuli, and procedural touch
Loss of ability to express oneself verbally when
intubated
Unfamiliar bodily sensations due to bed rest,
medications, surgery, or symptoms
Unanswered spiritual questions and concerns
about meaning of the events and life
Individual response to stressors depend on:
• Individual’s perception of the stressor
• Acute or chronic nature of the stressors
• Cumulative effect of multiple stressors
• Effectiveness of the person’s usual coping
strategies and style
• Degree of social support
STRATEGIES FOR COMMUNICATING WITH
PATIENTS AND FAMILY MEMBERS
Be patient. What is routine for caregivers can be
stressful and new to patients and family
members.
Repeat information as many times as necessary.
Stress reduces concentration, memory, and
comprehension, especially in unfamiliar
situations.
Assess patient and family knowledge level and
prior experience with critical care.
Use understandable language and interpret
medical terms, without talking down.
Asking clarifying questions to help validate
understanding.
Use a welcoming, open communication style.
Critical care units can feel intimidating to people
unfamiliar with the environment.
Offer frequent updates regarding patient’s
condition, even if not asked.
Engage in conversations of meaning with
patients and family members, even if brief. Often
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critical care conversations are reduced to
conveying only technical aspects of care.
Honor privacy and provide space for family
conferences.
Speak to patients, even if they are unconscious.
This conveys caring to family and words may
comfort the patient, even if there is no response.
Use communication boards or other devices with
patients unable to speak.
Give patients time to respond and ask questions
patient can likely answer easily.
Speak slowly and look at patients when
communicating. Gestures, lip movements, and
facial expressions convey important messages.
THE SYNERGY MODEL-PATIENT CHARACTERISTICS
The Synergy Model-patient characteristics are scored on
the health illness continuum from Level 1, which
describes a more compromised patient, to Level 5, which
indicates a patient who is less compromised.
The characteristics are:
1. Resiliency: “The ability to bounce back quickly
after insult.” Patients range along the continuum
from being unable to mount a response to having
strong reserves.
2. Vulnerability: “Susceptibility to actual or
potential stressors.” Patients range from being
fragile to being safe or “out of the woods.”
3. Stability: “The ability to maintain a steady state
equilibrium.” Patients vary from being
unresponsive to therapies and at high risk for
death to stable and responsive to therapy.
4. Complexity: “The intricate entanglement of two
or more systems (e.g., body, family).” Patients
span the gamut from having atypical presentations
of an illness or complex family dynamics to simple
clear-cut and typical presentation.
5. Predictability: “A characteristic that allows one
to predict a certain course of events or course of
ill- ness.” Patients range from having an unusual
or unexpected course of illness to following a
critical pathway.
6. Resource availability: “Extent of resources the
patient, family, and community bring to the
situation.” Patients may have few of the resources
necessary for recovery available to them or may
have extensive knowledge and skills.
7. Participation in care: “Extent to which patient
and/or family engage in care.” Patients and
families may vary from being unable or unwilling
to assist with care to being fully willing and able to
participate.
8. Participation in decision-making: “Extent to
which patient and/or family engage in decision-
making.” Patients and families may range from
requiring surrogate decision makers to having full
capacity and making decisions for themselves.
The Synergy Model proposes that when these
characteristics of the patients are met by the
competencies of the nurse, the patient will have the
following outcomes:
1. Comfort and healing
2. Satisfaction with care
3. Absence of complications
4. Perceived change in function
5. Perceived improvement in quality of life
6. Decreased recidivism
7. Effective cost resource utilization balance
PATIENTS UNDER SEDATION
When nurses communicate with their sedated patients,
it is usually for a specific purpose (Elliot & Wright, 1999)
usually to convey or obtain biopsychosocial information
(Slatore et al., 2012). Nurses communicate with or
around their sedated patients to:
1. Provide orientation or translate medical
information: Nurses believe that not knowing
who is providing care, and where the patient is
can be stressful to the patient. Grossback et al.
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 (2011) also emphasizes this by saying that
patients need reminders and explanations of
what has happened to them and why they are
intubated and in ICU.
2. State procedural and task intentions:
Studies indicate that nurses communicate more
with their sedated patients when the patients are
having procedures or tasks done. Patients state
that they would prefer to have nurses ask their
permission before such tasks and to give them
some indication of what they will experience.
3. Provide reassurance: Morse (2001) noted that
nurses use reassuring words to help a patient
hold on and endure a difficult procedure. The
nurse might say, “You’re doing well—it’s almost
done” even to a patient who appears
unresponsive.
4. Apologize and/or recognize discomfort: A
nurse might say as he prepares to suction a
patient, “I’m sorry, I know this is uncomfortable
but I need to clear these secretions now. It is
important to help your lungs to heal.”
5. Obtain a response: Determining if the patient
is able to respond to a request is important.
However, even when the patient does not
respond, it is quite possible he can still hear the
request and any other conversation.
6. Provide intentional and unintentional
distractions: Morse stated that nurses may use
intentional distractions as a way of providing
some comfort to patients who are undergoing
procedures. For example, nurses sometimes
sing, hum, or joke with their unresponsive
patients while they provide care.
7. Provide social information to colleagues:
Nurses sometimes have social conversations as
they are caring for unresponsive, sedated, or
ventilated patients. Patients have identified
overhearing such conversations as a source of
distress. They have felt removed from the
situation and less than human.
RESPONSIVE PATIENTS
A majority of responsive, ventilated patients identify
communication as highly frustrating (Patak et al.,
2004). They frequently modify requests or avoid
communication because the activity is so difficult
(Magnus & Turkington, 2006).
Intubated patients who are severely ill and are
probably dying have higher levels of anger and
frustration about their inability to communicate than
do less ill patients (Happ, Tuite, Dobbin, DiVirgilio-
Thomas, & Kitutu, 2004).
The most common means of communication used by
responsive ventilated patients are head nods in
response to yes/no questions, mouthing words,
gesturing, and writing.
Hand and arm movements are required for both
gesturing and writing, so the already limited
communication from patients is reduced when
patients’ hands and arms are restrained.
Happ et al. (2004) recommended limiting the use of
such restraints, believing it may be the most
effective way to facilitate communication with
responsive ventilated patients.
Communication with ventilated patients centers around
specific, predictable issues:
The most common reason for communication
between nurses and ventilated patients is the
patients’ experiences of pain.
Other common reasons for communication are:
○ Identifying patients’ emotions
○ Determining patients’ symptoms
○ Responding to patients’ needs for physical care
○ The physical environment of the ICU
○ The patients’ home and family
○ Treatment decision-making (Happ et al., 2004)
Patak et al. (2004) recommended evidence-based
interventions to facilitate communication with mechani-
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COLLEGE OF NURSING
cally ventilated, seriously ill patients. They stated that
healthcare providers should do the following:
• Be educated about the frustration that mechanically
ventilated patients experience when they are
attempting to communicate their needs and desires.
• When communicating with ventilated patients, they
should:
• Routinely ask patients about their feelings
and their state of mind.
• Ask permission before beginning nursing
care and procedures.
• Evaluate patients’ understanding of the
information conveyed to them by asking
simple yes/no questions.
• Demonstrate attention to the needs of their patients
by informing them of their surroundings, plan of
care, and when they will return after leaving the
bedside.
• Approach each patient with a kind, patient manner;
take the time to investigate and understand what the
patient is communicating; and respond to the
patient’s communicated needs.
USE OF RESTRAINTS
Nurses’ primary motivation in restraining these
patients was beneficence, acting to prevent patients
from the harm they might incur if they tried to pull
out an endotracheal tube or IV, move around in bed
unassisted, or inadvertently disconnect ventilator
tubing.
As researchers studied restraints, nurses learned
that restraining a patient causes physical harm.
When people are restrained, they are more likely to
become weak, incontinent, constipated, and to
develop nosocomial infections. They also recover
more slowly. Thus, there is reason to believe that in
acting to pre- vent a potential harm, such as the
disconnection of an IV, the nurses may be causing
actual physical harm as well as moral harm, such as
the deprivation of the patients’ autonomy.
Maccioli et al. (2003) list the following
recommendations developed by the American
College of Critical Care Medicine Task Force for the
use of restraining therapies:
Institutions and practitioners should strive to
create the least restrictive but safest
environment for patients regarding restraint
use.
Restraining therapies should be used only in
clinically appropriate situations and not as a
routine component of therapy. When
restraints are used, the risk of untoward
events must outweigh the physical,
psychological, and ethical risks of their use.
Patients must always be evaluated to
determine whether treatment of an existing
problem would obviate the need for restraint
use.
The choice of restraint should always be the
least invasive option capable of optimizing
patient safety, comfort, and dignity.
The rationale for restraint use must be
documented in the medical record. Orders
for a restraining order should be limited to a
24-hour period. New orders should be
written after 24 hours if the restraining
orders are to be continued.
Patients should be monitored for
development of com- plications from
restraining therapies every 4 hours, more
frequently if they are agitated.
Patients and their significant others should
receive ongoing education as to the need and
nature of restraining therapies.
Cho, Kim, Kim, and Choi (2006) determined that the
main factors in the nurses’ decisions to use restraints
were:
1. Glasgow Coma Scale score
2. restless behavior
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 3. emotional state
4. discomfort factors
5. medical devices
6. life-sustaining devices.
In their study, 31% of patients were restrained, with
more patients being restrained during the night than
during the day.
FACTORS AFFECTING THE WELLBEING OF
CRITICAL CARE NURSES
MORAL DISTRESS
In 1984, Jameton described a circumstance that
he called moral distress, wherein a nurse would
know the right thing to do, yet institutional
constraints such as lack of resources or personal
authority would prevent her from doing it.
In 2005, Elpern and colleagues learned that
critical care nurses commonly encounter
situations that are associated with high levels of
moral dis- tress. The primary source of moral
distress for nurses in their study was providing
aggressive care to patients whom the nurses did
not believe would benefit from the care.
Dracup (2008) identified the inability to achieve
appropriate pain control or relief of other patient-
specific symptom and aggressive treatment of
dying patients as the major causes of moral
distress for healthcare providers.
Nurses consistently state that when they do not
have a voice in the decision-making, they feel
powerless and that they cannot find meaning in
the patients’ or families’ suffering.
COMPASSION SATISFACTION/ FATIGUE
According to Figley, compassion fatigue is a
“state of tension and preoccupation with the
suffering of those being helped that is
traumatizing for the helper.”
It occurs in care providers who may be so selfless
and compassionate that they fail to pay sufficient
attention to their own needs.
The terminology for compassion fatigue has
evolved. What was once called compassion
fatigue was renamed secondary traumatic
stress, while compassion fatigue continues to be
used to describe the combined effect of
secondary traumatic stress and burnout.
Secondary traumatic stress differs from burnout
in that it may develop suddenly in response to a
specific incident of suffering, whereas burnout
tends to develop slowly and insidiously in
response to various stressors.
Secondary traumatic stress is primarily a
response to caring for people who are suffering,
whereas burnout is often a response to other
stressors such as poor morale in the work
environment.
Caregivers who are experiencing compassion fatigue
have many symptoms that often parallel the symptoms
of the suffering patients with whom they are working.
Some of the symptoms of compassion fatigue include:
Intrusive thoughts or images of patients’
situations or traumas
Difficulty separating work life from personal life
Lowered tolerance for frustration and/or
outbursts of anger or rage
Dread of working with certain patients
Depression
Increase in ineffective and/or self-destructive
self- soothing behaviors
Hypervigilance
Decreased functioning in nonprofessional
situations
Loss of hope
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COLEGIO SAN AGUSTIN – BACOLOD
COLLEGE OF NURSING
CHRONIC OBSTRUCTIVE PULMONARY DISEASE
COPD is the third leading cause of death and affects
>10 million persons in the United States. Estimates
suggest that COPD will rise to the third most common
cause of death worldwide by 2020.
persistent respiratory symptoms and airflow
limitation that is not fully reversible
a preventable and treatable slowly progressive
respiratory disease of airflow obstruction involving
the airways, pulmonary parenchyma, or both (Global
Initiative for Chronic Obstructive Lung Disease
[GOLD], 2015).
Most patients with COPD present with overlapping
signs and symptoms of emphysema and chronic
bronchitis, which are two distinct disease processes.
COPD may include diseases that cause airflow
obstruction (e.g., emphysema, chronic bronchitis) or
any combination of these disorders.
COPD includes emphysema, an anatomically defined
condition characterized by destruction of the lung
alveoli with air space enlargement; chronic
bronchitis, a clinically defined condition with chronic
cough and phlegm; and small airway disease, a
condition in which small bronchioles are narrowed
and reduced in number.
COPD can coexist with asthma. Both of these
diseases have the same major symptoms; however,
symptoms are generally more variable in asthma
than in COPD.
Asthma is considered a distinct, separate disorder
and is classified as an abnormal airway condition
characterized primarily by reversible inflammation.
Pathophysiology:
Airflow limitation, a major physiologic change in
COPD, can result from small airway disease and/or
emphysema.
Small airways may become narrowed by cells
(hyperplasia and accumulation), mucus, and fibrosis,
and extensive small airway destruction has been
demonstrated to be a hallmark of advanced COPD.
Persistent reduction in forced expiratory flow rates is
the most typical finding in COPD. Increases in the
residual volume and the residual volume/total lung
capacity ratio, non-uniform distribution of
ventilation, and ventilation-perfusion mismatching
also occur.
The inflammatory response occurs throughout the
proximal and peripheral airways, lung parenchyma,
and pulmonary vasculature (GOLD, 2015). Because
of the chronic inflammation and the body’s attempts
to repair it, changes and narrowing occur in the
airways.
o In the proximal airways (trachea and bronchi
greater than 2 mm in diameter), changes
include increased numbers of goblet cells
and enlarged submucosal glands, both of
which lead to hypersecretion of mucus.
o In the peripheral airways (bronchioles less
than 2 mm diameter), inflammation causes
thickening of the airway wall, peribronchial
fibrosis, exudate in the airway, and overall
airway narrowing (obstructive bronchiolitis).
o Over time, this ongoing injury-and-repair
process causes scar tissue formation and
narrowing of the airway lumen (GOLD,
2015).
Inflammatory and structural changes also occur in
the lung parenchyma (respiratory bronchioles and
alveoli).
Alveolar wall destruction leads to loss of alveolar
attachments and a decrease in elastic recoil. Finally,
the chronic inflammatory process affects the
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 pulmonary vasculature and causes thickening of the
lining of the vessel and hypertrophy of smooth
muscle, which may lead to pulmonary hypertension
(GOLD, 2015).
EMPHYSEMA
In emphysema, impaired oxygen and carbon dioxide
exchange results from destruction of the walls of
overdistended alveoli.
Emphysema is a pathologic term that describes an
abnormal distention of the airspaces beyond the
terminal bronchioles and destruction of the walls of
the alveoli (GOLD, 2015).
Pathophysiology of Emphysema:
1. Chronic exposure to cigarette smoke in
genetically susceptible individuals triggers
inflammatory and immune cell recruitment
within large and small airways and in the
terminal air spaces of the lung.
2. Inflammatory cells release proteinases that
damage the extracellular matrix supporting
airways, vasculature, and gas exchange surfaces
of the lung.
3. Structural cell death occurs through oxidant-
induced damage, cellular senescence, and
proteolytic loss of cellular-matrix attachments
leading to extensive loss of smaller airways,
vascular pruning, and alveolar destruction.
4. Disordered repair of elastin and other
extracellular matrix components contributes to
air space enlargement and emphysema.
As the walls of the alveoli are destroyed (a process
accelerated by recurrent infections), the alveolar
surface area in direct contact with the pulmonary
capillaries continually decreases.
This causes an increase in dead space (lung area
where no gas exchange can occur) and impaired
oxygen diffusion, which leads to hypoxemia.
In the later stages of disease, carbon dioxide
elimination is impaired, resulting in increased carbon
dioxide tension in arterial blood (hypercapnia)
leading to respiratory acidosis.
As the alveolar walls continue to break down, the
pulmonary capillary bed is reduced in size.
Consequently, resistance to pulmonary blood flow is
increased, forcing the right ventricle to maintain a
higher blood pressure in the pulmonary artery.
Hypoxemia may further increase pulmonary artery
pressures (pulmonary hypertension). Cor pulmonale,
one of the complications of emphysema, is right-
sided heart failure brought on by long-term high
blood pressure in the pulmonary arteries FEV1
(<25% of predicted) and chronic hypoxemia (Pao2
<55 mmHg).
This high pressure in the pulmonary arteries and
right ventricle lead to back up of blood in the venous
system, resulting in dependent edema, distended
neck veins, or pain in the region of the liver
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COLEGIO SAN AGUSTIN – BACOLOD
COLLEGE OF NURSING
Types of Emphysema:
Panlobular (panacinar) type of emphysema
there is destruction of the respiratory bronchiole,
alveolar duct, and alveolus.
All airspaces within the lobule are essentially
enlarged, but there is little inflammatory disease.
A hyperinflated (hyperexpanded) chest, marked
dyspnea on exertion, and weight loss typically occur.
To move air into and out of the lungs, negative
pressure is required during inspiration, and an
adequate level of positive pressure must be attained
and maintained during expiration. Instead being an
involuntary passive act, expiration becomes active
and requires muscular effort.
refers to abnormally large air spaces evenly
distributed within and across acinar units.
commonly observed in patients with 1AT deficiency,
which has a predilection for the lower lobes.
Centrilobular (Centroacinar) Emphysema
pathologic changes take place mainly in the center of
the secondary lobule, preserving the peripheral
portions of the acinus (i.e., the terminal airway unit
where gas exchange occurs).
Frequently, there is a derangement of ventilation–
perfusion ratios, producing chronic hypoxemia,
hypercapnia, polycythemia (i.e., an increase in red
blood cells), and episodes of right-sided heart failure.
This leads to central cyanosis and respiratory failure.
The patient also develops peripheral edema.
the type most frequently associated with cigarette
smoking, is characterized by enlarged air spaces
found (initially) in association with respiratory
bronchioles.
is usually most prominent in the upper lobes and
superior segments of lower lobes and is often quite
focal.
Airway Obstruction
Airflow limitation, also known as airflow obstruction, is
typically determined for clinical purposes by spirometry
Key parameters obtained from spirometry
include the volume of air exhaled within the first
second of the forced expiratory maneuver (FEV1)
and the total volume of air exhaled during the
entire spirometric maneuver (forced vital
capacity [FVC]).
Patients with airflow obstruction related to COPD
have a chronically reduced ratio of FEV1/FVC.
In contrast to asthma, the reduced FEV1 in COPD seldom
shows large responses to inhaled bronchodilators,
although improvements up to 15% are common.
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LARGE AIRWAYS
Cigarette smoking often results in mucus gland
enlargement and goblet cell hyperplasia, leading to
cough and mucus production that define chronic
bronchitis, but these abnormalities are not related to
airflow limitation.
Although not as prominent as in asthma, patients
may have smooth-muscle hypertrophy and bronchial
hyperreactivity leading to airflow limitation.
SMALL AIRWAYS
major site of increased resistance in most individuals
with COPD is in airways ≤2 mm diameter
Characteristic cellular changes include goblet cell
metaplasia, with these mucus-secreting cells
replacing surfactant-secreting Club cells
Narrowing and drop-out of small airways precede the
onset of emphysematous destruction.
HYPERINFLATION
In COPD there is often “air trapping” (increased
residual volume and increased ratio of residual
volume to total lung capacity) and progressive
hyperinflation (increased total lung capacity) late in
the disease.
Hyperinflation of the thorax during tidal breathing
preserves maximum expiratory airflow, because as
lung volume increases, elastic recoil pressure
increases, and airways enlarge so that airway
resistance decreases.
COPD RISK FACTORS:
1. Exposure to tobacco smoke accounts for an
estimated 80% to 90% of cases of chronic
obstructive pulmonary disease
2. Passive smoking (i.e., secondhand smoke)
3. Increased age
4. Occupational exposure—dust, chemicals
5. Indoor and outdoor air pollution
6. Genetic abnormalities, including a deficiency of
alpha1-antitrypsin, an enzyme inhibitor that
normally counteracts the destruction of lung tissue
by certain other enzymes
*Adapted from Global Initiative for Chronic Obstructive Disease.
(2015). Global strategy for the diagnosis, management and
prevention of COPD. Retrieved on 4/18/2016
www.goldcopd.org/uploads/users/files/GOLD_Report_2015.pdf
Emphysema – Risk factors:
1. Cigarette smoking
The most important environmental risk factor for
COPD worldwide is cigarette smoking. A dose–
response relationship exists between the
intensity of smoking (pack-year history) and the
decline in pulmonary function pack-years
(average number of packs of cigarettes smoked
per day multiplied by the total number of years
of smoking).
o Pack-years of cigarette smoking is the
most highly significant predictor of FEV1,
but only 15% of the variability in FEV1 is
explained by pack-years.
o Nonetheless, many patients with a
history of cigarette smoking with normal
spirometry have evidence for worse
health- related quality of life, reduced
exercise capacity, and emphysema and/
or airway disease on chest CT
evaluation; thus, they have not escaped
the harmful effects of cigarette smoking.
Other environmental risk factors include smoking
pipes, cigars, and other types of tobacco. Passive
smoking (i.e., secondhand smoke) also
contributes to respiratory symptoms and COPD
(GOLD, 2015).
Smoking depresses the activity of scavenger
cells and affects the respiratory tract’s ciliary
cleansing mechanism, which keeps breathing
passages free of inhaled irritants, bacteria, and
other foreign matter.
When smoking damages this cleansing
mechanism, airflow is obstructed and air
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COLEGIO SAN AGUSTIN – BACOLOD
COLLEGE OF NURSING
becomes trapped behind the obstruction. The
alveoli greatly distend, which diminishes lung
capacity.
Smoking also irritates the goblet cells and
mucous glands, causing an increased
accumulation of mucus, which in turn produces
more irritation, infection, and damage to the
lung (U.S. Department of Health and Human
Services [HHS], 2014a; HHS, 2014b).
In addition, carbon monoxide (a by-product of
smoking) combines with hemoglobin to form
carboxyhemoglobin. Hemoglobin that is bound
by carboxyhemoglobin cannot carry oxygen
efficiently.
Cigarette smoking is the best-studied COPD risk
factor; however, it is not the only risk factor and
studies have demonstrated nonsmokers may
also develop chronic airflow obstruction. Other
environmental risk factors for COPD include
prolonged and intense exposure to occupational
dusts and chemicals, indoor air pollution, and
outdoor air pollution (GOLD, 2015).
Alpha1-antitrypsin Deficiency
An enzyme inhibitor that protects the lung
parenchyma from injury. This deficiency may
lead to lung and liver disease.
Of patients with COPD, 1% to 2% are found to
have severe alpha1-antitrypsin deficiency
predisposes young people to rapid development
of lobular emphysema, even in the absence of
smoking. Among Caucasians, alpha1-antitrypsin
deficiency is one of the most common genetically
linked lethal diseases.
Genetically susceptible people are sensitive to
environmental factors (e.g., smoking, air
pollution, infectious agents, and allergens) and
eventually develop chronic obstructive
symptoms. Carriers must be identified so that
they can modify environmental risk factors to
delay or prevent overt symptoms of disease.
Alpha-protease inhibitor replacement
therapy, which slows the progression of the
disease, is available for patients with this
genetic defect and for those with severe
at:
disease
infusion therapy is costly and is required on
an ongoing basis
NATURAL HISTORY OF COPD
The effects of cigarette smoking on pulmonary
function appear to depend on:
1. the intensity of smoking exposure
2. the timing of smoking exposure during
growth
3. the baseline lung function of the individual
4. other environmental factors may have
similar effects.
The risk of eventual mortality from COPD is closely
associated with reduced levels of FEV 1
The rate of decline in pulmonary function can be
modified by changing environmental expo- sures
(i.e., quitting smoking), with smoking cessation at an
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 earlier age providing a more beneficial effect than
smoking cessation after marked reductions in
pulmonary function have already developed.
MANIFESTATIONS:
Although the natural history of COPD is variable, it is
generally a progressive disease characterized by
three primary symptoms: chronic cough, sputum
production, and dyspnea (GOLD, 2015)
As COPD advances, the principal feature is worsening
dyspnea on exertion with increasing intrusion on the
ability to perform vocational or avocational activities.
Chronic cough and sputum production often precede
the development of airflow limitation by many years.
o However, not all people with cough and
sputum production develop COPD.
o The cough may be intermittent and may be
unproductive in some patients (GOLD,
2015).
Dyspnea may be severe and interfere with the
patient’s activities and quality of life.
It is usually progressive, is worse with exercise, and
is persistent. As COPD progresses, dyspnea may
occur at rest.
Weight loss is common, because dyspnea interferes
with eating and the work of breathing is energy
depleting.
ASSESSMENT FINDINGS:
hyperinflation include a barrel chest
o results from a more fixed position of the ribs
in the inspiratory position (due to
hyperinflation) and from loss of lung
elasticity
Retraction of the supraclavicular fossae occurs on
inspiration, causing the shoulders to heave upward
In advanced emphysema, the abdominal muscles
may also contract on inspiration
enlarged lung volumes with poor diaphragmatic
excursion as assessed by percussion
Patients with severe airflow obstruction may also
exhibit use of accessory muscles of respiration,
sitting in the characteristic “tripod” position to
facilitate the actions of the sternocleidomastoid,
scalene, and intercostal muscles.
Patients may develop cyanosis, visible in the lips and
nail beds.
Advanced disease may be accompanied by cachexia,
with significant weight loss, bitemporal
American Thoracic Society’s Grade of Breathlessness Scale
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COLEGIO SAN AGUSTIN – BACOLOD
COLLEGE OF NURSING
wasting, and diffuse loss of subcutaneous adipose
tissue.
o This syndrome has been associated with
both inadequate oral intake and elevated
levels of inflammatory cytokines (TNF-).
o Such wasting is an independent poor
prognostic factor in COPD.
Some patients with advanced disease have
paradoxical inward movement of the rib cage with
inspiration (Hoover’s sign), the result of alteration of
the vector of diaphragmatic contraction on the rib
cage as a result of chronic hyperinflation.
Signs of overt right heart failure, termed cor
pulmonale, are relatively infrequent since the advent
of supplemental oxygen therapy.
Clubbing of the digits is not a sign of COPD, and its
presence should alert the clinician to initiate an
investigation for causes of clubbing.
DIAGNOSTICS
Pulmonary function studies/ SPIROMETRY
Pulmonary function studies are used to help confirm
the diagnosis of COPD, determine disease severity,
and monitor disease progression.
The hallmark of COPD is airflow obstruction
Spirometry is used to evaluate airflow obstruction,
which is determined by the ratio of FEV1 to forced
vital capacity (FVC).
Spirometric results are expressed as an absolute
volume and as a percentage of the predicted value
using appropriate normal values for gender, age, and
height. With obstruction, the patient either has
difficulty exhaling or cannot forcibly exhale air from
the lungs, reducing the FEV1.
Spirometry is also used to determine reversibility of
obstruction after the use of bronchodilators (GOLD,
2015).
Spirometry is initially performed, the patient is given
an inhaled bronchodilator treatment according to a
standard protocol, and then spirometry is repeated.
The patient demonstrates a degree of reversibility if
the pulmonary function values improve after
administration of the bronchodilator.
degree of airflow obstruction is an important
prognostic factor in COPD and is the basis for the
GOLD spirometric severity classification
ARTERIAL BLOOD GAS/ OXIMETRY
Arterial blood gases provide additional information
about alveolar ventilation and acid-base status by
measuring arterial Pco2 and pH.
o The change in pH with Pco2 is 0.08 units/10
mmHg acutely and 0.03 units/10 mmHg in
the chronic state.
Knowledge of the arterial pH therefore allows the
classification of ventilatory failure, defined as Pco 2
>45 mmHg, into acute or chronic conditions with
acute respiratory failure being associated with
acidemia.
RADIOGRAPHY
Obvious bullae, paucity of parenchymal markings, or
hyperlucency on chest x-ray suggests the presence
of emphysema.
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Increased lung volumes and flattening of the
diaphragm suggest hyperinflation but do not provide
information about chronicity of the changes.
CHEST CT SCAN
current definitive test for establishing the presence
or absence of emphysema, the pattern of
emphysema, and the presence of significant disease
involving medium and large airways
enables the discovery of coexisting interstitial lung
disease and bronchiectasis, which are common
complications in COPD.
Smokers with COPD are at high risk for development
of lung cancer, which can be identified on a chest CT
scan.
ALPHA1-ANTITRYPSIN SCREENING
may be performed for patients younger than 45
years and for those with a family history of COPD,
particularly if they have a family history of blood
relatives with alpha1-antitrypsin deficiency or COPD
that is primarily emphysematous in nature.
MANAGEMENT
Two main goals of therapy are:
to provide symptomatic relief
reduce respiratory symptoms
improve exercise tolerance
improve health status
to reduce future risk
prevent disease progression
prevent and treat exacerbations
reduce mortality).
Only three interventions have been demonstrated to
improve survival of patients with COPD.:
smoking cessation
oxygen therapy in chronically hypoxemic
patients
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COLLEGE OF NURSING
lung volume reduction surgery (LVRS) in
selected patients with emphysema
ASSESSMENT – HEALTH HISTORY:
1. Has the patient been exposed to risk factors (types,
intensity, duration)?
2. Does the patient have a past medical history of
respiratory diseases/problems, including asthma,
allergy, sinusitis, nasal polyps, or respiratory
infections?
3. Does the patient have a family history of chronic
obstructive pulmonary disease or other chronic
respiratory diseases?
4. How long has the patient had respiratory difficulty?
What is the pattern of symptom development?
5. Does exertion increase the dyspnea? What type of
exertion?
6. What are the limits of the patient’s tolerance for
exercise?
7. At what times during the day does the patient
complain most of fatigue and shortness of breath?
8. Does the patient describe any discomfort or pain in
any part of the body? If so, where does it occur, how
intense is this pain, when does it occur, and does it
interfere with activities of daily living? Is there any
intervention that helps to alleviate the pain or
discomfort?
9. Which eating and sleeping habits have been
affected?
10. What is the impact of respiratory disease on quality
of life?
11. What does the patient know about the disease and
their condition? What is the patient’s smoking history
(primary and secondary)?
12. Is there occupational exposure to smoke or other
pollutants?
13. What are the triggering events (e.g., exertion, strong
odors, dust, exposure to animals)?
14. Does the patient have a history of exacerbations or
previous hospitalizations for respiratory problems?
15. Are comorbidities present?
16. How appropriate are current medical treatments?
17. Does the patient have available social and family
support?
18. What is the potential for reducing risk factors (e.g.,
smoking cessation)?
Physical Assessment
1. What position does the patient assume during the
interview?
2. What are the pulse and the respiratory rates?
3. What is the character of respirations? Even and
without effort? Other?
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4. Can the patient complete a sentence without having
to take a breath?
5. Does the patient contract the abdominal muscles
during inspiration? Does the patient use accessory
muscles of the shoulders and neck when breathing?
6. Does the patient take a long time to exhale
(prolonged expiration)?
7. Is central cyanosis evident?
8. Are the patient’s neck veins engorged?
9. Does the patient have peripheral edema?
10. Is the patient coughing?
11. What are the color, amount, and consistency of the
sputum?
12. Is clubbing of the fingers present?
13. What types of breath sounds (i.e., clear, diminished
or distant, crackles, and wheezes) are heard?
Describe and document findings and locations.
14. Are there any sensory deficits?
15. Is there short- or long-term memory impairment?
16. Is there increasing stupor?
17. Is the patient apprehensive?
inhaler, by nebulization, or via the oral route in pill
or liquid form.
Bronchodilators are often given regularly throughout
the day as well as on an as-needed basis. They may
also be used prophylactically to prevent
breathlessness by having the patient use them
before participating in or completing an activity, such
as eating or walking.
Several devices are available to deliver medication
via the inhaled route. These include pMDIs, breath-
actuated pMDIs, dry powder inhalers, spacer or
valved-holding chambers, and nebulizers (also called
wet nebulizers; nebulization of liquid medication via
an air compressor) (Gardenhire, Ari, Hess et al.,
2013).

NURSING DIAGNOSES:
1. Ineffective Airway Clearance
2. Impaired Gas Exchange
3. Ineffective Breathing Pattern
4. Imbalanced Nutrition: Less Than Body
Requirements
5. Risk for Infection
6. Deficient Knowledge
7. Activity Intolerance
8. Other Possible Nursing Diagnosis

PHARMACOTHERAPY

SMOKING CESSATION
middle-aged smokers who were able to successfully
stop smoking experienced a significant improvement
in the rate of decline in pulmonary function, often
returning to annual changes similar to that of
nonsmoking patients.
smoking cessation improves survival
An emerging body of evidence demonstrates that
combining pharmacotherapy with traditional
supportive approaches considerably enhances the
chances of successful smoking cessation.
o There are three principal pharmacologic
approaches to the problem: nicotine
replacement therapy available as gum,
transdermal patch, lozenge, inhaler, and
nasal spray; bupropion; and varenicline, a
nicotinic acid receptor agonist/antagonist

BRONCHODILATORS
primary treatment for almost all patients with COPD
and are used for symptomatic benefit and to reduce
exacerbations.
inhaled route is preferred for medication delivery,
because side effects are less than with systemic
medication delivery.
In symptomatic patients, both regularly scheduled
use of long-acting agents and as-needed short-
acting medications are indicated.
Long-acting bronchodilators are more convenient for
patients to use, and combining bronchodilators with
different durations of action and different
mechanisms may optimize symptom management
(GOLD, 2015).
Bronchodilators relieve bronchospasm by improving
expiratory flow through widening of the airways and
promoting lung emptying with each breath.
o These medications alter smooth muscle tone
and reduce airway obstruction by allowing
increased oxygen distribution throughout
the lungs and improving alveolar ventilation.
o Although regular use of bronchodilators that
act primarily on the airway smooth muscle
does not modify the decline of function or
the prognosis of COPD, their use is central
in the management of COPD (GOLD, 2015).
These agents can be delivered through a pressurized
metered-dose inhaler (pMDI) or other type of
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• Attention to effective drug delivery and training in
proper inhaler technique is essential.
The choice of an inhaler device will depend on
availability, cost, prescribing physician, insurance
coverage and the skills and ability of the patient
(GOLD, 2015).
Several classes of bronchodilators are used: beta-
adrenergic agonists, anticholinergic agents, and
methylxanthines. These medications may be used in
combination to optimize the bronchodilation effect.
CORTICOSTEROIDS
Inhaled and systemic corticosteroids (oral or
intravenous) may also be used in COPD but are used
more frequently in asthma.
corticosteroids do not slow the decline in lung
function, these medications may improve symptoms.
A short trial course of oral corticosteroids may be
prescribed for patients with stage II or III COPD to
see if pulmonary function improves and symptoms
decrease. Inhaled corticosteroids via MDI may also
be used.
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Examples of corticosteroids in the inhaled form are
beclomethasone (Beclovent, Vanceril), budesonide
(Pulmicort), flunisolide (AeroBid), fluticasone
(Flovent), and triamcinolone (Azmacort).
Inhaled Corticosteroids
• main role of ICS is to reduce exacerbations
• use has been associated with increased rates of
oropharyngeal candidiasis and pneumonia and in
some studies an increased rate of loss of bone
density
• A trial of ICS should be considered in patients
with frequent exacerbations, defined as two or
more per year, and in patients with features of
asthma, such as eosinophilia
Anticholinergic Muscarinic Antagonists
• Short-acting ipratropium bromide improves
symptoms with acute improvement in FEV1.
• Long-acting muscarinic antagonists (LAMA,
including aclidinium, glycopyrrolate, tiotropium,
and umeclidinium) improve symptoms and
reduce exacerbations.
• In a large randomized clinical trial, there was a
trend toward reduced mortality rate in
tiotropium-treated patients that approached
statistical significance.
• Side effects are minor; dry mouth is the most
frequent side effect.
Beta Agonists
• Short-acting beta agonists ease symptoms with
acute improvements in lung function.
• Long-acting agents (LABA) provide symptomatic
benefit and reduce exacerbations, though to a
lesser extent than a LAMA.
• Currently available long-acting inhaled β
agonists are arformoterol, formoterol,
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14 Compiled by BJ SORRILLA, R.N., M.D.
 indacaterol, olodaterol, salmeterol, and
vilanterol.
• The main side effects are tremor and tachycardia
Combinations of Beta Agonist — Muscarinic
Antagonist
• combination inhaled beta agonist and muscarinic
antagonist therapy has been demonstrated to
provide improvement in lung function that is
greater than either agent alone and reduces
exacerbations
Medication regimens used to manage COPD are based on
disease severity (NIH, 2001):
• For stage I or mild COPD, a short-acting
bronchodilator may be prescribed.
• For stage II or moderate COPD, one or more
bronchodilators may be prescribed along with
inhaled corticosteroids, if symptoms are
significant.
• For stage III or severe COPD, medication therapy
includes regular treatment with one or more
bronchodilators and inhaled corticosteroids
Oral Glucocorticoids
• The chronic use of oral glucocorticoids for
treatment of COPD is not recommended because
of an unfavorable benefit/risk ratio.
• chronic use of oral glucocorticoids is associated
with significant side effects, including
osteoporosis, weight gain, cataracts, glucose
intolerance, and increased risk of infection
Antibiotics
• There are strong data implicating bacterial
infection as a precipitant of a substantial portion
of exacerbations.
• A randomized clinical trial of azithromycin,
chosen for both its anti-inflammatory and
antimicrobial properties, administered daily to
subjects with a history of exacerbation in the
past 6 months demonstrated a reduced
exacerbation frequency and longer time to first
exacerbation in the macrolide-treated cohort
(hazard ratio, 0.73).
Oxygen
• Supplemental O2 is the only pharmacologic
therapy demonstrated to unequivocally decrease
mortality rates in patients with COPD.
• For patients with resting hypoxemia (resting O2
saturation ≤88% in any patient or ≤89% with
signs of pulmonary hypertension or right heart
failure), the use of O2 has been demonstrated to
have a significant impact on mortality.
• NURSING ALERT:
o Because hypoxemia stimulates
respiration in the patient with severe
COPD, increasing the oxygen flow to a
high rate may greatly raise the patient’s
blood oxygen level. At the same time,
this will suppress the respiratory drive,
causing increased retention of carbon
dioxide and CO2 narcosis. The nurse
should closely monitor the patient’s
respiratory response to oxygen
administration via physical assessment,
pulse oximetry, and/or arterial blood
gases.
Oxygen Administration and Dyspnea Management in
Patients With AAT Deficiency (Knebel, A. R., Bentz, E., &
Barnes, P. (2000). Dyspnea management in alpha-1
antitrypsin deficiency: Effect of oxygen administration.
Nursing Research, 49(6), 333–338.
o Thirty-one Caucasian subjects participated in a
double-blind, crossover study.
o Oxygen saturation, 6-minute walk distance, and
end-of-walk dyspnea were measured during
three practice walks and during walks with nasal
cannula administration of oxygen (intervention)
and compressed air (control).
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o There was no difference in subjects’ walk
distance and severity of self-reported dyspnea
between oxygen and compressed air use.
The findings demonstrated that oxygen supplementation
did not significantly improve the sensation of dyspnea or
the distance walked in 6 minutes in the total sample of
patients with AAT deficiency.
Alpha1AT Augmentation Therapy
• Specific treatment in the form of IV α1AT
augmentation therapy is available for individuals
with severe α1AT deficiency.
• Despite sterilization procedures for these blood-
derived products and the absence of reported
cases of viral infection from therapy, some
physicians recommend hepatitis B vaccination
prior to starting augmentation therapy.
• Because only a fraction of individuals with severe
1AT deficiency will develop COPD, 1AT
augmentation therapy is not recommended for
severely 1AT-deficient persons with normal
pulmonary function and a normal chest CT scan.
Other Medications
• Patients should receive a yearly influenza
vaccine and the pneumococcal vaccine every 5
to 7 years as preventive measures.
• In most healthy adults, pneumococcal vaccine
titers persist for 5 or more years (George, San
Pedro & Stoller, 2000).
• Pneumococcal vaccines and vaccination for
Bordetella pertussis are recommended.
NON-PHARMACOLOGIC THERAPIES
Pulmonary Rehabilitation
• refers to a comprehensive treatment program
that incorporates exercise, education, and
psychosocial and nutritional counseling.
• In COPD, pulmonary rehabilitation has been
demonstrated to improve health-related quality
of life, dyspnea, and exercise capacity.
• It has also been shown to reduce rates of
hospitalization over a 6- to 12-month period.
• In both randomized and nonrandomized clinical
trials, pulmonary rehabilitation has been shown
to improve exercise tolerance, reduce dyspnea,
and increase health- related quality of life
(Rochester, 2000).
o The primary goal of re- habilitation is to
restore patients to the highest level of
independent function possible and to
improve their quality of life.
Lung Volume Reduction Surgery
• involves the removal of a portion of the diseased
lung parenchyma. This allows the functional
tissue to expand, resulting in improved elastic
recoil of the lung and improved chest wall and
diaphragmatic mechanics.
o This type of surgery does not cure the
disease, but it may decrease dyspnea,
improve lung function, and improve the
patient’s overall quality of life.
• In carefully selected patients with emphysema,
surgery to remove the most emphysematous
portions of lung improves exercise, lung
function, and survival.
• The anatomic distribution of emphysema and
post-rehabilitation exercise capacity are
important prognostic characteristics.
o Patients with upper lobe–predominant
emphysema and a low post-
rehabilitation exercise capacity are most
likely to benefit from LVRS.
o Patients with an FEV1 <20% of predicted
and either diffusely distributed
emphysema on CT scan or diffusing
capacity of lung for carbon monoxide
(DLCO) <20% of predicted have
increased mortality after the procedure,
and thus are not candidates for LVRS.
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Lung Transplantation
• COPD is currently the second leading indication
for lung transplantation.
• Current recommendations are that candidates
for lung transplantation should have very severe
airflow limitation, severe disability despite maxi-
mal medical therapy, and be free of significant
comorbid conditions such as liver, renal, or
cardiac disease.
EXACERBATIONS OF COPD
o Exacerbations are episodic acute worsening of
respiratory symptoms, including increased
dyspnea, cough, wheezing, and/ or change in the
amount and character of sputum.
o They may or may not be accompanied by other
signs of illness, including fever, myalgias, and
sore throat.
o The strongest single predictor of exacerbations is
a history of a previous exacerbation.
o The frequency of exacerbations increases as
airflow obstruction worsens; patients with severe
(FEV1 <50% predicted) or very severe airflow
obstruction (FEV1 <30% predicted) on average
have 1–3 episodes per year. However, some
individuals with very severe airflow obstruction
do not have frequent exacerbations.
o Other factors, such as an elevated ratio of the
diameter of the pulmonary artery to aorta on
chest CT, and gastroesophageal reflux, are also
associated with increased risk of COPD
exacerbations.
o Studies suggest that acquiring a new strain of
bacteria is associated with increased near-term
risk of exacerbation and that bacterial
infection/super- infection is involved in >50% of
exacerbations.
o Viral respiratory infections are present in
approximately one-third of COPD exacerbations.
HISTORY TAKING:
o The history should include quantification of the
degree and change in dyspnea by asking about
breathlessness during activities of daily living
and typical activities for the patient.
o The patient should be asked about fever; change
in character of sputum; and associated
symptoms such as wheezing, nausea, vomiting,
diarrhea, myalgias, and chills.
o Inquiring about the frequency and severity of
prior exacerbations can provide important
information
o the single greatest risk factor for hospitalization
with an exacerbation is a history of previous
hospitalization.
PE:
o tachycardia, tachypnea, use of accessory
muscles, signs of perioral or peripheral cyanosis,
the ability to speak in complete sentences, and
the patient’s mental status.
o The chest examination should establish the
presence or absence of focal findings, degree of
air movement, presence or absence of wheezing,
asymmetry in the chest examination (suggesting
large airway obstruction or pneumothorax
mimicking an exacerbation), and the presence or
absence of paradoxical motion of the abdominal
wall.
Management of Exacerbations:
Chest X-ray
Approximately 25% of x-rays in this clinical
situation will be abnormal, with the most
frequent findings being pneumonia and
congestive heart failure.
ABG
o advanced COPD, a history of hypercarbia,
mental status changes (confusion,
sleepiness), or those in significant distress
o
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CRITERIA FOR ADMISSION:
o presence of respiratory acidosis and
hypercarbia
o new or worsening hypoxemia
o severe underlying disease
o living situation is not conducive to careful
observation and the delivery of prescribed
treatment.
Bronchodilators
Antibiotics:
o Bacteria frequently implicated in COPD
exacerbations include Streptococcus
pneumoniae, Haemophilus influenzae, and
Moraxella catarrhalis.
o In addition, Mycoplasma pneumoniae or
Chlamydia pneumoniae are found in 5–10%
of exacerbations.
Systemic glucocorticoids
o reduces the length of stay, hastens recovery,
and reduces the chance of subsequent
exacerbation or relapse.
o One study demonstrated that 2 weeks of
glucocorticoid therapy produced benefit
indistinguishable from 8 weeks of therapy.
(Watch out for hyperglycemia)
Mechanical ventilatory support
o Non-invasive positive-pressure ventilation
Contraindications to NIPPV include
cardiovascular instability, impaired
mental status, inability to cooperate,
copious secretions or the inability to
clear secretions, craniofacial
abnormalities or trauma precluding
effective fitting of mask, extreme
obesity, or significant burns.
o Invasive intubation
indicated for patients with severe
respiratory distress despite initial
therapy, life-threatening hypoxemia,
severe hypercarbia and/or acidosis,
markedly impaired mental status,
respiratory arrest, hemodynamic
instability, or other complications.
Factors to consider during
mechanical ventilatory support
include the need to provide sufficient
expiratory time in patients with
severe airflow obstruction and the
presence of auto-PEEP (positive end-
expiratory pressure), which can
result in patients having to generate
significant respiratory effort to
trigger a breath during a demand
mode of ventilation.
NURSING MANAGEMENT:
Patient Education
topics may include normal anatomy and
physiology of the lung, pathophysiology and
changes with COPD, medications and home
oxygen therapy, nutrition, respiratory therapy
treatments, symptom alleviation, smoking
cessation, sexuality and COPD, coping with
chronic disease, communicating with the health
care team, and planning for the future (advance
directives, living wills, informed decision making
about health care alternatives).
Breathing Exercises
Breathing pattern of most people with COPD is
shallow, rapid, and inefficient; the more severe
the disease, the more inefficient the breathing
pattern.
diaphragmatic breathing, which reduces the
respiratory rate, increases alveolar ventilation,
and sometimes helps expel as much air as
possible during expiration
Pursed- lip breathing helps to slow expiration,
prevents collapse of small airways, and helps the
patient to control the rate and depth of
respiration. It also promotes relaxation, enabling
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16 Compiled by BJ SORRILLA, R.N., M.D.
 the patient to gain control of dyspnea and reduce Ineffective airway clearance related to
feelings of panic bronchoconstriction, increased mucus
production, ineffective cough, broncho-
Inspiratory muscle training pulmonary infection, and other complications
Diaphragmatic breathing - program requires that Ineffective breathing pattern related to
the patient breathe against resistance for 10 to shortness of breath, mucus, bronchoconstriction,
15 minutes every day. As the resistance is and airway irritants
gradually increased, the muscles become better Activity intolerance due to fatigue, ineffective
conditioned. breathing patterns, and hypoxemia
Deficient knowledge of self-care strategies to be
Activity pacing performed at home.
Activities requiring the arms to be supported Ineffective coping related to reduced
above the level of the thorax may produce socialization, anxiety, depression, lower activity
fatigue or respiratory distress but may be level, and the inability to work
tolerated better after the patient has been up
and moving around for an hour or more. COLLABORATIVE PROBLEMS/ POTENTIAL
planning self-care activities and determining the COMPLICATIONS
best time for bathing, dressing, and daily Based on the assessment data, potential complications
activities that may develop include:
Respiratory insufficiency or failure
Self-care activities Atelectasis
patient is taught to coordinate diaphragmatic Pulmonary infection
breathing with activities such as walking, Pneumonia
bathing, bending, or climbing stairs. Pneumothorax
The patient should bathe, dress, and take short Pulmonary hypertension
walks, resting as needed to avoid fatigue and
excessive dyspnea. Sources:
Fluids should always be readily available, and the 1. J.L. Hinkle, K.H. Cheever. Brunner & Suddarths’
patient should begin to drink fluids without Textbook of Medical & Surgical Nursing. Lippincott
Williams & Wilkins.
having to be reminded.
2. Harrisons’ Principles of Internal Medicine, 20th Ed.
If postural drainage is to be done at home, the
nurse instructs and supervises the patient before
discharge or in the outpatient setting.

Physical conditioning PULMONARY EMBOLISM

breathing exercises and general exercises
intended to conserve energy and increase
refers to the obstruction of the pulmonary artery or
pulmonary ventilation
one of its branches by a thrombus (or thrombi) that
Any physical activity that can be done regularly
originates somewhere in the venous system or in the
is helpful. Lightweight portable oxygen systems
right side of the heart.
are available for ambulatory patients who require
Most commonly, PE is due to a blood clot or
oxygen therapy during physical activity
thrombus. However, there are other types of emboli:
air, fat, amniotic fluid, and septic (from bacterial
Nutritional Therapy
invasion of the thrombus).
Approximately 25% of patients with COPD are
PE is a common disorder and often is associated with
undernourished (NIH, 2001; Ferreira, Brooks,
trauma, surgery (orthopedic, major abdominal,
Lacasse & Gold- stein, 2001)
pelvic, gynecologic), pregnancy, heart failure, age
thorough assessment of caloric needs and
older than 50 years, hypercoagulable states, and
counseling about meal planning and
prolonged immobility.
supplementation are part of the rehabilitation
It also may occur in an apparently healthy person.
process
ORIGIN
COPING MEASURES
most thrombi originate in the deep veins of the legs,
Any factor that interferes with normal breathing
other sites include the pelvic veins and the right
quite naturally induces anxiety, depression, and
atrium of the heart.
changes in behavior.
A venous thrombosis can result from slowing of blood
Restricted activity (and reversal of family roles
flow (stasis), secondary to damage to the blood
due to loss of employment), the frustration of
vessel wall (particularly the endothelial lining) or
having to work to breathe, and the realization
changes in the blood coagulation mechanism.
that the disease is prolonged and unrelenting
Atrial fibrillation is also a cause of pulmonary
may cause the patient to react with anger,
embolism.
depression, and demanding behavior.
An enlarged right atrium in fibrillation causes blood
Sexual function may be compromised, which also
to stagnate and form clots in this area. These clots
diminishes self-esteem. In addition, the nurse
are prone to travel into the pulmonary circulation.
needs to provide education and support to the
spouse/significant other and family because the
caregiver role in end-stage COPD can be difficult. RISK FACTORS FOR PE:
Venous Stasis (slowing of blood flow in veins)
PROGNOSIS: Prolonged immobilization (especially
Following a hospitalization for COPD, about 20% postoperative)
of patients are re-hospitalized in the subsequent Prolonged periods of sitting/traveling
30 days and 45% are hospitalized in the next Varicose veins
year. Spinal cord injury
Mortality following hospital discharge is about Hypercoagulability (due to release of tissue
20% in the following year thromboplastin after injury/surgery)
Injury
NURSING DIAGNOSES: Tumor (pancreatic, GI, GU, breast, lung)
Impaired gas exchange and airway clearance Increased platelet count (polycythemia,
due to chronic inhalation of toxins splenectomy)
Impaired gas exchange related to ventilation– Venous Endothelial Disease
perfusion inequality Thrombophlebitis
Vascular disease
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 Foreign bodies (IV/central venous catheters)
Certain Disease States (combination of stasis,
coagulation alterations, and venous injury)
Heart disease (especially heart failure)
Trauma (especially fracture of hip, pelvis,
vertebra, lower extremities)
Postoperative state/postpartum period Diabetes
mellitus
Chronic obstructive pulmonary disease
Other Predisposing Conditions
Advanced age
Obesity
Pregnancy
Oral contraceptive use
History of previous thrombophlebitis, pulmonary
embolism
Constrictive clothing
PATHOPHYSIOLOGY
Inflammation & Platelet Activation
Virchow’s triad of venous stasis,
hypercoagulability, and endothelial injury leads
to recruitment of activated platelets, which
release microparticles. These microparticles
contain proinflammatory mediators that bind
neutrophils, stimulating them to release their
nuclear material and form web-like extracellular
networks called neutrophil extracellular traps.
These prothrombotic networks contain histones
that stimulate platelet aggregation and promote
platelet-dependent thrombin generation. Venous
thrombi form and flourish in an environment of
stasis, low oxygen tension, and upregulation of
proinflammatory genes.
Prothrombic States
two most common autosomal dominant genetic
mutations are factor V Leiden, which causes
resistance to the endogenous anticoagulant,
activated protein C (which inactivates clotting
factors V and VIII), and the prothrombin gene
mutation, which increases the plasma
prothrombin concentration
Antiphospholipid antibody syndrome is the most
common acquired cause of thrombophilia and is
associated with venous or arterial thrombosis.
Other common predisposing factors include
cancer, obesity, cigarette smoking, systemic
arterial hypertension, chronic obstructive
pulmonary disease, chronic kidney disease,
blood transfusion, long-haul air travel, air
pollution, estrogen-containing contraceptives,
pregnancy, postmenopausal hormone
replacement, surgery, and trauma.
Embolization
When deep venous thrombi detach from their
site of formation, they embolize to the vena
cava, right atrium, and right ventricle, and lodge
in the pulmonary arterial circulation, thereby
causing acute PE.
Paradoxically, these thrombi occasionally
embolize to the arterial circulation through a
patent foramen ovale or atrial septal defect.
Many patients with PE have no evidence of DVT
because the clot has already embolized to the
lungs.
PHYSIOLOGY
The most common gas exchange abnormalities
are arterial hypoxemia and an increased
alveolar-arterial O2 tension gradient, which
represents the inefficiency of O2 transfer across
the lungs.
Anatomic dead space increases because
breathed gas does not enter gas exchange units
of the lung.
Physiologic dead space increases because
ventilation to gas exchange units exceeds
venous blood flow through the pulmonary
capillaries.
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Increased pulmonary vascular resistance
due to vascular obstruction or platelet secretion
of vasoconstricting neurohumoral agents such as
serotonin.
release of vasoactive mediators can produce
ventilation-perfusion mismatching at sites
remote from the embolus, thereby accounting
for discordance between a small PE and a large
alveolar-arterial O2 gradient.
Impaired gas exchange
due to increased alveolar dead space from
vascular obstruction, hypoxemia from alveolar
hypoventilation relative to perfusion in the non-
obstructed lung, right-to-left shunting, or
impaired carbon monoxide transfer due to loss of
gas exchange surface.
Alveolar hyperventilation
due to reflex stimulation of irritant receptors
Increased airway resistance
due to constriction of airways distal to the
bronchi
Decreased pulmonary compliance
due to lung edema, lung hemorrhage, or loss of
surfactant.
Pulmonary Hypertension, RV Dysfunction, and RV
Microinfarction
Pulmonary artery obstruction and neurohumoral
mediators cause a rise in pulmonary artery
pressure and in pulmonary vascular resistance.
When RV wall tension rises, RV dilation and
dysfunction ensue, with release of the cardiac
biomarker, brain natriuretic peptide, due to
abnormal RV stretch. The interventricular
septum bulges into and compresses an
intrinsically normal left ventricle (LV).
Diastolic LV dysfunction reduces LV distensibility
and impairs LV filling. Increased RV wall tension
also compresses the right coronary artery, limits
myocardial oxygen supply, and precipitates right
coronary artery ischemia and RV microinfarction,
with release of cardiac biomarkers such as
troponin.
Underfilling of the LV may lead to a fall in LV
cardiac output and systemic arterial pressure,
with consequent circulatory collapse and death.
When a thrombus completely or partially obstructs a
pulmonary artery or its branches, the alveolar dead
space is increased.
The area, although continuing to be ventilated,
receives little or no blood flow. Thus, gas
exchange is impaired or absent in this area.
In addition, various substances are released
from the clot and surrounding area, causing
regional blood vessels and bronchioles to
constrict.
This causes an increase in pulmonary vascular
resistance. This reaction compounds the
ventilation–perfusion imbalance.
hemodynamic consequences are increased
pulmonary vascular resistance from the regional
vasoconstriction and reduced size of the
pulmonary vascular bed
o This results in an increase in pulmonary
arterial pressure and, in turn, an
increase in right ventricular work to
maintain pulmonary blood flow.
o When the work requirements of the right
ventricle exceed its capacity, right
ventricular failure occurs, leading to a
decrease in cardiac output followed by a
decrease in systemic blood pressure and
the development of shock.
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Deep Venous Thrombosis discoloration, and superficial vein
Lower extremity DVT distention.
usually begins in the calf and propagates o The pain is usually relieved with
proximally to the popliteal vein, femoral vein, elevation.
and iliac veins. The diagnostic workup includes:
Leg DVT is about 10 times more common than o ventilation–perfusion scan
upper extremity DVT o pulmonary angiography
Upper extremity DVT o chest x-ray
often precipitated by placement of pacemakers, infiltrates, atelectasis, elevation
internal cardiac defibrillators, or indwelling of the diaphragm on the affected
central venous catheters side, or a pleural effusion
The likelihood of upper extremity DVT increases Well-established abnormalities
as the catheter diameter and number of lumens include focal oligemia
increase. (Westermark’s sign), a
Superficial venous thrombosis usually presents with peripheral wedged-shaped
erythema, tenderness, and a “palpable cord.” Patients density usually located at the
are at risk for extension of the thrombosis to the deep- pleural base (Hampton’s hump),
venous system. and an enlarged right
descending pulmonary artery
MANIFESTATION: (Palla’s sign).
The most common symptom is unexplained
breathlessness.
o When occult PE occurs concomitantly
with overt congestive heart failure or
pneumonia, clinical improvement often
fails to ensue despite standard medical
treatment of the concomitant illness.
This scenario presents a clinical clue to
the possible coexistence of PE
The symptoms of PE depend on the size of the
thrombus and the area of the pulmonary artery
occluded by the thrombus; they may be
nonspecific.
Dyspnea is the most frequent symptom;
tachypnea (very rapid respiratory rate) is the
most frequent sign (Goldhaber, 1998).
The duration and intensity of the dyspnea
depend on the extent of embolization. Chest pain
is common and is usually sudden and pleuritic.
It may be substernal and mimic angina pectoris
or a myocardial infarction.
Other symptoms include anxiety, fever,
tachycardia, apprehension, cough, diaphoresis,
hemoptysis, and syncope.
A massive embolism is best defined by the
degree of hemodynamic instability rather than
the percentage of pulmonary vasculature o ECG
occlusion. sinus tachycardia, PR-interval
o It is described as an occlusion of the depression, and nonspecific T-
outflow tract of the main pulmonary wave changes
artery or the bifurcation of the S1Q3T3 sign: an S wave in lead
pulmonary arteries that produces I, a Q wave in lead III, and an
pronounced dyspnea, sudden sub- inverted T wave in lead III
sternal pain, rapid and weak pulse, o peripheral vascular studies
shock, syncope, and sudden death. o impedance plethysmography
With DVT, the most common symptom is a o arterial blood gas analysis
cramp or “charley horse” in the lower calf that hypoxemia and hypocapnia
persists and intensifies over several days. (from tachypnea)
o Not all leg pain is due to DVT, and not all o ventilation-perfusion scan
dyspnea is due to PE. test of choice in patients with
o Fever and chills usually herald cellulitis suspected PE
rather than DVT. Physical findings, if perfusion portion of the scan
present, may consist only of mild may indicate areas of diminished
palpation discomfort in the lower calf. or absent blood flow and is the
o However, massive DVT often presents most useful test to rule out
with marked thigh swelling, tenderness, clinically important PE
and erythema. A ventilation scan may show
whether there is also a
ASSESSMENT, DIAGNOSTICS ventilation abnormality present
Death from PE commonly occurs within 1 hour of normal perfusion scan rules out
symptoms; thus, early recognition and diagnosis the diagnosis of PE
are priorities. If there is a ventilation–
Because the symptoms of PE can vary from few perfusion mismatch, the
to severe, a diagnostic workup is performed to probability of PE is high
rule out other diseases. o pulmonary angiography
Deep venous thrombosis is closely associated is invasive and is performed in
with the development of PE. Typically, the interventional radiology
o patients report sudden onset of pain department
and/or swelling and warmth of the contrast agent is injected into
proximal or distal extremity, skin the pulmonary arterial system,
allowing visualization of

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COLLEGE OF NURSING 19 Compiled by BJ SORRILLA, R.N., M.D.
 obstructions to blood flow and
abnormalities.
o Chest CT with IV contrast
principal imaging test for the
diagnosis of PE
The CT scan also provides an
excellent four-chamber view of
the heart. RV enlargement on
chest CT indicates an increased
likelihood of death within the
next 30 days compared with PE
patients who have normal RV
size.
PREVENTION
most effective approach to preventing PE is to
prevent deep venous thrombosis
o Active leg exercises to avoid venous stasis
o early ambulation
o use of elastic compression stockings
Describe the underlying process leading to
pulmonary embolism.
Describe the need for continued anticoagulant
therapy after the initial embolism.
Name the anticoagulant prescribed and identify
dosage and schedule of administration.
Describe potential side effects of coagulation such as
bruising and bleeding and identify ways to prevent
bleeding.
Avoid the use of sharps (razors, knives, etc.) to
prevent cuts; shave with an electric shaver.
Use a toothbrush with soft bristles to prevent gum
injury.
Do not take aspirin or antihistamines while taking
warfarin sodium (Coumadin).
Always check with health care provider before taking
any medicine, including over-the-counter
medications. Avoid laxatives, because they may
affect vitamin K absorption.
Report the occurrence of dark, tarry stools to the
health care provider immediately.
Wear an identification bracelet or carry a medicine
card stating that you are taking anticoagulants. •
Describe strategies to prevent recurrent deep venous
thrombosis and pulmonary emboli:
Continue to wear elastic pressure stockings
(compression hose) as long as directed.
o For patients with swelling of the legs when
acute DVT is diagnosed, below-knee
graduated compression stockings may be
pre- scribed, usually 30–40 mmHg, to lessen
patient discomfort.
o They should be replaced every 3 months
because they lose their elasticity.
o However, prescription of vascular
compression stockings in asymptomatic
newly diagnosed acute DVT patients does
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not prevent the development of post-
thrombotic syndrome.
Avoid sitting with legs crossed or sitting for
prolonged periods of time.
When traveling, change position regularly, walk
occasionally, and do active exercises of moving the
legs and ankles while sitting.
Drink fluids, especially while traveling and in warm
weather, to avoid hemoconcentration due to fluid
deficit.
Describe the signs and symptoms of lower extremity
circulatory compromise and potential deep venous
thrombosis: calf or leg pain, swelling, pedal edema.
Describe the signs and symptoms of pulmonary
compromise related to recurrent pulmonary
embolism.
Describe how and when to contact the health care
provider if symptoms of circulatory compromise or
pulmonary compromise are identified.
Patients who are older than 40, whose hemostasis is
adequate, and who are undergoing major elective
abdominal or thoracic surgery may receive anticoagulant
therapy.
Low doses of heparin may be given before
surgery to reduce the risk of postoperative deep
venous thrombus and PE.
Heparin should be administered subcutaneously
2 hours before surgery and continued every 8 to
12 hours until the patient is discharged.
Low-dose heparin is thought to enhance the
activity of antithrombin III, a major plasma
inhibitor of clotting factor X.
This regimen is not recommended for patients
with an active thrombotic process or for those
undergoing major orthopedic surgery, open
prostatectomy, or surgery on the eye or brain.
Low-molecular-weight heparin (eg, enoxaparin)
is an alternative therapy. It has a longer half-life,
enhanced subcutaneous absorption, a reduced
incidence of thrombocytopenia, and reduced
interaction with platelets as compared to
unfractionated heparin (Ansell, Hickey,
Kleinschmidt et al., 2000).
The intermittent pneumatic leg compression device is
useful in preventing thromboembolism.
The device inflates a bag that intermittently
compresses the leg from the calf to the thigh,
thereby improving venous return.
It may be applied before surgery and continued
until the patient is ambulatory.
The device is particularly useful for patients who
are not candidates for anticoagulant therapy
(Clagett, Anderson, Geerts et al., 1998).
MANAGEMENT
PRIMARY THERAPY
consists of clot dissolution with pharmaco-
mechanical therapy that usually includes low-
dose catheter-directed thrombolysis.
This approach is reserved for patients with
extensive femoral, iliofemoral, or upper
extremity DVT.
SECONDARY PREVENTION
Anticoagulation or placement of an inferior vena
caval (IVC) filter constitutes secondary
prevention of VTE.
EMERGENCY MANAGEMENT
Immediate objective is to stabilize the
cardiopulmonary system.
A sudden rise in pulmonary resistance increases the
work of the right ventricle, which can cause acute
right-sided heart failure with cardiogenic shock.
o Most patients who die of massive PE do so in
the first 1 to 2 hours after the embolic event.
Emergency management consists of the following:
• Nasal oxygen is administered immediately to
relieve hypoxemia, respiratory distress, and
central cyanosis.
CRITICAL CARE NURSING (NCM 118)
20 Compiled by BJ SORRILLA, R.N., M.D.
 • Intravenous infusion lines are started to
establish routes for medications or fluids that will
be needed.
• A perfusion scan, hemodynamic measurements,
and arterial blood gas determinations are
performed. Spiral (helical) CT or pulmonary
angiography may be performed. Spiral CT is
more advanced and quicker than routine
tomography. With spiral CT, the patient
continuously moves as the x-ray tube rotates.
With this type of CT, images can be
reconstructed at select levels and locations for
diagnostic purposes.
• Hypotension is treated by a slow infusion of
dobutamine (which has a dilating effect on the
pulmonary vessels and bronchi) or dopamine.
• The ECG is monitored continuously for
dysrhythmias and right ventricular failure, which
may occur suddenly.
• Digitalis glycosides, intravenous diuretics, and
antiarrhythmic agents are administered when
appropriate.
• Blood is drawn for serum electrolytes, complete
blood count, and hematocrit.
• If clinical assessment and arterial blood gas
analysis indicate the need, the patient is
intubated and placed on a mechanical ventilator.
• If the patient has suffered massive embolism and
is hypotensive, an indwelling urinary catheter is
inserted to monitor urinary output.
• Small doses of intravenous morphine or
sedatives are administered to relieve the
patient’s anxiety, to alleviate chest discomfort,
to improve tolerance of the endotracheal tube,
and to ease adaptation to the mechanical
ventilator.
PHARMACOLOGIC MANAGEMENT
Anticoagulation therapy is contraindicated in patients
who are at risk for bleeding (eg, those with GI conditions
or with postoperative or postpartum bleeding).
Anticoagulation Therapy
Anticoagulant therapy (heparin, warfarin sodium)
has traditionally been the primary method for
managing acute deep vein thrombosis and PE
(Goldhaber, 1998).
Heparin/ Unfractionated Heparin (UFH) is used
to prevent recurrence of emboli but has no effect on
emboli that are already present.
UFH anticoagulates by binding to and accelerating
the activity of antithrombin, thus preventing
additional thrombus formation.
administered as an IV bolus of 5,000 to
10,000 units, followed by a continuous
infusion initiated at a dose of 18 U/kg per
hour, not to exceed 1,600 U/hour in
otherwise healthy patients (Goldhaber,
1998).
The rate is reduced in patients with a high risk of
bleeding. The goal is to keep the partial
thromboplastin time 1.5 to 2.5 times normal (or 46
to 70 seconds). Heparin is usually administered for 5
to 7 days. Low-molecular-weight heparin (eg,
enoxaparin) may also be used.
major advantage of UFH is its short half-life, which is
especially useful in patients in whom hour-to-hour
control of the intensity of anticoagulation is desired.
Heparin also has pleiotropic effects that may
decrease systemic and local inflammation.
Warfarin sodium (Coumadin)
In an average-size adult, warfarin is often initiated in
a dose of 5 mg.
o The prothrombin time is standardized by
calculating the international normalized ratio
(INR), which assesses the anticoagulant
effect of warfarin.
o The target INR is usually 2.5, with a range of
2.0–3.0.
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begun within 24 hours after the start of heparin
therapy because its onset of action is 4 to 5 days.
Warfarin is usually continued for 3 to 6 months. The
prothrombin time is maintained at 1.5 to 2.5 times
normal (or an INR [international normalized ratio] of
2.0 to 3.0).
Thrombolytic Therapy
Thrombolytic therapy (urokinase, streptokinase,
alteplase, anistreplase, reteplase) also may be used
in treating PE, particularly in patients who are
severely compromised (eg, those who are
hypotensive and have significant hypoxemia despite
oxygen supplementation).
Thrombolytic therapy resolves the thrombi or emboli
more quickly and restores more normal
hemodynamic functioning of the pulmonary
circulation, thereby reducing pulmonary
hypertension, and improving perfusion, oxygenation,
and cardiac output.
Bleeding, however, is a significant side effect.
Contraindications to thrombolytic therapy include:
o cerebrovascular accident within the past 2
months
o other active intracranial processes, active
bleeding, surgery within the past 10 days of
the thrombotic event
o recent labor and delivery, trauma, or severe
hypertension
Consequently, thrombolytic agents are advocated
only for PE affecting a significant area of blood flow
to the lung and causing hemodynamic instability.
Novel Oral Anticoagulants
Novel oral anticoagulants (NOACs) are administered
in a fixed dose, establish effective anticoagulation
within hours of ingestion, require no laboratory
coagulation monitoring, and have few of the drug-
drug or drug-food interactions.
o Betrixaban, a direct factor Xa inhibitor, was
approved by the FDA in 2017 for VTE
prophylaxis in acutely ill medical patients
during hospitalization and continuing for a
total duration of 5 to 6 weeks.
o Rivaroxaban and apixaban, direct factor Xa
inhibitors, are approved as monotherapy for
acute and extended treatment of DVT and
PE, without a parenteral “bridging”
anticoagulant.
o Dabigatran, a direct thrombin inhibitor, and
edoxaban, a factor Xa inhibitor, are
approved for treatment of VTE after an initial
5-day course of parenteral anticoagulation.
Before thrombolytic therapy is started:
prothrombin time, partial thromboplastin time,
hematocrit values, and platelet counts are
obtained.
Heparin is stopped prior to administration of a
thrombolytic agent.
During therapy, all but essential invasive
procedures are avoided because of potential
bleeding.
If necessary, fresh whole blood, packed red cells,
cryoprecipitate, or frozen plasma is administered
to replace blood loss and reverse the bleeding
tendency.
After the thrombolytic infusion is completed
(which varies in duration according to the agent
used and the condition being treated), the
patient is given anticoagulants.
SURGICAL MANAGEMENT
Surgical embolectomy
rarely performed but may be indicated if the
patient has a massive PE or hemodynamic
instability or if there are contraindications to
thrombolytic therapy
Pulmonary embolectomy
requires a thoracotomy with cardiopulmonary
by-pass technique
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21 Compiled by BJ SORRILLA, R.N., M.D.
Transvenous catheter embolectomy
technique in which a vacuum-cupped catheter is
introduced transvenously into the affected
pulmonary artery
Interrupting the inferior vena cava
when PE recurs or when the patient is intolerant
of anticoagulant therapy
approach prevents dislodged thrombi from being
swept into the lungs while allowing adequate
blood flow.
The preferred approach is the application of
Teflon clips to the inferior vena cava to divide the
lumen into small channels without occluding
caval blood flow.
NURSING MANAGEMENT
MINIMIZING THE RISK OF PULMO. EMBOLISM
nurse must have a high degree of suspicion for
PE in any patient, but particularly in those with
conditions predisposing to a slowing of venous
return
PREVENTING THROMBUS FORMATION
Preventing thrombus formation is a major
nursing responsibility.
The nurse encourages ambulation and active and
passive leg exercises to prevent venous stasis in
patients on bed rest.
The nurse instructs the patient to move the legs
in a “pumping” exercise so that the leg muscles
can help increase venous flow.
The nurse also advises the patient not to sit or
lie in bed for prolonged periods, not to cross the
legs, and not to wear constricting clothing.
Legs should not be dangled or feet placed in a
dependent position while the patient sits on the
edge of the bed; instead, the patient’s feet
should rest on the floor or on a chair.
In addition, intravenous catheters (for parenteral
therapy or measurements of central venous
pressure) should not be left in place for
prolonged periods.
ASSESSING POTENTIAL FOR PULMO. EMBOLISM
The nurse examines patients who are at risk for
developing PE for a positive Homans’ sign, which may or
may not indicate impending thrombosis of the leg veins.
To test for Homans’ sign, the patient assumes a
supine position, lifts the leg, and dorsiflexes the
foot.
The nurse asks the patient to report whether calf
pain occurs during this maneuver. The
occurrence of pain—a positive Homans’ sign—
may indicate deep venous thrombosis.
turn the patient frequently and reposition the
patient to improve the ventilation–perfusion
ratio in the lung.
The nurse administers opioid analgesics as
prescribed for severe pain.
MANAGING OXYGEN THERAPY
nurse assesses the patient frequently for signs of
hypoxemia and monitors the pulse oximetry
values to evaluate the effectiveness of the
oxygen therapy.
Deep breathing and incentive spirometry are
indicated for all patients to minimize or prevent
atelectasis and improve ventilation.
Nebulizer therapy or percussion and postural
drainage may be used for management of
secretions.
MONITORING FOR COMPLICATIONS
nurse must be alert for the potential complication
of cardiogenic shock or right ventricular failure
subsequent to the effect of PE on the
cardiovascular system
PROVIDING POSTOPERATIVE NURSING CARE
After surgery, the nurse measures the patient’s
pulmonary arterial pressure and urinary output.
nurse assesses the insertion site of the arterial
catheter for hematoma formation and infection.
It is important to maintain the blood pressure at
a level that supports perfusion of vital organs.
To prevent peripheral venous stasis and edema
of the lower extremities, the nurse elevates the
foot of the bed and encourages isometric
exercises, use of elastic compression stockings,
and walking when the patient is permitted out of
bed.
Sitting is discouraged because hip flexion
compresses the large veins in the legs.
RELIEVING ANXIETY
nurse encourages the stabilized patient to talk
about any fears or concerns related to this
frightening episode, answers the patient’s and
family’s questions concisely and accurately,
explains the therapy, and describes how to
recognize untoward effects early.

MONITORING THROMBOLYTIC THERAPY

The nurse is responsible for monitoring thrombolytic and
anticoagulant therapy.
During thrombolytic infusion, the patient
remains on bed rest, vital signs are assessed
every 2 hours, and invasive procedures are
limited.
Tests to determine prothrombin time or partial
thromboplastin time are performed 3 to 4 hours
after the thrombolytic infusion is started to
confirm that the fibrinolytic systems have been
activated.
o Because of the prolonged clotting time,
only essential arterial punctures or
venipunctures are performed, and
manual pressure is applied to any
puncture site for at least 30 minutes.
o Pulse oximetry is used to monitor
changes in oxygenation. The nurse
immediately discontinues the infusion if
uncontrolled bleeding occurs.

MANAGING PAIN
Chest pain, if present, is usually pleuritic rather
than cardiac in origin. A semi-Fowler’s position
provides a more comfortable position for
breathing.
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COLLEGE OF NURSING 22 Compiled by BJ SORRILLA, R.N., M.D.
 o Dyspnea develops, with a sensation of
rapid shallow breathing and an inability
to get enough air.
o Tachypnea and increased work of
breathing result frequently in respiratory
fatigue and ultimately in respiratory
failure.
o alveolar capillary endothelial cells and type I
pneumocytes (alveolar epithelial cells) are
injured, with consequent loss of the normally
tight alveolar barrier to fluid and macromolecules
o Edema fluid that is rich in protein accumulates in
the interstitial and alveolar spaces
o condensed plasma proteins aggregate in the air
spaces with cellular debris and dysfunctional
pulmonary surfactant to form hyaline mem-
brane whorls. Pulmonary vascular injury also
occurs early in ARDS, with vascular obliteration
by microthrombi and fibrocellular proliferation
o Alveolar edema predominantly involves
dependent portions of the lung with diminished
aeration.
o Collapse of large sections of dependent
lung can contribute to decreased lung
compliance.
o intrapulmonary shunting and hypoxemia
WELL’S POINT SCORING FOR DVT, PE develop and the work of breathing
increases, leading to dyspnea
o chest radiograph usually reveals opacities
consistent with pulmonary edema and often
involves at least three-quarters of the lung fields
ACUTE RESPIRATORY DISTRESS SYNDROME o chest x-ray in ARDS may not
demonstrate cardiomegaly, pleural
a clinical syndrome of severe dyspnea of rapid
effusions, or pulmonary vascular
onset, hypoxemia, and diffuse pulmonary
redistribution as is often present in pure
infiltrates leading to respiratory failure
cardiogenic pulmonary edema.
caused by diffuse lung injury from many
underlying medical and surgical disorders
PROLIFERATIVE PHASE
lung injury may be direct, as occurs in toxic
usually lasts from day 7 to day 21
inhalation, or indirect, as occurs in sepsis
most patients recover rapidly and are liberated
annual incidence of ARDS is estimated to be as
from mechanical ventilation during this phase.
high as 60 cases/100,000 population.
Despite this improvement, many patients still
Approx. 10% of all intensive care unit (ICU)
experience dyspnea, tachypnea, and hypoxemia.
admissions involve patients with ARDS
Some patients develop progressive lung injury
and early changes of pulmonary fibrosis during
the proliferative phase
Histologically, the first signs of resolution are
often evident in this phase, with the initiation of
lung repair, the organization of alveolar
exudates, and a shift from neutrophil- to
lymphocyte-predominant pulmonary infiltrates.
o As part of the reparative process, type II
pneumocytes proliferate along alveolar
basement membranes. These specialized
epithelial cells synthesize new
pulmonary surfactant and differentiate
into type I pneumocytes.

FIBROTIC PHASE
most cases (>80%) are caused by a relatively
small number of clinical disorders: pneumonia
and sepsis (~40–60%), followed in incidence by
aspiration of gastric contents, trauma, multi- ple
transfusions, and drug overdose
o Among patients with trauma, the most
frequently reported surgical conditions in
ARDS are pulmonary contusion, multiple
bone fractures, and chest wall
trauma/flail chest, whereas head
trauma, near-drowning, toxic inhalation,
and burns are rare causes.
Other clinical variables have been associated
with the development of ARDS: older age,
chronic alcohol abuse, metabolic acidosis,
pancreatitis, and severity of critical illness

PATHOPHYSIOLOGY
EXUDATIVE PHASE
o exudative phase encompasses the first 7 days of
illness after exposure to a precipitating ARDS risk
factor, with the patient experiencing the onset of
respiratory symptoms.
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COLLEGE OF NURSING 23 Compiled by BJ SORRILLA, R.N., M.D.
 While many patients with ARDS recover lung
function 3–4 weeks after the initial pulmonary
injury, some enter a fibrotic phase that may
require long-term support on mechanical
ventilators and/or supplemental oxygen.
Histologically, the alveolar edema and
inflammatory exudates of earlier phases convert
to extensive alveolar-duct and interstitial
fibrosis.
Marked disruption of acinar architecture leads to
emphysema-like changes, with large bullae.
Intimal fibroproliferation in the pulmonary
microcirculation causes progressive vascular
occlusion and pulmonary hypertension.
The physiologic consequences include:
o an increased risk of pneumothorax
o reductions in lung compliance
o increased pulmonary dead space
Patients in this late phase experience a
substantial burden of excess morbidity.
o Lung biopsy evidence for pulmonary
fibrosis in any phase of ARDS is
associated with increased mortality risk.
The normal alveolus (left) and the injured alveolus in the acute
phase of acute lung injury and the acute respiratory distress
syndrome (right). In the acute phase of the syndrome (right), there
is sloughing of both the bronchial and alveolar epithelial cells, with
the formation of protein-rich hyaline membranes on the denuded
basement membrane. Neutrophils are shown adhering to the injured
capillary endothelium and transmigrating through the interstitium
into the air space, which is filled with protein-rich edema fluid. In
the air space, an alveolar macrophage is secreting pro-inflammatory
cytokines—i.e., interleukins 1, 6, 8 (IL-1, 6, 8) and tumor necrosis
factor  (TNF-)—that act locally to stimulate chemotaxis and activate
neutrophils. IL-1 can also stimulate the production of extracellular
matrix by fibroblasts. Neutrophils can release oxidants, proteases,
leukotrienes, and other proinflammatory molecules, such as
platelet-activating factor (PAF). A number of anti-inflammatory
mediators are also present in the alveolar milieu, including the IL-1-
receptor antagonist, soluble TNF- receptor, autoantibodies to IL-8,
and cytokines such as IL-10 and IL-11 (not shown). The influx of
protein-rich edema fluid into the alveolus can lead to the inactivation
of surfactant. MIF, macrophage inhibitory factor. (Adapted from
LB Ware, MA Matthay: N Engl J Med 342:1334, 2000,
with permission.)
MEDICAL MANAGEMENT
GENERAL PRINCIPLES:
1. the recognition and treatment of underlying
medical and surgical disorders (e.g., pneumonia,
sepsis, aspiration, trauma)
2. the minimization of unnecessary procedures and
their complications
3. standardized “bundled care” approaches for ICU
patients, including prophylaxis against venous
thromboembolism, gastrointestinal bleeding,
aspiration, excessive sedation, prolonged
mechanical ventilation, and central venous
catheter infections
4. prompt recognition of nosocomial infections
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5. provision of adequate nutrition via the enteral
route when feasible.
Minimizing Ventilator-Induced Lung Injury
Despite its life- saving potential, mechanical
ventilation can aggravate lung injury.
o ventilator-induced lung injury can arise
from at least two principal mechanisms:
“volutrauma” from repeated alveolar
overdistention from excess tidal volume
and “atelectrauma” from recurrent
alveolar collapse.
o compliance differs in affected versus
more “normal” areas of the lung,
attempts to fully inflate the consolidated
lung may lead to overdistention of and
injury to the more normal areas.
Ventilator-induced injury can be
demonstrated in experimental models of
acute lung injury, in particular with high-
tidal-volume (VT) ventilation.
A large-scale, randomized controlled trial
sponsored by the National Institutes of Health
and conducted by the ARDS Network compared
low VT ventilation (6 mL/kg of predicted body
weight) to conventional VT ventilation (12 mL/kg
predicted body weight). Lower airway pressures
were also targeted in the low tidal volume group
(i.e., plateau pressure measured on the
ventilator after a 0.5-s pause after inspiration)
≤30 cm H2O versus ≤50 cm H2O in the high tidal
volume group.
o The mortality rate was significantly lower
in the low VT patients (31%) than in the
conventional VT patients (40%). This
improvement in survival represents a
substantial ARDS-mortality benefit
Minimizing Atelectrauma by Prevention of Alveolar
Collapse
In ARDS, the presence of alveolar and interstitial
fluid and the loss of surfactant can lead to a
marked reduction of lung compliance
o Without an increase in end-expiratory
pressure, significant alveolar collapse
can occur at end-expiration, with
consequent impairment of oxygenation.
o In most clinical settings, positive end-
expiratory pressure (PEEP) is adjusted to
minimize Fio2 (inspired O2 per- centage)
and provide adequate Pao2 (arterial
partial pressure of O2) without causing
alveolar overdistention.
Prone Positioning
While several prior trials demonstrated that mechanical
ventilation in the prone position improved arterial
oxygenation without a mortality benefit, a recent trial
demonstrated a significant reduction in 28-day mortality
with prone positioning (32.8 to 16%) for patients with
severe ARDS (Pao2/Fio2 <150 mm Hg).
many centers are increasing the use of prone
positioning in severe ARDS, with the
understanding that this maneuver requires a
critical-care team that is experienced in
“proning,” as repositioning critically ill patients
can be hazardous, leading to accidental
endotracheal extubation, loss of central venous
catheters, and orthopedic injury.
Fluid Management
Fluid restriction, diuretics
Increased pulmonary vascular permeability
leading to interstitial and alveolar edema fluid
rich in protein is a central feature of ARDS.
limited only by hypotension and hypoperfusion of
critical organs such as the kidneys
Maintaining a low left atrial filling pressure:
minimizes pulmonary edema
prevents further decrements in arterial
oxygenation and lung compliance
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24 Compiled by BJ SORRILLA, R.N., M.D.
 improves pulmonary mechanics
shortens ICU stay and the duration of mechanical
ventilation
NEUROMUSCULAR BLOCKADE
In severe ARDS, sedation alone can be inadequate for
the patient- ventilator synchrony required for lung-
protective ventilation.
In a multicenter, randomized, placebo-controlled
trial of early neuromuscular blockade (with
cisatracurium besylate) for 48 h, patients with
severe ARDS had increased survival and
ventilator-free days without increasing ICU-
acquired paresis.
These promising findings support the early
administration of neuromuscular blockade if
needed to facilitate mechanical ventilation in
severe ARDS.
NURSING MANAGEMENT
Respiratory modalities are used: oxygen
administration, nebulizer therapy, chest
physiotherapy, endotracheal intubation or
tracheostomy, mechanical ventilation,
suctioning, bronchoscopy)
Frequent assessment of the patient’s status is
necessary to evaluate the effectiveness of
treatment
nurse should turn the patient frequently to
improve ventilation and perfusion in the lungs
and enhance secretion drainage. However, the
nurse must closely monitor the patient for
deterioration in oxygenation with changes in
position.
The nurse should explain all procedures and
provide care in a calm, reassuring manner. It is
important to reduce the patient’s anxiety
because anxiety pre- vents rest and increases
oxygen expenditure. Rest is essential to reduce
oxygen consumption, thereby reducing oxygen
needs.
Nursing assessment is important to assess for
problems with ventilation that may be causing
the anxiety reaction: tube blockage by kinking or
retained secretions; other acute respiratory
problems (eg, pneumothorax, pain); a sudden
drop in the oxygen level; the patient’s level of
dyspnea; or ventilator malfunction.
Use of paralytic agents has many dangers and
side effects. The nurse must be sure the patient
does not become disconnected from the
ventilator, because respiratory muscles are
paralyzed and the patient will be apneic.
Consequently, the nurse ensures that the patient
is closely monitored at all times.
All ventilator and patient alarms should be on at
all times.
Eye care is important as well because the patient
cannot blink, increasing the risk of corneal
abrasions.
Neuromuscular blockers predispose patients to
the development of deep venous thrombi,
muscle atrophy, and skin breakdown. Nursing
assessment is essential to minimize the com-
plications related to neuromuscular blockade.
The patient may have discomfort or pain but
cannot communicate these sensations. is usually
administered concurrently with neuromuscular
blocking agents.
The nurse must anticipate the patient’s needs
regarding pain and comfort. The nurse checks
the patient’s position to ensure it is comfortable
and in normal alignment and talks to, and not
about, the patient while in the patient’s
presence.
Improving ventilation & oxygenation
Administer high Fio2 levels with high-flow
system using face mask or nasal cannula if able
to oxygenate noninvasively.
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COLEGIO SAN AGUSTIN – BACOLOD
COLLEGE OF NURSING
Initiate mechanical ventilation if cardiovascular
instability is present, severe hypoxemia
persists, or if respiratory fatigue develops.
Oxygen support at high Fio2 levels with PEEP is
usually required to achieve an acceptable Pao2
(> 50 mm Hg). Monitor for hemodynamic
compromise when using PEEP greater than 5
cm H20 and titrate oxygen if possible to less
than .6 to prevent secondary lung injury. The
goal is not to achieve a normal Pao2 but to
keep it above 50 mm Hg
Decrease work of breathing initially by using
ventilator modes and ventilator rates to
decrease respiratory effort by the patient.
Prevent "volutrauma." Studies have
demonstrated that large tidal volumes, which
contribute to high plateau pressures, caused
damage to the alveoli if used for prolonged
periods (48 hours) in patients with ARDS. The
use of small tidal volumes (4-8 mL/kg predicted
body weight) is recommended to maintain
plateau pressures of 30 cm H20 or less.
Sedation and analgesia maybe necessary after
intubation to maximize gas exchange and
minimize oxy- gen consumption.
"Patient/ventilator dyssynchrony" is a common
complication of ventilatory support in the
severely dyspneic, hypoxemic patient.
While transfusions may improve oxygen-
carrying capacity, evidence has shown that
transfusion itself is a cause of ARDS and
increases the risk of mortality (TRALI-
transfusion-related acute lung injury).
Transfusions are reserved for hemoglobin below
7 g/dL unless underlying cardiac disease exists.
Enteral is the preferred route of nutrition and may help
decrease bacterial translocation across the gut and
provide prophylaxis for GI bleeding
PROGNOSIS
In the recent report from the Large Observational Study
to Understand the Global Impact of Severe Acute
Respiratory Failure (LUNG SAFE) trial, hospital mortality
estimates for ARDS range from:
34.9% for mild ARDS
40.3% for moderate ARDS
46.1% with severe ARDS
PNEUMONIA
inflammation of the lung parenchyma that is caused
by a microbial agent
“Pneumonitis” is a more general term that describes
an inflammatory process in the lung tissue that may
predispose a patient to or place a patient at risk for
microbial invasion
results from the proliferation of microbial pathogens
at the alveolar level and the host’s response to those
pathogens
Mechanical factors for host defense:
CRITICAL CARE NURSING (NCM 118)
25 Compiled by BJ SORRILLA, R.N., M.D.
 o hairs and turbinates of the nares
o branching architecture of the
tracheobronchial tree traps microbes on the
airway lining
o mucociliary clearance and local antibacterial
factors
o gag and cough reflexes offer critical
protection from aspiration
o normal flora adhering to mucosal cells of the
oropharynx prevents pathogenic bacteria
from binding
When these barriers are overcome or when
microorganisms are small enough to be inhaled to
the alveolar level, resident alveolar macrophages are
extremely efficient at clearing and killing pathogens.
Macrophages are assisted by proteins that are
produced by the alveolar epithelial cells (e.g.,
surfactant proteins A and D) and that have intrinsic
opsonizing properties or antibacterial or antiviral
activity.
Once engulfed by the macrophage, the pathogens—
even if they are not killed—are eliminated via either o erythrocytes can cross the alveolar–capillary
the mucociliary elevator or the lymphatics and no membrane, with consequent hemoptysis
longer represent an infectious challenge. bacterial pathogens appear to interfere with the
o Only when the capacity of the alveolar hypoxemic vasoconstriction that would normally
macrophages to ingest or kill the occur with fluid- filled alveoli, and this interference
microorganisms is exceeded does clinical can result in severe hypoxemia
pneumonia become manifest increased respiratory drive in the systemic
inflammatory response syndrome leads to
PATHOPHYSIOLOGY respiratory alkalosis
results from the proliferation of microbial pathogens decreased compliance due to capillary leak,
at the alveolar level and the host’s response to those hypoxemia, increased respiratory drive, increased
pathogens secretions, and occasionally infection-related
Microorganisms gain access to the lower respiratory bronchospasm all lead to dyspnea
tract in several ways: if severe enough, the changes in lung mechanics
o The most common is by aspiration from the secondary to reductions in lung volume and
oropharynx - small-volume aspiration occurs compliance and the intrapulmonary shunting of blood
frequently during sleep (especially in the may cause respiratory failure and death.
elderly) and in patients with decreased levels
of consciousness PATHOLOGY
o Rarely, pneumonia occurs via hematogenous *phases may not apply to pneumonia of all etiologies,
spread (e.g., from tricuspid endocarditis) or especially viral or Pneumocystis pneumonia
by contiguous extension from an infected 1. Edema phase
pleural or mediastinal space. with the presence of a proteinaceous
exudate—and often of bacteria—in the
alveoli
2. Red hepatization phase
presence of erythrocytes in the cellular
intra-alveolar exudate gives this second
stage its name, but neutrophil influx is
more important with regard to host
defense
bacteria are occasionally seen in
pathologic specimens collected during
this phase.
3. Gray hepatization
no new erythrocytes are extravasating,
and those already present have been
lysed and degraded
neutrophil is the predominant cell, fibrin
deposition is abundant, and bacteria
have disappeared
phase corresponds with successful
alveolar macrophages initiate the inflammatory
containment of the infection and
response to bolster lower respiratory tract defenses.
improvement in gas exchange
o the host inflammatory response, rather than 4. Resolution
proliferation of microorganisms, triggers the
macrophage reappears as the dominant
clinical syndrome of pneumonia
cell type in the alveolar space, and the
release of interleukin 1 and tumor necrosis factor
debris of neutrophils, bacteria, and fibrin
results in fever
has been cleared, as has the
interleukin 8 and granulocyte colony-stimulating
inflammatory response
factor, stimulate the release of neutrophils and their
attraction to the lung, producing both peripheral
In VAP, respiratory bronchiolitis may precede the
leukocytosis and increased purulent secretions.
development of a radiologically apparent
Inflammatory mediators released by macrophages
infiltrate.
and the newly recruited neutrophils create an
Because of the microaspiration mechanism, a
alveolar capillary leak equivalent to that seen in
bronchopneumonia pattern is most common in
ARDS syndrome
nosocomial pneumonias, whereas a lobar pattern
capillary leak results in a radiographic
is more common in bacterial CAP
infiltrate and rales detectable on
auscultation, and hypoxemia results from
alveolar filling
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COLEGIO SAN AGUSTIN – BACOLOD CRITICAL CARE NURSING (NCM 118)
COLLEGE OF NURSING 26 Compiled by BJ SORRILLA, R.N., M.D.
Definition of terms:
(Data from Anand N, Kollef MH: The alphabet soup of pneumonia:
CAP, HAP, HCAP, NHAP, and VAP. Semin Respir Crit Care Med
30(1):3–9, 2009.)
Community-Acquired Pneumonia (CAP):
o Pneumonia diagnosed in people who have
limited contact with the health care system
and are at low risk for developing MDR
infections.
Hospital-Acquired Pneumonia (HAP):
o Pneumonia occurring more than 48 hours
after a hospital admission.
Health Care–Associated Pneumonia (HCAP):
o HCAP is defined as a patient who having
been hospitalized in the last 90 days and who
received antimicrobial therapy; a nursing
home or extended-care facility resident,
dialysis dependent, immunosuppressed
and/or receiving immune suppressing
therapy.
Ventilator-Associated Pneumonia (VAP):
o Pneumonia occurring in patients who have
been intubated for more than 48 hours.
Although Streptococcus pneumoniae is most
common, other organisms must also be considered
in light of the patient’s risk factors and severity of
illness.
o Typical organisms:
o S. pneumoniae, Haemophilus
influenzae, and (in selected patients)
S. aureus and gram-negative bacilli
such as Klebsiella pneumoniae and
Pseudomonas aeruginosa.
o Atypical organisms:
o Mycoplasma pneumoniae,
Chlamydia pneumoniae, and
Legionella species as well as
respiratory viruses such as influenza
viruses, adenoviruses, human
metapneumovirus, and respiratory
syncytial viruses.
Anaerobes play a significant role only when an
episode of aspiration has occurred days to weeks
before presentation for pneumonia.
The combination of an unprotected airway
(e.g., in patients with alcohol or drug
overdose or a seizure disorder) and
significant gingivitis constitutes the major
risk factor.
MRSA has been reported as a primary etiologic agent
of CAP; potentially serious consequence: necrotizing
pneumonia
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COLEGIO SAN AGUSTIN – BACOLOD
COLLEGE OF NURSING
Risk Factors
Risk factors for CAP include alcoholism, asthma,
immunosuppression, institutionalization, and an age
of ≥70 years.
Risk factors for pneumococcal pneumonia include
dementia, seizure disorders, heart failure,
cerebrovascular disease, alcoholism, tobacco
smoking, chronic obstructive pulmonary disease
(COPD), and HIV infection.
P. aeruginosa is a particular problem in patients with
severe structural lung disease, such as
bronchiectasis, cystic fibrosis, or severe COPD.
Risk factors for Legionella infection include diabetes,
hematologic malignancy, cancer, severe renal
disease, HIV infection, smoking, male gender, and a
recent hotel stay or ship cruise.
MANIFESTATIONS
frequently febrile with tachycardia
may have a history of chills and/or sweats
Cough may be either nonproductive or productive of
mucoid, purulent, or blood-tinged sputum.
o Gross hemoptysis is suggestive of CA-MRSA
pneumonia
Pleuritic chest pain
20% of patients may have GI symptoms such as
nausea, vomiting, and/or diarrhea
increased respiratory rate and use of accessory
muscles of respiration are common
Palpation may reveal increased or decreased tactile
fremitus, and the percussion note can vary from dull
to flat, reflecting underlying consolidated lung and
pleural fluid, respectively
Crackles, bronchial breath sounds, and possibly a
pleural friction rub may be heard on auscultation.
The clinical presentation may not be so obvious in
the elderly, who may initially display new-onset or
CRITICAL CARE NURSING (NCM 118)
27 Compiled by BJ SORRILLA, R.N., M.D.
 worsening confusion and few other manifestations.
Severely ill patients may have septic shock and
evidence of organ failure.
o The usual symptoms (fever, chills, increased
white blood count) may be absent.
o Confusion and tachypnea are common
presenting symptoms in older patients with
pneumonia. Other symptoms in the older
o weakness, lethargy, failure to thrive,
anorexia, abdominal pain, episodes of
falling, incontinence, headache, delirium,
and nonspecific deterioration.
• Prevention. People 65 years of age and older should
receive both the pneumococcal and influenza vaccines
based upon CDC recommendations
DIAGNOSTICS
the sensitivity and specificity of the findings on
physical examination are less than ideal, averaging
58% and 67%, respectively
the elderly may initially present with confusion alone.
Therefore, chest radiography is often necessary to
differentiate CAP from other conditions
Identification of an unexpected pathogen allows
narrowing of the initial empirical regimen, thereby
decreasing antibiotic selection pressure and
lessening the risk of resistance
o Pathogens with important public safety
implications, such as Mycobacterium
tuberculosis and influenza virus, may be
found in some cases.
o without culture and susceptibility data,
trends in resistance cannot be followed
accurately
GRAM STAIN & CULTURE
main purpose of the sputum Gram’s stain is to
ensure that a sample is suitable for culture.
Gram’s staining may also identify certain pathogens
(e.g., S. pneumoniae, S. aureus, and gram-
negative bacteria) by their characteristic
appearance.
To be adequate for culture, a sputum sample must
have >25 neutrophils and <10 squamous epithelial
cells per low-power field
Even in cases of proven bacteremic pneumococcal
pneumonia, the yield of positive cultures from
sputum samples is ≤50%.
Others may already have started a course of
antibiotics that can interfere with culture results at
the time a sample is obtained. I
o Inability to produce sputum can result from
dehydration, and its correction may result
in increased sputum production and a more
obvious infiltrate on chest radiography.
o For patients admitted to the ICU and
intubated, a deep-suction aspirate or
bronchoalveolar lavage sample (obtained
either via bronchoscopy or non-
bronchoscopically) has a high yield on
culture when sent to the microbiology
laboratory as soon as possible
BLOOD CULTURES
The yield from blood cultures, even when samples
are collected before antibiotic therapy, is
disappointingly low.
o Only 5–14% of cultures of blood from
patients hospitalized with CAP are positive,
and the most frequently isolated pathogen
is S. pneumoniae
Certain high- risk patients—including those with
neutropenia secondary to pneumonia, asplenia,
complement deficiencies, chronic liver disease, or
severe CAP—should have blood cultured.
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COLEGIO SAN AGUSTIN – BACOLOD
COLLEGE OF NURSING
URINARY ANTIGEN TESTS
Two commercially available tests detect pneumococcal
and Legionella antigen in urine.
o The sensitivity and specificity of the Legionella
urine antigen test are as high as 70% and 99%,
respectively. The pneumococcal urine antigen
test is also quite sensitive and specific (70%
and >90%, respectively).
POLYMERASE CHAIN REACTION
PCR tests, which amplify a microorganism’s DNA or
RNA, are available for a number of pathogens.
o PCR of nasopharyngeal swabs, for example, has
become the standard for diagnosis of
respiratory viral infection.
o In addition, PCR can detect the nucleic acid of
Legionella species, M. pneumoniae, C.
pneumoniae, and mycobacteria.
o In patients with pneumococcal pneumonia, an
increased bacterial load documented in whole
blood by PCR is associated with an increased
risk of septic shock, the need for mechanical
ventilation, and death
SEROLOGY
A fourfold rise in specific IgM antibody titer between
acute- and convalescent-phase serum samples is
generally considered diagnostic of infection with the
pathogen in question
BIOMARKERS
The two most commonly in use are C-reactive protein
(CRP) and procalcitonin (PCT).
o Levels of these acute-phase reactants increase
in the presence of an inflammatory response,
particularly to bacterial pathogens.
o CRP may be of use in the identification of
worsening disease or treatment failure, and PCT
may play a role in distinguishing bacterial from
viral infection, determining the need for
antibacterial therapy, or deciding when to
discontinue treatment. PCT testing can result in
less antibiotic use in CAP with no concomitant
increase in treatment failure or mortality risk.
These tests should not be used on their own, but, when
interpreted in conjunction with other findings from the
history, physical examination, radiology, and laboratory
tests, may help with antibiotic stewardship and
appropriate management of seriously ill patients with
CAP.
MEDICAL MANAGEMENT
The CURB-65 criteria include five variables: confusion
(C); urea >7 mmol/L (U); respiratory rate ≥30/min (R);
blood pressure, systolic ≤90 mmHg or diastolic ≤60
mmHg (B); and age ≥65 years.
o Patients with a score of 0, among whom the 30-
day mortality rate is 1.5%, can be treated
outside the hospital.
o With a score of 1 or 2, the patient should be
hospitalized unless the score is entirely or in part
attributable to an age of ≥65 years. In such
cases, hospitalization may not be necessary.
CRITICAL CARE NURSING (NCM 118)
28 Compiled by BJ SORRILLA, R.N., M.D.
 o Among patients with scores of ≥3, mortality
rates are 22% overall; these patients may
require ICU admission
FAILURE TO IMPROVE
Patients slow to respond to therapy should be
reevaluated at about day 3 (sooner if their condition is
worsening rather than simply not improving), and
several possible scenarios should be considered.
o noninfectious conditions mimic pneumonia,
including pulmonary edema, pulmonary
embolism, lung carcinoma, radiation and
hypersensitivity pneumonitis, and connective
tissue disease involving the lungs
o The pathogen may be resistant to the drug
selected, or a sequestered focus (e.g., lung
abscess or empyema) may be blocking access
of the antibiotic(s) to the pathogen.
o The patient may be getting either the wrong
drug or the correct drug at the wrong dose or
frequency of administration. Another possibility
is that CAP is the correct diagnosis but an
unsuspected pathogen (e.g., CA-MRSA, M.
tuberculosis, or a fungus) is the cause.
Nosocomial superinfections—both pulmonary and
extrapulmonary—are other possible explanations for a
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COLEGIO SAN AGUSTIN – BACOLOD
COLLEGE OF NURSING
hospitalized patient’s failure to improve or
deterioration.
o In all cases of delayed response or worsening
condition, the patient must be carefully
reassessed and appropriate studies initiated,
possibly including procedures such as CT or
bronchoscopy.
COMPLICATIONS
Complications of severe CAP include respiratory failure,
shock and multiorgan failure, coagulopathy, and
exacerbation of comorbid illnesses.
o Three particularly noteworthy conditions are
metastatic infection, lung abscess, and
complicated pleural effusion.
o Lung abscess may occur in association with
aspiration or with infection caused by a single
CAP pathogen, such as CA-MRSA, P. aeruginosa,
or (rarely) S. pneumoniae.
o Aspiration pneumonia is typically a polymicrobial
infection involving both aerobes and anaerobes.
o A significant pleural effusion should be tapped for
both diagnostic and therapeutic purposes.
o If the fluid has a pH of <7, a glucose level
of <2.2 mmol/L, and a lactate
dehydrogenase concentration of >1000
U/L or if bacteria are seen or cultured, it
should be completely drained; a chest
tube is often required, and video-
assisted thoracoscopy may be needed
FOLLOW-UP
Fever and leukocytosis usually resolve within 2–4
days in otherwise healthy patients with CAP, but
physical findings may persist longer.
Chest radiographic abnormalities are slowest to
resolve (4–12 weeks), with the speed of clearance
depending on the patient’s age and underlying lung
disease.
Patients may be discharged from the hospital once
their clinical conditions, including comorbidities, are
stable.
The site of residence after discharge (nursing home,
home with family, home alone) is an important
discharge consideration, particularly for elderly
patients.
o For a hospitalized patient, a follow-up
radiograph ~4–6 weeks later is
recommended.
o If relapse or recurrence is documented,
particularly in the same lung segment, the
possibility of an underlying neoplasm must
be considered.
PROGNOSIS
The overall mortality rate for the outpatient group is
<5%. For patients requiring hospitalization, the
overall mortality rate ranges from 2 to 40%,
depending on the category of patient and the
processes of care, particularly the administration of
appropriate antibiotics as soon as possible.
PREVENTION
Pneumococcal polysaccharide vaccine (PPSV23)
o contains capsular material from 23
pneumococcal serotypes
Protein con- jugate pneumococcal vaccine (PCV13)
o capsular polysaccharide from 13 of the most
common pneumococcal pathogens affecting
children is linked to an immunogenic protein
Administration of this vaccine to children has led to
an overall decrease in the prevalence of
antimicrobial-resistant pneumococci and in the
incidence of invasive pneumococcal disease among
both children and adults.
CRITICAL CARE NURSING (NCM 118)
29 Compiled by BJ SORRILLA, R.N., M.D.
 Practice Guidelines for the Management of Community-Acquired
Pneumonia in Adults by John G Bartlett, Scott F Dowell, Lionel A
Mandell, Thomas M File, Jr., Daniel M Musher, Michael J Fine
VENTILATOR PNEUMONIA
Pneumonia is a common complication among
patients requiring mechanical ventilation. Prevalence
estimates vary between 6 and 52 cases per 100
patients, depending on the population studied.
Three factors are critical in the pathogenesis of VAP:
o colonization of the oropharynx with
pathogenic microorganisms
o aspiration of these organisms from the
oropharynx into the lower respiratory tract
o compromise of the normal host defense
mechanisms.
The most obvious risk factor is the endotracheal
tube, which bypasses the normal mechanical factors
preventing aspiration.
o microaspiration is actually exacerbated by
secretions pooling above the cuff
o The endotracheal tube and the concomitant
need for suctioning can damage the tracheal
mucosa, thereby facilitating tracheal
colonization
o pathogenic bacteria can form a glycocalyx
biofilm on the tube’s surface that protects
them from both antibiotics and host
defenses
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COLEGIO SAN AGUSTIN – BACOLOD
COLLEGE OF NURSING
In a high percentage of critically ill patients, the normal
oropharyngeal flora is replaced by pathogenic
microorganisms.
o The most important risk factors are:
o antibiotic selection pressure
o cross-infection from other
infected/colonized patients or
contaminated equipment
o malnutrition
o Of these factors, antibiotic exposure poses the
greatest risk by far. Pathogens such as P.
aeruginosa almost never cause infection in
patients without prior exposure to antibiotics
Severely ill patients with sepsis and trauma appear to
enter a state of immunoparalysis several days after
admission to the ICU—a time that corresponds to the
greatest risk of developing VAP
o mechanism of this immunosuppression is not
clear, although several factors have been
suggested
o Hyperglycemia and more frequent transfusions
adversely affect the immune response
MANIFESTATIONS:
o The clinical manifestations are generally the
same in VAP as in all other forms of pneumonia:
fever, leukocytosis, increase in respiratory
secretions, and pulmonary consolidation on
physical examination, along with a new or
changing radiographic infiltrate.
o Other clinical features may include tachypnea,
tachycardia, worsening oxygenation, and
increased minute ventilation.
DIAGNOSIS:
Application of the clinical criteria typical for CAP
consistently results in overdiagnosis of VAP, largely
because of three common findings in at-risk patients:
1. frequent tracheal colonization with
pathogenic bacteria in patients with
endotracheal tubes
CRITICAL CARE NURSING (NCM 118)
30 Compiled by BJ SORRILLA, R.N., M.D.
 2. multiple alternative causes of radiographic
infiltrates in mechanically ventilated patients
3. the high frequency of other sources of fever
in critically ill patients.
Clinical findings in ventilated patients with fever and/or
leukocytosis may have alternative causes, including:
1. antibiotic-associated diarrhea
2. central line–associated infection
3. sinusitis
4. urinary tract infection
5. pancreatitis
6. drug fever
o The more distal in the respiratory tree the diagnostic
sampling, the more specific the results and therefore
the lower the threshold of growth necessary to
diagnose pneumonia and exclude colonization.
MANAGEMENT
o Frequent use of β-lactam drugs, especially
cephalosporins, appears to be the major risk factor
for infection with MRSA and extended-spectrum β-
lactamase–positive strains.
o P. aeruginosa has demonstrated the ability to
develop resistance to all routinely used antibiotics
o The majority of patients without risk factors for MDR
infection can be treated with a single agent
o The major difference from CAP is the
markedly lower incidence of atypical
pathogens in VAP; the exception is
Legionella, which can be a nosocomial
pathogen, especially with breakdowns in the
treatment of potable water in the hospital.
o The standard recommendation for patients
with risk factors for MDR infection is for three
antibiotics: two directed at P. aeruginosa and
one at MRSA.
NURSING MANAGEMENT
According to the evidence-based directive from AACN, in
all patients receiving mechanical ventilation as well as
those at high risk for aspiration:
o the head of the bed should be elevated at 30 to
45 degrees unless medically contraindicated
o endotracheal tubes should have dorsal lumens
above the cuff to allow drainage and continuous
tracheal secretions
o patient ventilator circuits should be changed
based on need because of contamination rather
than by routine.
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COLEGIO SAN AGUSTIN – BACOLOD
COLLEGE OF NURSING
o In addition to these guidelines, the AACN has
also published guidelines for aggressive oral care
in patients with mechanical ventilation.
o Humidified oxygen should be administered by
mask or endotracheal tube to promote adequate
ventilation.
o Aggressive pulmonary toilet is indicated to
mobilize secretions, open closed alveoli, and
promote oxygenation.
o Adequate nutritional support is critical. In
addition, a nutritional consult should be initiated
with implementation of appropriate enteral or
parenteral therapy.
COMPLICATIONS
Apart from death, the major complication of VAP is
prolongation of mechanical ventilation, with
corresponding increases in the duration of ICU stay and
hospitalization.
o In most studies, an additional week of
mechanical ventilation resulting from VAP is
common.
o In rare cases, necrotizing pneumonia (e.g., that
due to P. aeruginosa) can cause significant
pulmonary hemorrhage. More commonly,
necrotizing infections result in the long-term
complications of bronchiectasis and parenchymal
scarring leading to recurrent pneumonia.
FOLLOW-UP
Clinical improvement, if it occurs, is usually evident
within 48–72 h of the initiation of antimicrobial
treatment.
PREVENTION
o Because of the significance of endotracheal
intubation as a risk factor for VAP, the most
important preventive intervention is to avoid
intubation or minimize its duration.
o Aggressive attempts to extubate early may
result in reintubation(s) and increase aspiration,
posing a risk of VAP.
o Heavy continuous sedation increases VAP risk,
but self-extubation because of insufficient
sedation is also a risk.
o Minimizing microaspiration around the
endotracheal tube cuff is also a strategy for
avoidance of VAP. Simply elevating the head of
the bed (at least 30° above horizontal but
preferably 45°) decreases VAP rates.
o The risk-to-benefit ratio of transporting the
patient outside the ICU for diagnostic tests or
procedures should be carefully considered, since
VAP rates are increased among transported
patients
o emphasis on controlling overgrowth of the bowel
flora by avoidance of agents that raise gastric pH
may be relevant only in certain populations, such
as liver transplant recipients and patients who
have undergone other major intraabdominal
procedures or who have bowel obstruction.
Decrease the risk of cross-contamination or
colonization via the hands of hospitalized personnel.
Hand hygiene is the most effective strategy.
Implement a comprehensive oral hygiene program
that includes oral suctioning, teeth brushing, and use
of oral 0.12% chlorhexidine gluconate.
Maintain a closed system on ventilator/humidifier
circuits, and avoid pooling of condensation or
secretions in the tubing. Do not routinely change the
ventilator circuit, except when visibly soiled or
malfunctioning. Use sterile water or saline for use
with any respiratory equipment.
Use sterile technique for endotracheal suctioning and
suction only when necessary to clear secretions from
large airways.
Provide nutritional support to improve host defenses
and reduce the risk for pneumonia.
Remove invasive devices and equipment as soon as
possible.
CRITICAL CARE NURSING (NCM 118)
31 Compiled by BJ SORRILLA, R.N., M.D.
 Assess weaning readiness daily with a spontaneous
breathing protocol and limit the use of sedatives.
Decrease the risk of aspiration: Avoid supine
positioning and keep the head of the bed elevated to
30° to 45° at all times, unless medically
contraindicated. Use an endotracheal tube with a
dorsal lumen above the endotracheal cuff to remove
drainage with continuous suction. Suction above the
endotracheal tube cuff before removing or
repositioning the tube. Assess for, and correct,
gastric reflux problems.
Use a progressive mobility protocol and in
collaboration with other members of the healthcare
team, promote exercise and mobility early in the
course of a critical illness.
HOSPITAL ACQUIRED PNEUMONIA
HAP in non-intubated patients—both inside and outside
the ICU—is similar to VAP.
o The main differences are the higher frequency of
non-MDR pathogens and the generally better
underlying host immunity in non-intubated
patients
o The greater risk of macroaspiration by
non-intubated patients and the lower
oxygen tensions in the lower respiratory
tract of these patients increase the
likelihood of a role for anaerobes.
o The only pathogens that may be more common
in the non-VAP population are anaerobes.
o Many of the underlying diseases that predispose
a patient to HAP are also associated with an
inability to cough adequately.
NURSING PROCESS
ASSESSMENT
The nurse should monitor the following:
Changes in temperature and pulse
Amount, odor, and color of secretions
Frequency and severity of cough
Degree of tachypnea or shortness of breath
Changes in physical assessment findings
(primarily assessed
by inspecting and auscultating the chest)
Changes in the chest x-ray findings
In addition, it is important to assess the elderly
patient for unusual behavior, altered mental
status, dehydration, excessive fatigue, and
concomitant heart failure
DIAGNOSIS
Based on the assessment data, the patient’s major
nursing diagnoses may include:
Ineffective airway clearance related to copious
tracheobronchial secretions
Activity intolerance related to impaired
respiratory function
Risk for deficient fluid volume related to fever
and dyspnea
Imbalanced nutrition: less than body
requirements
Deficient knowledge about the treatment
regimen and preventive health measures
COLLABORATIVE PROBLEMS/
POTENTIAL COMPLICATIONS
Based on the assessment data, collaborative problems
or potential complications that may occur include:
Continuing symptoms after initiation of therapy
Shock
Respiratory failure
Atelectasis
Pleural effusion
Confusion
Superinfection
Nursing Interventions
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COLEGIO SAN AGUSTIN – BACOLOD
COLLEGE OF NURSING
IMPROVING AIRWAY PATENCY
The nurse encourages hydration (2 to 3 L/day)
because adequate hydration thins and loosens
pulmonary secretions.
Humidification may be used to loosen secretions and
improve ventilation. A high-humidity facemask
(using either compressed air or oxygen) delivers
warm, humidified air to the tracheobronchial tree,
helps to liquefy secretions, and relieves
tracheobronchial irritation.
Coughing can be initiated either voluntarily or by
reflex. Lung expansion maneuvers, such as deep
breathing with an incentive spirometer, may induce
a cough. A directed cough may be necessary to im-
prove airway patency.
The nurse encourages the patient to perform an
effective, directed cough, which includes correct
positioning, a deep inspiratory maneuver, glottic
closure, contraction of the expiratory muscles
against the closed glottis, sudden glottic opening,
and an explosive expiration.
The nurse may assist the patient by placing both
hands on the patient’s lower rib cage (anteriorly or
posteriorly) to focus the patient on a slow deep
breath, and then manually assisting the patient by
applying external pressure during the expiratory
phase.
Chest physiotherapy (percussion and postural
drainage) is important in loosening and mobilizing
secretions.
o Indications for chest physiotherapy include
sputum retention not responsive to
spontaneous or directed cough, a history of
pulmonary problems previously treated with
chest physiotherapy, continued evidence of
retained secretions (decreased or abnormal
breath sounds, change in vital signs),
abnormal chest x-ray findings consistent
with atelectasis or infiltrates, or deterioration
in oxygenation.
o The patient is placed in the proper position
to drain the involved lung segments, and
then the chest is percussed and vibrated
either manually or with a mechanical
percussor.
o After each position change, the nurse
encourages the patient to breathe deeply
and cough.
o If the patient is too weak to cough
effectively, the nurse may need to remove
the mucus by nasotracheal suctioning. It
may take time for secretions to mobilize and
move into the central airways for
expectoration. Thus, it is important for the
nurse to monitor the patient for cough and
sputum production after the completion of
chest physiotherapy.
The nurse administers and titrates oxygen therapy
as pre- scribed. The effectiveness of oxygen therapy
is monitored by improvement in clinical signs and
symptoms, and adequate oxygenation values
measured by pulse oximetry or arterial blood gas
analysis.
PROMOTING REST AND CONSERVING ENERGY
The nurse encourages the debilitated patient to rest
and avoid overexertion and possible exacerbation of
symptoms.
The patient should assume a comfortable position
to promote rest and breathing (eg, semi-Fowler’s)
and should change positions frequently to enhance
secretion clearance and ventilation/perfusion in the
lungs.
It is important to instruct outpatients not to
overexert themselves and to engage in only
moderate activity during the initial phases of
treatment.
CRITICAL CARE NURSING (NCM 118)
32 Compiled by BJ SORRILLA, R.N., M.D.
PROMOTING FLUID INTAKE
The respiratory rate of a patient with pneumonia
increases because of the increased workload
imposed by labored breathing and fever.
An increased respiratory rate leads to an increase in
insensible fluid loss during exhalation and can lead
to dehydration.
Therefore, it is important to encourage increased
fluid intake (at least 2 L/day), unless
contraindicated.
MAINTAINING NUTRITION
Patients with shortness of breath and fatigue often
have a decreased appetite and will take only fluids.
Fluids with electrolytes may help provide fluid,
calories, and electrolytes. Other nutritionally
enriched drinks or shakes may be helpful. In
addition, fluids and nutrients may be administered
intravenously if necessary.
PULMONARY HYPERTENSION
a spectrum of diseases involving the pulmonary
vasculature, and defined as an elevation in
pulmonary arterial pressures (mean pulmonary
artery pressure [PAP] >22 mmHg or an estimated
systolic PAP >36 mmHg)
Pulmonary arterial hyper- tension (PAH) is a
relatively rare form of PH and is characterized by
symptoms of dyspnea, chest pain, and syncope.
o If left untreated, the disease carries a high
mortality rate, with the most common cause
of death being decompensated right heart
failure
o A delay in diagnosis results in an obvious
delay in the initiation of appropriate
treatment.
PATHOPHYSIOLOGY
Vasoconstriction, vascular proliferation, thrombosis,
and inflammation appear to underlie the
development of PAH
Intimal proliferation and fibrosis, medial
hypertrophy, and in situ thrombosis characterize
the pathological findings in the pulmonary
vasculature.
Vascular remodeling at earlier stages may be
confined to the small distal pulmonary arteries.
As the disease advances, intimal proliferation and
pathologic remodeling progress resulting in
decreased compliance of the pulmonary
vasculature.
The outcome is a progressive increase in the right
ventricular afterload or total pulmonary vascular
resistance (PVR), and, thus, right ventricular work.
In subjects with moderate to severe pulmonary
vascular disease, as the resting PVR increases,
there will be a corresponding increase in mean PAP
until the cardiac output (CO) is compromised and
starts to fall. With a decline in CO, the PAP will fall.
As CO declines as a result of increased afterload
and decreased contractility, tachycardia is a
compensatory response. Tachycardia decreases
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COLEGIO SAN AGUSTIN – BACOLOD
COLLEGE OF NURSING
filling time and, thus, preload, and results in a
reduced fraction of stroke volume available to
distend the pulmonary vascular tree.
DIAGNOSIS AND CLASSIFICATION
Most patients will present with dyspnea and/or fatigue,
whereas edema, chest pain, presyncope, and syncope
are less common and associated with more advanced
disease.
In early phases of PAH, the physical examination
is often unrevealing. As the disease progresses
there may be evidence of right ventricular failure
with elevated jugular venous pressure, lower
extremity edema, and ascites.
Additionally, the cardiovascular examination
may reveal an accentuated P2 component of the
second heart sound, a right-sided S3or S4, and
a holosystolic tricuspid regurgitant murmur.
It is also important to seek signs of the diseases
that are often concurrent with PH: clubbing may
be seen in some chronic lung diseases,
sclerodactyly and telangiectasia may signify
scleroderma, and crackles on examination of the
lungs and systemic hypertension may be clues to
left-sided systolic or diastolic heart failure.
An echocardiogram with bubble study is the most
important initial screening test. Echocardiography is also
important for determining specific causes. All forms of PH
may demonstrate a hypertrophied and dilated right
ventricle with elevated estimated pulmonary artery
systolic pressure. Important additional information can
be gleaned about specific etiologies of PH
MANIFESTATIONS
Signs and symptoms include pallor, dyspnea, fatigue,
chest pain, and syncope. Cor pulmonale or enlargement
of the right ventricle can be a result of PAH and may lead
to right ventricular failure. The diagnostic strategy is
related to both establishing the diagnosis of PH versus
PAH and if possible the underlying cause.
DIAGNOSTICS
Echocardiogram: Valvular heart disease, left
ventricular dysfunction, and intracardiac shunts
Chest x-ray: Enlarged hilar and pulmonary arterial
shadows and enlargement of the right ventricle.
12-lead ECG: Right ventricular strain, right
ventricular hypertrophy, and right axis deviation.
CTPA, ventilation-perfusion scan, pulmonary
angiogram: These are done to rule out
thromboembolism.
CT chest: Assess for presence or absence of
parenchymal lung disease.
6-minute-walk test: Measurement of distance used
to monitor exercise tolerance, response to therapy,
and progression of disease.
Right-heart cardiac catheterization: Gold standard
for diagnosis with vasodilator (adenosine, nitric
oxide, epoprostenol) testing for benefit from long-
term therapy with calcium channel blockers. Positive
response is a decrease in mean PAP of 10 to 40
mmHg with an increased or unchanged CO from
baseline values.
CRITICAL CARE NURSING (NCM 118)
33 Compiled by BJ SORRILLA, R.N., M.D.
 The definition of precapillary PH or PAH by RHC
requires:
1. an increased mean PAP (mPAP >25 mmHg)
2. a pulmonary capillary wedge pressure (PCWP),
left atrial pressure, or left ventricular end-
diastolic pressure (LVEDP) ≤15 mmHg
3. PVR >3 Wood units. Post capillary PH is
differentiated from precapillary PH by the PCWP
being ≥15 mmHg; this is further differentiated
into passive, based on a transpulmonary
gradient <12 mmHg, or reactive, based on a
transpulmonary gradient >12 mmHg and an
increased PVR. In either case, the CO may be
normal or reduced.
Serology testing: Antinuclear antibodies.
Pulmonary function testing: Used to rule out any
other diseases contributing to shortness of breath.
Sleep study: Done as a screen for sleep apnea, which
may also contribute to the PH
PRINCIPLES OF MANAGEMENT
Provide anticoagulation therapy to prevent
thrombosis and patient education about the long-
term use of anticoagulants.
Avoid betablockers, decongestants, or other
medications that worsen PH or decrease right heart
function.
Encourage physical activity as tolerated alternating
periods of activity with periods of rest.
Administer oxygen to treat hypoxemia and prevent
increased pulmonary vasoconstriction due to low
oxygen levels.
Maintain Sao2 greater than 90% if possible.
Give diuretics to control edema and ascites if right-
sided heart failure is present.
Use calcium channel blockers in patients who show a
positive response to vasodilator therapy during right
heart catheterization
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COLEGIO SAN AGUSTIN – BACOLOD
COLLEGE OF NURSING
Medical Treatment Options
Prior to 1995, there was no medical therapy for P AH
other than continuous oxygen. Epoprostenol was the first
medication for PAH and was approved in 1995. Patients
must be preapproved through their insurance prior to
starting many of these costly medications and be able to
self-administer.
In general, these medications should not be stopped and
require expertise in administration. There are five
medication classifications.
Phosphodiesterase inhibitors block phosphodiesterase
type five, which is responsible for the degradation of
cyclic guanosine monophosphate (cGMP).
Increased cGMP concentration results in
pulmonary vasculature relaxation; vasodilation
in the pulmonary bed and the systemic
circulation (to a lesser degree) may occur.
Endothelin receptor antagonists block the
neurohormone endothelin from binding in the
endothelium and vascular smooth muscle.
Prostacyclin receptor agonists stimulate the
endogenous production of prostacyclin to
potentiate vasodilatation.
Soluble guanylate cyclase stimulator acts
synergistically with endogenous nitric oxide and
also independently to produce vasodilatory
effects, reduce pulmonary smooth muscle
proliferation and acts against platelet inhibition.
Prostacyclin is a potent vasodilator of both
systemic and pulmonary arterial vascular beds
and is an inhibitor of platelet aggregation.
Surgical Treatment Options
Atrial septostomy creates a right-to-left shunt to help
decompress a failing right ventricle in select patients
who are unresponsive to medical therapies. This also
leads to significant hypoxemia in an already
compromised patient.
Pulmonary thromboendarterectomy for those with
chronic thromboembolic pulmonary hypertension
CRITICAL CARE NURSING (NCM 118)
34 Compiled by BJ SORRILLA, R.N., M.D.
 (CTEPH) to improve hemodynamics and functional
status.
Lung transplantation is indicated when the PH has
progressed despite optimal medical and surgical
therapy.
Panel (A) is a representative echocardiogram showing
the apical 4-chamber view from a patient with pulmonary
hypertension demonstrating an enlarged right atrium
and ventricle with some compression of the left side of
the heart. Panel (B) is the same echocardiographic view
showing a normal echocardiogram.
Sleep-disordered breathing is another important cause of
mild PH, but a sleep study is generally necessary only
when indicated by the patient’s history.
Nocturnal desaturation is a common finding in
PH, even in the absence of sleep-disordered
breathing.
Thus, all patients should undergo nocturnal
oximetry screening, regardless of whether
classic symptoms of obstructive sleep apnea or
obesity- hypoventilation syndrome are observed.
PNEUMOTHORAX
It is the presence of gas in the pleural space.
Spontaneous pneumothorax is one that occurs
without antecedent trauma to the thorax.
o Primary spontaneous pneumothorax
occurs in the absence of underlying lung
disease
o Secondary pneumothorax occurs in its
presence
o Traumatic pneumothorax results from
penetrating or non- penetrating chest
injuries
o Tension pneumothorax is a pneumothorax
in which the pressure in the pleural space is
positive throughout the respiratory cycle.
Primary Spontaneous Pneumothorax
usually due to rupture of apical pleural blebs, small
cystic spaces that lie within or immediately under the
visceral pleura.
Primary spontaneous pneumothoraxes occur almost
exclusively in smokers; this suggests that these
patients have subclinical lung disease.
o Approximately one-half of patients with an
initial primary spontaneous pneumothorax
will have a recurrence.
o The initial recommended treatment for
primary spontaneous pneumothorax is
simple aspiration. If the lung does not
expand with aspiration or if the patient has a
recurrent pneumothorax, thoracoscopy with
stapling of blebs and pleural abrasion is
indicated.
o Thoracoscopy or thoracotomy with pleural
abrasion is almost 100% successful in
preventing recurrences.
Secondary Pneumothorax
Most are due to chronic obstructive pulmonary
disease, but pneumothoraxes have been
reported with virtually every lung disease.
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COLEGIO SAN AGUSTIN – BACOLOD
COLLEGE OF NURSING
Pneumothorax in patients with lung disease is
more life-threatening than it is in normal
individuals because of the lack of pulmonary
reserve in these patients.
Nearly all patients with secondary pneumothorax
should be treated with tube thoracostomy.
Most should also be treated with thoracoscopy or
thoracotomy with the stapling of blebs and
pleural abrasion.
o If the patient is not a good operative
candidate or refuses surgery,
pleurodesis should be attempted by the
intrapleural injection of a sclerosing
agent such as doxycycline
Traumatic Pneumothorax
can result from both penetrating and
nonpenetrating chest trauma
should be treated with tube thoracostomy unless
they are very small.
o If a hemopneumothorax is present, one
chest tube should be placed in the
superior part of the hemithorax to
evacuate the air and another should be
placed in the inferior part of the
hemithorax to remove the blood.
Iatrogenic pneumothorax is a type of traumatic
pneumothorax that is becoming more common.
o The leading causes are transthoracic
needle aspiration, thoracentesis, and the
insertion of central intravenous
catheters. Most can be managed with
supplemental oxygen or aspiration, but if
these measures are unsuccessful, a tube
thoracostomy should be performed.
Tension Pneumothorax
usually occurs during mechanical ventilation or
resuscitative efforts
The positive pleural pressure is life-threatening both
because ventilation is severely compromised and
because the positive pressure is transmitted to the
mediastinum, resulting in decreased venous return
to the heart and reduced cardiac output.
Difficulty in ventilation during resuscitation or high
peak inspiratory pressures during mechanical
ventilation strongly suggest the diagnosis.
The diagnosis is made by physical examination
showing an enlarged hemithorax with no breath
sounds, hyperresonance to percussion, and shift of
the mediastinum to the contralateral side.
Tension pneumothorax must be treated as a medical
emergency. If the tension in the pleural space is not
relieved, the patient is likely to die from inadequate
cardiac output or marked hypoxemia.
CRITICAL CARE NURSING (NCM 118)
35 Compiled by BJ SORRILLA, R.N., M.D.
 A large-bore needle should be inserted into the
pleural space through the second anterior intercostal
space. If large amounts of gas escape from the
needle after insertion, the diagnosis is confirmed.
The needle should be left in place until a
thoracostomy tube can be inserted
Management
1. Supplemental oxygen should be administered to all
patients with pneumothorax because oxygen
accelerates the rate of air resorption from the
pleural space.
2. If the pneumothorax is 15% to 20%, no medical
intervention is required.24 If the pneumothorax is
greater than 20%, a chest tube is placed in the
apical and anterior aspect of the pleural space to
assist air removal.
3. Connecting the chest tube to underwater seal
drainage alone is usually adequate to resolve the
pneumothorax.
4. If the pneumothorax persists after 12 to 24 hours
of underwater seal drainage, 15 to 20 cm H2O
suction should be applied to facilitate closure.
5. When treating tension pneumothorax, if a chest
tube is not immediately available, a large-bore (16-
or 18-gauge) needle should be placed into the
anterior second intercostal space.
a. After needle insertion, a chest tube is
placed and connected to underwater seal
drainage.
b. When the tension pneumothorax is relieved,
the effect is rapid and is evidenced by an
improvement in oxygenation, a decrease in
heart rate, and an increase in blood
pressure.
ACUTE RESPIRATORY FAILURE
Respiratory failure is one of the most common reasons
for ICU admission. In some ICUs, ≥75% of patients
require mechanical ventilation during their stay.
TYPE I: ACUTE HYPOXEMIC RESPIRATORY
FAILURE
occurs with alveolar flooding and subsequent
intrapulmonary shunt physiology.
Alveolar flooding may be a consequence of
pulmonary edema, lung injury, pneumonia, or
alveolar hemorrhage. Pulmonary edema can be
further categorized as occurring due to elevated
pulmonary microvascular pressures, as seen in heart
failure and intravascular volume overload or ARDS
(“low-pressure pulmonary edema”)
acute onset (≤1 week) of bilateral opacities on
chest imaging that are not fully explained by
cardiac failure or fluid overload and of shunt
physiology requiring positive end-expiratory
pressure (PEEP)
occurs in clinical settings such as sepsis, gastric
aspiration, pneumonia, near-drowning, multiple
blood transfusions, and pancreatitis
TYPE II RESPIRATORY FAILURE
a consequence of alveolar hypoventilation and
results from the inability to eliminate carbon dioxide
effectively
Mechanisms are categorized by impaired central
nervous system (CNS) drive to breathe, impaired
strength with failure of neuromuscular function in the
respiratory system, and increased load(s) on the
respiratory system
o Reasons for diminished CNS drive to breathe
include drug overdose, brainstem injury,
sleep-disordered breathing, and severe
hypothyroidism.
o Reduced strength can be due to impaired
neuromuscular transmission (e.g.,
myasthenia gravis, Guillain-Barré syndrome,
amyotrophic lateral sclerosis) or respiratory
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COLEGIO SAN AGUSTIN – BACOLOD
COLLEGE OF NURSING
muscle weak- ness (e.g., myopathy,
electrolyte derangements, fatigue
overall load on the respiratory system can be
subclassified into resistive loads (e.g.,
bronchospasm), loads due to reduced lung
compliance (e.g., alveolar edema, atelectasis,
intrinsic positive end-expiratory pressure [auto-
PEEP]—see below), loads due to reduced chest wall
compliance (e.g., pneumothorax, pleural effusion,
abdominal distention), and loads due to increased
minute ventilation requirements (e.g., pulmonary
embolus with increased dead-space fraction)
mainstays of therapy for type II respiratory failure
are directed at reversing the underlying cause(s) of
ventilatory failure. Noninvasive positive-pressure
ventilation with a tight-fitting facial or nasal mask,
with avoidance of endotracheal intubation, often
stabilizes these patients
TYPE III RESPIRATORY FAILURE
results from lung atelectasis
atelectasis occurs so commonly in the perioperative
period, this form is also called perioperative
respiratory failure
After general anesthesia, decreases in functional
residual capacity lead to collapse of dependent lung
units
frequent changes in position, chest physiotherapy,
upright positioning, and control of incisional and/or
abdominal pain. Noninvasive positive-pressure
ventilation may also be used to reverse regional
atelectasis
TYPE IV RESPIRATORY FAILURE
results from hypoperfusion of respiratory muscles in
patients in shock
Patients in shock often experience respiratory
distress due to pulmonary edema (e.g., in
cardiogenic shock), lactic acidosis, and anemia.
o In this setting, up to 40% of cardiac output
may be distributed to the respiratory
muscles.
o Intubation and mechanical ventilation can
allow redistribution of the cardiac output
away from the respiratory muscles and back
to vital organs while the shock is treated.
Manifestations
Early signs are those associated with impaired
oxygenation and may include restlessness, fatigue,
headache, dyspnea, air hunger, tachycardia, and
increased blood pressure.
As the hypoxemia progresses, more obvious signs
may be present, including confusion, lethargy,
tachycardia, tachypnea, central cyanosis,
diaphoresis, and finally respiratory arrest.
Physical findings are those of acute respiratory
distress, including use of accessory muscles,
decreased breath sounds if the patient cannot
adequately ventilate, and other findings related
specifically to the underlying disease process and
cause of ARF.
Medical Management
The objectives of treatment are to correct the
underlying cause and to restore adequate gas
exchange in the lung.
Intubation and mechanical ventilation may be
required to maintain adequate ventilation and
oxygenation while the underlying cause is corrected.
Improving oxygenation & ventilation
Most causes of ARF are treatable, with a return of normal
respiratory function following resolution of the
pathophysiologic condition. Aggressive support of
respiratory function is required until there is resolution
of the underlying condition.
Provide supplemental 02 to maintain Pao2 greater
than 60 mmHg. The use of noninvasive methods for
O2 administration (high flow nasal cannula or face
CRITICAL CARE NURSING (NCM 118)
36 Compiled by BJ SORRILLA, R.N., M.D.
 masks) is preferable if acceptable Pao2 levels can be o Place one hand on the patient's abdomen.
achieved. Instruct the patient to inhale deeply, causing
Continued hypoxemia despite noninva sive 02 the hand on the abdomen to rise.
delivery methods necessitates intubation and o During exhalation, have the patient feel the
mechanical ventilation. hand on the belly sink down toward the
Improve ventilation with the administration of spine. Explain that the chest moves
bronchodilators, suctioning, positioning, and minimally.
mobilization aa indicated. The routine use of chest o After a minute or two, ask the patient to
physiotherapy has not been shown to be supported place his or her hands on the belly to
by literature and is not recommended. continue the exercise.
Intubate and initiate mechanical ventilation if non- o If necessary, administer mild doses of
invasive methods fail to correct hypoxemia and anxiolytics (ie, lorazepam or alprazolam)
hypercarbia or if cardiovascular instability develops. that do not depress respiration. Use a
o In patients with COPD exacerbation, a trial of validated sedation assessment tool to
non- invasive positive pressure mechanical measure the patient's anxiety and evaluate
ventilation may be appropriate prior to the medication's effect.
intubation. The mode of mechanical
ventilation, rate, and tidal volume vary, Preventing complications
depending on the underlying cause of Pulmonary aspiration: Ensure proper inflation
respiratory failure and a variety of clinical of endotracheal tube cuff at all times.
factors. Gastrointestinal (GI) bleeding: Protect
o Modes of ventilation that decrease the work gastric mucosa and increase gastric pH in
of breathing (control, assist/control, SIMV ventilator patients by using stress ulcer
with high minute ventilation [MV] rates, and prophylaxis and/or tube feedings after assessing
pressure support [PS]) are typically used for the patient's risk for GI bleeding
the first 24 hours because respiratory muscle Barotrauma: Avoid unnecessary increases in
fatigue is common. airway pressures (eg, patient/ventilator
dyssynchrony, excessive coughing) and assess
o PEEP levels more than 5 cm H20 may be
for signs and symptoms of pneumothorax,
required if Fio2 levels above 0.5 are needed
pneumomediastinum, and other barotrauma
to eliminate hypoxemia.
complications
o Closely monitor the cardiovascular status
Volutrauma: Prevent alveolar damage from
during increases of PEEP, which may
excessive tidal volumes.
decrease venous return and cardiac output.
Institute analgesia and sedation for patient
comfort. Neuromuscular blockade may be
END OF PULMONARY MODULE
needed initially to prevent ventilator
dyssynchrony and to maximize gas
exchange.
During suctioning, closely observe for signs and
symptoms of complications: drop in oxygenation
(Spo2, Svo2) , cardiac dysrhythmias, respiratory dis-
tress (bronchospasm, increased respiratory rate),
increased blood pressure or intracranial pressure,
anxiety, pain, agitation, or change in mental status.
o Hyperoxygenate with 100% Fio2, preferably
by using the manual 100% Fio2 button on the
ventilator.
o An alternative is the use of a manual
resuscitation bag (MRB) that delivers 100%
02 and can be used with a PEEP valve when
the ventilator PEEP levels are more than 5
cm H20.
o Suctioning is only be performed when
clinically indicated, and never on a routine
schedule.
o The use of in-line suction catheters is
encouraged as the catheters do not affect
oxygenation as dramatically as complete
disconnection and they decrease the
potential contamination of the clinician doing
the suctioning.
Prior to intrahospital transport, verify adequacy of
ventilatory support equipment to maintain
cardiopulmonary stability.
o Verify that PEEP levels are maintained during
transport. Some ventilators used for
transport do not have the capability to
provide more advanced ventilatory modes
(eg, PS, reverse inspiratory : expiratory (I:E)
ratio, pressure release, pressure-regulated
volume control).
o Thus when transitioning from an advanced
mode to a more traditional mode prior to
transport, allow for a brief "stabilization"
period prior to leaving the critical care unit.

Teach diaphragmatic breathing to slow the rate and

increase the depth of respirations.

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COLEGIO SAN AGUSTIN – BACOLOD CRITICAL CARE NURSING (NCM 118)
COLLEGE OF NURSING 37 Compiled by BJ SORRILLA, R.N., M.D.
 Colegio San Agustin - Bacolod City
College of Nursing – NCM 118 LECTURE
CARDIOLOGY MODULE
Compiled by S. S. Sorrilla, R.N., M.D.
NON-ST-SEGMENT ELEVATION ACUTE
CORONARY SYNDROME (NON-ST-SEGMENT
ELEVATION MYOCARDIAL INFARCTION AND
UNSTABLE ANGINA)
caused by an imbalance between myocardial oxygen
supply and demand resulting from one or more of the
following four processes that lead to thrombus
formation:
1. disruption of an unstable coronary plaque
due to plaque rupture, erosion, or a calcified
protruding nodule that leads to intracoronary
thrombus formation and an inflammatory
response
2. coronary arterial vasoconstriction
3. gradual intraluminal narrowing
4. increased myocardial oxygen demand
produced by conditions such as fever,
tachycardia, and thyrotoxicosis in the
presence of fixed epicardial coronary
obstruction.
While plaque rupture remains the most common
etiology of coronary thrombosis, erosion of an
intracoronary plaque is increasing in frequency,
perhaps related to the above mentioned shifts in the
underlying risk factors for ACS
Among patients with NSTE-ACS studied at
angiography, ~10% have stenosis of the left main
coronary artery, 35% have three-vessel CAD, 20%
have two-vessel disease, 20% have single-vessel
disease, and 15% have no apparent critical epicardial
coronary artery stenosis; some of the latter may
have obstruction of the coronary microcirculation
and/or spasm of the epicardial vessels.
Vulnerable plaques are composed of a lipid-rich core
with a thin fibrous cap. Patients with NSTE-ACS
frequently have multiple such plaques that are at risk
of disruption.
One study showed that 2% of patients who
eventually were diagnosed with an acute MI were
incorrectly dis- charged and sent home from the
emergency department (Pope et al., 2000).
HISTORY & PE EVALUATION
Typically, chest discomfort is severe and has at least
one of three features:
1. occurrence at rest (or with minimal
exertion), lasting >10 min
2. relatively recent onset (i.e., within the prior
2 weeks)
3. a crescendo pattern, i.e., distinctly more
severe, prolonged, or frequent than previous
episodes
chest discomfort is typically located in the substernal
region and radiates to the left arm, left shoulder,
and/or superiorly to the neck and jaw
Anginal equivalents such as dyspnea, epigastric
discomfort, nausea, or weakness may occur instead
of chest discomfort
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COLEGIO SAN AGUSTIN – BACOLOD
COLLEGE OF NURSING
They appear to be more frequent in women, the
elderly, and patients with diabetes mellitus
if the patient has a large area of myocardial ischemia
or a large NSTEMI, the physical findings can include
diaphoresis; pale, cool skin; sinus tachycardia; a
third and/or fourth heart sound; basilar rales; and,
sometimes, hypotension
The Framingham Heart Study revealed that 50% of
the men and 63% of the women who died suddenly
of cardio- vascular disease had no previous
symptoms (Kannel, 1986)
Electrocardiogram
New ST-segment depression occurs in about one-
third of patients with NSTE-ACS
It may be transient but may persist for several days
following NSTEMI.
T-wave changes are more common but are less
specific signs of ischemia, unless they are new and
deep T-wave inversions (≥0.3 mV)
CARDIAC BIOMARKERS
Patients with NSTEMI have elevated biomarkers of
necrosis, such as cardiac troponin (cTn) I or T, which
are specific, sensitive, and the preferred markers of
myocardial necrosis
The MB isoform of creatine kinase (CK-MB) is a less
sensitive alternative
DIAGNOSTIC EVALUATION
In addition to the clinical examination, three major
noninvasive tools are used in the evaluation of
NSTEMI-ACS: the ECG, cardiac biomarkers, and
stress testing. In equivocal cases, coronary
computed tomographic angiography (CCTA) may be
useful to improve the accuracy and speed of the
diagnostic evaluation. The goals are to:
recognize or exclude myocardial infarction (MI)
using cardiac biomarkers, preferably cTn
detect rest ischemia (using serial or continuous
ECGs)
detect significant coronary obstruction at rest
with CCTA and/ or myocardial ischemia using
stress testing
PRINCIPLES OF MANAGEMENT
Because most complications of acute ischemic
heart disease directly result from reduced
coronary flow, a primary objective in patient
management is to optimize blood flow to the
myocardium. Additional goals are to prevent
complications of ischemia and infarction,
alleviate chest discomfort/pain, and reduce
anxiety
MEDICAL MANAGEMENT
Patients should be placed at bed rest with continuous
ECG monitoring for ST-segment deviation and
cardiac arrhythmias, preferably on a specialized
cardiac unit.
Ambulation is permitted if the patient shows no
recurrence of ischemia (symptoms or ECG changes)
and does not develop an elevation of a biomarker of
necrosis for 12–24 h.
To provide relief and prevention of recurrence of
ischemic discomfort, initial treatment should include
bed rest, nitrates, beta adrenergic blockers, and
inhaled oxygen in patients with arterial O2 saturation
(<90%) and/or in those with heart failure and rales.
CRITICAL CARE NURSING (NCM 118)
1 Compiled by BJ SORRILLA, R.N., M.D.
 pressure falls to <90 mmHg, or the dose
reaches 200 μg/min)
o Topical or oral nitrates (Chap. 267) can be
used when the pain has resolved, or they
may replace intravenous nitroglycerin when
the patient has been symptom-free for 12–
24 h.
o The only absolute contraindications to the
use of nitrates are hypotension or the recent
use of a phosphodiesterase type 5 (PDE-5)
inhibitor, sildenafil or vardenafil (within 24
h), or tadalafil (within 48 h).

BETA-ADRENERGIC BLOCKERS
may be started by the intravenous route in patients
with severe ischemia
should be avoided in the presence of acute or severe
heart failure, low cardiac output, hypotension, or
contraindications to beta-blocker therapy (e.g., high-
degree atrioventricular block, active bronchospasm).
oral beta blockade targeted to a heart rate of 50–60
beats/ min is recommended

OTHER DRUGS
HMG-CoA reductase inhibitors (statins)
atorvastatin 80 mg/d, prior to percutaneous
coronary intervention (PCI), and continued
thereafter, has been shown to reduce peri-
procedural MI and recurrences of ACS
In patients who do not have an adequate response
to maximally tolerated statin (i.e., <50% decrease
in LDL-C from untreated baseline or LDL-C on
treatment >70 mg/dL), addition of ezetimibe 10 mg
daily to reduce further the LDL-C has been shown to
reduce future cardiovascular events

ANTI-PLATELET DRUGS
Initial treatment should begin with the
NITRATES cyclooxygenase inhibitor aspirin with a dose of at
given sublingually or by buccal spray (0.3–0.6 mg) if least 162 mg of a rapidly acting preparation (oral
the patient is experiencing ischemic discomfort non-enteric coated or intravenous).
o If symptoms persists after three doses given Lower doses (75–100 mg/d) are recommended
5 min apart, intravenous nitroglycerin (5–10 thereafter, since they maintain efficacy while causing
μg/min using non-absorbing tubing) is less bleeding.
recommended (rate of the infusion may be Contraindications are severe active bleeding or
increased by 10 μg/min every 3–5 min until aspirin allergy.
symptoms are relieved, systolic arterial
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COLEGIO SAN AGUSTIN – BACOLOD CRITICAL CARE NURSING (NCM 118)
COLLEGE OF NURSING 2 Compiled by BJ SORRILLA, R.N., M.D.
 CLOPIDOGREL
thienopyridine clopidogrel is an inactive prodrug that ST-SEGMENT ELEVATION ACUTE CORONARY
is converted into an active metabolite that causes SYNDROME (ST-SEGMENT ELEVATION
irreversible blockade of the platelet P2Y12 receptor MYOCARDIAL INFARCTION)
loading dose of clopidogrel is 600 or 300 mg while
the maintenance dose is 75 mg daily. About half of AMI-related deaths occur before the
o When clopidogrel is added to aspirin, so- stricken individual reaches the hospital.
called dual antiplatelet therapy (DAPT), has The 1-year mortality rate after AMI is about 15%.
been shown to confer a 20% relative Mortality is approximately fourfold higher in elderly
reduction in cardiovascular death, MI, or patients (aged >75) as compared with younger
stroke, compared to aspirin alone, but to be patients.
associated with a moderate (absolute 1%)
increase in major bleeding
o DAPT should continue for at least 1 year in
patients with NSTE- ACS, especially those
with a drug-eluting stent, to prevent stent
thrombosis.

ANTICOAGULANTS
Four options are available for anticoagulant therapy
to be added to antiplatelet agents:
1. unfractionated heparin (UFH), long the mainstay
of therapy
2. low-molecular-weight heparin (LMWH),
enoxaparin, which has been shown to be superior
to UFH in reducing recurrent cardiac events,
especially in patients managed by a conservative
strategy (with a slight increase in bleeding
compared to UFH)
3. bivalirudin, a direct thrombin inhibitor that is
similar in efficacy to either UFH or LMWH but Acute coronary syndromes. Following disruption of a
causes less bleeding and is used just prior to vulnerable plaque, patients experience ischemic
and/or during PCI discomfort resulting from a reduction of flow through
4. indirect factor Xa inhibitor, fondaparinux, which the affected epicardial coronary artery. The flow
is equivalent in efficacy to enoxaparin but has a reduction may be caused by a completely occlusive
lower risk of major bleeding. thrombus (right) or subtotally occlusive thrombus
(left). Patients with ischemic discomfort may present
ACE inhibitors (ACE-I) with or without ST-segment elevation. Of patients
prevent the conversion of angiotensin from I to II. In with ST-segment elevation, the majority (wide red
the absence of angiotensin II, the blood pressure arrow) ultimately develop a Q wave on the ECG (Qw
decreases and the kidneys excrete sodium and fluid MI), while a minority (thin red arrow) do not develop
(diuresis), decreasing the oxygen demand of the Q wave and, in older literature, were said to have
heart. sustained a non-Q-wave MI (NQMI).
Use of ACE inhibitors in patients after MI decreases
the mortality rate and prevents the onset of heart The 12-lead electrocardiogram (ECG) is a pivotal
failure. diagnostic and triage tool because it is at the center
It is important to ensure that the patient is not of the decision pathway for management; it permits
hypotensive, hyponatremic, hypovolemic, or distinction of those patients presenting with ST-
hyperkalemic before ACE-I ad- ministration. Blood segment elevation from those presenting without ST-
pressure, urine output, and serum sodium, segment elevation.
potassium, and creatinine levels need to be Serum cardiac biomarkers are obtained to
monitored closely. distinguish unstable angina (UA) from non-ST-
segment elevation myocardial infarction (NSTEMI)
SUMMARY OF MANAGEMENT: and to assess the magnitude of an ST-segment
elevation myocardial infarction (STEMI).
Decrease activity of coagulation system with
pharmacologic therapy: PATHOPHYSIOLOGY
o Antiplatelet agents: aspirin, glycoprotein Ilb/Illa STEMI usually occurs when coronary blood flow
receptor blocking agents (eg, abciximab decreases abruptly after a thrombotic occlusion of a
[Reopro], eptifibatide [Integrilin], and tirofiban coronary artery previously affected by
[Aggra-stat]), thienopyridine agents (eg, atherosclerosis.
clopidogrel [Plavix] or tacagrelor [Brilinta]) Slowly developing, high-grade coronary artery
o Antithrombin agents: indirect (eg, stenoses do not typically precipitate STEMI
unfractionated heparin, low-molecular-weight because of the development of a rich collateral
heparin), direct (eg, bivalirudin [Angiomax]) network over time.
Increase ventricular filling time (decrease heart Instead, STEMI occurs when a coronary artery
rate): thrombus develops rapidly at a site of vascular
o Beta-blockers injury.
o Bed rest for 24 hours This injury is produced or facilitated by factors
Decrease preload: such as cigarette smoking, hypertension, and
o Nitrates lipid accumulation.
o Diuretics In most cases, STEMI occurs when the surface of
o Morphine sulfate 4. an atherosclerotic plaque becomes disrupted
Decrease afterload: (exposing its contents to the blood) and
o Angiotensin-converting enzyme (ACE) inhibitors conditions (local or systemic) favor
if EF ~ 40% thrombogenesis.
o Hydralazine A mural thrombus forms at the site of plaque
Decrease myocardial oxygen consumption (MV02): disruption, and the involved coronary artery
o Beta-blockers becomes occluded.
o Bedrestfor24hours Coronary plaques prone to disruption are those with
a rich lipid core and a thin fibrous cap

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COLEGIO SAN AGUSTIN – BACOLOD CRITICAL CARE NURSING (NCM 118)
COLLEGE OF NURSING 3 Compiled by BJ SORRILLA, R.N., M.D.
 After an initial platelet monolayer forms at the
site of the disrupted plaque, various agonists
(collagen, ADP, epinephrine, serotonin) promote PHYSICAL EXAM
platelet activation.
After agonist stimulation of platelets,
thromboxane A2 (a potent local vasoconstrictor)
is released, further platelet activation occurs,
and potential resistance to fibrinolysis develops.
activation of platelets by agonists promotes a
conformational change in the glycoprotein
IIb/IIIa receptor
Once converted to its functional state, this
receptor develops a high affinity for soluble
adhesive proteins (i.e., integrins) such as
fibrinogen. Since fibrinogen is a multivalent
molecule, it can bind to two different platelets
simultaneously, resulting in platelet cross-linking
and aggregation.
Factors VII and X are activated, ultimately
leading to the conversion of prothrombin to
thrombin, which then converts fibrinogen to
fibrin
culprit coronary artery eventually becomes
occluded by a thrombus containing platelet
aggregates and fibrin strands

The amount of myocardial damage caused by

coronary occlusion depends on:
1. the territory supplied by the affected vessel
2. whether or not the vessel becomes totally
occluded
3. the duration of coronary occlusion
4. the quantity of blood supplied by collateral
vessels to the affected tissue
5. the demand for oxygen of the myocardium
whose blood supply has been suddenly limited
6. endogenous factors that can produce early
spontaneous lysis of the occlusive thrombus
7. the adequacy of myocardial perfusion in the
infarct zone when flow is restored in the occluded
epicardial coronary artery

MANIFESTATIONS combination of substernal chest pain persisting for

up to one-half of cases, a precipitating factor appears >30 min and diaphoresis strongly suggests STEMI
to be present before STEMI, such as vigorous about one-fourth of patients with anterior infarction
physical exercise, emotional stress, or a medical or have manifestations of sympathetic nervous system
surgical illness hyperactivity (tachycardia and/or hypertension), and
Although STEMI may commence at any time of the up to one-half with inferior infarction show evidence
day or night, circadian variations have been reported of parasympathetic hyperactivity (bradycardia
such that clusters are seen in the morning within a and/or hypotension).
few hours of awakening. precordium is usually quiet, apical impulse may be
Pain is the most common presenting complaint in difficult to palpate
patients with STEMI. In patients with anterior wall infarction, an abnormal
systolic pulsation caused by dyskinetic bulging of
The pain is deep and visceral; adjectives commonly infarcted myocardium may develop in the periapical
used to describe it are heavy, squeezing, and area within the first days of the illness and then may
crushing; although, occasionally, it is described as resolve.
stabbing or burning. fourth and third heart sounds, decreased intensity of
commonly occurs at rest, is usually more severe, and the first heart sound, and paradoxical splitting of the
lasts longer second heart sound
typically, the pain involves the central portion of the carotid pulse is often decreased in volume, reflecting
chest and/or the epigastrium, and, on occasion, it
radiates to the arms.
Less common sites of radiation include the abdomen,
back, lower jaw, and neck.
The pain of STEMI may radiate as high as the
occipital area but not below the umbilicus. It is often
accompanied by weakness, sweating, nausea,
vomiting, anxiety, and a sense of impending doom.
The pain may commence when the patient is at rest,
but when it begins during a period of exertion, it does
not usually subside with cessation of activity, in
contrast to angina pectoris.
Radiation of discomfort to the trapezius is not seen
in patients with STEMI and may be a useful
distinguishing feature that suggests pericarditis is
the correct diagnosis.
However, pain is not uniformly present in patients
with STEMI. The proportion of painless STEMIs is reduced stroke volume
greater in patients with diabetes mellitus, and it temperature elevations up to 38°C may be observed
increases with age. during the first week after STEMI

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COLEGIO SAN AGUSTIN – BACOLOD CRITICAL CARE NURSING (NCM 118)
COLLEGE OF NURSING 4 Compiled by BJ SORRILLA, R.N., M.D.
 in most patients with transmural infarction, systolic
pressure declines by ~10–15 mmHg from the
preinfarction state
LABORATORY FINDINGS
STEMI progresses through the following temporal
stages:
o acute (first few hours–7 days)
o healing (7–28 days)
o healed (≥29 days)
When evaluating the results of diagnostic tests for
STEMI, the temporal phase of the infarction must be
considered.
The laboratory tests of value in confirming the
diagnosis may be divided into four groups:
o ECG
o serum cardiac biomarkers
o cardiac imaging
o nonspecific indices of tissue necrosis and
inflammation
ELECTROCARDIOGRAM
During the initial stage, total occlusion of an
epicardial coronary artery produces ST-segment
elevation.
o Most patients initially presenting with ST-
segment elevation ultimately evolve Q waves on
the ECG.
o However, Q waves in the leads overlying the
infarct zone may vary in magnitude and even
appear only transiently, depending on the
reperfusion status of the ischemic myocardium
and restoration of transmembrane potentials
over time.
o Contemporary studies using magnetic
resonance imaging (MRI) suggest that the
development of a Q wave on the ECG is more
dependent on the volume of infarcted tissue
rather than the transmurality of infarction.
SERUM CARDIAC BIOMARKERS
Cardiac biomarkers become detectable in the
peripheral blood once the capacity of the cardiac
lymphatics to clear the interstitium of the infarct
zone is exceeded and spillover into the venous
circulation occurs.
The zone of necrosing myocardium is shown at
the top of the figure, followed in the middle portion
of the figure by a diagram of a cardiomyocyte that is
in the process of releasing biomarkers. The
biomarkers that are released into the interstitium are
first cleared by lymphatics followed subsequently by
spillover into the venous system. After disruption of
the sarcolemmal membrane of the cardiomyocyte,
the cytoplasmic pool of biomarkers is released first
(left-most arrow in bottom portion of figure).
Markers such as myoglobin and CK isoforms are
rapidly released, and blood levels rise quickly above
the cutoff limit; this is then followed by a more
protracted release of biomarkers from the
disintegrating myofilaments that may continue for
several days. Cardiac troponin levels rise to about
20–50 times the upper reference limit (the 99th
percentile of values in a reference control group) in
patients who have a “classic” acute myocardial
infarction (MI) and sustain sufficient myocardial
necrosis to result in abnormally elevated levels of the
MB fraction of creatine kinase (CK-MB). Clinicians
can now diagnose episodes of microinfarction by
sensitive assays that detect cardiac troponin
elevations above the upper reference limit, even
though CK-MB levels may still be in the normal
reference range (not shown). CV, coefficient of
variation. (Modified from EM Antman: Decision making with cardiac
troponin tests. N Engl J Med 346:2079, 2002 and AS Jaffe, L Babiun, FS
Apple: Biomarkers in acute cardiac disease: The present and the future.
J Am Coll Cardiol 48:1, 2006.)
MANAGEMENT
The prognosis in STEMI is largely related to the
occurrence of two general classes of complications:
(1) electrical complications (arrhythmias)
(2) mechanical complications (“pump failure”)
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COLEGIO SAN AGUSTIN – BACOLOD
COLLEGE OF NURSING
Most out-of-hospital deaths from STEMI are due to
the sudden development of ventricular fibrillation
The greatest delay usually occurs not during
transportation to the hospital but, rather, between
the onset of pain and the patient’s decision to call for
help
transfer from a non-PCI hospital to one that is PCI
capable, with a goal of initiating PCI within 120 min
of first medical contact
Aspirin administration (160-325mg/tablet buccal) -
rapid inhibition of cyclooxygenase-1 in platelets
followed by a reduction of thromboxane A 2 levels;
then 75-162mg daily
when hypoxemia is present, O2 should be
administered by nasal prongs or face mask (2–4
L/min) for the first 6–12 h after infarction; the
patient should then be reassessed
Glucocorticoids and nonsteroidal anti-inflammatory
agents, with the exception of aspirin, should be
avoided in patients with STEMI.
o impair infarct healing and increase the risk of
myocardial rupture, and their use may result
in a larger infarct scar
o can increase coronary vascular resistance,
thereby potentially reducing flow to ischemic
myocardium
Elevation of the head is beneficial for the following
reasons:
o Tidal volume improves because of reduced
pressure from abdominal contents on the
diaphragm and better lung expansion and
gas exchange.
o Drainage of the upper lung lobes improves.
o Venous return to the heart (preload)
decreases, which reduces the work of the
heart
Scrupulous attention to fluid volume status prevents
overloading the heart and lungs. Encouraging the
patient to breathe deeply and change position
frequently helps keep fluid from pooling in the bases
of the lungs.
Music therapy, in which the patient listens to selected
music for a predetermined duration and at a set time,
has been found to be an effective method for
reducing anxiety and managing stress (Chlan &
Tracy, 1999; Evans, 2002)
Developing a trusting and caring relationship with
the patient is critical in reducing anxiety. Providing
information to the patient and family in an honest
and supportive manner invites the patient to be a
partner in care and greatly assists in developing a
positive relationship.
Ensuring a quiet environment, preventing
interruptions that disturb sleep, using a caring and
appropriate touch, teaching the patient the
relaxation response, using humor and assisting the
patient to laugh, and providing the appropriate
prayer book and assisting the patient to pray if
consistent with the patient’s beliefs are other nursing
interventions that can be used to reduce anxiety.
CONTROL OF DISCOMFORT
Sublingual nitroglycerin
given safely to most patients with STEMI.
Up to three doses of 0.4 mg should be
administered at about 5-min intervals.
In addition to diminishing or abolishing chest
discomfort, nitroglycerin may be capable of both
decreasing myocardial oxygen demand (by
lowering preload) and increasing myocardial
oxygen sup- ply (by dilating infarct-related
coronary vessels or collateral vessels)
Contraindications: low systolic arterial pressure
(<90 mmHg) or in whom there is clinical
suspicion of RV infarction (inferior infarction on
ECG, elevated jugular venous pressure, clear
lungs, and hypotension), intake of
phosphodiesterase-5 inhibitor for erectile
dysfunction within the preceding 24 h
Morphine
CRITICAL CARE NURSING (NCM 118)
5 Compiled by BJ SORRILLA, R.N., M.D.
 administered by repetitive (every 5 min)
intravenous injection of small doses (2–4 mg)
reduce sympathetically mediated arteriolar and
venous constriction, and the resulting venous
pooling may reduce cardiac output and arterial
pressure
has a vagotonic effect and may cause
bradycardia or advanced degrees of heart block,
particularly in patients with inferior infarction.
These side effects usually respond to atropine
(0.5 mg intra- venously)
IV Beta-Blockers
control pain effectively in some patients,
presumably by diminishing myocardial O2
demand and hence ischemia
there is evidence that intravenous beta blockers
reduce the risks of reinfarction and ventricular
fibrillation
5 mg every 2–5 min for a total of three doses,
provided the patient has a heart rate >60
beats/min, systolic pressure >100 mmHg, a PR
interval <0.24 s, and rales that are no higher
than 10 cm up from the diaphragm. Fifteen
minutes after the last intravenous dose, an oral
regimen is initiated of 50 mg every 6 h for 48 h,
followed by 100 mg every 12 h
NURSING DIAGNOSES
Based on the clinical manifestations, history, and
diagnostic assessment data, the patient’s major
nursing diagnoses may include:
Ineffective cardiopulmonary tissue perfusion
related to reduced coronary blood flow from
coronary thrombus and atherosclerotic plaque
Potential impaired gas exchange related to fluid
overload from left ventricular dysfunction
Potential altered peripheral tissue perfusion
related to de- creased cardiac output from left
ventricular dysfunction
Anxiety related to fear of death
Deficient knowledge about post-MI self-care
CONGESTIVE HEART FAILURE
inability of the heart to pump sufficient blood to meet
the needs of the tissues for oxygen and nutrients
The current American College of Cardiology
Foundation (ACCF)/American Heart Association
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COLEGIO SAN AGUSTIN – BACOLOD
COLLEGE OF NURSING
(AHA) guidelines define HF as a complex clinical
syndrome that results from structural or functional
impairment of ventricular filling or ejection of blood,
which in turn leads to the cardinal clinical symptoms
of dyspnea and fatigue and signs of HF, namely
edema and rales.
ETIOLOGY
An assessment of the ejection fraction (EF) is
performed to assist in determining the type of HF.
EF is the percentage of the end-diastolic blood
volume in the ventricle minus the end-systolic
blood volume in the ventricle divided by the end-
diastolic blood volume in the ventricle—an
indication of the amount of blood that was
ejected and the contractile ability of the
ventricle.
The EF is normal in diastolic HF, whereas the EF
is less than 40% in systolic HF.
PROGNOSIS
Despite recent advances in the management of HF,
the development of symptomatic HF still carries a
poor prognosis.
Community-based studies indicate that 30–40%
of patients die within 1 year of diagnosis and 60–
70% die within 5 years, mainly from worsening
HF or as a sudden event (probably because of a
ventricular arrhythmia).
patients with symptoms at rest (New York Heart
Association [NYHA] class IV) have a 30–70%
annual mortality rate, whereas patients with
symptoms with moderate activity (NYHA class II)
have an annual mortality rate of 5–10%.
Thus, functional status is an important predictor
of patient outcome
CRITICAL CARE NURSING (NCM 118)
6 Compiled by BJ SORRILLA, R.N., M.D.
 reorganization of the extracellular matrix with
PATHOGENESIS dissolution of the organized structural collagen
HF is a progressive disorder that is initiated after an weave surrounding myocytes and subsequent
index event either damages the heart muscle, with a
resultant loss of functioning cardiac myocytes, or,
alternatively, disrupts the ability of the myocardium
to generate force, thereby pre- venting the heart
from contracting normally.
Regardless of the nature of the inciting event, the
feature that is common to each of these index events
is that they all in some manner produce a decline in
the pumping capacity of the heart
Patients with LV dysfunction may remain
asymptomatic in the presence of cardiac injury
and/or LV dysfunction allowing patients to sustain
and modulate LV function for a period of months to
years.
The compensatory mechanisms that have been
described thus far include:
o activation of the renin-angiotensin-
aldosterone system (RAAS) and the
adrenergic nervous system, which are
responsible, respectively, for maintaining
cardiac output through increased retention of
salt and water
o increased myocardial contractility. In
addition, a family of countervailing
vasodilatory molecules are activated,
including the atrial and brain natriuretic
peptides (ANP and BNP), bradykinin, replacement by an interstitial collagen matrix
prostaglandins (PGE2 and PGI2), and nitric that does not provide structural support to the
oxide (NO), that offset the excessive myocytes.
peripheral vascular vasoconstriction. Many of Myocardial relaxation is an adenosine tri- phosphate
these vasodilatory peptides, including (ATP)-dependent process that is regulated by uptake
bradykinin and natriuretic peptides, are of cytoplasmic calcium into the SR by SERCA2A and
degraded by a neprilysin, which is a extrusion of calcium by sarcolemmal pumps.
membrane-bound peptidase. o Accordingly, reductions in ATP concentration, as
the transition to symptomatic HF is accompanied by occurs in ischemia, may interfere with these
increasing activation of neurohormonal, adrenergic, processes and lead to slowed myocardial
and cytokine systems that lead to a series of relaxation.
adaptive changes within the myocardium o Alternatively, if LV filling is delayed because LV
collectively referred to as LV remodeling. compliance is reduced (e.g., from hypertrophy or
fibrosis), LV filling pressures will similarly remain
HF WITH REDUCED EJECTION FRACTION elevated at end diastole. An increase in heart
(HFrEF) rate disproportionately shortens the time for
LV remodeling develops in response to a series of diastolic filling, which may lead to elevated LV
complex events that occur at the cellular and filling pressures, particularly in noncompliant
molecular levels: ventricles. Elevated LV end- diastolic filling
o myocyte hypertrophy pressures result in increases in pulmonary
o alterations in the contractile properties of the capillary pressures, which can contribute to the
myocyte dyspnea experienced by patients with diastolic
o progressive loss of myocytes through necrosis, dysfunction.
apoptosis, and autophagic cell death
o β-adrenergic desensitization LV Remodelling
o abnormal myocardial energetics and metabolism Ventricular remodeling refers to the changes in LV
mass, volume, and shape and the composition of the
heart that occur after cardiac injury and/or abnormal
hemodynamic loading conditions.
o LV remodeling contributes to the progression of
HF by virtue of the mechanical burdens that are
engendered by the changes in the geometry of
the remodeled LV
o The increase in wall thinning, along with the
increase in afterload created by LV dilation, leads
to a functional afterload mis- match that may
contribute further to a decrease in stroke
volume.

MANIFESTATIONS
cardinal symptoms of HF are fatigue and shortness
of breath
o skeletal-muscle abnormalities and other
noncardiac comorbidities (e.g., anemia)
also contribute to fatigue
dyspnea - most important mechanism is pulmonary
congestion with accumulation of interstitial or intra-
alveolar fluid, which activates juxtacapillary J
receptors, which in turn stimulate the rapid, shallow
breathing characteristic of cardiac dyspnea
o Dyspnea may become less frequent with the
onset of right ventricular (RV) failure and
tricuspid regurgitation.
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COLLEGE OF NURSING 7 Compiled by BJ SORRILLA, R.N., M.D.

ORTHOPNEA
dyspnea occurring in the recumbent position, is
usually a later manifestation of HF than is exertional
dyspnea
It results from redistribution of fluid from the
splanchnic circulation and lower extremities into the
central circulation during recumbency, with a
resultant increase in pulmonary capillary pressure
Orthopnea generally is relieved by sitting upright or
sleeping with additional pillows. Although orthopnea
is a relatively specific symptom of HF, it may occur
in patients with abdominal obesity or ascites and
patients with pulmonary disease whose lung
mechanics favor an upright posture.
PAROXYSMAL NOCTURNAL DYSPNEA (PND)
o refers to acute episodes of severe shortness of
breath and coughing that generally occur at night
and awaken the patient from sleep, usually 1–3 h
after the patient retires
o may manifest as coughing or wheezing, possibly
because of increased pressure in the bronchial
arteries leading to airway compression, along with
interstitial pulmonary edema that leads to increased
airway resistance
o patients with PND often have persistent coughing
and wheezing even after they have assumed the
upright position
o Cardiac asthma is closely related to PND, is
characterized by wheezing secondary to
bronchospasm, and must be differentiated from
primary asthma and pulmonary causes of wheezing.
CHEYNE-STOKES RESPIRATION
o also referred to as periodic respiration or cyclic
respiration, Cheyne-Stokes respiration is present in
40% of patients with advanced HF and usually is
associated with low cardiac output
o caused by an increased sensitivity of the respiratory
center to arterial Pco2 and a lengthy circulatory time.
There is an apneic phase, during which arterial Po2
falls and arterial Pco2 rises.
o These changes in the arterial blood gas content
stimulate the respiratory center, resulting in
hyperventilation and hypocapnia, followed by
recurrence of apnea.
OTHER SYMPTOMS
o Anorexia, nausea, and early satiety associated with
abdominal pain and fullness (edema of the bowel wall
and/or a congested liver)
o Congestion of the liver and stretching of its capsule
may lead to right upper-quadrant pain
o Cerebral symptoms such as confusion,
disorientation, and sleep and mood disturbances
may be observed in patients with severe HF,
particularly elderly patients with cerebral
arteriosclerosis and reduced cerebral perfusion.
o Nocturia is common in HF and may contribute to
insomnia
PHYSICAL EXAMINATION
o In mild or moderately severe HF - patient appears to
be in no distress at rest except for feeling
uncomfortable when lying flat for more than a few
minutes
o In more severe HF, the patient must sit upright, may
have labored breathing, and may not be able to finish
a sentence because of shortness of breath.
o SBP may be normal or high in early HF, but it
generally is reduced in advanced HF because of
severe LV dysfunction.
o The pulse pressure may be diminished, reflecting a
reduction in stroke volume.
o Sinus tachycardia is a nonspecific sign caused by
increased adrenergic activity.
o Peripheral vasoconstriction leading to cool peripheral
extremities and cyanosis of the lips and nail beds is
also caused by excessive adrenergic activity.
JVP
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o The jugular venous pressure is best appreciated with
the patient lying recumbent, with the head tilted at
45°.
o The jugular venous pressure should be
quantified in centimeters of water (normal
≤8 cm) by estimating the height of the
venous column of blood above the sternal
angle in centimeters and then adding 5 cm.
o In the early stages of HF, the venous
pressure may be normal at rest but may
become abnormally elevated with sustained
(~15 s) pressure on the abdomen (positive
abdominojugular reflux).
o Giant v waves indicate the presence of
tricuspid regurgitation.
Pulmonary Examination
o result from the transudation of fluid from the
intravascular space into the alveoli
o In patients with pulmonary edema, rales may be
heard widely over both lung fields and may be
accompanied by expiratory wheezing (cardiac
asthma).
o When present in patients with- out
concomitant lung disease, rales are specific
for HF.
o Importantly, rales are frequently absent in
patients with chronic HF, even when LV filling
pressures are elevated, because of increased
lymphatic drainage of alveolar fluid.
o Pleural effusions result from the elevation of
pleural capillary pressure and the resulting
transudation of fluid into the pleural cavities.
o Since the pleural veins drain into both the
systemic and the pulmonary veins, pleural
effusions occur most commonly with
biventricular failure.
o Although pleural effusions are often bilateral
in HF, when they are unilateral, they occur
more frequently in the right pleural space.
Cardiac Examination
Examination of the heart, although essential,
frequently does not provide useful information
about the severity of HF.
o If cardiomegaly is present, the point of
maximal impulse (PMI) usually is displaced
below the fifth intercostal space and/or
lateral to the midclavicular line, and the
impulse is palpable over two interspaces.
o Severe LV hypertrophy leads to a sustained
PMI.
o In some patients, a third heart sound (S3) is
audible and palpable at the apex.
o Patients with enlarged or hypertrophied right
ventricles may have a sustained and
prolonged left parasternal impulse extending
throughout systole.
o An S3 (or protodiastolic gallop) is most
commonly present in patients with volume
overload who have tachycardia and
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8 Compiled by BJ SORRILLA, R.N., M.D.
 tachypnea, and it often signifies severe
hemodynamic compromise.
o A fourth heart sound (S4) is not a specific
indicator of HF but is usually present in
patients with diastolic dysfunction.
o The murmurs of mitral and tricuspid
regurgitation are frequently present in
patients with advanced HF.
Abdomen and Extremities
Hepatomegaly is an important sign in patients with
HF.
o When it is present, the enlarged liver is
frequently tender and may pulsate during systole
if tricuspid regurgitation is present.
o Ascites, a late sign, occurs as a consequence of
increased pressure in the hepatic veins and the
veins draining the peritoneum.
o Jaundice, also a late finding in HF, results from
impairment of hepatic function secondary to
hepatic congestion and hepatocellular
hypoxemia and is associated with elevations of
both direct and indirect bilirubin.
Peripheral edema is a cardinal manifestation of HF,
but it is nonspecific and usually is absent in patients
who have been treated adequately with diuretics.
o Peripheral edema is usually symmetric and
dependent in HF and occurs predominantly in the
ankles and the pretibial region in ambulatory
patients.
o In bedridden patients, edema may be found in
the sacral area (presacral edema) and the
scrotum.
o Long-standing edema may be associated with
indurated and pigmented skin.
Cardiac Cachexia
With severe chronic HF, there may be marked weight
loss and cachexia. Although the mechanism of
cachexia is not entirely understood, it is probably
multifactorial. When present, cachexia augurs a poor
overall prognosis.
DIAGNOSTICS
o Routine exams: complete blood count, a panel
of electrolytes, blood urea nitrogen, serum
creatinine, hepatic enzymes, and a urinalysis.
Selected patients should have assessment for
diabetes mellitus (fasting serum glucose or oral
glucose tolerance test), dyslipidemia (fasting
lipid panel), and thyroid abnormalities (thyroid-
stimulating hormone level).
o ECG - to assess cardiac rhythm and determine
the presence of LV hypertrophy or a prior MI
(presence or absence of Q-waves) as well as to
determine QRS width to ascertain whether the
patient may benefit from resynchronization
therapy (see below). A normal ECG virtually
excludes LV systolic dysfunction.
o Chest X-ray: cardiac size and shape, as well as
the state of the pulmonary vasculature, and may
identify noncardiac causes of the patient’s
symptoms.
o 2D-Echo: provide a semiquantitative
assessment of LV size 1767 and function as well
as the presence or absence of valvular and/or
regional wall motion abnormalities (indicative of
a prior MI).
o Cardiac Magnetic resonance imaging (MRI):
provides a comprehensive analysis of cardiac
anatomy and function and is now the gold
standard for assessing LV mass and volumes.
MRI also is emerging as a useful and accurate
imaging modality for evaluating patients with HF,
both in terms of assessing LV structure and for
determining the cause of HF (e.g., amyloidosis,
ischemic cardiomyopathy, hemochromatosis).
o The most useful index of LV function is
the EF (stroke volume divided by end-
diastolic volume)
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o Biomarkers - B-type natriuretic peptide (BNP)
and N-terminal pro-BNP (NT-proBNP), which are
released from the failing heart, are relatively
sensitive markers for the presence of HF with
depressed EF; they also are elevated in HF
patients with a preserved EF, albeit to a lesser
degree; useful for establishing prognosis or
disease severity in chronic HF and can be useful
to achieve optimal dosing of medical therapy in
select clinically euvolemic patients.
o Exercise Testing: not routinely advocated for
patients with HF, but either is useful for
assessing the need for cardiac transplantation in
patients with advanced HF
HEART FAILURE WITH PRESERVED EJECTION
FRACTION (HFpEF)
o Therapeutic targets in HFpEF include control of
congestion, stabilization of heart rate and blood
pressure, and efforts at improving exercise
tolerance.
o Candesartan in Heart Failure—Assessment of
Mortality and Morbidity (CHARM) Preserved study
showed a statistically significant reduction in
hospitalizations but no difference in all-cause
mortality in patients with HFpEF who were treated
with the angiotensin receptor blocker (ARB),
candesartan.
o A small trial demonstrated that the
phosphodiesterase-5 inhibitor sildenafil improved
filling pressures and right ventricular function in a
cohort of HFpEF patients with pulmonary venous
hypertension.
o This finding led to the phase II trial,
Phosphodiesterase-5 Inhibition to Improve
Clinical Status and Exercise Capacity in
Diastolic Heart Failure (RELAX), in HFpEF
patients (left ventricular ejection fraction
[LVEF] >50%) with New York Heart
Association (NYHA) functional class II or III
symptoms, who received sildenafil at 20 mg
three times daily for 3 months, followed by
60 mg three times daily for another 3
months, compared with a placebo. There was
no improvement in functional capacity,
quality of life (QOL), or other clinical and
surrogate parameters.
ACUTE DECOMPENSATED HEART FAILURE
(ADHF)
o first principle of management of these patients is to
identify and tackle known precipitants of
decompensation
o dentification and management of medication
nonadherence and use of prescribed
medicines such as nonsteroidal anti-
inflammatory drugs, cold and flu
preparations with cardiac stimulants, and
herbal preparations, including licorice,
ginseng, and herbal forms of ephedrine (now
banned in most places), are required
o arrhythmias should be corrected by controlling
heart rate or restoring sinus rhythm in patients with
poorly tolerated rapid atrial fibrillation and by
correcting ongoing ischemia with coronary
revascularization or by correcting offenders such as
ongoing bleeding in demand-related ischemia
o Analysis of in-hospital registries has identified
several parameters associated with worse
outcomes:
o a blood urea nitrogen level >43 mg/dL (to
convert to mmol/L, multiply by 0.357)
o SBP <115 mmHg
o a serum creatinine level >2.75 mg/dL (to
convert to μmol/L, multiply by 88.4)
o elevated troponin I level
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 Volume Management
o When high doses of diuretic agents are required or
when the effect is suboptimal, a continuous infusion
may be needed to reduce toxicity and maintain
stable serum drug levels
o Change in weight is often used as a surrogate for
adequate diuresis, but this objective measure of
volume status may be surprisingly difficult to
interpret, and weight loss during hospitalization does
not necessarily correlate closely with outcomes.
Cardiorenal syndrome
o recognized increasingly as a complication of ADHF.
o interplay between abnormalities of heart and kidney
function, with deteriorating function of one organ
while therapy is administered to preserve the other
o Continued use of diuretic therapy may be associated
with a reduction in glomerular filtration rate and a
worsening of the cardiorenal syndrome when right-
sided filling pressures remain elevated. In patients in
the late stages of disease characterized by profound
low cardiac output state, inotropic therapy or
mechanical circulatory support has been shown to
preserve or improve renal function in selected
individuals in the short term until more definitive
therapy such as assisted circulation or cardiac
transplantation is implemented.
INOTROPIC THERAPY
o pharmacologic agents that increase intracellular
concentration of cyclic adenosine monophosphate via
direct or indirect pathways, such as
sympathomimetic amines (dobutamine) and
phosphodiesterase-3 inhibitors (milrinone),
respectively, serve as positive inotropic agents.
o their activity leads to an increase in cytoplasmic
calcium.
o Inotropic therapy in those with a low-output state
augments cardiac output, improves perfusion, and
relieves congestion acutely.
o Studies are in universal agreement that
long-term inotropic therapy increases
mortality.
o However, the short-term use of inotropic
agents in ADHF is also associated with
increased arrhythmia, hypotension, and no
beneficial effects on hard outcomes.
o Inotropic agents are currently indicated as
bridge therapy (to either left ventricular
assist device support or to transplant) or as
selectively applied palliation in end-stage
heart failure.
HFrEF MANAGEMENT
Neurohormonal Antagonism
Patients treated with beta blockers provide a further
35% reduction in mortality on top of the benefit
provided by ACEIs alone.
o Increased experience with both agents in a broad
range of patients with HFrEF has demonstrated
the safety of ACEIs in treating patients with mild
renal insufficiency and the tolerability of beta
blockers in patients with moderately controlled
diabetes, asthma, and obstructive lung disease.
The benefits of ACEIs and beta blockers extend
to advanced symptoms of disease (NYHA class
IIIb–IV).
o On the basis of investigations, beta blocker use
in HFrEF should ideally be restricted to
carvedilol, bisoprolol, and metoprolol
succinate—agents tested and proven to improve
survival in clinical trials.
MINERALOCORTICOID ANTAGONISTS
Aldosterone antagonism is associated with a
reduction in mortality in all stages of symptomatic
NYHA class II to IV HFrEF.
Elevated aldosterone levels in HFrEF promote sodium
retention, electrolyte imbalance, and endothelial
dysfunction and may directly contribute to
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myocardial fibrosis. The selective agent eplerenone
(tested in NYHA class II and post–myocardial
infarction heart failure) and the nonselective
antagonist spironolactone (tested in NYHA class III
and IV heart failure) reduce mortality and
hospitalizations, with significant reductions in
sudden cardiac death (SCD).
Hyperkalemia and worsening renal function are
concerns, especially in patients with underlying
chronic kidney disease, and renal function and serum
potassium levels must be closely monitored.
NOVEL NEUROHORMONAL ANTAGONISM
More recently, the introduction of LCZ696, an ARB
(valsartan) with an endopeptidase inhibitor
(sacubitril), has shown a survival benefit in a large
trial versus ARB alone.
o The drug, referred to as an angiotensin
receptor–neprilysin inhibitor (ARNI) (and
denoted Entrezto), was tested in the
PARADIGM-HF trial as an alternate to
optimally dosed ACEI and demonstrated an
incremental improvement in survival when
compared to ACEI alone.
Most guidelines now advocate switching ACEI to this
drug as a standard in patients with mild-moderate
systolic heart failure when they remain symptomatic
despite fully tolerated doses of conventional therapy.
HEART RATE MODIFICATION
Ivabradine, an inhibitor of the I current in the
sinoatrial node, slows the heart rate without a
negative inotropic effect.
The Systolic Heart Failure Treatment with Ivabradine
Compared with Placebo Trial (SHIFT) was conducted
in patients with class II or III HFrEF, a heart rate >70
beats/min, and history of hospitalization for heart
failure during the previous year.
o Ivabradine reduced hospitalizations and the
combined endpoint of cardiovascular-related
death and heart failure hospitalization.
DIGOXIN
Digitalis glycosides exert a mild inotropic effect,
attenuate carotid sinus baroreceptor activity, and are
sympatho-inhibitory
These effects decrease serum norepinephrine levels,
plasma renin levels, and possibly aldosterone levels.
o The DIG trial demonstrated a reduction in
heart failure hospitalizations in the treatment
group (patients with heart failure and sinus
rhythm) but no reduction in mortality or
improvement in QOL.
o digoxin levels should be checked to minimize
toxicity
o digoxin is now relegated as therapy for
patients who remain profoundly
symptomatic despite optimal neurohormonal
blockade and adequate volume control
ORAL DIURETICS
o often required because of their increased potency,
and frequent dose adjustments may be necessary
because of variable oral absorption and fluctuations
in renal function
o no data suggest that these agents improve survival
CALCIUM CHANNEL ANTAGONISTS
o Amlodipine and felodipine, second-generation
calcium channel–blocking agents, safely and
effectively reduce blood pressure in HFrEF but do
not affect morbidity, mortality, or QOL.
STATINS
o Potent lipid-altering and pleiotropic effects of statins
reduce major cardiovascular events and improve
survival in non–heart failure populations.
o Once heart failure is well established, this therapy
may not be as beneficial and theoretically could
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 even be detrimental by depleting ubiquinone in the
electron transport chain.
o If statins are required to treat progressive coronary
artery disease in the background setting of heart
failure, then they should be employed. However, no
rationale appears to exist for routine statin therapy
in nonischemic heart failure.
ANTICOAGULATION AND ANTIPLATELET
THERAPY
o HFrEF is accompanied by a hypercoagulable state
and therefore a high risk of thromboembolic events,
including stroke, pulmonary embolism, and
peripheral arterial embolism
o data are insufficient to support the use of
warfarin in patients in normal sinus rhythm
without a history of thromboembolic events
or echocardiographic evidence of left
ventricular thrombus.
o A reduced risk of ischemic stroke with
warfarin was offset by an increased risk of
major hemorrhage. Aspirin blunts ACEI-
mediated prostaglandin synthesis, but the
clinical importance of this finding remains
unclear.
FISH OIL
o Treatment with long-chain omega-3 polyunsaturated
fatty acids (ω-3 PUFAs) has been shown to be
associated with modestly improved clinical outcomes
in patients with HFrEF.
MICRONUTRIENTS
o Reversible heart failure has been described as a
consequence of severe thiamine and selenium
deficiency.
o Thiamine deficiency has received attention in heart
failure due to the fact that malnutrition and diuretics
are prime risk factors for thiamine loss.
o Small exploratory randomized studies have
suggested a benefit of supplementation of thiamine
in HFrEF with evidence of improved cardiac function.
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o This finding is restricted to chronic heart
failure states and does not appear to be
beneficial in the ADHF phenotype.
ENHANCED EXTERNAL COUNTERPULSATION
(EECP)
o Peripheral lower extremity therapy using graded
external pneumatic compression at high pressure is
administered in 1-h sessions for 35 treatments (7
weeks) and has been proposed to reduce angina
symptoms and extend time to exercise-induced
ischemia in patients with coronary artery disease.
o The Prospective Evaluation of Enhanced
External Counterpulsation in Congestive
Heart Failure (PEECH) study assessed the
benefits of enhanced external
counterpulsation in the treatment of patients
with mild-to-moderate heart failure.
o This randomized trial improved exercise
tolerance, QOL, and NYHA functional
classification but without an accompanying
increase in peak oxygen consumption.
EXERCISE
o The Heart Failure: A Controlled Trial Investigating
Outcomes of Exercise Training (HF-ACTION) study
investigated short-term (3-month) and long-term
(12-month) effects of a supervised exercise training
program in patients with moderate HFrEF.
o Exercise was safe, improved patients’ sense of well-
being, and correlated with a trend toward mortality
reduction.
o Maximal changes in 6-min walk distance were
evident at 3 months with significant improvements
in cardiopulmonary exercise time and peak oxygen
consumption persisting at 12 months.
o Therefore, exercise training is recommended as an
adjunctive treatment in patients with heart failure.
MANAGING CHF AND COMORBIDITIES
DEPRESSION
o Depression is common in HFrEF, with a reported
prevalence of one in five patients, and is associated
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 with a poor QOL, limited functional status, and
increased risk of morbidity and mortality in this
population.
o However, the largest randomized study of depression
in HFrEF, the Sertraline Against Depression and
Heart Disease in Chronic Heart Failure (SADHART-
CHF) trial, showed that although sertraline was safe,
it did not provide greater reduction in depression or
improve cardiovascular status among patients with
heart failure and depression compared with nurse-
driven multidisciplinary management.
Sleep-disordered breathing is common in HF and
particularly in HFrEF. A range of presentations
exemplified by obstructive sleep apnea, central sleep
apnea, and its extreme form of Cheyne-Stokes
breathing are noted.
o Treatment with nocturnal positive airway
pressure improves oxygenation, and 6-min walk
distance. However, no conclusive data exist to
support this therapy as a disease-modifying
approach with reduction in mortality.
o The recognition that hibernating myocardium,
defined as myocardial tissue with abnormal
function but maintained cellular function, could
recover after revascularization led to the notion
that revascularization with CABG would be useful
in those with living myocardium.
o The Surgical Treatment for Ischemic Heart
Failure (STICH) trial in patients with an ejection
fraction of ≤35% and coronary artery disease
amenable to CABG demonstrated no significant
initial benefit compared to medical therapy.
o However, patients assigned to CABG had lower
rates of death from cardiovascular causes and of
death from any cause or hospitalization for
cardiovascular causes over 10 years than among
those who received medical therapy alone.

DIABETES MELLITUS
o Recently, the drug empagloflozin was tested in
the EMPA-REG study and demonstrated a
decrease in cardiovascular mortality as well as
hospitalizations for heart failure.
o This drug, a sodium–glucose cotransporter 2
(SGLT2), induces an osmotic diuresis as well as
ketosis

NON-PHARMACOLOGIC MANAGEMENT

CARDIAC RESYNCHRONIZATION THERAPY

o Nonsynchronous contraction between the walls
of the left ventricle (intraventricular) or between
the ventricular chambers (interventricular)
impairs systolic function, decreases mechanical
efficiency of contraction, and adversely affects
ventricular filling.
o Mechanical dyssynchrony results in an increase
in wall stress and worsens functional mitral
regurgitation.
o The single most important association of extent
of dyssynchrony is a widened QRS interval on the
surface electrocardiogram, particularly in the
presence of a left bundle branch block pattern.
o With placement of a pacing lead via the coronary
sinus to the lateral wall of the ventricle, cardiac
resynchronization therapy (CRT) enables a more
synchronous ventricular contraction by aligning
the timing of activation of the opposing walls.

SUDDEN CARDIAC DEATH PREVENTION IN

HEART FAILURE
SCD due to ventricular arrhythmias is the mode of
death in approximately half of patients with heart
failure and is particularly proportionally prevalent in
HFrEF patients with early stages of the disease.
o Patients who survive an episode of SCD are
considered to be at very high risk and qualify for
placement of an implantable cardioverter-
defibrillator (ICD).
o Currently, patients with NYHA class II or III
symptoms of heart failure and an LVEF <35%,
irrespective of etiology of heart failure, are
appropriate candidates for ICD prophylactic
therapy. NURSING DIAGNOSES
o In patients with a myocardial infarction and Based on the assessment data, major nursing
optimal medical therapy with residual LVEF diagnoses for the patient with HF may include the
≤30% (even when asymptomatic), placement of following:
an ICD is appropriate.

SURGICAL APPROACH TO CHF

CORONARY ARTERY BYPASS GRAFT (CABG)

o considered in patients with ischemic
cardiomyopathy with multivessel coronary artery
disease.
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COLLEGE OF NURSING 12 Compiled by BJ SORRILLA, R.N., M.D.
 Based on the assessment data, potential complications
that may develop include the following:
1. Cardiogenic shock
2. Dysrhythmias
3. Thromboembolism
4. Pericardial effusion and cardiac tamponade

NURSING MANAGEMENT
1. Keeping an intake and output record to identify
a negative balance (more output than input)
2. Weighing the patient daily at the same time and
on the same scale, usually in the morning after
urination; monitoring for a 2- to 3-lb gain in a
day or 5-lb gain in week
3. Auscultating lung sounds at least daily to detect
an increase or decrease in pulmonary crackles
4. To reduce the risk for hypokalemia, the nurse
advises patients to increase their dietary intake
of potassium. Dried apricots, bananas, beets,
figs, orange or tomato juice, peaches, and
prunes (dried plums), potatoes, raisins, spinach,
squash, and watermelon are good dietary
sources of potassium. An oral potassium
supplement (potassium chloride) may also be
prescribed for patients receiving diuretic
medications. If the patient is at risk for
hyperkalemia, the nurse advises the patient to
avoid the above products, including salt
substitutes.
5. Grapefruit (fresh and juice) is a good dietary
source of potassium but has serious drug–food
interactions. Patients are advised to consult their
physician or pharmacist before including
grapefruit in their diet.
6. Periodic assessment of the patient’s electrolyte
levels will alert health team members to
hypokalemia, hypomagnesemia, and
hyponatremia. Serum levels are assessed
frequently
when the patient starts diuretic therapy and then
usually every 3 to 12 months. It is important to
remember that serum potassium levels do not
always indicate the total amount of potassium
within the body.

CARDIOMYOPATHIES
1. Activity intolerance (or risk for activity
intolerance) related to imbalance between disease of the heart muscle. It is estimated that
oxygen supply and demand because of cardiomyopathy accounts for 5–10% of the heart
decreased CO failure in the 5–6 million patients carrying that
2. Excess fluid volume related to excess fluid or diagnosis in the US
sodium intake and retention of fluid because of ischemic cardiomyopathy is sometimes applied to
HF and its medical therapy describe diffuse dysfunction attributed to multivessel
3. Anxiety related to breathlessness and coronary artery disease, and nonischemic
restlessness from inadequate oxygenation cardiomyopathy to describe cardiomyopathy from
4. Powerlessness related to inability to perform role other causes.
responsibilities because of chronic illness and As of 2013, cardiomyopathies are defined as
hospitalizations “disorders characterized by morphologically and
5. Noncompliance related to lack of knowledge functionally abnormal myocardium in the absence of
any other disease that is sufficient, by itself, to cause
COLLABORATIVE PROBLEMS/ POTENTIAL the observed phenotype.” It was further specified
COMPLICATIONS that many cardiomyopathies will be attributable to
genetic disease.1
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GENERAL PRESENTATION
For all cardiomyopathies, the early symptoms often
relate to exertional intolerance with breathlessness
or fatigue, usually from inadequate cardiac reserve
during exercise.
As fluid retention leads to elevation of resting filling
pressures, shortness of breath may occur during
routine daily activity such as dressing and may
manifest as dyspnea or cough when lying down at
night
All three types of cardiomyopathy can be associated
with atrioventricular (AV) valve regurgitation, typical
and atypical chest pain, atrial and ventricular
tachyarrhythmias, and embolic events

GENETIC CAUSES
Well-recognized in hypertrophic cardiomyopathy,
heritability is also present in at least 30% of dilated
cardiomyopathy (DCM) without other clear etiology.

Careful family history should elicit not only known

cardiomyopathy and heart failure, but also family
members who have had sudden death, often
incorrectly attributed to “a massive heart attack,”
who have had atrial fibrillation or pacemaker
implantation by middle age, or who have muscular
dystrophy.
Most familial cardiomyopathies are inherited in an
autosomal dominant pattern, with occasional
autosomal recessive and X-linked inheritance
Missense mutations with amino acid substitutions are
the most common in cardiomyopathy
defining phenotype of cardiomyopathy is rarely
present at birth and, in some individuals, may never
manifest
Sex appears to play a role, as penetrance and clinical
severity may be greater in men for most
cardiomyopathies.

GENES AND PATHWAYS IN CARDIOMYOPATHIES

The most commonly recognized genetic causes of
DCM are truncating mutations of the giant protein
titin, encoded by TTN, which maintains sarcomere
structure and acts as a key signaling molecule.
cytoskeletal proteins play crucial roles in the
structure, connection, and stability of the myocyte,
multiple defects in these proteins can lead to
cardiomyopathy, usually with a dilated phenotype.
o desmin forms intermediate filaments that
connect the nuclear and plasma membranes,
Z-lines, and the intercalated disks between
muscle cells.
o Desmin mutations impair the transmission of
force and signaling for both cardiac and
skeletal muscle and may cause combined
cardiac and skeletal myopathy.

Defects in the sarcolemmal membrane proteins are

associated with DCM.
o The best known is dystrophin, encoded by
the X chromosome gene DMD, abnormalities
of which cause Duchenne’s and Becker’s
muscle dystrophy.
o abnormal dystrophin can be acquired when
the coxsackie virus cleaves dystrophin
during viral myocarditis. This protein
provides a network that supports the
sarcolemma and also connects to the
sarcomere.
Intercalated disks contribute to intracellular
connections, allowing mechanical and electrical
coupling between cells and also connections to
desmin filaments within the cell.
o Mutations in proteins of the desmosomal
complex compromise attachment of the
myocytes, which can become disconnected
and die, to be replaced by fat and fibrous
tissue.
o These areas are highly arrhythmogenic and
may dilate to form aneurysms. Although
more often noted in the right ventricle
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(arrhythmogenic right ventricular
cardiomyopathy), this condition can affect
both ventricles and has also been termed
“arrhythmogenic cardiomyopathy.”
For any patient with suspected or proven genetic
disease, family members should be considered and
evaluated in a longitudinal fashion.
Screening includes an echocardiogram and
electrocardiogram (ECG)
DILATED CARDIOMYOPATHY (DCM)
An enlarged left ventricle with reduced systolic
function as measured by left ventricular ejection
fraction characterizes DCM
Systolic failure is more prominent than diastolic
dysfunction.
Dynamic remodeling of the interstitial scaffolding
affects diastolic function and the amount of
ventricular dilation. Mitral regurgitation commonly
develops as the valvular apparatus is distorted and
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14 Compiled by BJ SORRILLA, R.N., M.D.

is usually substantial by the time heart failure is
severe.
Even with long-standing disease, some patients have
dramatic improvement to near-normal ejection
fractions during pharmacologic therapy, particularly
notable with the b-adrenergic antagonists coupled
with renin-angiotensin system inhibition.
HYPERTROPHIC CARDIOMYOPATHY
• defined as left ventricular hypertrophy that develops
in the absence of causative hemodynamic factors,
such as hypertension, aortic valve disease, or
systemic infiltrative or storage diseases
• previously been termed hypertrophic obstructive
cardiomyopathy (HOCM), asymmetric septal
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COLLEGE OF NURSING
hypertrophy (ASH), and idiopathic hypertrophic
subaortic stenosis (IHSS).
• the leading cause of sudden death in the young and
is an important cause of heart failure. Although
pediatric presentation is associated with increased
early morbidity and mortality, the prognosis for
patients diagnosed as adults is generally favorable.
• Echocardiographic screening of families revealed an
autosomal dominant pattern of inheritance.
• Initial genetic studies using linkage analysis in large
families identified disease-causing mutations in
sarcomeric genes.
o A sarcomere mutation is present in ~60% of
patients with hyper- trophic cardiomyopathy
and is more common in those with familial
disease and characteristic asymmetric septal
hypertrophy.
o More than nine different sarcomere genes
with >1400 mutations have been implicated,
although ~80% of patients have a mutation
in either MYH7 or MYBPC3
• In MYBPC3 mutation carriers, the average age of
disease development is 40 years, while 30% remain
free from hypertrophy after 70 years.
• HCM is characterized by age-dependent and
incomplete penetrance. The defining phenotype of
left ventricular hypertrophy is rarely present at birth
and usually develops later in life.
PATHOPHYSIOLOGY:
• At the level of the sarcomere, hypertrophic
cardiomyopathy mutations lead to enhanced calcium
sensitivity, maximal force generation, and ATPase
activity. Calcium handling is affected through
modification of regulatory proteins. Sarcomere
mutations lead to abnormal energetics and impaired
relaxation, both directly and as a result of
hypertrophy. Hypertrophic cardiomyopathy is
characterized by misalignment and disarray of the
enlarged myofibrils and myocytes, which can also
occur to a lesser extent in other cardiac diseases.
Although hypertrophy is the defining feature of
hypertrophic cardiomyopathy, fibrosis and
microvascular disease are also present. Interstitial
fibrosis is detectable before overt hypertrophy
develops and likely results from early activation of
profibrotic pathways. In the majority of patients with
overt cardiomyopathy, focal areas of replacement
fibrosis can be readily detected with MRI. These
areas of “scar” may represent substrate for the
development of ventricular arrhythmias.
• Increased thickness and decreased luminal area of
the intramural vessels in hypertrophied myocardium
contribute to microvascular ischemia and angina.
Microinfarction of hypertrophied myocardium is a
hypothesized mechanism for replacement scar
formation.
CRITICAL CARE NURSING (NCM 118)
15 Compiled by BJ SORRILLA, R.N., M.D.
• Macroscopically, hypertrophy is typically manifest as
nonuniform ventricular thickening (Fig. 254-15). The
interventricular septum is the typical location of
maximal hypertrophy, although other patterns of
hypertrophic remodeling include concentric and
midventricular.
• Left ventricular outflow tract obstruction represents
the most common focus of diagnosis and
intervention, although diastolic dysfunction,
myocardial fibrosis, and microvascular ischemia also
contribute to contractile dysfunction and elevated
intracardiac pressures.
• Obstruction is present in ~30% of patients at rest
and can be provoked by exercise in another ~30%.
Systolic obstruction is initiated by drag forces, which
push an anteriorly displaced and enlarged anterior
mitral leaflet into contact with the hypertrophied
ventricular septum.
• Mitral leaflet coaptation may ensue, leading to
posteriorly directed mitral regurgitation. In order to
maintain stroke volume across outflow tract
obstruction, the ventricle generates higher
pressures, leading to higher wall stress and
myocardial oxygen demand.
• Smaller chamber size and increased contractility
exacerbate the severity of obstruction. Conditions of
low preload, such as dehydration, and low afterload,
such as arterial vasodilation, may lead to transient
hypotension and near-syncope.
• The systolic ejection murmur of left ventricular
outflow tract obstruction is harsh and late peaking
and can be enhanced by bedside maneuvers that
diminish ventricular volume and transiently worsen
obstruction, such as standing from a squatting
position or the Valsalva maneuver.
DIAGNOSIS:
• Patients may be diagnosed after undergoing
evaluations triggered by the abnormal physical
findings (murmur) or symptoms of exertional
dyspnea, angina, or syncope.
• Cardiac imaging is central to diagnosis due to the
insensitivity of examination and ECG and the need to
exclude other causes for hyper- trophy.
• The identification of a disease-causing mutation in a
proband can focus family evaluations on mutation
carriers, but this strategy requires a high degree of
certainty that the mutation is truly pathogenic and
not a benign DNA variant.
• Biopsy is not needed to diagnose hypertrophic
cardiomyopathy but can be used to exclude
infiltrative and metabolic diseases.
• Rigorous athletic training (athlete’s heart) may cause
intermediate degrees of physiologic hypertrophy
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COLEGIO SAN AGUSTIN – BACOLOD
COLLEGE OF NURSING
difficult to differentiate from mild hypertrophic
cardiomyopathy.
• Unlike hyper- trophic cardiomyopathy, hypertrophy
in the athlete’s heart regresses with cessation of
training, and is accompanied by supernormal
exercise capacity (VO2max >50 mL/kg per min), mild
ventricular dilation, and normal diastolic function.
TREATMENT
• Management focuses on treatment of symptoms and
prevention of sudden death and stroke
• -Adrenergic blocking agents and L-type calcium
channel blockers (e.g., verapamil) are first-line
agents that reduce the severity of obstruction by
slowing heart rate, enhancing diastolic filling, and
decreasing contractility. Persistent symptoms of
exertional dyspnea or chest pain can sometimes be
controlled with the addition of disopyramide, an
antiarrhythmic agent with potent negative inotropic
properties.
• Patients with or without obstruction may develop
heart failure symptoms due to fluid retention and
require diuretic therapies for venous congestion.
• Severe medically refractory symptoms develop in
~5% of patients, for whom surgical myectomy or
alcohol septal ablation may be effective. Developed
over 50 years ago, surgical myectomy effectively
relieves outflow tract obstruction by excising part of
the septal myocardium involved in the dynamic
obstruction.
• Mitral valve repair or replacement is usually
unnecessary as associated eccentric mitral
regurgitation resolves with myectomy alone. Alcohol
septal ablation in patients with suitable coronary
anatomy can relieve outflow tract obstruction via a
con- trolled infarction of the proximal septum, which
produces simi- lar periprocedural outcomes and
gradient reduction as surgical myomectomy.
o Neither procedure has been shown to
improve outcomes other than symptoms.
o With both procedures, the most common
complication is the development of complete
heart block necessitating permanent pacing.
• Patients with hypertrophic cardiomyopathy have an
increased risk of sudden cardiac death from
ventricular tachyarrhythmias.
• Vigorous physical activity and competitive sport are
prohibited. Factors that increase the risk of sudden
death from a baseline of 0.5% per year are
presented in Table 254-6 below.
• As sudden death has not been reduced by medical or
procedural interventions, an implantable
cardioverter-defibrillator is advised for patients with
two or more risk factors and is advised on a selected
basis for patient with one risk factor.
• Atrial fibrillation is common in patients with
hypertrophic cardiomyopathy and may lead to
hemodynamic deterioration and embolic stroke.
o Rapid ventricular response is poorly
tolerated and may worsen outflow tract
obstruction.
o -Adrenergic blocking agents and L-type
calcium channel blockers slow AV nodal
conduction and improve symptoms;
o cardiac glycosides should be avoided, as
they may increase contractility and worsen
obstruction.
• Symptoms exacerbated by atrial fibrillation may
persist despite adequate rate control due to loss of
AV synchrony and may require restoration of sinus
rhythm.
• Disopyramide and amiodarone are the preferred
antiarrhythmic agents, with radiofrequency ablation
considered for medically refractory cases.
• Anticoagulation to prevent embolic stroke in atrial
fibrillation is recommended.
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16 Compiled by BJ SORRILLA, R.N., M.D.

PROGNOSIS:
• For patients diagnosed as adults, survival is
comparable to an age-matched population without
cardiomyopathy.
• The sudden death risk is <1% per year; however, up
to 1 in 20 patients will progress to overt systolic
dysfunction with a reduced ejection fraction with or
without dilated remodeling (“burned out” or end-
stage hypertrophic cardiomyopathy).
• These patients suffer from low cardiac output and
have a high risk of death from progressive heart
failure and sudden death unless they undergo
cardiac transplantation.
ISCHEMIC HEART DISEASE
• condition in which there is an inadequate supply of
blood and oxygen to a portion of the myocardium; it
typically occurs when there is an imbalance between
myocardial oxygen supply and demand.
• The most common cause of myocardial ischemia is
atherosclerotic disease of an epicardial coronary
artery (or arteries) sufficient to cause a regional
reduction in myocardial blood flow and inadequate
perfusion of the myocardium supplied by the
involved coronary artery.
EPIDEMIOLOGY
• IHD is the most common, serious, chronic, life-
threatening illness in the United States, where 15.5
million persons have IHD, and 3.4 million people
aged ≥40 years have angina pectoris.
• Although there is regional variation, about 4% of the
population has sustained a myocardial infarction.
• Genetic factors, a high-fat and energy-rich diet,
smoking, and a sedentary lifestyle are associated
with the emergence of IHD
• epidemiologic data show a decline in the rate of
deaths due to IHD, about half of which is attributable
to treatments and half to prevention by risk factor
modification.
• Obesity, insulin resistance, and type 2 diabetes
mellitus are increasing and are powerful risk factors
for IHD. These trends are occurring in the general
context of population growth and as a result of the
increase in the average age of the world’s population
• Population subgroups that appear to be particularly
affected are men in South Asian countries, especially
India and the Middle East. In light of the projection
of large increases in IHD throughout the world, IHD
is likely to become the most common cause of death
worldwide by 2020.
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COLLEGE OF NURSING
PATHOPHYSIOLOGY
• In normal conditions, for any given level of a demand
for oxygen, the myocardium will control the supply
of oxygen-rich blood to prevent under- perfusion of
myocytes and the subsequent development of
ischemia and infarction.
• The major determinants of myocardial oxygen
demand (MVO2) are heart rate, myocardial
contractility, and myocardial wall tension (stress).
o An adequate supply of oxygen to the
myocardium requires a satisfactory level of
oxygen-carrying capacity of the blood
(determined by the inspired level of oxygen,
pulmonary function, and hemoglobin
concentration and function) and an adequate
level of coronary blood flow.
• Blood flows through the coronary arteries in a phasic
fashion, with the majority occurring during diastole.
About 75% of the total coronary resistance to flow
occurs across three sets of arteries: (1) large
epicardial arteries (Resistance 1 = R1), (2)
prearteriolar vessels (R2), and (3) arteriolar and
intramyocardial capillary vessels (R3).
o In the absence of significant flow-limiting
atherosclerotic obstructions, R1 is trivial; the
major determinant of coronary resistance is
found in R2 and R3
The normal coronary circulation is dominated and
controlled by the heart’s requirements for oxygen.
This need is met by the ability of the coronary
vascular bed to vary its resistance (and, therefore,
blood flow) considerably while the myocardium
extracts a high and relatively fixed percentage of
oxygen. Normally, intramyocardial resistance
vessels demonstrate a great capacity for dilation (R2
and R3 decrease).
For example, the changing oxygen needs of the heart
with exercise and emotional stress affect coronary
vascular resistance and in this manner regulate the
supply of oxygen and substrate to the myocardium
(metabolic regulation).
The coronary resistance vessels also adapt to
physiologic alterations in blood pressure to maintain
coronary blood flow at levels appropriate to
myocardial needs (autoregulation).
By reducing the lumen of the coronary arteries,
atherosclerosis limits appropriate increases in
perfusion when the demand for flow is augmented,
as occurs during exertion or excitement. When the
luminal reduction is severe, myocardial perfusion in
the basal state is reduced.
Myocardial ischemia also can occur if myocardial
oxygen demands are markedly increased and
particularly when coronary blood flow may be
limited, as occurs in severe left ventricular
hypertrophy (LVH) due to aortic stenosis.
o A reduction in the oxygen-carrying
capacity of the blood, as in extremely
severe anemia or in the presence of
carboxyhemoglobin, rarely causes
myocardial ischemia by itself but may
lower the threshold for ischemia in
patients with moderate coronary
obstruction.
CRITICAL CARE NURSING (NCM 118)
17 Compiled by BJ SORRILLA, R.N., M.D.
CORONARY ATHEROSCLEROSIS in atherosclerosis), pathologic spasm
(Prinzmetal’s angina), or small platelet-
Epicardial coronary arteries are the major site of rich plugs also can upset the critical
atherosclerotic dis- ease. balance between oxygen supply and
The major risk factors for atherosclerosis (high levels demand and thereby precipitate
of plasma low-density lipoprotein [LDL], low plasma myocardial ischemia.
high-density lipoprotein [HDL], cigarette smoking,
hypertension, and diabetes mellitus vary in their
relative impact on disturbing the normal functions of
the vascular endothelium.
These functions include local control of vascular tone,
maintenance of an antithrombotic surface, and
control of inflammatory cell adhesion and diapedesis.
o The loss of these defenses leads to
inappropriate constriction, luminal
thrombus formation, and abnormal
interactions between blood cells,
especially monocytes and platelets, and
the activated vascular endothelium.
Atherosclerosis develops at irregular rates in
different segments of the epicardial coronary tree
and leads eventually to segmental reductions in
cross-sectional area, i.e., plaque formation.
There is also a predilection for atherosclerotic
plaques to develop at sites of increased turbulence
in coronary flow, such as at branch points in the
epicardial arteries.
When a stenosis reduces the diameter of an
epicardial artery by 50%, there is a limitation of the
ability to increase flow to meet increased myocardial
demand.
When the diameter is reduced by ~80%, blood flow
at rest may be reduced, and further minor decreases
in the stenotic orifice area can reduce coronary flow
dramatically to cause myocardial ischemia at rest or
with minimal stress.
Segmental atherosclerotic narrowing of epicardial
coronary arteries is caused most commonly by the
formation of a plaque, which is subject to rupture or
erosion of the cap separating the plaque from the
bloodstream.
Upon exposure of the plaque contents to blood, two
important and interrelated processes are set in
motion: During ischemia, regional disturbances of ventricular
(1) platelets are activated and aggregate, and contractility cause segmental hypokinesia, akinesia,
(2) the coagulation cascade is activated, leading or, in severe cases, bulging (dyskinesia), which can
to deposition of fibrin strands. A thrombus reduce myocardial pump function.
composed of platelet aggregates and fibrin The abrupt development of severe ischemia, as
strands traps red blood cells and can reduce occurs with total or subtotal coronary occlusion, is
coronary blood flow, leading to the clinical associated with almost instantaneous failure of
manifestations of myocardial ischemia. normal muscle relaxation and then contraction. The
Chronic severe coronary narrowing and myocardial relatively poor perfusion of the subendocardium
ischemia frequently are accompanied by the causes more intense ischemia of this portion of the
development of collateral vessels, especially when wall (compared with the subepicardial region).
the narrowing develops gradually. When well Ischemia of large portions of the ventricle causes
developed, such vessels can by themselves provide transient left ventricular (LV) failure, and if the
sufficient blood flow to sustain the viability of the papillary muscle apparatus is involved, mitral
myocardium at rest but not during conditions of regurgitation can occur. When ischemia is transient,
increased demand. it may be associated with angina pectoris; when it is
With progressive worsening of a stenosis in a prolonged, it can lead to myocardial necrosis and
proximal epicardial artery, the distal resistance scarring with or without the clinical picture of acute
vessels (when they function normally) dilate to myocardial infarction
reduce vascular resistance and maintain coronary The normal myocardium metabolizes fatty acids and
blood flow. glucose to carbon dioxide and water. With severe
o A pressure gradient develops across the oxygen deprivation, fatty acids cannot be oxidized,
proximal stenosis, and post-stenotic and glucose is converted to lactate; intracellular pH
pressure falls. When the resistance is reduced, as are the myocardial stores of high-
vessels are maximally dilated, energy phosphates, i.e., ATP and creatine
myocardial blood flow becomes phosphate. Impaired cell membrane function leads
dependent on the pressure in the to the leakage of potassium and the uptake of
coronary artery distal to the obstruction. sodium by myocytes as well as an increase in
o In these circumstances, ischemia, cytosolic calcium. The severity and duration of the
manifest clinically by angina or imbalance between myocardial oxygen supply and
electrocardiographically by ST-segment demand deter- mine whether the damage is
deviation, can be precipitated by reversible (≤20 min for total occlusion in the absence
increases in myocardial oxygen demand of collaterals) or permanent, with subsequent
caused by physical activity, emotional myocardial necrosis (>20 min).
stress, and/or tachycardia. Transient T-wave inversion probably reflects
o Changes in the caliber of the stenosed nontransmural, intramyocardial ischemia; transient
coronary artery resulting from ST-segment depression often reflects patchy
physiologic vasomotion, loss of subendocardial ischemia; and ST-segment elevation
endothelial control of dilation (as occurs is thought to be caused by more severe transmural
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COLLEGE OF NURSING 18 Compiled by BJ SORRILLA, R.N., M.D.
 ischemia. Another important consequence of
myocardial ischemia is electrical instability, which
may lead to isolated ventricular premature beats or
even ventricular tachycardia or ventricular fibrillation
Most patients who die suddenly from IHD do so as a
result of ischemia- induced ventricular
tachyarrhythmias
• Patients with IHD also can present with cardiomegaly
and heart failure secondary to ischemic damage of
the LV myocardium that may have caused no
symptoms before the development of heart failure;
this condition is referred to as ischemic
cardiomyopathy
STABLE ANGINA PECTORIS
This episodic clinical syndrome is due to transient
myocardial ischemia
Males constitute ~70% of all patients with angina
pectoris and an even greater proportion of those
aged <50 years.
HISTORY
The typical patient with angina is a man >50 years
or a woman >60 years of age who complains of
episodes of chest discomfort, usually described as
heaviness, pressure, squeezing, smothering, or
choking and only rarely as frank pain. When the
patient is asked to localize the sensation, he or she
typically places a hand over the sternum, some-
times with a clenched fist, to indicate a squeezing,
central, substernal discomfort (Levine’s sign).
Angina is usually crescendo-decrescendo in nature,
typically lasts 2–5 min, and can radiate to either
shoulder and to both arms (especially the ulnar
surfaces of the forearm and hand). It also can arise
in or radiate to the back, interscapular region, root
of the neck, jaw, teeth, and epigastrium. Angina is
rarely localized below the umbilicus or above the
mandible. A useful finding in assessing a patient with
chest discomfort is the fact that myocardial ischemic
discomfort does not radiate to the trapezius muscles;
that radiation pattern is more typical of pericarditis.
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COLEGIO SAN AGUSTIN – BACOLOD
COLLEGE OF NURSING
• Exertional angina typically is relieved in 1–5 min by
slowing or ceasing activities and even more rapidly
by rest and sublingual nitroglycerin. Indeed, the
diagnosis of angina should be suspect if it does not
respond to the combination of these measures.
Sharp, fleeting chest pain or a prolonged, dull ache
localized to the left submammary area is rarely due
to myocardial ischemia. However, especially in
women and diabetic patients, angina pectoris may be
atypical in location and not strictly related to
provoking factors. In addition, this symptom may
exacerbate and remit over days, weeks, or months.
Its occurrence can be seasonal, occurring more
frequently in the winter in temperate climates.
Anginal “equivalents” are symptoms of myocardial
ischemia other than angina. They include dyspnea,
nausea, fatigue, and faintness and are more common
in the elderly and in diabetic patients.
It is also important to uncover a family history of
premature IHD (<55 years in first-degree male
relatives and <65 in female relatives) and the
presence of diabetes mellitus, hyperlipidemia,
hypertension, cigarette smoking, and other risk
factors for coronary atherosclerosis.
The history of typical angina pectoris establishes the
diagnosis of IHD until proven otherwise. The
coexistence of advanced age, male sex, the
postmenopausal state, and risk factors for
atherosclerosis increase the likelihood of
hemodynamically significant coronary dis- ease. A
particularly challenging problem is the evaluation
and management of patients with persistent
ischemic-type chest discomfort but no flow-limiting
obstructions in their epicardial coronary arteries.
This situation arises more often in women than in
men. Potential etiologies include microvascular
coronary disease (detectable on coronary reactivity
testing in response to vasoactive agents such as
intracoronary adenosine, acetylcholine, and
nitroglycerin) and abnormal cardiac nociception.
Treatment of microvascular coronary disease should
focus on efforts to improve endothelial function,
including nitrates, beta blockers, calcium
antagonists, statins, and angiotensin-converting
enzyme (ACE) inhibitors.
CRITICAL CARE NURSING (NCM 118)
19 Compiled by BJ SORRILLA, R.N., M.D.
PHYSICAL EXAMINATION
• The physical examination is often normal in patients
with stable angina when they are asymptomatic.
However, because of the increased likelihood of IHD
in patients with diabetes and/or peripheral arterial
disease, clinicians should search for evidence of
atherosclerotic disease at other sites, such as an
abdominal aortic aneurysm, carotid arterial bruits,
and diminished arterial pulses in the lower
extremities.
• The physical examination also should include a
search for evidence of risk factors for atherosclerosis
such as xanthelasmas and xanthomas.
Evidence for peripheral arterial disease should be
sought by evaluating the pulse contour at multiple
locations and comparing the blood pressure between
the arms and between the arms and the legs (ankle-
brachial index). Examination of the fundi may reveal
an increased light reflex and arteriovenous nicking as
evidence of hypertension. There also may be signs of
anemia, thyroid disease, and nicotine stains on the
fingertips from cigarette smoking.
Palpation may reveal cardiac enlargement and
abnormal contraction of the cardiac impulse (LV
dyskinesia). Auscultation can uncover arterial bruits,
a third and/or fourth heart sound, and, if acute
ischemia or previous infarction has impaired
papillary muscle function, an apical systolic murmur
due to mitral regurgitation. These auscultatory signs
are best appreciated with the patient in the left
lateral decubitus position.
Tenderness of the chest wall, localization of the
discomfort with a single fingertip on the chest, or
reproduction of the pain with palpation of the chest
makes it unlikely that the pain is caused by
myocardial ischemia. A protuberant abdomen may
indicate that the patient has the metabolic syndrome
and is at increased risk for atherosclerosis.
for IHD and may be useful in therapeutic decision-
making about the initiation of hypolipidemic
treatment. The major benefit of high-sensitivity CRP
is in reclassifying the risk of IHD in patients in the
“intermediate” risk category on the basis of
traditional risk factors.
• ECG: presence of LVH is a significant indication of
increased risk of adverse outcomes from IHD.
Dynamic ST-segment and T-wave changes that
accompany episodes of angina pectoris and
disappear thereafter are more specific.
• STRESS TESTING:
most widely used test for both the diagnosis of IHD
and the estimation of risk and prognosis involves
recording of the 12-lead ECG before, during, and
after exercise, usually on a treadmill
Exercise duration is usually symptom-limited,
and the test is discontinued upon evidence of
chest discomfort, severe shortness of breath,
dizziness, severe fatigue, ST-segment
depression >0.2 mV (2 mm), a fall in systolic
blood pressure >10 mmHg, or the development
of a ventricular tachyarrhythmia.
used to discover any limitation in exercise
performance, detect typical ECG signs of myocardial
ischemia, and establish their relationship to chest
discomfort. The ischemic ST-segment response
generally is defined as flat or downsloping depression
of the ST segment >0.1 mV below baseline (i.e., the
PR segment) and lasting longer than 0.08 s (Fig.
267-2). Upsloping or junctional ST-segment changes
are not considered characteristic of ischemia and do
not constitute a positive test.
A medical professional should be present throughout
the exercise test. It is important to measure total
duration of exercise, the times to the onset of
ischemic ST-segment change and chest discomfort,
the external work performed (generally expressed as
the stage of exercise), and the internal cardiac work
performed, i.e., by the heart rate–blood pressure
product. The depth of the ST-segment depression
and the time needed for recovery of these ECG
changes are also important. Because the risks of
exercise testing are small but real—estimated at one
fatality and two nonfatal complications per 10,000
tests—equipment for resuscitation should be
available.
CARDIAC IMAGING: When the resting ECG is
abnormal (e.g., preexcitation syndrome, >1 mm of
resting ST- segment depression, left bundle branch
block, paced ventricular rhythm), information gained
from an exercise test can be enhanced by stress
myocardial radionuclide perfusion imaging after the
intra- venous administration of thallium-201 or 99m-
technetium sestamibi during exercise (or with
pharmacologic) stress.

DIAGNOSTICS
• urine should be examined for evidence of diabetes
mellitus and renal disease (including
microalbuminuria) since these conditions accelerate
atherosclerosis.
• examination of the blood should include
measurements of lipids (cholesterol—total, LDL,
HDL—and triglycerides), glucose (hemoglobin A1C),
creatinine, hematocrit, and, if indicated based on the
physical examination, thyroid function.
• chest x-ray is important as it may show the
consequences of IHD, i.e., cardiac enlargement,
ventricular aneurysm, or signs of heart failure. These
signs can support the diagnosis of IHD and are
important in assessing the degree of cardiac
damage.
• Evidence exists that an elevated level of high-
sensitivity C-reactive protein (CRP) (specifically,
between 0 and 3 mg/dL) is an independent risk factor
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COLEGIO SAN AGUSTIN – BACOLOD CRITICAL CARE NURSING (NCM 118)
COLLEGE OF NURSING 20 Compiled by BJ SORRILLA, R.N., M.D.
• ECHOCARDIOGRAPHY: used to assess LV function in
patients with chronic stable angina and patients with
a history of a prior myocardial infarction, pathologic
Q waves, or clinical evidence of heart failure. Two-
dimensional echocardiography can assess both
global and regional wall motion abnormalities of the
left ventricle that are transient when due to
ischemia. Stress (exercise or dobutamine)
echocardiography may cause the emergence of
regions of akinesis or dyskinesis that are not present
at rest. Stress echocardiography, like stress
myocardial perfusion imaging, is more sensitive than
exercise electrocardiography in the diagnosis of IHD.
• CORONARY ARTERIOGRAPHY: diagnostic method
outlines the lumina of the coronary arteries and can
be used to detect or exclude serious coronary
obstruction. However, coronary arteriography
provides no information about the arterial wall, and
severe atherosclerosis that does not encroach on the
lumen may go undetected.
• Indicated in (1) patients with chronic stable angina
pectoris who are severely symptomatic despite
medical therapy and are being considered for
revascularization, i.e., a percutaneous coronary
intervention (PCI) or coronary artery bypass grafting
(CABG); (2) patients with troublesome symptoms
that present diagnostic difficulties in whom there is a
need to confirm or rule out the diagnosis of IHD; (3)
patients with known or possible angina pectoris who
have survived cardiac arrest; (4) patients with
angina or evidence of ischemia on noninvasive
testing with clinical or laboratory evidence of
ventricular dysfunction; and (5) patients judged to
be at high risk of sustaining coronary events based
on signs of severe ischemia on noninvasive testing,
regardless of the presence or severity of symptoms
• Angina pectoris of recent onset, unstable angina
(Chap. 268), early postmyocardial infarction angina,
angina that is unresponsive or poorly responsive to
medical therapy, and angina accompanied by
symptoms of congestive heart failure all indicate an
increased risk for adverse coronary events.
• Same is true for the physical signs of heart failure,
episodes of pulmonary edema, transient third heart
sounds, and mitral regurgitation and for
echocardiographic or radio- isotopic (or
roentgenographic) evidence of cardiac enlargement
and reduced (<0.40) ejection fraction.
On cardiac catheterization, elevations of LV end-
diastolic pressure and ventricular volume and
reduced ejection fraction are the most important
signs of LV dysfunction and are associated with a
poor prognosis. Patients with chest discomfort but
normal LV function and normal coronary arteries
have an excellent prognosis. Obstructive lesions of
the left main (>50% luminal diameter) or left
anterior descending coronary artery proximal to the
origin of the first septal artery are associated with a
greater risk than are lesions of the right or left
circumflex coronary artery because of the greater
quantity of myocardium at risk. Atherosclerotic
plaques in epicardial arteries with fissuring or filling
defects indicate increased risk.
The greater the number and severity of risk factors
for coronary atherosclerosis (advanced age [>75
years], hypertension, dyslipidemia, diabetes, morbid
obesity, accompanying peripheral and/or
cerebrovascular disease, previous myocardial
infarction), the worse the prognosis of an angina
patient.

Other conditions warranting CA:

1. Patients with chest discomfort suggestive of angina
pectoris but a negative or nondiagnostic stress test
who require a definitive diagnosis for guiding medical
management, alleviating psychological stress, career
or family planning, or insurance purposes.
2. Patients who have been admitted repeatedly to the
hospital for a suspected acute coronary syndrome,
but in whom this diagnosis has not been established
and in whom the presence or absence of CAD should
be determined.
3. Patients with careers that involve the safety of others
(e.g., pilots, firefighters, police) who have
questionable symptoms or suspicious or positive
noninvasive tests and in whom there are reasonable
doubts about the state of the coronary arteries.
4. Patients with aortic stenosis or hypertrophic
cardiomyopathy and angina in whom the chest pain
could be due to IHD.
5. Male patients >45 years and females >55 years who
are to undergo a cardiac operation such as valve
replacement or repair and who may or may not have
clinical evidence of myocardial ischemia.
6. Patients after myocardial infarction, especially those
who are at high risk after myocardial infarction
because of the recurrence of angina or the presence
of heart failure, frequent ventricular premature con-
tractions, or signs of ischemia on the stress test.
7. Patients with angina pectoris, regardless of severity,
in whom noninvasive testing indicates a high risk of
coronary events (poor exercise performance or
severe ischemia).
8. Patients in whom coronary spasm or another
nonatherosclerotic cause of myocardial ischemia
(e.g., coronary artery anomaly, Kawasaki disease) is
suspected.

PROGNOSIS:
• The principal prognostic indicators in patients known
to have IHD are age, the functional state of the left
ventricle, the location(s) and severity of coronary
artery narrowing, and the severity or activity of
myocardial ischemia.

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COLLEGE OF NURSING 21 Compiled by BJ SORRILLA, R.N., M.D.
A 45-year-old avid jogger who began experiencing
classic substernal chest pressure underwent an
exercise echo study. With exercise the patient’s
heart rate increased from 52 to 153 beats/min. The
left ventricular chamber dilated with exercise, and
the septal and apical portions became akinetic to
dyskinetic (red arrow). These findings are strongly
suggestive of a significant flow-limiting stenosis in
the proximal left anterior descending artery, which
was confirmed at coronary angiography. (Modified
from SD Solomon, in E. Braunwald et al [eds]:
Primary Cardiology, 2nd ed, Philadelphia, Saunders,
2003.)
C. Stress and rest myocardial perfusion single-photon
emission computed tomography images obtained
with 99m-technetium sestamibi in a patient with
chest pain and dyspnea on exertion. The images
demonstrate a medium-size and severe stress
perfusion defect involving the inferolateral and basal
inferior walls, showing nearly complete reversibility,
consistent with moderate ischemia in the right
coronary artery territory (red arrows). (Images
provided by Dr. Marcello Di Carli, Nuclear Medicine
Division, Brigham and Women’s Hospital, Boston,
MA.)
GERONTOLOGIC CONSIDERATIONS:
The older adult with angina may not exhibit a typical
pain profile because of the diminished pain
transmission that can occur with aging. Often the
presenting symptom in older adults is dyspnea.
Sometimes there are no symptoms (“silent” CAD),
making recognition and diagnosis a clinical
challenge. Older patients should be encouraged to
recognize their chest pain–like symptom (e.g.,
weakness) as an indication that they should rest or
take prescribed medications. Pharmacologic stress
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COLEGIO SAN AGUSTIN – BACOLOD
COLLEGE OF NURSING
testing and cardiac catheterization may be used to
diagnose CAD in older patients.
• Medications used to manage angina are given
cautiously in older adults because they are
associated with an increased risk of adverse
reactions (Burchum & Rosenthal, 2016). Invasive
procedures (e.g., PCI) that were once considered too
risky in older adults may be considered; when these
procedures are performed, many older adults benefit
from symptom relief and longer survival (Shan,
Saxena, & McMahon, 2014).
MANAGEMENT
NITROGLYCERIN
• standard treatment for angina pectoris.
• Nitroglycerin is a potent vasodilator that improves
blood flow to the heart muscle and relieves pain.
Nitroglycerin dilates primarily the veins and, to a
lesser extent, the arteries.
• Dilation of the veins causes venous pooling of blood
2069 throughout the body. As a result, less blood
returns to the heart, and filling pressure (preload) is
reduced. If the patient is hypovolemic (does not have
adequate circulating blood volume), the decrease in
filling pressure can cause a significant decrease in
cardiac output and blood pressure (Burchum &
Rosenthal, 2016)
• Nitrates also relax the systemic arteriolar bed,
lowering blood pressure and decreasing afterload.
These effects decrease myocardial oxygen
requirements, bringing about a more favorable
balance between supply and demand.
• Nitroglycerin may be given by several routes:
sublingual tablet or spray, oral capsule, topical
agent, and intravenous (IV) administration.
Sublingual nitroglycerin is generally placed under the
tongue or in the cheek (buccal pouch) and ideally
alleviates the pain of ischemia within 3 minutes.
o Oral preparations and topical patches are
used to provide sustained effects. A regimen
in which the patches are applied in the
morning and removed at bedtime allows for
a nitrate-free period to prevent the
development of tolerance.
o A continuous or intermittent IV infusion of
nitroglycerin may be given to the
hospitalized patient with recurring signs and
symptoms of ischemia or after a
revascularization procedure. The rate of
infusion is titrated to the patient’s pain level
and blood pressure. It usually is not given if
the systolic blood pressure is less than 90
mm Hg.
• Generally, after the patient is symptom-free, the
nitroglycerin may be switched to an oral or topical
preparation within 24 hours. A common adverse
effect of nitroglycerin is headache, which may limit
the use of this drug in some patients.
Self-administration of Nitroglycerin
1. Instruct the patient to make sure that the mouth is
moist, the tongue is still, and saliva is not swallowed
until the nitroglycerin tablet dissolves. If the pain is
severe, the patient can crush the tablet between the
teeth to hasten sublingual absorption.
2. Advise the patient to carry the medication at all times
as a precaution. However, because nitroglycerin is
very unstable, it should be carried securely in its
original container (e.g., capped dark glass bottle);
tablets should never be removed and stored in metal
or plastic pillboxes.
3. Explain that nitroglycerin is volatile and is inactivated
by heat, moisture, air, light, and time. Instruct the
patient to renew the nitroglycerin supply every 6
months.
4. Inform the patient that the medication should be
taken in anticipation of any activity that may produce
pain. Because nitroglycerin increases tolerance for
exercise and stress when taken prophylactically (i.e.,
before angina-producing activity, such as exercise,
CRITICAL CARE NURSING (NCM 118)
22 Compiled by BJ SORRILLA, R.N., M.D.
 stair-climbing, or sexual intercourse), it is best taken
before pain develops.
5. Recommend that the patient note how long it takes
for the nitroglycerin to relieve the discomfort. Advise
the patient that if pain persists after taking three
sublingual tablets at 5-minute intervals, emergency
medical services should be called.
6. Discuss possible side effects of nitroglycerin,
including flushing, throbbing headache, hypotension,
and tachycardia.
7. Advise the patient to sit down for a few minutes when
taking nitroglycerin to avoid hypotension and
syncope.
Beta-Adrenergic Blocking Agents
• Beta-blockers such as metoprolol (Lopressor) reduce
myocardial oxygen consumption by blocking beta-
adrenergic sympathetic stimulation to the heart.
o The result is a reduction in heart rate, slowed
conduction of impulses through the
conduction system, decreased blood
pressure, and reduced myocardial
contractility (force of contraction).
• Because of these effects, beta-blockers balance the
myocardial oxygen needs (demands) and the
amount of oxygen available (supply). This helps
control chest pain and delays the onset of ischemia
during work or exercise. Beta-blockers reduce the
incidence of recurrent angina, infarction, and cardiac
mortality.
• The dose can be titrated to achieve a resting heart
rate of 50 to 60 bpm (Burchum & Rosenthal, 2016)
• Side effects include depressed mood, fatigue,
decreased libido, and dizziness. Patients taking beta-
blockers are cautioned not to stop taking them
abruptly, because angina may worsen and MI may
develop. Beta-blocker therapy should be decreased
gradually over several days before being
discontinued. Patients with diabetes who take beta-
blockers are instructed to monitor their blood glucose
levels as prescribed because beta-blockers can mask
signs of hypoglycemia.
• Beta-blockers that are not cardioselective also affect
the beta-adrenergic receptors in the bronchioles,
causing bronchoconstriction, and therefore are
contraindicated in patients with significant chronic
pulmonary disorders, such as asthma.

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COLLEGE OF NURSING 23 Compiled by BJ SORRILLA, R.N., M.D.