Download Course: Handout Adult CCRN / CCRN-E Certification

Adult CCRN / CCRN-E Certification
Review Course:
Handout
Presented by:
Mary Kay Bader, RN, MSN, CCRN, CNRN, CCNS, FAHA
Suzi Burns, RN, MSN, RRT, CCRN, ACNP, FAAN, FCCM, FAANP
Bobbi Leeper, RN, MN, CCRN, FAHA
Carol A. Rauen, RN, MS, CCNS, CCRN, PCCN
An AACN Critical Care Publication
101 Columbia
Aliso Viejo, CA 92656-1491
2011 American Association of Critical-Care Nurses
©
All rights reserved. AACN grants permission for a single individual to print one copy of
this electronic publication. No additional copies are permitted. No part of this electronic
publication may be reproduced, uploaded, stored in a retrieval system, or transmitted, in
any form or by any means (electronic, photocopying, recording or otherwise) without the
prior written permission of AACN.
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Adult CCRN / CCRN-E Certification
Review Course:
Handout
Overview, Caring Practices,
Behavioral, and Endocrine
Presented by:
Carol A. Rauen, RN, MS, CCNS, CCRN, PCCN
An AACN Critical Care Publication
101 Columbia
Aliso Viejo, CA 92656-1491
2011 American Association of Critical-Care Nurses
©
All rights reserved. AACN grants permission for a single individual to print one copy of
this electronic publication. No additional copies are permitted. No part of this electronic
publication may be reproduced, uploaded, stored in a retrieval system, or transmitted, in
any form or by any means (electronic, photocopying, recording or otherwise) without the
prior written permission of AACN.
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Professional Caring and Ethical Practice
I.
Introduction
A. AACN-CCRN Blueprint
Professional Caring and Ethical Practices……………..
20%
 Advocacy/Moral Agency ………………………………
 Caring Practices……………… ………………………
 Collaboration………………………………………….
 Systems Thinking……………………………………..
 Response to Diversity…………………………………
 Clinical Inquiry……………………………………….
 Facilitation of Learning………………………………
B.
3%
4%
4%
2%
2%
2%
3%
Synergy Model of Certified Practice (taken directly from
AACN web page. Synergy Model Basic Information. (bullets
added for emphasis)
The core concept of the re-conceptualized model of certified practice
- the AACN Synergy Model for Patient Care - is that the needs or
characteristics of patients and families influence and drive the
characteristics or competencies of nurses. Synergy results when the
needs and characteristics of a patient, clinical unit or system are
matched with a nurse’s competencies.
All patients have similar needs and experience these needs across
wide ranges or continuums from health to illness. Logically, the more
compromised patients are, the more severe or complex are their
needs. The dimensions of a nurse's practice are driven by the needs
of a patient and family. This requires nurses to be proficient in the
multiple dimensions of the nursing continuums. When nurse
competencies stem from patient needs and the characteristics of the
nurse and patient synergize, optimal patient outcomes can result.
The AACN Synergy Model and Certification Examinations
The AACN Synergy Model for Patient Care was developed to link
clinical practice with patient outcomes. The integration of the Synergy
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Model into the AACN Certification Corporation credentialing programs
puts an emphasis on the patient, and says to the world that patients
come first. Nurses make a unique contribution to outcomes, quality of
care and containment of costs.
Recognizing the additional components that comprise critical care
nursing, 20% of the CCRN examination is now based on
Advocacy/Moral Agency, Caring Practices, Collaboration, Systems
Thinking, Response to Diversity, Clinical Inquiry and Facilitation of
Learning knowledge and skills. These nursing characteristics are
referred to collectively as "Professional Caring and Ethical Practice."
The remaining 80% of the CCRN examination continues to be based
on clinical judgment.
Since July 1, 1999, the CCRN examination has included the following
component: Professional Caring and Ethical Practice, which is based
on the AACN Synergy Model for Patient Care. Prior to the application
of the Synergy Model framework to the CCRN certification program,
the examination was based solely on clinical judgment. The Synergy
Model, and its incorporation into the CCRN, CCNS and PCCN
exams, is not to have nurses memorize the various patient or nurse
characteristics, or their levels. They are presented here to help you
begin to comprehend the model. Test questions cover application
of the Synergy Model, not its terminology.
1.
Patient Characteristics: Each patient and family, clinical unit
and system is unique, with a varying capacity for health and
vulnerability to illness. Each one brings a set of unique
characteristics to the care situation. These characteristics span
the health-illness continuum.
 Resiliency--the capacity to return to a restorative level of
functioning using compensatory/coping mechanisms; the ability to
bounce back quickly after an insult.
Level 1 - Minimally resilient - Unable to mount a response; failure of
compensatory/coping mechanisms; minimal reserves; brittle
Level 3 - Moderately resilient - Able to mount a moderate response; able to
initiate some degree of compensation; moderate reserves
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Level 5 - Highly resilient - Able to mount and maintain a response; intact
compensatory/coping mechanisms; strong reserves; endurance
 Vulnerability--susceptibility to actual or potential stressors that
may adversely affect patient outcomes.
Level 1 - Highly vulnerable - Susceptible; unprotected, fragile
Level 3 - Moderately vulnerable - Somewhat susceptible;
somewhat protected
Level 5 - Minimally vulnerable - Safe; out of the woods;
protected, not fragile
 Stability--the ability to maintain a steady-state equilibrium.
Level 1 - Minimally stable - Labile; unstable; unresponsive to
therapies; high risk of death
Level 3 - Moderately stable - Able to maintain steady state for
limited period of time; some responsiveness to therapies
Level 5 - Highly stable - Constant; responsive to therapies; low
risk of death
 Complexity--the intricate entanglement of two or more systems
(e.g., body, family, therapies).
Level 1 - Highly complex - Intricate; complex patient/family
dynamics; ambiguous/vague; atypical presentation
Level 3 - Moderately complex - Moderately involved
patient/family dynamics
Level 5 - Minimally complex - Straightforward; routine
patient/family dynamics; simple/clear cut; typical presentation
 Resource Availability--extent of resources (e.g., technical, fiscal,
personal, psychological, and social) the patient/family/community
bring to the situation.
Level 1 - Few resources - Necessary knowledge and skills not
available; necessary financial support not available; minimal
personal/psychological supportive resources; few social
systems resources
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Level 3 - Moderate resources - Limited knowledge and skills
available; limited financial support available; limited
personal/psychological supportive resources; limited social
systems resources
Level 5 - Many resources - Extensive knowledge and skills
available and accessible; financial resources readily
available; strong personal/psychological supportive resources;
strong social systems resources
 Participation in Care--extent to which patient/family engages in
aspects of care.
Level 1 - No participation - Patient and family unable or
unwilling to participate in care
Level 3 - Moderate level of participation - Patient and family
need assistance in care
Level 5 - Full participation - Patient and family fully able to
participate in care
 Participation in Decision-Making--extent to which patient/family
engages in decision-making.
Level 1 - No participation - Patient and family have no capacity
for decision-making; requires surrogacy
Level 3 - Moderate level of participation - Patient and family
have limited capacity; seeks input/advice from others in
decision-making
Level 5 - Full participation - Patient and family have capacity,
and makes decision for self
 Predictability--a characteristic that allows one to expect a certain
course of events or course of illness.
Level 1 - Not predictable - Uncertain; uncommon patient
population/illness; unusual or unexpected course; does not
follow critical pathway, or no critical pathway developed
Level 3 - Moderately predictable - Wavering; occasionally-noted
patient population/illness
Level 5 - Highly predictable - Certain; common patient
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population/illness; usual and expected course; follows critical
pathway
For example:
A healthy, uninsured, 40-year-old woman undergoing a preemployment physical is likely to be: (a) stable (b) not complex
(c) very predictable (d) resilient (e) not vulnerable (f) able to
participate in decision-making and care, but (g) has inadequate
resource availability.
A critically ill infant with multisystem organ failure is likely to be:
(a) unstable (b) highly complex (c) unpredictable (d) highly
resilient (e) vulnerable (f) unable to become involved in
decision-making and care, but (g) has adequate resource
availability.
2.
Nurse Characteristics:
Nurse Competencies of Concern to Patients, Clinical Units
and Systems Nursing care reflects an integration of knowledge,
skills, experience, and attitudes needed to meet the needs of
patients and families. Thus, continuums of nurse characteristics
are derived from patient needs. The following are levels of
expertise ranging from competent (1) to expert (5):
 Clinical Judgment--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 education, experiential knowledge, and evidencebased guidelines.
Level 1 - Collects basic-level data; follows algorithms, decision
trees, and protocols with all populations and is uncomfortable
deviating from them; matches formal knowledge with clinical
events to make decisions; questions the limits of one's ability to
make clinical decisions and delegates the decision-making to
other clinicians; includes extraneous detail
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Level 3 - Collects and interprets complex patient data; makes
clinical judgments based on an immediate grasp of the whole
picture for common or routine patient populations; recognizes
patterns and trends that may predict the direction of illness;
recognizes limits and seeks appropriate help; focuses on key
elements of case, while shorting out extraneous details
Level 5 - Synthesizes and interprets multiple, sometimes
conflicting, sources of data; makes judgment based on an
immediate grasp of the whole picture, unless working with new
patient populations; uses past experiences to anticipate
problems; helps patient and family see the "big picture;"
recognizes the limits of clinical judgment and seeks multidisciplinary collaboration and consultation with comfort;
recognizes and responds to the dynamic situation
 Clinical Inquiry (Innovator/Evaluator)--the ongoing process of
questioning and evaluating practice and providing informed
practice. Creating changes through evidence-based practice,
research utilization and experiential knowledge.
Level 1 - Follows standards and guidelines; implements clinical
changes and research-based practices developed by others;
recognizes the need for further learning to improve patient care;
recognizes obvious changing patient situation (e.g.,
deterioration, crisis); needs and seeks help to identify patient
problem
Level 3 - Questions appropriateness of policies and guidelines;
questions current practice; seeks advice, resources, or
information to improve patient care; begins to compare and
contrast possible alternatives
Level 5 - Improves, deviates from, or individualizes standards
and guidelines for particular patient situations or populations;
questions and/or evaluates current practice based on patients'
responses, review of the literature, research and
education/learning; acquires knowledge and skills needed to
address questions arising in practice and improve patient care;
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(The domains of clinical judgment and clinical inquiry converge
at the expert level; they cannot be separated)
 Facilitation of Learning--the ability to facilitate learning for
patients/families, nursing staff, other members of the healthcare
team, and community. Includes both formal and informal
facilitation of learning.
Level 1 - Follows planned educational programs; sees
patient/family education as a separate task from delivery of
care; provides data without seeking to assess patient's
readiness or understanding; has limited knowledge of the
totality of the educational needs; focuses on a nurse's
perspective; sees the patient as a passive recipient
Level 3 - Adapts planned educational programs; begins to
recognize and integrate different ways of teaching into delivery
of care; incorporates patient's understanding into practice; sees
the overlapping of educational plans from different healthcare
providers' perspectives; begins to see the patient as having
input into goals; begins to see individualism
Level 5 - Creatively modifies or develops patient/family
education programs; integrates patient/family education
throughout delivery of care; evaluates patient's understanding
by observing behavior changes related to learning; is able to
collaborate and incorporate all healthcare providers' and
educational plans into the patient/family educational program;
sets patient-driven goals for education; sees patient/family as
having choices and consequences that are negotiated in
relation to education
 Collaboration--working with others (e.g., patients, families,
healthcare providers) in a way that promotes/encourages each
person's contributions toward achieving optimal/realistic
patient/family goals. Involves intra- and inter-disciplinary work with
colleagues and community.
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Level 1 - Willing to be taught, coached and/or mentored;
participates in team meetings and discussions regarding
patient care and/or practice issues; open to various team
members' contributions
Level 3 - Seeks opportunities to be taught, coached, and/or
mentored; elicits others' advice and perspectives; initiates and
participates in team meetings and discussions regarding
patient care and/or practice issues; recognizes and suggests
various team members' participation
Level 5 - Seeks opportunities to teach, coach, and mentor and
to be taught, coached and mentored; facilitates active
involvement and complementary contributions of others in
team meetings and discussions regarding patient care and/or
practice issues; involves/recruits diverse resources when
appropriate to optimize patient outcomes
 Systems Thinking--body of knowledge and tools that allow the
nurse to manage whatever environmental and system resources
exist for the patient/family and staff, within or across healthcare
and non-healthcare systems.
Level 1 - Uses a limited array of strategies; limited outlook sees the pieces or components; does not recognize
negotiation as an alternative; sees patient and family within the
isolated environment of the unit; sees self as key resource
Level 3 - Develops strategies based on needs and strengths of
patient/family; able to make connections within components;
sees opportunity to negotiate but may not have strategies;
developing a view of the patient/family transition process;
recognizes how to obtain resources beyond self
Level 5 - Develops, integrates, and applies a variety of
strategies that are driven by the needs and strengths of the
patient/family; global or holistic outlook - sees the whole rather
than the pieces; knows when and how to negotiate and
navigate through the system on behalf of patients and families;
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anticipates needs of patients and families as they move
through the healthcare system; utilizes untapped and
alternative resources as necessary
 Advocacy and Moral Agency--working on another's behalf and
representing the concerns of patient/family and nursing staff;
serving as a moral agent in identifying and helping to resolve
ethical and clinical concerns within and outside the clinical setting.
Level 1 - Works on behalf of patient; self assesses personal
values; aware of ethical conflicts/issues that may surface in
clinical setting; makes ethical/moral decisions based on rules;
represents patient when patient cannot represent self; aware of
patients' rights
Level 3 - Works on behalf of patient and family; considers
patient values and incorporates in care, even when differing
from personal values; supports colleagues in ethical and
clinical issues; moral decision-making can deviate from rules;
demonstrates give and take with patient's family, allowing them
to speak/represent themselves when possible; aware of patient
and family rights
Level 5 - Works on behalf of patient, family, and community;
advocates from patient/family perspective, whether similar to or
different from personal values; advocates ethical conflict and
issues from patient/ family perspective; suspends rules - patient
and family drive moral decision-making; empowers the patient
and family to speak for/represent themselves; achieves
mutuality within patient/professional relationships
 Caring Practices--the constellation of nursing activities that create
a compassionate, supportive, and therapeutic environment for
patients and staff, with the aim of promoting comfort and healing
and preventing unnecessary suffering. Includes, but is not limited
to, vigilance, engagement, and responsiveness of caregivers,
including family and healthcare personnel.
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Level 1 - Focuses on the usual and customary needs of the
patient; no anticipation of future needs; bases care on
standards and protocols; maintains a safe physical
environment; acknowledges death as a potential outcome
Level 3 - Responds to subtle patient and family changes;
engages with the patient as a unique patient in a
compassionate manner; recognizes and tailors caring practices
to the individuality of patient and family; domesticates the
patient's and family's environment; recognizes that death may
be an acceptable outcome
Level 5 - Has astute awareness and anticipates patient and
family changes and needs; fully engaged with and sensing how
to stand alongside the patient, family, and community; caring
practices follow the patient and family lead; anticipates hazards
and avoids them, and promotes safety throughout patient's and
family's transitions along the healthcare continuum;
orchestrates the process that ensures patient's/family's comfort
and concerns surrounding issues of death and dying are met
 Response to Diversity- the sensitivity to recognize, appreciate
and incorporate differences into the provision of care. Differences
may include, but are not limited to, cultural differences, spiritual
beliefs, gender, race, ethnicity, lifestyle, socioeconomic status,
age, and values.
Level 1 - Assesses cultural diversity; provides care based on
own belief system; learns the culture of the healthcare
environment
Level 3 -Inquires about cultural differences and considers their
impact on care; accommodates personal and professional
differences in the plan of care; helps patient/family understand
the culture of the healthcare system
Level 5 - Responds to, anticipates, and integrates cultural
differences into patient/family care; appreciates and
incorporates differences, including alternative therapies, into
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care; tailors healthcare culture, to the extent possible, to meet
the diverse needs and strengths of the patient/family
For example:
If the gestalt of a patient were stable but unpredictable, minimally
resilient, and vulnerable, primary competencies of the nurse would be
centered on clinical judgment and caring practices, (which includes
vigilance).
If the gestalt of a patient were vulnerable, unable to participate in
decision-making and care, and inadequate resource availability, the
primary competencies of the nurse would focus on advocacy and
moral agency, collaboration, and systems thinking.
All eight competencies are essential for contemporary nursing
practice, but each assumes more or less importance depending on a
patient’s characteristics.
Synergy results when the needs and characteristics of a patient,
clinical unit or system are matched with a nurse’s competencies.
II.
Practice Questions
1.
Which of the following actions by a nurse might decrease a
patient’s self-esteem?
A. Discussing the negative consequences of the patient’s condition.
B. Requiring the patient to participate in all treatments.
C. Providing opportunities to discuss issues important to the patient.
D. Indicating his or her acceptance of the patient’s condition.
2.
A 22-year-old patient with end-stage liver failure secondary to
Hepatitis C virus has been declared brain dead. The parents
decide to discontinue feedings and donate their daughter’s
organs. In response to the parents’ request, the most
appropriate action by the nurse would be to:
A. Contact the organ procurement agency.
B. Convene a multidisciplinary care conference.
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C. Tell the parents that their daughter’s condition precludes organ
donation.
D. Discontinue feedings per the parents’ request.
3.
A patient in the ICU is confused about time and place, despite
frequent reorientation. For the patient’s safety, the nurse would
initially:
A. Put a vest restraint on the patient.
B. Ask a family member to stay with the patient.
C. Administer a mild sedative.
D. Increase the frequency of observation of the patient.
4.
A patient transferring out of the ICU says, “Why can’t I just stay
a few days longer? I don’t feel strong enough.” Which of the following
is the most appropriate response?
A. “There’s a very sick patient who needs this bed.”
B. “You sound concerned about leaving the ICU.”
C. “Most people do just fine after transfer.”
D. “Your insurance limits the time you can stay in the ICU.”
5.
Six members of a trauma patient’s family arrive at the ICU
asking questions about their loved one’s condition. The nurse’s most
appropriate initial response would be to:
A. Ensure that the chaplain is available.
B. Include the family in patient care.
C. Offer the family a tour of the ICU.
D. Identify a family spokesperson.
6.
A patient’s family expresses anxiety regarding the meaning of
numbers on the patient’s monitor, and asks the nurse for clarification.
The nurse’s most appropriate response would be:
A. “The numbers indicate when the patient is having problems.”
B. “The numbers help us determine the best treatment.”
C. “Which numbers on the monitor concern you?”
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D. “What don’t you understand about the monitor?”
7.
A patient has been waiting in the ICU for 2 months for a heart
transplant. A family member angrily tells the nurse, "This is
hopeless!" the nurse's actions should be based on the knowledge
that:
A. Expressions of frustration are normal and usually require no
nursing intervention.
B. Since expressions of hopelessness may be harmful to the patient,
the family member should be encouraged to keep those statements
out of the patient care area.
C. The integrity of the family system is crucial in the transplant
process.
D. Encouraging discussion of negative emotions can impede their
resolution.
8.
A major trauma victim is transported from a rural hospital. The
patient died prior to the wife's arrival to the ICU. The nurse would
best prepare for the wife's arrival by:
A. Arranging for a physician to speak with her when she enters the
unit.
B. Planning to escort her to the waiting room to await the physician's
arrival.
C. Preparing to give her information about the care her husband
received prior to death.
D. Planning to escort her to the morgue to see her husband.
9.
A patient with Type I insulin-dependent diabetes mellitus is
admitted in diabetic ketoacidosis (DKA). Since admission to the ICU,
the patient’s glucose levels have been in the range of 400 – 500
mg/dl, and regular insulin has been administered on a sliding dosage
scale. Given these findings, the most appropriate initial nursing
intervention is to:
A. Consult with the physician about changing the regimen to regular
insulin via continuous drip.
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B. Arrange for nutritional consult to enhance adherence to ADA diet.
C. Consult with the physician about increasing the maximum dosage
of regular insulin on the sliding scale.
D. Request evaluation by diabetic educator.
10. An AMI patient is in critical condition in the CCU. His significant
other has been at the bedside providing reassurance and support
since his admit 12 hours ago. His estranged wife arrives and
demands that the significant other not be allowed to visit or be given
condition updates. The nurse should:
A. Ask the physician to write an order to allow the significant other to
have visitation privileges.
B. Request a multidisciplinary care conference to discuss visitation
and communication of patient status.
C. Contact the hospital's medical- legal department and request that
the hospital attorney speak to the wife.
D. Encourage the patient to express his desire to spend time with his
significant other to his wife.
11. A nurse is caring for a patient with a T5 spinal cord injury. To
facilitate the patient’s safe transfer to a rehabilitation facility, the nurse
would:
A. Ensure that the patient is functionally independent prior to transfer.
B. Ensure that the patient has bowel and bladder control.
C. Consult with the rehabilitation staff regarding transfer criteria.
D. Request a psychiatric evaluation of the patient’s coping skills.
12. The family of a patient moved to a lower acuity area verbalizes
feelings of mistrust, disappointment and rejection by the ICU staff.
These are signs of:
A. Poor self-esteem.
B. Hopelessness.
C. Transfer anxiety.
D. Powerlessness.
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13. After cardiac surgery, a patient who is a Jehovah’s Witness has
an HCT of 18% and accumulated chest tube drainage of 1800cc in
the first 3 hours. The most appropriate action would be to:
A. Begin continuous-circuit autotransfusion.
B. Administer donated directed PRBCs.
C. Administer donated autologous whole blood.
D. Administer 500cc of albumin.
14. A Russian patient who does not speak or understand English
has just undergone an aortic valve replacement. The nurse notices
he is increasingly restless and splinting his chest with both hands. An
effective means of communication with this patient would be by:
A. Using a letter board.
B. Contacting the patient’s family.
C. Touch and gestures.
D. Using “yes” or “no” questions.
15. When teaching a family member to perform an aspect of patient
care, the nurse understands that family members:
A. Are unaffected by the timing of teaching.
B. Learn best if they perceive a need to learn.
C. Learn best if shown a complex procedure all at once.
D. Learn unrelated tasks first.
16. A blind patient is to be transferred to the neuroscience unit after
unsuccessful thrombolytic therapy for a right middle cerebral artery
stroke. The nurse would prepare the patient for transition by:
A. Offering to answer the patient’s questions about the transfer.
B. Giving the patient a brief, factual introduction to the unit.
C. Providing written materials about the receiving unit to the patient’s
family.
D. Arranging for the patient’s family to tour the receiving unit.
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17. The daughter of a mechanically ventilated patient is to be
taught how to suction. When developing a teaching plan, the nurse
must first:
A. Obtain written information about the procedure.
B. Determine a schedule for demonstrating the technique
C. Assess the knowledge and skills the daughter needs to learn.
D. Encourage the daughter to observe the procedure on other
patients.
18. A physician instructs an orientee to level an ICP transducer to
the Foramen of Magnum. The critical care nurse should:
A. Tell the orientee to level the transducer to the Foramen of Monroe.
B. Help the orientee plan and carry out an appropriate response.
C. Help the orientee identify the correct anatomical landmarks.
D. Reinforce the physician’s instructions to the orientee.
19. To assess discomfort in a patient with chronic dementia, the
nurse should:
A. Consistently use a visual or numerical pain rating scale.
B. Analyze the amount of pain medication given to the patient.
C. Monitor the patient’s behaviors and physiologic data.
D. Speak slowly while looking directly at the patient.
20. A patient with cerebral edema after a subarachnoid
hemorrhage has been ordered nifedipine 10 mg PO q4h. The
patient’s blood pressure is 150/85. How should the nurse respond to
this order?
A. Ask the pharmacist to clarify the order.
B. Discuss the purpose of the order with the physician.
C. Research the indications and safety of nifedipine.
D. Administer the medication to control blood pressure.
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21.
When caring for a 15-year-old patient, the nurse would:
A. Address worries about the future.
B. Use games as a teaching strategy.
C. Encourage the patient to talk about life experiences.
D. Allow the patient’s peers to visit.
22. A patient has just been informed of the diagnosis of liver failure.
Clutching a rosary, the patient says to the nurse, “I am going to die.”
The nurse’s best response would be:
A. “Do you want me to call the chaplain?”
B. “Don’t give up your will to live.”
C. “You think you are going to die?”
D. “Have faith in God’s will.”
23.
Providing culture-specific care includes understanding:
A. That identifying the changes that need to occur, and who will be
involved, is part of developing a therapeutic plan.
B. Health beliefs among members of a cultural group are the same.
C. Delineating standard goals of therapy will help enhance patient
adherence to a therapeutic regimen.
D. Use of non-specific methods will enhance patient problem solving.
24. A patient who does not speak or understand English is admitted
to the ICU. Guidelines for using a translator may include:
A. Having the translator ask questions that you don’t feel comfortable
asking.
B. Standing next to the translator and as close to the patient as
possible.
C. Providing all of the information; then allowing for translation and
asking of questions.
D. Allowing time for the translator to decode the medical jargon used
in the teaching.
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25. You are caring for a patient experiencing a fourth bout of
congestive heart failure. The patient states “I cannot take it anymore.
I wish I could end all of this.” A priority when caring for this patient’s
response to stress is to:
A. Place the patient in a hospital gown or pajamas.
B. Explore suicidal intent with the patient.
C. Manage the patient in a restrictive environment for the first 48
hours.
D. Allow the patient to have only short periods alone once in a safe
environment.
26. An alert patient is emergently intubated during an episode of
pulmonary edema. When family members come to visit the patient,
they cry out, “Talk to me; talk to me!” The nurse should tell the family
that:
A. They must not excite the patient while visiting.
B. Communication is not a priority at this time.
C. The patient is too exhausted to converse with them.
D. The breathing tube temporarily prevents the patient from speaking.
27. The nurse is instructing a patient’s family about the significant
complications of a ventriculoperitoneal shunt. Which of the following
would be most important for the family to report to nursing staff?
A. An increase in temperature to 99 degrees F (37.2 degrees C)
B. A change from alert to drowsy
C. Some loss of short-term memory
D. Redness at the incision site
28. A patient who is stable after AMI is to be transferred from the
ICU to a telemetry unit. The patient’s spouse says, “I don’t want my
spouse moved; it’s too soon.” Discussion with this patient and spouse
should focus on:
A. Improvements in the patient’s condition.
B. Reviewing the acuity of the other patients.
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C. The spouse’s ability to act as caregiver.
D. The contrasting staffing ratios of the units.
29. A teenager post cardiac arrest has a new diagnosis of
hypertrophic cardiomyopathy. The parents are concerned about what
to do if the patient collapses again. The nurse’s best response would
be:
A. “Now that your son has been diagnosed and treated, you need not
worry.”
B. “Would teaching you CPR help ease your anxieties?”
C. “Do you know how to access the EMS system?”
D. “I will have your son’s cardiologist talk to you.”
30. A patient with receptive aphasia and dementia is to be enrolled
in a clinical trial. How should the critical care nurse proceed to ensure
that informed consent is ethically obtained?
A. Involve the patient’s legal guardian in the consent process.
B. Ensure that the investigator is aware of the patient’s condition.
C. Inform the institutional review board (IRB) of the potential risk to
the patient.
D. Obtain a copy of the consent form to place in the patient’s chart.
31. A patient recalls a near-death experience (NDE) that occurred
during resuscitation and wishes to tell the nurse about it. What is the
optimal response by the nurse?
A. Let the patient know that NDE’s are often hallucinations.
B. Compare the patient’s story to the actual resuscitation events.
C. Encourage the patient to describe the NDE to his family.
D. Make time to listen actively while the patient tells the story.
21 | P a g e
REFERENCES
(Rauen updated original list taken from aacn.org)
Alspach, J. Core Curriculum for Critical Care Nursing. Saunders, 2006.
Alspach, J. AACN Certification and Core Review for High Acuity and
Critical Care 6th ed. Saunders (2008)
Antoi-Otong, D. Psychiatric Nursing: Biologic and Behavioral Concepts.
Saunders, 1995.
Barry, P.D. Psychosocial Nursing: Care of the Physically Ill Patients and
Their Families. Lippincott, 1996.
Chulay, M., Burns, S. AACN Essentials of Critical Care Nursing. McGraw
Hill, 2010.
Hickey, J. The Clinical Practice of Neurological and Neurosurgical Nursing.
Lippincott, 1997.
Morton, P., Fontaine, D. Critical Care Nursing: A Holistic Approach. 9th ed.
Lippincot, Williams and Wilkins. 2007
Lipson, et al. Culture and Nursing Care, UCSF Press, 1998.
Thelan, et al. Critical Care Nursing: Diagnosis and Management. Mosby,
2006.
Wirtz, et al. Managing chronic spinal cord injury, Critical Care Nurse, Vol.
16, No. 4.
1. B
2. A
3. D
4. B
5. D
6. C
7. C
8. C
9. A
10. B
22 | P a g e
11.C
12.C
13.A
14.C
15.B
16.B
17.C
18.B
19.C
20.B
21.D
22.C
23.A
24.B
25.B
26.D
27.B
28.A
29.B
30.A
31.D
III.
Caring & Ethical Practices
A.
Ethical Principles
 Patient Autonomy: Self determination, freedom of choice
 Justice: Fair treatment without discrimination
 Veracity: Truth, honesty and integrity
 Fidelity: Obligation to care to the best of ones ability
 Beneficence: Doing good for others
 Non-maleficence: Do no harm
 Paternalism: Deciding what is right (best) for others
B.
Moral Concepts
 Respect for Persons
 Justice
 Values
 Rights
C.
Family Theories
1.
Family Needs: Nancy Molter
 Need for Accurate and Regular Information
 Need to See the Patient
 Need to be Helpful to the Patient
 Need to Understand the Hospital Environment
 Need to Preserve a Reasonable Emotional Balance
 Need to Relive the Incident (common for trauma
families)
 Need for Realistic Hope and Assurance
 Need to Have Personal Needs Met
 Need for Support
 Need to Maintain or Develop Confidence in Care
2.
23 | P a g e
Phases of Family Recovery: Epperson
 High Anxiety
 Denial
 Anger
 Remorse
 Grief
 Reconciliation
24 | P a g e
3.
Functional Coping: Fogerty’s Model
 Family Adapts to Change
 Connectedness is Maintained
 Minimum of Fusion: distance is not used to solve
problems
 Triangling is Discouraged
 Differences are tolerated and encouraged
 Preservation of a positive emotional climate takes
precedence over what “should” be done and what is
“right”
 Members of a family use each other for feedback and
learning, not as the enemy
4.
Dysfunctional Coping
 Prolonged Denial
 Disruption of Family Routines
 Blaming- Increased Conflict
 Dysfunctional Behaviors: agitation, depression,
hostility, guilt, addictions
 Forgetting critical facts or necessary information
 Not Hearing- decreased crisis or non-resolution of
crisis
 Scapegoating – projecting all the problems onto one
family member to relieve the overall anxiety in the
system
 Unhealthy communication patterns: secrets, deception,
double messages, evasiveness
D.
Adult Learning Principles: Malcolm Knowles
 The Need to Know
 The Learner’s Self-Concept
 The Role of Experience
 Readiness to Learn
 Orientation to Learning
 Motivation
E.
Pain
 Definition
“A personal, private sensation of hurt. A harmful stimulus which
signals current or impending tissue damage. A pattern of responses
to protect the organism from harm.” Sternback (1979)
“Pain is whatever the experiencing person says it is and exists
whenever he/she says it does.” McCaffery (1979)

Acute vs. Chronic

Assessment

Treatment
F.
Growth and Development: Erik Erikson’s Stages of Life Cycle
 Trust vs. Mistrust
0-2 yr
Hope
 Autonomy vs. Shame
2-3 yr
Will
 Initiative vs. Guilt
3-6 yr
Purpose
 Industry vs. Inferiority
6-12 yr
Competence
 Identity vs. Role Confusion
13-20yr
Fidelity
 Intimacy vs. Isolation
21-45 yr Love
 Generativity vs. Stagnation
45-65 yr Care
 Ego Integrity vs. Despair
>65 yr
Wisdom
H.
Human Needs: Maslow
 Physiologic
 Safety and Security
 Love and Belonging
 Self-Esteem
 Self-Actualization
25 | P a g e
I.
IV.
Stages of Death & Dying: Elizabeth Kubler-Ross
 Denial or Isolation
 Anger
 Bargaining
 Depression
 Acceptance
Summary
26 | P a g e
Behavioral
I.
Introduction
AACN-CCRN Blueprint 4%
 Abuse/Neglect
 Antisocial Behaviors, Aggression, Violence
 Delirium and Dementia
 Developmental Delays
 Failure to Thrive
 Mood Disorders and Depression
 Substance Dependence (e.g. withdrawal, drug-seeking
behavior, chronic alcohol or drug dependence)
 Suicidal Behavior
AACN Synergy Model Patient Characteristic
 Resiliency
 Vulnerability
 Stability
 Complexity
 Resource Availability
 Participation in Care
 Participation in Decision Making
 Predictability
II.
Assessment
A.
Psychosocial Assessment
 Acute Care Hospitalization is a Potential Crisis for Patient
and Family
 Pre-Existing Mental Health Diagnosis
 Undiagnosed Mental Health Problems
 Pre Hospitalization Coping Skills
 Anxiety Level
 Scope of Control/Powerlessness
 Sources of Support
 Family Stress
27 | P a g e








Cognitive Level
Sleep Deprivation
Pain Level
Grief and Loss
Fear Level
Attention Level
Ability to Retain Information
Physical Symptoms of Mental Stress
B. Growth and Development:
Erik Erikson’s Stages of Life Cycle
 Trust vs. Mistrust
0-2 yr
 Autonomy vs. Shame
2-3 yr
 Initiative vs. Guilt
3-6 yr
 Industry vs. Inferiority
6-12 yr
 Identity vs. Role Confusion
13-20yr
 Intimacy vs. Isolation
21-45 yr
 Generatively vs. Stagnation
45-65 yr
 Ego Integrity vs. Despair
>65 yr
Hope
Will
Purpose
Competence
Fidelity
Love
Care
Wisdom
Human Needs: Maslow
 Physiologic
 Safety and Security
 Love and Belonging
 Self-Esteem
 Self-Actualization
D.
Coping Assessment
1.







28 | P a g e
Functional Coping: Fogerty’s Model
Family Adapts to Change
Connectedness is Maintained
Minimum of Fusion: distance is not used to solve problems
Triangling is Discouraged
Differences are tolerated and encouraged
Preservation of a positive emotional climate takes
precedence over what “should” be done and what is “right”
Members of a family use each other for feedback and
learning, not as the enemy
2.








Dysfunctional Coping
Prolonged Denial
Disruption of Family Routines
Blaming- Increased Conflict
Dysfunctional Behaviors: agitation, depression, hostility,
guilt, addictions
Forgetting critical facts or necessary information
Not Hearing- decreased crisis or non-resolution of crisis
Scapegoating – projecting all the problems onto one family
member to relieve the overall anxiety in the system
Unhealthy communication patterns: secrets, deception,
double messages, evasiveness
III. Delirium
A. Definitions
Delirium
“A sudden, fluctuating, and usually reversible disturbance of
mental function. It is characterized by inability to pay attention,
disorientation, an inability to think clearly, and fluctuations in the
level of alertness”
Merck Manual
“Rapid onset and fluctuating course, the symptoms of delirium
include disturbances in consciousness and attention and
changes in cognition, such as memory deficits or perceptual
disturbances.” American Psychiatric Association DSM-IV
Perceptual changes such as hallucination, illusions and
delusions are not required for the diagnosis of delirium. Not
psychosis and must be assessed on a regular basis.
Dementia
Gradual onset of memory impairment and cognitive
disturbances. Slow steady decline in cognitive function. Can
be organic or metabolic in etiology but typically not reversible
and often not treatable.
29 | P a g e
B.





C.














30 | P a g e
Incidence: (delirium)
20– 50% of All Hospitalized Patients
Undiagnosed in 66-84% of Hospitalized Patients
20-80% Rate in ICU Patients
87% of Ventilated Patients
Associated with Increased Mortality, Morbidity, Hospital Stay
and Over All Costs
Etiologies and Predisposing Factors
Cognitive Impairment
Electrolyte Imbalance
Dehydration
Hyperthermia
Sleep Deprivation
Restraint Use
Medications
Vision and/or Hearing Problems
Infection
Malnutrition
Age >65
Withdraw Syndromes
Acute CNS Problems
History of:
 Depression
 Dementia
 Stroke
 Seizures
 ETOH Abuse
 Medical History of
 Renal Failure
 Liver Failure
 CHF
 HIV
 Endocrine Disorders
B.
Clinical Presentation
 Disorientation/Confusion
 Decreased Attention Span and Ability to Focus
 Hyperactive Type
 Restlessness
 Agitation
 Does Not Follow Commands (leave catheter alone or
in place)
 Wide Mood Swings
 Attempting to Get Out of Bed
 Hypoactive Type (more common, worse outcome)
 Lethargy
 Withdrawal
 Decreased Responsiveness
C.
Treatment Options
Prevention!
Early Identification of Risk Factors
Accurate Assessment/Diagnosis (Delirium Scales)
Treatment/Modification of Risk Factors/Cause
Review all Medications as Possible Cause
Treat Electrolyte and Metabolic Derangements
Non-Pharmacological
 Repeat Orientation
 Sleep Protocol
 Early Mobilization
 Minimal Restraint Use
 Pain Control
 Cognitive Stimulation
 Pharmacological (can cause and/or treat)
 Benzodiazepines
 Narcotics
 Neuroleptics - Haloperidol (FDA approved for
Delirium)
 Antipsychotics







31 | P a g e
IV.
Depression
A.
Definition
An abnormal emotional state characterized by exaggerated
feelings of sadness, melancholy, dejection, worthlessness,
emptiness and hopelessness that are inappropriate and out of
proportion to reality. The overt manifestations, which are
extremely variable, range from a slight lack of motivation and
inability to concentrate to severe physiologic alterations of body
functions and may represent symptoms of variety of mental and
physical conditions, a syndrome of related symptoms
associated with a particular disease, or a specific mental
illness. Mosby’s Medical Dictionary
B.
Etiology and Predisposing Factors
 Fear and Anxiety Related to Current Events/Illness
 Response to Loss and/or Grief and/or Deprivation
 Diminished Self-Esteem
 Guilt – Real or Perceived
 Metabolic Causes
 Electrolyte Imbalances
 Endocrine Dysfunction
 Neurotransmitter Imbalance
 Medication Derived
 Chronic Pain
 Sleep Deprivation
C.
Clinical Presentation
 Agitation  Lethargy
 Inability to Concentrate
 Inability to Focus
 Change in Sleep Patterns
 Severe Fatigue
 Signs of Sadness/Hopelessness
 Thoughts of Death
 Suicide Ideations
32 | P a g e
D.
Treatment Options
 Counseling
 Significant Other Support
 Rule Out Organic/Metabolic Causes
 Antidepressants
V.
Mental Illness
Mental illness might be a chronic comorbidity of the hospitalized
adult. This adds an increase challenge to nursing care requirements
for patients. Informed consent, adherence and patient education are
more difficult if the patient does not have a full concept of reality.
A.
Types of Disorders (DSM IV)
 Psychotic – ex. Schizophrenia
 Personality Disorders – ex. Antisocial, borderline, narcissistic
 Anxiety – ex. panic attacks, phobias, obsessive compulsive
 Developmental/Learning – ex. autism, ADHA, retardation
 Cognitive – ex. dementia and delirium
 Mood – ex. depression
B.
Nursing Priorities
 Identify and seek appropriate and timely psychiatric
assistance
 Safe Environment
 Identify and treat cause (if possible)
 Determine if There is a Risk of Injury
 Orientation
 Assist with
 Crisis Management
 Stress Management
 Coping Skills
 Social Support
 Pharmacological Management- antidepressants,
antipsychotics, antianxiety agents
 Patient/Family/Support System Education
 Discharge Planning
33 | P a g e
VI.
Substance Dependence
A.
Commonly Abused Substances
 Alcohol
 Nicotine
 Narcotics
 Marijuana
 Amphetamines
 Benzodiazepine
 Cocaine
B.
Nursing Care Concerns/Priorities
 Physical and/or Mental Dependence
 Physical and or Mental Withdraw Symptoms
 Assessment of Cause (recreational vs. medical vs. pain
management)
 Current State of Health
 Current Nutritional State
 Pharmacological Considerations i.e. tolerance and cross
tolerance
 Diagnosed or Undiagnosed Mental Health Issues
 Ability for Self Care Post Discharge
 Patient Education and Adherence
 Appropriate Addiction Referral
 Community and Social Support
C.
Alcohol Withdrawal
Autonomic hyperactivity symptoms such as tachycardia,
anxiety/agitation, dysphoric mood, diaphoresis, hypertension,
sleeplessness and fine tremor are common physical findings
when alcohol is abruptly stopped and typically will present
within 2 days of cessation. Nausea, vomiting and hallucination
may also occur.
34 | P a g e
Clinical Presentation for Delirium Tremors (72-96 hr. Post
drink)
 Anxiety and/or Panic Attacks
 Disorientation/Confusion
 Insomnia
 Disorganized Thought Processes
 Visual and/or Auditory Hallucinations or Illusions
 Tactile Hallucinations
 Delirium
 Tachycardia
 Tachypnea
 Fever
 Seizure Activity
Treatment Options
 Anticipate/Prevent – Prophylactic Withdraw Regimen
 Safety Measures for Patient, Family, Staff and Therapeutic
Devices
 Decrease Stimulation
 Utilize Short Directed Conversations
 Nonthreatening and Supportive Approach
 Hydration
 Monitor Vital Signs and LOC
 Medications
 Benzodiazepines (Lorazepam, Diazepam,
Chlordiazeposide, Oxazepam)
 Nutrition Support (MVI, Thiamine, Folate)
 Neuroleptic (Haloperidol) (lacking research but used)
 IV Ethanol
 Propofol (lacking research but used)
D.
35 | P a g e
Sedative Withdrawal
Physical withdraw signs and symptoms similar to ETOH.
Treatment is different and will typically have to continue post
discharge from the critical care setting. The patient is slowly
“weaned” off the drug or transitioned to a longer acting agent
like Chlordiazeposide (Librium) or Diazepam (Valium) and then
tapered off drug.
E.
Opiate Withdrawal
Clinical Presentation
 Yawning
 Extra Fluid Production (Tearing, Rhinorrhea, Diaphoresis)
 Mydriasis and Myalgia
 Tremors
 Abdominal Cramps, Nausea, Vomiting, Diarrhea
 Involuntary Leg Movements (kicking)
 Piloerection
 Muscle Cramping
 Vital Sign Changes: Fever, Hypertension, Tachycardia
Treatment Options
 Methadone – switch to longer acting agent  wean
 Clonidine – block sympathetic hyperactivity
 Buprenorphine – alpha opiate receptor partial agonist
VII. Suicidal Behavior
When a patient is admitted to the ICU with suicidal behavior the
physical needs, hemodynamic instability and organ dysfunction are
typically the primary concern and focus of the health care team. As
soon as the patient is able to participate in counseling/psychotherapy
it should begin. Note that not all suicide attempts are obvious
especially in the elderly and chronically or terminally ill. It is essential
that the family and support system (as always) be included in the
treatment plan. Discussion of overdoses is included in Multisystem.
VIII. Antisocial Behaviors, Aggression and Violence
Aggressive or violent behavior from patients, family members or
hospital staff is a safety concern for everyone in the ICU.
Risk Factors
 High levels of stress with poor coping skills
 Lack of resources
 Mental Illness
 Substance abuse or withdrawal
 Males > Females
36 | P a g e
 History of violent behavior
Clinical Presentation (Warning Signs)
 Not thinking clearly
 Paranoia
 Shouting and Profanity Use
 Agitation, Anxiety, Anger
 Verbal Threats
 Tachycardia
 Tachypnea
 Hypertension
Treatment Options
 Evaluate Medication List and Consider Cause
 Rule Out Organic Cause
 Review History
 Identify Trigger (if any) and Remove
 Decrease Stimulation
 Involve Social Service and Security if Necessary
 Restraints if Needed
 Anxiolytics and Neuroleptics
 SAFETY FIRST
IX.
Summary
37 | P a g e
References
Alspach, J. (2006). Core Curriculum for Critical Care Nursing. AACN &
Saunders
Devlin, J. et al (2008). Assessment of delirium in the intensive care unit:
Nursing practices and perceptions. AJCC;17,6,555-566.
Gagnon, L. (2010). Behavioral Health Emergencies. In Sheehy’s
Emergency Nursing Principles and Practice. Mosby.
Sona, C. (2009). Assessing delirium in the intensive care unit.
CCN;29,2;103–105.
Sweeny, S., et al. (2008). Care of the patient with delirium. AJN:108,5,7275
Truman, B., Ely, W. (2003). Monitoring delirium in critically ill patients:
Using the confusion assessment method for the intensive care unit.
CCN;23:25-35.
Welsh, c. Kurt, H., Hirsch, M., Beebe J. (2009). Substance abuse and
trauma care. In McQuillan, Makic & Whalen ed. Trauma Nursing From
Resuscitation Through Rehabilitation. Saunders.
Mosby’s Dictionary
Merck Manual
APA DMS IV
38 | P a g e
The Body Harmony
Endocrine Disorders & Emergencies
I.
Introduction
Disorders of the Endocrine System are Related to Either an Excess
of a Deficiency of a Specific Hormone or Defect at its Receptor Site.
AACN CCRN Exam Blueprint 5%
 Acute Hypoglycemia
 Diabetes Insipidus (DI)
 Diabetic Ketoacidosis
 Hyperglycemic Hyperosmolar Nonketotic Syndrome (HHNK)
 Syndrome of Inappropriate Secretion of Antidiuretic
Hormone (SIADH)
Every Cell in the Body is Under Endocrine Influence
II.
Acute Complications of Diabetes
 Acute Hypoglycemia
 Diabetic Ketoacidosis
 Hyperglycemia Hyperosmolar Nonketotic Coma
A.
Acute Hypoglycemia
 Serum Glucose < 50mg/dL
 Causes:
 Too Much Insulin
 Not Enough Calories
 Signs & Symptoms
 Tachycardia
  LOC: Irritable, Confused, Unconscious
 Skin: Pale, Cool, Clammy
 Seizures
 Blurred Vision
39 | P a g e
 Treatment
 Give Glucose
 Enteral
 Parental (if SG < 20mg/dL)
 Determine Cause
B.
Diabetic Ketoacidosis (DKA)
 Epidemiology
 Occurs in 2-5% of Type I DM/yr
 Most often precipitated by illness (infection)
 1-10% of DKA victims will die
 Mortality is highest in > 60 yo
 Diagnosis
 Metabolic derangement resulting from
absolute or relative insulin deficiency
 Blood Glucose > 500
 pH < 7.32
 HCO3 < 15mEq/L
 Increase Anion Gap
 + Ketones in Urine
 Azotemia
Anion Gap = Na+ - (Cl- + HC03) Normal 8-16mEq/L
 Signs & Symptoms
 Hypotension
 Tachycardia
 Tachypnea
 Kussmaul’s Respirations
 Decreased Skin Turgor
 Dry Mucous Membranes
 ? Abd Pain, Nausea & Vomiting
40 | P a g e
 Fluid Therapy
 Restore Circulating Volume
 1-2 L of Isotonic Saline in 2 hr
 D5 .45%NS after BS down to 250
 May get 8-10L in 1st 24 hr
 Drug Therapy
 Continuous IV or Bolus Regular Insulin
 Lower 100mg/dl/hr
 Monitor K Levels Carefully
 Bicarbonate for Severe Acidosis
C.
Hyperglycemic Hyperosmolar Nonketotic Coma (HHNK)
A hyperosmolar state from severe hyperglycemia without
ketosis. Predominantly older adults and type II DM.
 Diagnosis
 Glucose > 800mg/dL
 Osmolality > 350mlOsm
 Ketones neg
 pH > 7.3
 Severe Dehydration
 Fluid Therapy
 2 L of Normal Saline in 1 hr
 Followed by Fluid Replacement
 Drug Therapy
 Continuous IV Regular Insulin (10U/hr)
 Monitor K+ closely
III.
Acute Complications of Water Regulation
 Diabetes Insipidus
 Syndrome of Inappropriate ADH
A.
41 | P a g e
Diabetes Insipidus
A Problem of Impaired Conservation of H20 by the Kidneys
 Polyuria
 Low Urine SG
 Hypernatremia
 Fluid Deficit/Dehydration
Neurogenic or Central DI
Lack of ADH from the Hypothalamus or Posterior Pituitary
gland. Normal regulatory mechanisms are not functioning
typically from some type of neuro dysfunction.
 Causes:
 Idiopathic – autoimmune
 Head Trauma
 Hypoxic or Ischemic Encephalopathy
 Surgery (neuro)
Nephrogenic DI
There is ADH but the Kidneys do not respond to the ADH
 Causes:




Osmotic Agents or States
Renal Failure
Decreased Osmotic Pressure
Pregnancy
 DI Signs & Symptoms
 Polyuria
 Polydipsia
 Dehydration/Hypovolemia
 Lab Data
 Plasma Osmolality
 High > 295mOsm/kg (normal 285-300)
 Serum Sodium
 Normal or > 145 mEq/L (normal 135-145)
 Urine Osmolality
 Low, < 250 mOsm/kg (300-1400)
 Urine SG
42 | P a g e
 Low < 1.005 (1.005 – 1.030)
 Treatment:
 Correct the Underlying Cause
 Free Water Replacement
 Neurogenic: ADH Replacement
 Nephrogenic: Thiazide Diuretics
 Nutrition
 Elimination Problems
B.
Syndrome of Inappropriate Antidiruetic Hormone (SIADH)
Too much release of ADH, stimulating the kidneys to retain
water resulting in water intoxication.
 Over Hydration
 Low Serum Osmolality
 Hyponatremia
 Causes:
 Malignancies: Lung, Pancreas, Duodenum, Lymph,
Prostate, Thymus
 Meningitis
 Brain Abscess or Tumors
 Head Injury (Blunt Trauma or Bleeds)
 Mechanical Ventilation
 Drugs (hypoglycemic meds, barbiturates, general
anesthesia, nicotine, chemotherapy agents, MS04,
Thiazide, Hormones, TCD)
 Signs & Syndrome:
 Wt. Gain
 Edema
 Signs of Over Hydration
 Lab Data:
 Plasma Osmolality
 Low < 280mOsm/kg
 Serum Sodium
 Low < 135 mEq/L
43 | P a g e
 Urine Osmolality
 Normal or High > 100 mOsm/kg
 Urine SG
 High > 1.030
 Treatment:
 Correct the Underlying Cause
 Fluid Restriction
 Give Na: Saline, Hypertonic Saline
 Diuretic Tx
IV.
Summary
44 | P a g e
Adult CCRN / CCRN-E Certification
Review Course:
Handout
Gastrointestinal and
Renal (Parts 1 and 2) Systems
Presented by:
Carol A. Rauen, RN, MS, CCNS, CCRN, PCCN
An AACN Critical Care Publication
101 Columbia
Aliso Viejo, CA 92656-1491
2011 American Association of Critical-Care Nurses
©
All rights reserved. AACN grants permission for a single individual to print one copy of
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Gastrointestinal
I.
Introduction
A.
AACN Blueprint: 6%
 Acute Abdominal Trauma
 Acute GI Hemorrhage
 Bowel Infarction/Obstruction/Perforation (e.g. mesenteric
ischemia, adhesions)
 GI Surgeries
 Hepatic Failure/Coma (e.g. portal hypertension, cirrhosis,
esophageal varicies)
 Malnutrition and Malabsorption
 Pancreatitis
B.
Structures/Function/Digestion
 Mouth
 Esophagus
 Stomach
 Small Intestine
 Pancreas
 Gallbladder
 Liver
 Spleen
 Portal Circulation
 Mesentery Circulation
 Large Intestine
 Digestive Hormones
 Digestive Enzymes
C.
Assessment
 Inspection
 Auscultation
 Palpation
 Percussion
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II.
The Hepatic System
A.
Liver Function
 Metabolic Factory & Waste Disposal Plant
 Carbohydrate, Fat & Protein Metabolism
 Production of Bile Salts
 Production of Clotting Factors
 Bilirubin Metabolism
 Detoxification: Nutrients, Drugs, Toxins, Bacteria, Everything
 Vitamin & Mineral Storage:
 Blood Reservoir: 10% of Total Blood Volume
Any time the liver is not functioning normally (hepatitis, cirrhosis, shock liver,
hepatic cancer, biliary duct obstruction, cholecystitis, etc.) many, if not all, of
these essential functions are impaired. Therefore liver dysfunction will impact
multiple bodily functions from wound healing, coagulation, substrate
metabolism to level of consciousness.
B.
Liver Function Tests
1. Serum Proteins:
Total Protein:
Serum Albumin:
Serum Globulins:
6.0 – 8.0 g/dL
3.5 – 5.0 g/dL
2.6 – 4.1g/dL
2. Serum Ammonia: 19 – 60 mcg/dL
3. Bilirubin:
Total Bilirubin:
0.1 – 1.2 mg/dL
Unconjugated Bilirubin:
0.1 – 1.0 mg/dL
Conjugated Bilirubin:
0.1 – 0.2 mg/dL
4. Coagulation Studies
PT, PTT, INR, Bleeding Time, ACT all
indirectly reflect liver function.
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5. Hepatic Enzymes:
ALP
GGT
AST
ALT
C.
42 – 136U/L
Men: 0–85 U/L Women: 0-70 U/L
Men: 15-40 U/L Women: 13-35U/L
Men: 10-55U/L Women: 7-30U/L
Liver Dysfunction and Failure
1.
Pathophysiology
 Liver Tissue (cells) are Destroyed and Replaced with
Fibrotic Tissue
 Functions are Altered
 Organ Changes Shape
 Vascular Flow is Obstructed
 Portal Hypertension
2.
Cirrhosis: A chronic progressive liver disease where
diffuse fibrotic bands of connective tissue, distort the liver’s
normal architecture and functional ability. The liver loses its
ability to regulate fluids, metabolize waste, regulate coagulation
and nutrition.
 Causes
 Alcoholic, Laennec's Portal, or Fatty
 Post Necrotic: Toxic, Nodular, or Post Hepatic
 Biliary: Cholangitic or Obstructive
3.
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Hepatitis: Widespread Inflammation of Liver Cells
 Causes
 Primary Viral – Most Common
 Hepatotoxins – Toxic or Drugs
 Secondary Viral, Low Mortality
Hepatitis Tests:
Serologic Tests for Hepatitis
 Presence of virus RNA or DNA
 Presence of virus antigen(s)
 Presence of anti-virus antibodies
 Presence of specific immunoglobins
 Evidence of liver damage/failure from LFTs
Hepatitis A: Enteral (oral-fecal) transmission with an
incubation period of 2-12wks. Jaundice is an early symptom.
The infection is usually acute and self-limiting. Vaccine
available. Tests: Anti-HAV-IgM, Anti-HAV-IgG. IgM denotes
acute phase of infection, IgG denotes recovery, past infection
or immunity.
Hepatitis B: Parenteral (IV and sexual) transmission with an
incubation period of 6 – 24 weeks. There are acute and chronic
stages to this disease and it is the leading cause of liver
carcinoma. Tests: HBV-DNA, HBsAg, Anti-HBs, HBeAg,
HbcAg, Anti-HBc-IgM, Anti-HBc. HBsAg is the earliest
indicator of HBV infection and is typically present for the first 12
weeks. It if followed by the anti-HBs antibody indicating
recovery or immunity. HBeAg appears during infection and is
present in the chronic carrier state. Anti-HBe denotes recovery.
The Anti-HBc-IgM indicates acute infection and the Anti-HBc
indicates that the individual has been infected and this serum
maker may be present for several years. There is a vaccine
available
Hepatitis C: Parenteral (IV and sexual) transmission with an
incubation period of 2 - 26 weeks. Cirrhosis due to HCV is the
most common reason for liver transplantation. Tests: HCVRNA, Anti-HCV, ALT, liver biopsy. One half of HCV infected
patients will become chronic carriers. High incidence of
cirrhosis and liver cancer from HCV. No vaccine available.
4.
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Clinical Presentation of Liver Dysfunction
a.
Hepatic Encephalopathy: the liver is unable to
perform its detoxification function and toxins build up. Primarily
ammonia causing altered LOC, behavior and motor abilities.
 Clinical Presentation
 Confusion  Coma
 Agitation  Unsafe Behavior
 Asterixis: Flap like Tremor of Hands
 Apraxia: Inability to Perform Purposeful Acts
 Elevated Ammonia
 Common Treatment Modalities
 Limit Protein Intact
 Limit Hepatotoxic Drugs
 Lactulose & Neomycin
 Safe Environment
b.
Malnutrition/Malabsorption: the liver is unable to
perform its function of carbohydrate, protein and fat metabolism. This
leads to malnutrition
 Clinical Presentation
 Common Treatment Modalities
 Need to tx the Cause of Liver Failure
 Parenteral Nutrition
 Limit Protein Intake
 Restrict Fluids
c.
Coagulopathy: the liver is unable to synthesize
fibrinogen, prothrombin and factors V, VII, IX, X, XI, XIII, fibrinolytic
factors and Vit. K. These are needed to maintain the ability to clot.
Platelet aggregation and adhesion are also effected by liver
dysfunction.
 Clinical Presentation
 Bleeding Tendencies
 Nonspecific Bleeding
 Common Treatment Modalities
 Monitor Coagulation Studies and Platelet Ct
 Decrease Bleeding and Bruising Risk
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 Administer Blood Products
d.
Portal Hypertension: increased pressure in the portal
vein occurs secondary to flow obstruction from
inflammation, bands, or fibrotic hepatic tissue. This
retrograde pressure leads to formation of varices in the
esophagus, stomach and rectal vault.
 Clinical Presentation
 Caput Medusae: dilated cutaneous veins
radiating from the umbilical (spider angiomas)
commonly seen in Cirrhosis
 Upper GI Bleeding
 Common Treatment Modalities
 Surgical Shunting
 TIPSS - Transjugular Intrahepatic
Portosytemic Stent Shunt
 Treat Bleeding
 Treat Cause
e.
Hepatorenal Syndrome: a form of pre-renal failure
caused by the liver dysfunction. Mortality of liver failure is very high
once renal failure develops.
 Clinical Presentation
 S&S of Renal Dysfunction
 Common Treatment Modalities
 Maintain Adequate Renal Perfusion
 Restrict Fluids
 Restrict Nephrotoxic Agents
 Continuous Renal Replacement Therapies
f.
Ascites: fluid accumulation in the peritoneal space
secondary to decreased production of albumin, decreased systemic
oncotic pressure, increased hepatic lymph production and increased
capillary permeability. The fluid accumulation impacts the respiratory
(diaphragm) and cardiac (hemodynamic) systems primarily as well as
comfort and body image.
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 Clinical Presentation
 Inc. Abdominal Girth
 Hypotension and Tachycardia
 Dyspnea, Orthopnea, Tachypnea
 S&S of Dehydration
 N&V
 Common Treatment Modalities
 Restrict PO Fluid
 Diuretics (if tolerated hemodynamically)
 Restrict Na
 Respiratory Support
 Paracentesis
 Peritoneovenous Shunt Surgery
g.
Infection: one of the functions of the liver cells (Kuppfer
cells) is to clean the blood of bacteria. With liver failure
this function is not provided and bacteria builds up
(primarily gram negative bugs) in the systemic circulation
increasing the risk of infection.
 Clinical Presentation
 Poor Wound Healing
 Increased Risk of Infection
 Common Treatment Modalities
 Heightened Prevention Measures
 Abx Therapy – w Caution
III.
The Pancreas
A.
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Function
 Endocrine Functions
 Synthesis and Release of Hormones: Glycogen,
Insulin, Gastrin
 Exocrine Functions
 Pancreatic Enzymes Break Down Protein, Starch
and Fat. > 2L/day
 Bicarbonate Raise pH
 PNS, Gastrin and Hormones Regulate Secretions
B.
Pancreatic Enzymes
 Trypsin: Aids in Protein Digestion
 Amylase: Aids in Carbohydrate Digestion
 Lipase: Aids in Fat Digestion
Amylase:
Serum:
Urine:
27 – 131 U/L
P type:
30 – 55%
S type:
45 – 70%
1 – 17 U/hr (need 24 hr urine)
The enzyme amylase comes from the pancreas, the salivary
glands. It is necessary to convert starch to sugar. Amylase had two isoenzymes:
P type from the pancreas and S type from the salivary glands. In addition to
serum levels, Amylase levels can also be measured in urine, ascitic fluid, pleural
effusion and saliva. Serum Amylase is frequently ordered to assess acute
abdominal pain and identify Pancreatitis.
Elevated Amylase:
Acute and chronic pancreatitis, obstruction of pancreatic duct, acute
cholecystitis, pancreatic cancer, alcoholism, medications that cause spasm at the
sphincter of Oddi, biliary tract disease, thiazide diuretic, diagnostic dyes, DKA,
renal failure, BPH, burns and trauma to the pancreas. Parotitis and mumps will
cause an elevation of the total Amylase from the S type increase.
Lipase: 20 – 180 U/L
Lipase is a pancreatic enzyme that is secreted into the duodenum to aid in the
digestion of fat. Lipase breaks down fat into glycerol and fatty acids. Lipase
only comes from the pancreas and therefore is specific to identify pancreatic
disorders. Lipase elevations will occur with pancreatic cancer, acute and
chronic pancreatitis, and obstructions of the pancreatic duct, injury or trauma to
the pancreas, acute cholecystitis and acute renal failure. Lipase will rise with
amylase in pancreatic disorders but the serum lipase elevation occurs later in the
course and remains elevated longer (up to 14 days after acute attack, amylase
only 3 days).
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C.
Acute Pancreatitis
 Pathophysiology
 Auto Digestion
 Tissue Damage
 Fat Necrosis
 Vascular Damage and Hemorrhage
 Increased Capillary Permeability
 Hypotension
 Forms/Types
 Edematous
 Hemorrhagic
 Classifications
 Acute Pancreatitis
 Recurrent Acute
 Recurrent Chronic
 Chronic Pancreatitis
 Cause (blocked enzyme release)
 Alcoholism
 Biliary Stones
 Hyperlipidemia
 Abdominal Trauma
 Infection (bacterial or viral)
 Shock
 Drugs (Most Common: Cyclosporine, Acetaminophen,
Cimetadine, Steroids, Salicylates, Furosemide, Thiazides,
Estrogens)
Necrotizing Pancreatitis
 Clinical Presentation
Cullen’s Sign:
Bluish Discoloration Umbilical
 Pain
Grey Turner’s Sign:
 Low Grade Fever
Bluish Discoloration Flanks
 N&V
 Distended/Tender/Rigid Abd
 Guarding with Rebound Tenderness
 Jaundice
 Hypoactive Bowel Sounds
 Steatorrhea: bulky, pale, foul-smelling stools
 ? Ascites
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 Hypovolemic Shock
 Labs (MOST diagnostic underlined)

 Hypocalcemia (classic sign)

 Low Ca, Mg, K

 Hyperglycemia

 Hyperbilirubinemia

 Hypertriglyceridemia
 Increased BUN & Creatinine 
Elevated Amylase
Elevated Lipase
Elevated LFTs
Elevated WBC
Decreased H/H
? Increased H/H
 Ranson’s Criteria
 On Admission
 Age > 55yr
 WBC > 16,000
 Glucose > 200
 LDH > 350
 AST > 250
During Initial 48 hr
HCT Dec > 10%
BUN > 5
Ca < 8
Pa02 < 60mmHg
Base Def > 4mEq/L
Fluid Seq. > 6L







 Treatment Options
 Fluid Resuscitation
 Rest the Pancreas: NPO, NGT
 Pain Management
 Monitor & Replace Electrolytes
 Tx Multisystem
 Nutritional Support
 Surgery
IV.
Gastrointestinal Bleeding
A.
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Lower GI Bleeding: Not Typically Life Threatening
 Causes
 Diverticulitis
 Angiodysplasia
 Cancer
 Hemorrhoids
 Inflammatory Bowel Disease (Ulcerative Colitis; Crohn's
Disease)
 Bowel Infarction
B.
Upper GI Bleeding
 Causes
 Peptic Ulcer Disease: Duodenal, Gastric and Stomal
ulcers account for 50% bleeding episodes
 Gastritis or Esophagitis
 Esophageal Varices
 Mallory -Weiss Syndrome
 Clinical Presentation
 Hematemesis
 Melona
 PUD
Distended and Tender Bbd
Hyperactive Bowel Sounds
 Hypovolemia
 Shock
 Assessment
 H&H
 Coags & Platelets
 Hemoconcentration
 Elevated BUN
 LFTs
 Endoscopy
 Angiography
 Raionuclide Scans
 Treatment
 NG Decompression/Lavage – Room Temp vs Iced
 Fluid Resuscitation
 Blood Product Admin
 Endoscopic Sclerotherapy
 Pharmacology
 H2 Blockers, Antacids, Proton Pump Inhibitors
 Sucralfate
 Vasopressin: constricts splanchnic inflow to reduce
portal pressure
 Somatostatin and Octreotide: vasoconstricts
splanchnic vessels to decrease blood flow
 Surgery
 Vagotomy and Pyloroplasty
 Oversew Ulcer or Tear
 Total and Subtotal Gastric Resection
 Billroth I: Vagotomy, Antrectomy,
AnastomosisStomach and Duodenum
 Billroth II: Vagotomy, Antrectomy, Anastomosis
Stomach and Jejunum
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 Whipple: Removal of the Distal 3rd of Stomach, Entire
duodenum, Head of Pancreas, Gastrojejunotomy
 Colon Resection
 Bleeding Esophageal Varices
 TIPSS: Transjugular Intrahepatic Portosytemic Stent
Shunt
 Beta Blocker – Decreases Pressure
 Blakemore Tube
 Portal Caval Shunt
V.
Disorders of the Bowel
A.
Bowel Infarction
 Etiology
 Embolic or Thrombotic Occlusion
 Typically from the Superior Mesenteric Artery
 Clinical Presentation
 Severe Epigastric Pain
 Rebound Tenderness
 Guarding and Rigidity
 Stimulated Sympathetic Response from Pain
 Treatment Options
 Angiography to Identify/Confirm Occlusion
 Surgery to Remove Occlusion and Dead Bowel
B.
Bowel Obstruction
 Etiology
 Internal Lumen Obstruction ex. Tumor
 External Lumen Obstruction ex. Adhesions
 Emboli: no blood flow
 Paralytic Ileus
Terms
Strangulated: Obstruction with diminished blood flow
Incarcerated, Volvulus, Herniated: Intestinal loops
over itself creating a closed off section.
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 Clinical Presentation
 Complete vs. Partial
 Distended Edematous Bowel
 Fluid and Electrolytes Leaking from Bowel
 Elevated WBC
 Fever
 Small Intestine
 Acute Pain w Sudden Onset
 N & V (movement on both ends)
 Wave-Like Hyperactive High Pitched Bowel Sounds
 May Have Some Gas or Feces
 Distention (mild)
 Large Intestine
 Slow Onset Pain Progression Mild  Severe, Lower
Abd
 No N & V (nothing moving)
 No Stool
 Low Pitched Bowel Sounds
 Distention (large amount)
 Treatment Options
 Diagnosis Obstruction by Hx, X-Ray, CT, Upper or Lower
Barium Radiology Tests
 Pain Management
 IV Fluids
 Decompress w NG, Rectal or Intestinal Tube
 Abx
 NPO and Time (rest the bowel)
 Surgery
C.
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Perforation/Peritonitis
 Etiology
 Gastric/Intestinal Contents Leak into Peritoneal Cavity
 Ulcer Perforation
 Diverticular Rupture
 Trauma
 Bowel Infarction
 Clinical Presentation
 Infection/Sepsis (all the S&S)
 Sudden Onset of Severe Pain
 Rigid Abdomen w Rebound Tenderness
 Hypoactive Bowel Sounds  No Bowel Sounds
 Treatment Options
 Surgery to Repair Cause & Clean Up
 ABX
 Fluids
 Tx of Sepsis
 Tx of MODS
VI.
GI Surgeries
A.
Types
 Ex lap with Lysis of Adhesions
 Colon Resection
 Colostomy vs Ileostomy
 Esophago-Gastrectomy
 Gastric Bypass
 Splenectomy
 Appendectomy
B.
Care Concerns
 Infection - Leaks
 Sepsis
 Third Spacing/Hypovolemia
 Bleeding
 Electrolyte Imbalance
 Nutrition
 Immobility
 Pain
 Potential for Respiratory Compromise
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VII. Abdominal Trauma
A.
Mechanism of Injury
 Blunt Trauma
 MVC
 Falls
 Assaults
 Crush
 Sports
 Penetrating Trauma
 GSW
 Stabbings
 Impalements
B.
Types of Injuries
 Organ Contusions
 Organ Laceration
 Spleen Common Site of Injury
 Solid Organs vs. Hallow Organs
 Crush w Tissue Damage
 Vascular Injury
 Hypoperfusion
 Hemorrhage
C.
Assessment
 Abdominal Exam
 Pain/Tenderness
 Firmness
 Discoloration
 Bowel Sounds
 Abdominal Sonogram
 CT
 Diagnostic Peritoneal Lavage
 Labs
 X-Ray
 Cullen’s Sign: Hemorrhagic Patches (bruising) Around the
Umbilicus (pancreatitis, GI Hemorrhage, ruptured ectopic
pregnancy)
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 Grey Turner’s Sign: Bruising Around the Flank Area
(Hemorrhagic Pancreatitis, Retroperitoneal Bleeding)
 Kehr’s Sign: Left Shoulder Pain from Irritation to the
Diaphragm From Blood as a Result of Splenic Rupture. Best
Elicited with patient Lying Flat or in Trendelenburg’s
Position.
 Abdominal Compartment Syndrome
D.
VIII.
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Treatment
 Fluid Resuscitation
 Diagnose Problem
 Plug Holes and/or Repair Lacerations
 Support Damaged Organ(s)
 Remove Damaged Tissue/Organ(s)
 Post Tx Concerns
 Infection/Sepsis
 Hemodynamic Status
 Organ Function
 ARDS, ATN, MODS
Summary
RENAL
I.
INTRODUCTION
AACN-CCRN Blueprint 6%
 Acute Renal Failure
 Chronic Renal Failure
 Life-Threatening Electrolyte Imbalance
II.
RENAL PHYSIOLOGY
Major Functions of the Kidney
1.
Excretion of Metabolic Wastes
2.
Urine Formation
3.
Acid-Base Balance Regulation
4.
Electrolyte Regulation
5.
Fluid Regulation
6.
Blood Pressure Regulation
7.
Erythropoietin Secretion/Anemia Regulation
Renal Assessment
1. Blood Work
 Blood Urea Nitrogen
 Creatinine
 Serum Electrolytes
 Hgb & Hct
 Serum Albumin
 Serum Osmolality
2. Urine Assessment
 Volume & Concentration
 Urinalysis (see table)
 Renal Clearance Studies
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3. Other Tests
 KUB X-ray
 Renal Arteriography
 IVP
 CT
 Ultrasound
 Biopsy
III.
CHRONIC RENAL FAILURE:
Acute renal failure affects many body systems.
Chronic renal failure affects EVERY body system.
Chronic renal failure (CRF) is a permanent, irreversible condition in which
the kidneys cease to remove metabolic wastes and excessive water from
the blood. (ESRF, ESRD, CRD, CKD)
 Etiology - more than 100 different diseases can cause
RF
 Glomerular Disease
 Tubular Diseases
 Vascular Kidney Diseases
 Urinary Tract Disease
 Infection (kidney)
 Systemic Vascular Diseases
 Metabolic Diseases
 Connective Tissue Diseases
A.
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Terms
1. Azotemia – Nitrogenous Waste Products in the Bloodstream
2. Uremic Syndrome – Systemic and Laboratory Manifestations
of ESRD
3. Renal Replacement Therapy – Treatment Options
B. Stages of Renal Failure
1. Diminished Renal Reserve
2. Renal Insufficiency
3. End Stage Renal Disease (ESRD) – Affects every system in the
body
C.
IV.
Treatment: Renal Replacement Therapies
 Medications
 Hemodialysis
 Peritoneal Dialysis
 Renal Transplant
ACUTE RENAL FAILURE:
A. Pathophysiology: a sudden deterioration in renal function usually
associated with the loss of the kidney’s ability to concentrated urine,
as well as the retention and accumulation of nitrogen wastes.
 Decreased Glomerular Filtration Rate
 Interstitial Inflammatory Changes
 Tubular Lumen Obstruction
 Oliguric, < 400 mL/day
 Non-Oliguric, Large Amt of Dilute Urine
B. Common Etiologies
 Severe Hypotension (all forms of shock)
 Heart Failure
 Dehydration
 Nephrotoxic Agents
 Complication of Infection
 Severe Hypertension
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Category
Cause/Conditions
Volume: Dehydration
Pre Renal
The problem is not actually with the
kidneys but with perfusion (blood flow)
to the kidneys
Ischemia: hypovolemic shock, cardiogenic
shock, septic shock, hypoxemia, low cardiac
output, heart failure, severe hypertension
Hemodynamic instability, multisystem organ
failure, trauma
Urethral: Stricture, Prostatic Hypertrophy
Post Renal
The problem is not actually with the
kidneys but after the kidneys.
Urethral: fibrosis, calculi, blood clots
Bladder: neurogenic problems,
neoplasms/cancer, obstruction
Trauma
Renal
The problem is in the kidney itself
effecting function. Kidney diseases
Glomerulus: acute glomerulonephritis, acute
cortical necrosis, hepatorenal syndrome
Tubule: acute tubular necrosis, acute
pyelonephritis
Nephrotoxins: heavy metals, antibiotics,
radiographic contrast media, anesthetics
Pigments: hemoglobin, myoglobin
Trauma, intravenous hemolysis,
rhabdomyolysis
C. Differentiating Pre-Renal From Renal Diagnosis for ATN
Assessment
Pre-Renal
Renal
(Hypoperfusion) (Tissue Damage)
Urinary Sodium
< 20mEq/L
> 20 mEq/L
BUN:Creatinine Ratio
> 20:1
10-20:1 (normal)
Responds (increase in
Positive
No Response
UO) to volume or
Response
diuretics
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D.
Phases of ARF
 Onset Phase
 BUN & Creatinine Rising
 Urine Output Dropping
 Diuretics Still Working
 Acidosis Beginning
 Oliguric Phase
 Alteration in Electrolyte Balance
 Potential for Infection
 Alteration in A-B Balance
 Alteration in Nutrition Status
 Uremic Syndrome
 Alteration in Pulmonary Status
 Alteration in GI Function
 Diuretic Phase
 Fluid Loss
 Goal is to maintain adequate fluid balance and
regulate electrolytes
 Alteration in Electrolytes
 Recovery Phase
 Goal is Supportive Care
 Prevent Further Insults
 Assessment of Renal Function
 Keep patient well hydrated and free from infection
 Prevent Further Insults
E.
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Systemic Response to Acute Failure
 Hypertension
 Tachycardia
 Decreased UO
 Lethargy
 Pulmonary Edema
 Depends on Type
 Very Similar to Chronic RF
F.
Nursing Care Needs
 Ensure Hydration
 Fluid Challenges
 Diuretics
 Monitor Fluid Status
 Weigh Daily & I & O
 Monitor Electrolyte Imbalance
 Support Renal Function
G.
Treatment Options/Alternatives
 Drug Therapy
 Diet Therapy
 Renal Replacement Therapies (CVVH, Hemodialysis,
Peritoneal Dialysis)
 Renal Transplant
H.
Support Therapy for ATN
Pt Problem
Treatment
Extracellular Volume
Restrict NaCl and H20
Overload
Diuretics
Dialysis
Hyponatremia
Restrict Oral H20
Restrict Hypotonic IV Solutions
Hyperkalemia
Restrict K intake
Dialysis
K Binding Resins
Glucose/Insulin
Eliminate K Supplements NaBicarb Ca
Gluconate
Metabolic Acidosis
Na Bicarb
Dialysis
Hyperphosphatemia
Hypocalcemia
Hypermagnesemia
Nutrition
Drug Dosage
67 | P a g e
Restrict PHO4
Dialysis
Phosphate Binding Agents
Calcium Carbonate
Calcium Gluconate
Phosphate Binding Agents
Dialysis
D/C Mg Containing Antacids
Dialysis
High Protein
Enteral or Parental Nutrition
Adjust Doses Around GFR
Avoid NSAIDS, ACE I, Dye, Nephrotoxic Abx
V.
Renal Replacement Therapies
Goal – to remove body waste and fluids in the presence of acute
or chronic renal failure
A. Terms –
 Diffusion: movement of particles from an area of greater
to an area of lesser concentration. During dialysis
diffusion results in the movement of urea, creatinine, and
uric acid from the patient’s blood in the dialysate
 Osmosis: the movement of water across a semipermeable membrane from an area of lesser to an area of
greater concentration (osmolality) of particles. During
dialysis osmosis results in extra fluid from the patient
being removed.
 Ultrafiltration: the movement of fluid across a semipermeable membrane as a result of an artificially created
pressure gradient. More efficient than osmosis for the
removal of water.
 Dialysis: involves the movement of fluid and particles
across a semipermeable membrane. It is a treatment that
can help restore fluid and electrolyte balance, control
acid-base balance, and remove waste and toxic material
from the body. It can sustain life successfully in both
acute and chronic situation where substitution for or
augmentation of normal renal function is needed.
B. Insurance Coverage – in 1972 the Congress enacted
legislation that provides for people with ESRD to receive
Medicare regardless of age. This is not true in all countries.
68 | P a g e
HEMODIALYSIS
Goal – involves shunting the patient’s blood from the body through
a dialyzer in which diffusion and ultrafiltration occur and then back
into the patient’s circulation. Requires access to the pt’s blood, a
mechanism to transport the blood to and from the dialyzer (where
exchange of fluid, electrolytes, and waste products occur). HD
can be used in the treatment of acute and chronic renal failure
Access – five different types of access can be used
 Arteriovenous Fistula
 Arteriovenous Graft
 External Arteriovenous Shunt
 Femoral Vein Catheterization
 Subclavian Vein Catheterization
Contraindications - Causes rapid fluid shifts
 Labile Cardiovascular States
 Recent MI
 Hypotension
Complications
 Hypotension
 Air Embolism
 Arrhythmias
 Infection
 Disequilibrium Syndrome -Rapid shifts in osmolality
between cerebral spinal fluid and blood can lead to
cerebral edema
 Coagulopathies - Heparin used during dialysis to
prevent clotting of blood outside of body
Chronic Care Needs –
 Patients are typically hemodialyzed 2-3 times a week for
2-4 hours
 Require many medication
 Encounter multiple acute and chronic health risks as a
result of the renal failure and dialysis
 Have dietary and fluid restrictions
 Safety concerns regarding access sites
 Assessment requirements for access sites
69 | P a g e
PERITONEAL DIALYSIS
Goal – The goal is the same as above but a machine is not used
to perform the “cleaning of the blood.” The dialyzing fluid is
instilled into the peritoneal cavity, and the peritoneum becomes
the dialyzing membrane. PD is used for acute and chronic renal
failure and can be done in the hospital or at home.
Access – an abd catheter is inserted into the peritoneal space. In
chronic use this catheter remains in place permanently and only
changed periodically should problems arise.
Procedure – Approximately 2 liters of sterile dialysate is instilled
into the peritoneal cavity and allowed to dwell for a period of time.
During this time osmosis and diffusion of particles takes place.
The catheter is then reopened and the fluid is drained from the
patient (entire process is called an exchange). This process is
done repeated during a 24 hr period.
Contraindications
 Peritonitis
 Abdominal Surgery
 Abdominal Adhesions
 Pregnancy
Complications
 Peritonitis
 Respiratory Distress
Chronic Care Needs – PD can be done independently at home
and the individual can lead a fairly normal schedule. Not as many
risks as
HD. Most common problem is infection of abd catheter.
 Continuous ambulatory peritoneal dialysis (CAPD) – 4 –5
exchanges are done a day.
 Continuous cyclic peritoneal dialysis (CCPD) –
exchanges are done with the use of a machine to control
the infusion, dwell and drain times and patients can set up
before going to sleep and have their PD occur
automatically whale they sleep. They are completely
independent the rest of the day.
70 | P a g e
CONTINUOUS RENAL REPLACEMENT THERAPY
Goal - CRRT provides continuous ultrafiltration of extracellular
fluid and clearance of uremic toxins. Only done in the critical care
setting.
Access – Arterial and venous cannulation sites are required or
two venous cannulation.
Procedure – the blood leaves the patient and flow through a
hemofilter where the ultrafiltration takes place and removal of
water and waste (collected into standard urine bag) and then the
blood is returned to the patient via the venous access. The flow
gradient to move the blood through the filter is the patient’s own
blood pressure. There are several types of processes that are
used in the critical care setting for CRRT. Not necessary to learn
this year. It will be covered in your acute care course next fall.
Contraindications:
 Inability to tolerate extracorporeal circulation
 Hypercoagulability
 Inability to tolerate anti-coagulation therapy (heparin)
 Fluid, electrolyte and acid-base shifts are less severe
than with hemodialysis and usually better tolerated
Complications
 Fluid Imbalance - Hypo/Hypervolemia (Depends on
ultrafiltration rate and intravascular volume requirements)
 Electrolyte Imbalance - Hypokalemia, Hyponatremia,
Hypocalcemia, and Hypomagnesaemia
 Metabolic Acidosis - Bicarbonate readily removed
 Drug removal - Potential for removing most drugs
 Hemorrhage - Heparin used as blood leaves body to
prevent coagulation
 Thrombosis/Infection
 Hypo/Hyperthermia
VI.
RENAL TRANSPLANTATION
71 | P a g e
VII.
SUMMARY
72 | P a g e
Adult CCRN / CCRN-E Certification
Review Course:
Handout
Renal, Part 2
Presented by:
Carol A. Rauen, RN, MS, CCNS, CCRN, PCCN
An AACN Critical Care Publication
101 Columbia
Aliso Viejo, CA 92656-1491
2011 American Association of Critical-Care Nurses
©
All rights reserved. AACN grants permission for a single individual to print one copy of
this electronic publication. No additional copies are permitted. No part of this electronic
publication may be reproduced, uploaded, stored in a retrieval system, or transmitted, in
any form or by any means (electronic, photocopying, recording or otherwise) without the
prior written permission of AACN.
73 | P a g e
Electrolyte
Disturbances
I.
INTRODUCTION
Fluid and electrolyte monitoring are an essential
component of patient assessment. These factors regulate
most physiological functions and the acid-base balance.
II.
PHYSIOLOGIC FLUID BALANCE
A. Total Body Water – 60% of body weight (approximately 40L)
1. Intracellular – 67% of total body H20
a. Primarily made up of intracellular electrolytes
2. Extracellular – 33% of total body H20
a. Plasma Water – 8%, Water, proteins and lipids
b. Interstitial Fluid & Lymph – 20%, Fluid bathing the cells
c. Transcellular Fluid – 7%, Pleural, pericardial, peritoneal,
synovial and fluids in secretions (GI, respiratory, salivary)
B. Osmolarity – the concentration of particles within a solution
1. Plasma osmolarity avg. 290 + 5 mOsm/kg
Na is the primary regulator of extracellular osmolarity
K is the primary regulator of intracellular osmolarity
2. Calculated osmolarity = 2(Na) + BG + BUN
18
2.8
III. ELECTROLYTE BALANCE
A. Physiology:
Electrolytes are particles or solutes found throughout the body in
fluids. They carry an electrical charge and are essential for fluid and
acid base balance within the body. The cations (positively charged
ions) are sodium (Na+), potassium (K+), magnesium (Mg++), and
74 | P a g e
calcium (Ca++). The anions (negatively charged ions) are chloride (Cl), bicarbonate (HCO3-), sulfate (SO4=), and phosphate (PO4-).
The four major functions of electrolytes are:
1. Regulate Acid Base Balance
2. Maintain Fluid Balance and Osmolarity
3. Distribute the Body Fluid and H20 Between the Compartments
4. Promote Neuromuscular Function/Irritability
B. Distribution:
Electrolytes are found in the intracellular and extracellular fluid. They
are concentrated in one of these two compartments and exert osmotic
properties within that compartment. Electrolytes help to maintain
total body fluid balance and also help to regulate fluid movement in
and out of the cell. For example K+ is the major intracellular ion and
Na+ is the major extracellular ion and they each play a significant role
in maintaining homeostasis within each of their compartments. Each
electrolyte serves a unique physiologic function and concentrations
above or below the “normal” range can affect homeostasis or specific
organ function detrimentally.
ELECTROLYTE or
COMPOUND
PRIMARY
COMPARTMENT
EXTRACELLULAR
CONCENTRATION
(plasma or intravascular)
Sodium (Na+)
Extracellular
135 – 146 mEq/L
10 – 15 mEq/L
Potassium (K+)
Intracellular
3.5 – 5.5 mEq/L
140 - 150 mEq/L
Calcium (Ca++)
Extracellular
0 - 2 mg/dL
Magnesium (Mg++)
Intracellular
T 8.5 – 10.5 mg/dL
I 4.0 – 5.0 mg/dL
1.5 – 2.5 mEq/L
Phosphate (PH04=)
Intracellular
100 mEq/L
Chloride (Cl-)
Bicarbonate (HC03-)
or Serum C02
Extracellular
Extracellular
2.5 – 4.5 mg/dL
1.7 – 2.6 mEq/L
96 – 109 mEq/L
22 – 26 mEq/L
C.
INTRACELLULAR
CONCENTRATION
30 – 40 mEq/L
1 – 4 mEq/L
4 – 10 mEq/L
Sodium: Na+ 135 – 146 mEq/L
1. Function: Sodium is the major extracellular cation. Its osmotic
properties make it very important in both fluid and acid-base balance
within the body. There is a close relationship between water and
75 | P a g e
sodium. Sodium is also essential for physiologic activities, the active
and passive transport mechanism across the cell membrane and
intracellular metabolism.
2. Hyponatremia: Na+ < 135 mEq/L
Causes - Fluid Excess or Sodium Deficit:
thiazide diuretics, decreased Na+ dietary intake, vomiting, diarrhea,
SIADH, adrenal insufficiency, NG suctioning, profuse diaphoresis,
draining fistulas, overhydration, congested heart failure, renal failure,
salt-losing nephritis, liver failure, hyperglycemia (osmotic diuresis)
Signs & Symptoms: muscle weakness, headache, fatigue, apathy,
malaise, orthostatic hypotension, poor skin turgor, wt. loss, nausea,
anorexia, vomiting, decreased CVP, abdominal cramps, seizures,
respiratory distress, confusion up to coma.
Treatment: oral or IV replacement of sodium. 0.9% Sodium Chloride
or Lactated Ringer‟s solutions. Hypertonic Saline can be used for
emergency situations.
Clinical Pearl
Hyponatremia is the most frequent electrolyte imbalance seen in
hospitalized patients.
3.
Hypernatremia: Na+ > 146 mEq/L
Cause: Fluid Deficit or Sodium Excess:
excess dietary intake, mineral corticoids, excessive adrencorticord
secretions, diabetes insipidus, strict fluid restrictions, hypothalamic
dysfunction, osmotic diuretics, hypercalcemia or hypokalemia,
excessive IV infusion of sodium chloride solutions, pregnancy.
Signs & Symptoms: muscle weakness, restlessness, tachycardia, low
urine output, orthostatic hypotension, dry mucous membranes, flushed
skin, irritability, lethargy, seizures, dyspnea, dehydration, confusion to
coma.
Treatment: replace volume and treat underlining cause.
76 | P a g e
Free H20 deficit (L) = (.6 X kg) X Na – 140
140
Example: 70kg patient with Na of 160
(.6 X 70) X 160 – 140 = 42 X 0.14 = 5.88L H20 deficit
140
77 | P a g e
D.
Potassium: K+ = 3.5 – 5.5 mEq/L
1.
Function: Major intracellular cation contributes to cell homeostasis and
function by maintaining its osmolarity and electro neutrality. Potassium
plays a principle role in electrical conductivity by influencing neuromuscular
transmission of nerve impulses and cardiac muscle contractility. Also helps
to maintain acid-base balance and normal kidney function.
2. Hypokalemia: K+ < 3.5 mEq/L
Cause: Decreased Intake, Increase Loss or Shift of K into Cells:
starvation, dehydration, massive fluid infusion lacking in K+, decreased
dietary intake, vomiting, diarrhea, corticosteroids therapy, draining fistula,
diuretics, some antibiotics, laxative overuse, NG suctioning, hypernatremia,
metabolic alkalosis (relative hypokalemia), aldosteronism.
Signs & Symptoms: ECG Changes – depressed ST segments, flat or
inverted T waves, presence of U waves, dysrhythmias, cardiac arrest, dilute
urine, anorexia, nausea, vomiting, ileus, lethargy, mental depression,
paralysis, confusion, muscle weakness, respiratory arrest, can precipitate
digitalis toxicity.
Treatment: Oral or Parenteral Replacement of K+
3. Hyperkalemia: K+ > 5.5 mEq/L
Cause: Excess Intake, Decreased Loss, Shift of K out of Cells: movement
of K out of the cells (acidosis, sepsis, fever, trauma, hyperglycemia,
rhabdomyolysis, catecholamines, insulin deficiency, tissue necrosis),
excessive dietary intake, renal failure (decreased excretion), Addison‟s
disease (adrenal insufficiency), large volume of stored blood products,
potassium sparing diuretics, medications that promote K+ retention (ACE
inhibitors, beta blockers, NSAIDS, heparin), hyperosmolar states, excessive
potassium administration.
Signs & Symptoms: ECG changes – tall, peaked, tented T waves, flattened
or absent P waves, widening QRS, asystole, alteration of
depolarization/repolarization of cardiac muscle, oliguria, nausea, vomiting,
diarrhea, calf pain, numbness or paresthesia, hyporeflexia up to flaccid
paralysis.
78 | P a g e
Treatment: Three-Part Therapy
1. Cardiac Protect: 10ml of Calcium Chloride or Calcium Gluconate
slow IV push. Renders the myocardium less excitable by decreasing
the effects of excess extracellular K+.
2. Shift K+ into the Cell:
 1 amp Sodium Bicarbonate
 5-10U Regular Insulin
 50ml Bolus 50% Dextrose
 Albuterol 10 – 20mg inhalation or intravenous (beta2
adrenergic agent – stimulates B2 receptor in the pancreas to
release more insulin).
+
3. Removal of K :
 Loop Diuretic
 Sodium Polystyrene Sulfonate (Kayexalate) a cation exchange
resin given orally or by retention enema. Oral administration is
more effective. Each 1gm will lower the K+ 1mEq with orally
administration, and 0.5mEq with rectal administration. Sorbitol
prevents constipation.
+
 Dialysis can also be utilized to remove K from the body.
79 | P a g e
80 | P a g e
E.
Calcium Total 8.5 – 10.5 mg/dL,
Ionized (biologically active) 4.0 – 5.0mg/dL
Total = 45% ionized + 40% protein bound + 15% complexed
Corrected Ca++ = Total Ca++ + 0.8(4.0 – serum albumin)
Function: Calcium is necessary for many physiologic
and metabolic processes. The transmission of nerve impulses,
and cardiac muscle contractility are calcium dependent. Because Ca++
lines the pores of the cell membrane it plays an important role with action
potential and pacemaker function. Calcium is needed for activation of
the clotting mechanisms and in teeth and bone formation. Vascular
smooth muscle is affected by Ca++ and therefore it plays a role in muscle
contraction and vasodynamics.
Calcium Regulation: Ca++ Homeostasis is Maintained by Organ
Regulation and Hormonal Control.
 Organ Regulation: Bone, Intestinal and Kidney
 Parathyroid glands secrete parathyroid hormone (PHT) which
regulates movement of Ca++ into and out of the bone, GI tract and
kidney
 Vit D is necessary for PHT assistance in Ca++ regulation
 Calcitriol (hormone) stimulates absorption and reabsorption of
Ca++
 Calcitonin (thyroid hormone) is secreted in hypercalcemia to
inhibit bone reabsorption and increase renal excretion.
 Acid-Base Regulation. Alkalosis = Hypocalcemia, Acidosis =
Hypercalcemia
 Hyperphosphatemia = Hypocalcemia
 Hypomagnesemia = Hypocalcemia
81 | P a g e
Hypocalcemia:
Total Ca++ < 8.5 mg/dL
Ionized < 4.0 mg/dL
Cause: Excess Loss, Inadequate Intake, Decreased Ionized Ca,
Decreased GI/Bone Absorption, Movement of Ca into Cell (Alkalosis):
Alkalosis, renal disease, large transfusions of PRBC
(citrate), hypoparathryroidism, hypomagnesemia, liver failure, sepsis,
pancreatitis, burns, diarrhea, diuretics, malabsorption syndromes, Vit. D
deficiency, medications (radiographic contrast, NaHC03, protamine,
aminoglycosides), inadequate dietary intake of Ca++, Hypothyroidism,
metabolic bone disease, hyperphosphatemia (including rapid infusion of
PHO4=), elevated calcitonin, alcoholism, post op thyroid, parathyroid or
radical neck surgeries.
Signs & Symptoms: ECG Changes – prolonged ST segment, torsades
de pointes, catecholamine insensitivity, and bradycardia. Osteoporosis,
paresthesia, numbness, tingling, muscle weakness, twitching and/or
hyperreflexia, tetany, seizures, larynogospasm and bronchospasm,
bruising/bleeding.
Chvostek’s Sign – Twitching of the lip and/or muscles on the side of
the face simulated from tapping the facial nerve (CNVII) on that same
side.
Trousseau’s Sign – Palmar flexion of the hand simulated from
inflating a blood pressure cuff (3 minutes) on that arm. The cuff
induces ulnar nerve ischemia.
Treatment: Oral or IV replacement of Ca++ (calcium gluconate or
calcium chloride), administer Vit. D, aluminum hydroxide gel for
Hyperphosphatemia, Mg for Hypomagnesemia, monitor pt carefully.
Clinical Pearl
Calcium chloride has more Ca++ than calcium gluconate but is also
more irritating to the vein
82 | P a g e
4.
Hypercalcemia: Total Ca++> 10.5 mg/dL
Ionized > 5.0 mg/dL
Cause: Excess Intake, Loss from Bones, Increased mobilization from
Bones, Movement of Ca out of Cell (Acidosis):
Metastatic carcinoma (breast, bone, multiple myeloma, osteolytic
metastases) and hyperparathyroidism account for 80% of all hypercalcemia.
Also acidosis, immobilization, thiazide diuretics, renal failure, tuberculosis,
sarcoidosis, excessive dietary intake, steroid therapy, Grave‟s disease
(hyperthyroidism).
Signs & Symptoms: ECG Changes – shortening of the ST & QT segments,
heart blocks. Muscle weakness, hypotonia, hyporeflexia, seizures, confusion
up to coma, anorexia, nausea, vomiting, constipation, peptic ulcer, renal
failure flank and leg pain, fatigue.
Treatment: Volume expansion with normal saline, loop diuretics or
corticosteroids, calcitonin and/or mithramycin (prevent bone reabsorption),
treat underlying cause.
83 | P a g e
84 | P a g e
F.
Magnesium: Mg++ = 1.5 – 2.5 mEq/L
Function: Magnesium is essential for the production and use of energy, all
ATP reactions involve Mg++. The Na+/K+ ATPase pump is dependent on
Mg++, therefore making it an important component in the action potential
and depolarization and repolarization of the cardiac muscle. Mg++ appears to
play a role in membrane stabilization decreasing the likelihood of cardiac
cell irritability or ectopy. It also has vasodilating effects, and it influences
the release of neurotransmitters at the neuromuscular junction by stabilizing
the nerve axon.
Hypomagnesemia: Mg++ < 1.5 mEq/L
Cause: Excess Loss, Decreased Intake, Impaired Absorption, Movement of
Mg into the Cell (Alkalosis):
Excessive diuretic therapy, starvation, malabsorption, medications (digitalis,
cyclosporine, cisplatin), endocrine disorders (DKA, HHNK,
hyperaldosteronism, hyperthyroidism), chronic alcoholism, pancreatitis,
alkalosis, vomiting, NG suctioning, citrate-chelation, decreased intake
(enteral or parenteral).
Signs & Symptoms: (very similar to hypocalcemia) ECG Changes – flat or
inverted T waves, ST segment depression, prolonged QT interval,
supraventricular and/or ventricular ectopy including torsades de pointes and
Vfib. Chvostek‟s & Trousseau‟s signs, hyperreflexia, vertigo, seizures,
confusion, hallucinations, depression up to coma, increased SVR and
hypertension, nausea & vomiting.
Treatment: IV administration of Mg++ with close monitoring. 1–4g MgS04
over 2 minutes to 6 hr (depending on severity of depletion). Common side
effects of MgS04 administration are flushed feeling or sweating, bradycardia,
hypotension and IV site burning.
Clinical Pearl
When low Mg and low K+ are both present the patient will be
unresponsive to KCL therapy until the hypomagnesaemia is treated.
++
85 | P a g e
Hypermagnesemia: Mg++ > 2.5mEq/L
Cause: Excess Mg++ intake (MgS04, laxatives, antacids), Renal
Insufficiency or Failure, Movement of Mg out of Cell (Acidosis)
Signs & Symptoms: ECG Changes – peaked T waves, shortened QT
interval, prolonged PR & QRS intervals, bradycardia, heart blocks, asystole.
Hyporeflexia, respiratory depression to apnea, lethargy to coma, seizure,
hypotension, hypocalcaemia, hyperkalemia, flushed/warm skin.
Treatment: Volume administration, diuretics, decrease Mg++ intake, IV
insulin and glucose will drive Mg++ back into cell, treat acidosis,
hemodialysis or CAPD with Mg-free dialysate.
V.
SUMMARY
Na
K
86 | P a g e
Cl
Glucose
CO2
87 | P a g e
Adult CCRN / CCRN-E Certification
Review Course:
Handout
Hematology/Immunology and Multisystem
Presented by:
Carol A. Rauen, RN, MS, CCNS, CCRN, PCCN
An AACN Critical Care Publication
101 Columbia
Aliso Viejo, CA 92656-1491
2011 American Association of Critical-Care Nurses
©
All rights reserved. AACN grants permission for a single individual to print one copy of
this electronic publication. No additional copies are permitted. No part of this electronic
publication may be reproduced, uploaded, stored in a retrieval system, or transmitted, in
any form or by any means (electronic, photocopying, recording or otherwise) without the
prior written permission of AACN.
88 | P a g e
Hematology & Immunology
I.
INTRODUCTION
AACN-CCRN Blueprint 2%
 Coagulopathies (e.g. ITP, DIC, HIT)
PHYYSIOLOGY OF HEMATOPOIETIC SYSTEM
A.
B.
C.
D.
E.
89 | P a g e
Purpose
 Circulate
 Provide Nutrition
 Provide Oxygen
 Remove Waste Products (carbon dioxide and metabolic wastes)
 Maintain Hemostasis
Location
 Veins & Venules
66%
 Pulmonary Loop
12%
 Arteries & Arterioles
11%
 Heart
6%
 Capillaries
5%
Composition
4-6 liters of blood
 Plasma
55%
 Cellular Components
45%
 Erythrocytes (red blood cells)
 Leukocytes (white blood cells)
 Thrombocytes (platelets)
Function & Assessment (see review information at end of this section)
Transfusions (see review information at end of this section)
II.
BLEEDING DISORDERS
A.
B.
Causes for Bleeding
1.
Vessel Integrity Disruption
 Surgical
 Trauma
2.
Platelet Disorders
 Quantitative
 Qualitative
3.
Coagulation Disorders
 Acquired
 Congenital
Coagulation Disorders
1.
Acquired
 Malnutrition
 Liver Dysfunction (decrease synthesis of factors)
 Vitamin K Deficiency
 GI Dysfunction (unable to absorb Vit K)
 Uremia
 Medications (heparin, Coumadin)
 Massive Transfusions
 Consumptive Coagulopathies (DIC)
2.
90 | P a g e
Congenital
 Abnormal Structure or Function of Blood Vessels
Rendu-Osler-Weber Disease
 Platelet Coagulation Abnormality
Kasabach-Merrit Syndrome
vonWillebrand‟s Disease
Hemophilia A or B
Afibrinogenemia
 Hyper-Coagulable Disorders
Protein C or S Deficiency
C.
DIC - Disseminated Intravascular Coagulation
Definition - DIC is a secondary disorder resulting from a primary
pathophysiologic state or disease. It is complex because it presents as an over
stimulation of both bleeding and thrombosis. The victim has microvascular
thrombi and bleeding occurring simultaneously. The disorder can be lifethreatening, acute or chronic and has a mortality rate of 50%-80%. When DIC
is a complication of sepsis or shock the mortality rate can be as high as 90%. It
frequently is associated with MODS.
Risk Factors - There does not appear to be one common risk factor for this
acquired coagulation disorder
General
Classifications
Primary Event/Disorder
Primary Event/Disorder
Tissue Damage
Major Surgery
Major Trauma
Heat Stroke
Head Injury
Burns
Transplant Rejection
Extracorporeal Circulation
Snake Bites
Obstetric
Complications
HELLP
Amniotic Emboli
Abruptio Placenta
Fetal Demise
NS Abortion
Eclampsia
Placenta Accreta
Placenta Previa
Shock States
Cardiogenic Shock
Septic Shock (severe infection
or inflammation)
Hemorrhagic Shock
Dissecting Aneurysm
Massive blood and volume
resuscitation
Drowning
Anaphylaxis
Neoplasms
Acute & Chronic Leukemia
Acute & Chronic Lymphoma
Solid Tumors
Hematologic
Disorders
Thrombotic
Thrombocytopenic Purpura
(TTP)
Collagen Vascular Disorders
Thrombocythemia
Sickle Cell Crisis
Specific System
Dysfunction
Acute & Chronic Renal Dis
Ulcerative Colitis
DKA, Acid Ingestion
HIV Disease
Cirrhosis
Acute Pancreatitis
Liver Dysfunction/Failure
SIRS & MODS
Pulmonary Embolism
Fat Embolism
91 | P a g e
Common Physiologic Response
 Tissue damage
 Platelet damage
 Endothelial damage
Pathophysiology











Tissue Damage Occurs
Healing is Stimulated (Clotting)
Hemopoietic Chaos
Fibrinolytic Mediators Released
Initially Microvascular Thrombi
Consumption Exceeds Synthesis
Ability to Clot is Lost
Fibrinolytic Mediators “Run a Muck”
Lyse all Clots
Bleeding State
Consumption Coagulopathy
Physical Assessment and Findings: the primary problem and pre-existing
condition certainly play a major role in the presentation. All systems are
at risk for dysfunction. The most common problems occur in the
pulmonary, renal and hematopoietic systems. Any bleeding patient who
does not have a history of or “reason” for to bleed should be suspected of
DIC.
 Laboratory Findings
Test
Elevated Decreased
Hgb
HCT
Platelet Ct
PT
PTT
Fibrinogen
FDP/FSP
D-Dimer
92 | P a g e
Treatment: No definitive treatment exists for DIC. The major goal is to treat
primary disorder – stopping the hemapoietic chaos. In addition patient
and family emotional support is paramount for quality nursing care.
 Support/Treat the Primary Problem – Eradicate the Cause of
DIC
 Early Recognition
 Decrease Bleeding Risk
 Treat Pain
 Transfusion Therapy – PRBC, FFP, Platelets, Cyro
 Vit K
 Anticoagulation Therapy – Heparin
 General Critical Care Management
D.
HELLP Syndrome - Hemolysis, Elevated Liver enzymes & Low Platelets
Atypical variant of severe preeclampsia-eclampsia. Presenting with distinct
physical and laboratory abnormalities.
Risk Factors:
 Second Trimester  Postpartum
 70% btw 27-37 Weeks Gestation
 Pregnancy-Induced Hypertension
 Older Multiparas
Pathophysiology:
 Preeclampsia: Vasoconstriction, Platelet Aggregation, Altered
Thromboxane-to-Prostacyclin Ratio
 Microvascular Injury
 ? Inflammatory Condition of Hepatocytes
 The Physiological Response is Similar to Autoimmune Diseases
Treatment:
 Deliver the Baby
 Control Blood Pressure
 Hydralazine, Labetalol, Nipride
 Post Partum Nifedipine
 Hemotherapy
 Assess Liver
 Prevent Seizures: MgS04
 Dexamethasome
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 Antapartum 10mg IV q12
 Postpartum 10mg Q12 X2, 5mg q12 X2
 PP Monitor for S&S of MODS
 Future Pregnancies?
E.
Heparin Induced Thrombocytopenia (HIT)
 Acquired Allergy to Heparin
 Antibodies are Produced to Heparin
 With Heparin Admin the Antibodies „attack‟ Heparin and
Thrombocytes
 Pt‟s Platelet Count Drops: 50% drop from baseline typically
between day 4-10 of Heparin Administration
 Treatment is to Stop all Heparin, Admin a Non-Heparin
Anticoagulant & Admin Platelets Only if Needed
F.
Thrombotic Thrombocytopenic Purpura (TTP)
 Drop in Platelet Ct
 Hemolytic Anemia
 Classically Presents with Neuro Symptoms or Renal
Dysfunction and Fever
 Difficult Diagnosis
 Causes: Drugs or BMT, Autoimmune Dis, AIDS, Depressed
Bone Marrow, DIC, HIT, Bleeding, Extracorporeal Cir.,
Medications, Artificial Heart Valve, Hemodilution
 Treatment
 Stop Cause
 Admin Platelets or Neumega
 Plasmapheresis
H.
Idiopathic Thrombocytopenic Purpura (ITP)
 Thrombocytopenia < 150,000
 Unable to Determine Cause
II.
SUMMARY
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MULTISYSTEM
I.
Introduction
A.
II.
AACN Blueprint 8%
 Asphyxia
 Distributive Shock (e.g. anaphylaxis)
 Multi-Organ Dysfunction Syndrome (MODS)
 Multisystem Trauma
 Septic Shock/Septic Shock
 System Inflammatory Response Syndrome (SIRS)
 Toxic Ingestions/Inhalations (e.g., drug/alcohol overdose)
 Toxin/Drug Exposure
Toxic Exposure (Ingestions/Inhalations)
A.
Pathophysiology
 Absorption
 Distribution
 Metabolism
 Elimination
B.
Assessment
 ABCs …ALWAYS….ALWAYS….ALWAYS
 DE and Poison Control
 Secondary Survey (full assessment)
 Vital Signs
 LOC
 Heart Rate and Rhythm
 Temperature:
Hyperthermia - Salicylates & Cocaine
Hypothermia - Barbiturates & Opiates
 Respiratory Rate
 Blood Pressure
 Full System Assessment
 History
 Environment/Bystanders
 AMPLE: Allergies, Medications, Past Illnesses, Last Meal, Events
 Diagnostic Work
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




B.
Toxicology Screens: Blood, Urine, Gastric Aspirate
CBC, Chemistry, LFTs, Coags, ABG
Chest X-Ray, ECG
Abd X-Ray (body packing/stuffing)
Pregnancy Test
Treatment Options
 Rapid Response: Unknown Substance, Unconscious Victim
 Ampule
 D50 IV: Hypoglycemia
 Thiamine 100mg IV: Prevent Wernicke-Korakoff‟s Syndrome
 Naloxone 2mg IV, IM or ET: Narcotic Antagonist
 Antidote When Known and Available (see below)
 Prevent Absorption & Enhance Elimination
 Oralgastric Lavage
 Emetics (not recommended)
 Activated Charcoal
 Diuresis
 Whole Bowel Irrigation
 Hemodialysis
 Don‟t Negate Psycho/Social and Family Indications
C.
Common Toxins (Review Complete Toxicology Table in Patho Book or
AACN Core Curriculum)
Toxin
Problem/
Presentation
Antidote
Assessment &
Treatment
Acetaminophen
Liver Failure
NAcetylcysteine
(NAC)
(Mucomyst)
PO, IV
No Direct
N/V, Right UQ Pain, Bleeding
Elevating LFTs
IV Fluids
Helpful
Protect Airway, NTG – Lavage (within
1hr)
ABGs, IV Fluids, Seizure Precautions,
Monitor and Tx Electrolyte Imbalance
Altered LOC, Headache, Seizures, Coma,
Alcohol
Carbon
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Respiratory Depression
Seizures
Liver Failure
(chronic)
Hypoxia
Removal
NAC, Gastric Lavage, Charcoal
Altered LOC, ETOH on Breath, Hx
Monoxide
Cocaine
Cyclic
Antidepressants
Replaces 02 on Hgb
Oxygen
Admin
Stimulates Sympathetic None
System
HTN, CP, ECG
s, Headache, Stroke,
Seizures, Hyperthermia
CNS: Seizure, Coma
CV: Rhythm
Disturbance
Anticholinergic:
Decreased Gastric
Emptying, Urinary
Retention
Opiates
Cardiac and
Respiratory Depression
Salicylate
(aspirin, pepto
bismal,
cough/cold
preps)
Acute: Central
Stimulation of
Respiratory System
(hyperventilation)
Metabolic: Met
Acidosis,
Hyperthermia,
Hypoglycemia, Platelet
Dysfunction (bleeding)
Chronic: Bleeding
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From
Exposure
Sodium
Bicarbonate
Flu-Like Complaints
100% Oxygen
Hyperbaric Oxygen
OD Levels Look Like Hypoxia, Stroke,
Head Injuries, MI, Hyperthermia
Treat the Physical Presenting Problem
(MI, Stroke etc.)
Protect Airway – Admin O2
Benzodiazepines: Sedation
Vasodilators: HTN
ACS Tx: see Cardiac Section
Provide Cooling
Seizure Tx and/or Prophylactic
ECG s: Tachy, Vent Dysrhythmias,
Heart Blocks, Wide QRS
Hypotension
Physostigmine
(Antilirium)
Altered LOC: Confusion, Agitation,
(Reverses
Hallucinations, Seizures, Coma
CNS effects)
Admin NaBicarb, GI Evacuation: Lavage
and Charcoal
Monitor ECG and Tx PRN
Naloxane
Decreased HR, BP, RR
(Narcan)
Administer Naloxane
No Direct
Hyperventilation, Resp Alk & Met
Acidosis, Dehydration, N&V,
Sodium
Hyperpyrexia, Bleeding
Bicarbonate
for Met
ABG, Get Blood Levels, Chemistry,
Acidosis
Platelet Ct, Coags
Gastric Lavage, Charcoal,
IV Fluids
Tx Metabolic Derangements
Cool Temp, Seizure Precautions
Hemodialysis
III. Toxic Exposures (External)
Chemical Exposure
 Identify if Possible
 Antidote if Possible
 Remove Chemical
 Brush if Power
 Flush if Liquid- large volumes of NS or H20
 Cover w Sterile Damp Dressing
 Never Rub Area
IV. Asphyxia
Severe oxygen deprivation (hypoxia) secondary to decreased air flow
 Drop in Pa02
 Rise PaC02
 Decreased Level of Consciousness
 MODS Death
Common Causes
 Physical Suffocation/Hanging
 Foreign Body/Obstruction in Upper Airway
 Drowning
 Electrical Shock
 Gastric Aspiration
 Smoke or Toxic Gas Inhalation
Treatment Priorities
 Open Airway
 Oxygenate and Ventilate
 Monitor
 Lactate Level
 Consider Therapeutic Hypothermia
 Organ Support & Surgery if Required
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V.
Shock
A. Definitions
Clinical Definition for Shock
The inability of the circulatory system to supply oxygen and
nutrients to the cells of the body.
The oxygen demands are greater than the supply.
B.
CLASSIFICATIONS OF SHOCK
Hypovolemic Shock:
1. Definition:
Hypovolemic Shock is the most common type of shock. It also is the easiest
to treat if identified early. Shock develops when blood volume is
insufficient to fill the intravascular space causing a preload deficit and
ultimately a decreased cardiac output.
2. Cause:
Absolute/Direct or Relative/Indirect Loss of Volume
Absolute/Direct Loses
External Hemorrhage
Gastrointestinal Volume Losses
 Diarrhea
 Vomited
 Gastric Suction
 Ostomies
Renal Volume Losses
 Massive Diuresis
 Hyperglycemic Osmotic
Diuresis
 Diabetes Insipidus
Plasma Losses
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 Burns
 Skin Lesions
 Fistulas
 Excessive Sweating
 High Fever
Relative/Indirect Losses
Sequestration of Fluid
 Cirrhosis
 Intestinal Obstruction
 Ileus
 Peritonitis
Internal Hemorrhage/Volume Losses
 Hemothorax
 Hemorrhagic Pancreatitis
 Ruptured Spleen
 Long Bone or Pelvic Fx
 Arterial Dissection
 Hemoperitoneum
 Ascites
 Extra Uterine Pregnancy
Vasodilation
 Sepsis
 Anaphylaxis
 Spinal Shock
Salt Depletion
Addisonian Crisis
Hypopituitarism
Adapted with Additions from Rauen & Munro (1998). Shock. In Kinney, M., et al. AACN Clinical Reference for
Critical Care Nursing. Mosby: Philadelphia
3. Clinical Presentation:
Patient presentation will depend
1. Percent volume loss
2. Duration of hypovolemia
3. Activation and response of compensatory mechanisms
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4. Therapeutic Goal:
Restore adequate intravascular volume as quickly as possible and stop
losses. The fluid options and crystalloid vs colloid controversy will be
addressed in the management section of this seminar.
Neurogenic Shock
1. Definition:
A loss of vasomotor tone secondary to inhibition of neural output. The loss
of sympathetic tone allows the parasympathetic nervous system to dominate,
which causes a drop in systemic vascular resistance (massive vasodilation)
and bradycardia. Cardiac output drops because of the lack of preload and
slow heart rate.
2. Causes:
The most common cause of neurogenic shock is spinal cord injury at or
above the T6 level. This injury can be complete or incomplete and the shock
state typically occurs quickly after the injury and maybe self limiting or
transient. The shock state may last up to three weeks.
 Spinal Cord Injury
 Deep General Anesthesia
 Spinal Anesthesia
 Damage to the Basal Regions of the Brain
 Prolonged Medullary Ischemia
 Central Nervous System Problems
3. Clinical Presentation:
Parasympathetic dominance is the hallmark of spinal shock. Vasodilation
and bradycardia are the classic clinical presentation.
During the shock state the patient will typically have no motor or sensory
function below the level of the lesion. Long term disability/function can not
be determined until the shock state has subsided.
4. Therapeutic Goal:
Stop the initiating cause and stabilize the spine as soon as possible. During
the shock state therapies revolve around administering volume (fill the tank),
beta stimulation (increase heart rate), alpha stimulation (vasoconstriction).
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Anaphylactic Shock
1. Definition:
Massive vasodilation occurs because of an antigen-antibody reaction which
activates mast cells and basophils triggering the release of
vasoactive mediators (histamine, serotonin, bradykinin, eosinophil
chemotactic factor, prostaglandlins, heparin, leukotrinenes, plateletactivating factors, adenosine and various proteolytic enzymes) which
stimulates a systemic response. This results in tremendous vasodilation and
increased capillary permeability, with loss of fluid into the interstitial space
and resultant hypotension from the relative hypovolemia.
2. Cause:
The initial activating response can be immunoglobulin E (IgE) or non-IgE
mediated. Anaphylaxis is IgE mediated and is typically the result of a
specific antigen exposure. An anaphylatoid response is mediated by a nonIgE reaction. There is direct activation of the mediators listed above (not
antigen-antibody) from a source. A wide range of agents can cause this
response: anti-inflammatory drugs, contrast media, opiates, polysaccharide
volume expanders and anesthetics.
Foods
 Eggs
 Milk
 Nuts
 Legumes
Venoms
 Bees
 Wasps
 Snakes
 Spiders
Blood Products
COMMON CAUSES
Antibiotics
Chemotherapy
 Penicillins
 Cisplatin
 Cephalosporins  Cyclophosphamde
 Tetracyclines
 Daunorubicin
 Erythromycin  Methotrexate
NSADs
Insulin
 Salicylates
 Pork
 Buprofen
 Beef
 Indomethacin
 Human
Local Anesthetics
General Anesthetics
Other Drugs
 Protamine
 Thiazides
 Chlorpropamide
Diagnostic Agents
 Iodinated
Radiocontrast
Agents
Narcotics
3. Clinical Presentation:
The release of the vasoactive mediators cause an array of systemic effects
which lead to decreased oxygen delivery and shock.
 Hypotension
 Generalized Edema (increased capillary permeability)
 Laryngeal Edema
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 Severe Bronchoconstriction
 Difficulty Breathing
 Coronary Vasoconstriction
 Urticaria
 Angioedema
 Itching
 Fever
 Flushed or Warm Skin
 Anxiety
4. Therapeutic Goal:
Identify and stop the exposure to the causative agent. Block the effects of
the vasoactive mediators. Treatment options are typically anti-histamines,
vasoconstrictors, bronchodilators, and fluid resuscitation.
Septic Shock
1.
Definition:
1992 ACCP/SCCM Definitions Bone, R. et al (1992) Chest, 101, pg 1644-1655
 Sepsis: the systemic response to infection, manifested by two or
more of the following conditions as a result of infection:
 Temperature > 38o C or < 36oC
 Heart Rate > 90 beats per minute
 Respiratory Rate > 20 bpm or PaC02 < 32mmHg
 WBC > 12,000 or < 4,000, or > 10% immature (bands) forms
 Systemic Inflammatory Response Syndrome (SIRS): The
systemic inflammatory response to a variety of severe clinical
insults. The response is manifested by two or more of the
following conditions:

Temperature > 38o C or < 36oC

Heart Rate > 90 beats per minute

Respiratory Rate > 20 bpm or PaC02 < 32mmHg

WBC > 12,000 or < 4,000, or > 10% immature (bands)
forms
 Severe Sepsis: Sepsis associated with organ dysfunction,
hypoperfusion, or hypotension. Hypoperfusion and perfusion
abnormalities may include, but are not limited to
 Lactic acidosis
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 Oliguria
 Acute alteration in mental status
 Septic Shock: Sepsis-induced with hypotension despite adequate fluid
resuscitation along with the presence of perfusion abnormalities that
may include, but are not limited to:
 Lactic Acidosis
 Oliguria
 Acute alteration in mental status
Pt who is receiving inotropic or vaspressor agents may not be
hypotensive at the time that perfusion abnormalities are measured.
 MODS: Multiple Organ Dysfunction Syndrome: the presence of
altered organ function in an acutely ill patient such that
homeostasis cannot be maintained without intervention.
2001 SCCM/ESICM/ACCP/ATS/SIS
International Sepsis Definitions Conference
Levy, M., et al. (2003). 2001 SCCM/ESICM/ATS/SIS International sepsis definitions conference. CCM
31(4), 1250-1256.
 Approved and supported 1992 definitions. Offered S&S for sepsis
and staging system (lacks evidence at this time).
 General Variables:
 Fever (core >38.3C)
 Hypothermia (core < 36C)
 Heart Rate > 90min or > 2 SD above the normal value for age
 Tachypnea
 Altered mental status
 Significant edema or positive fluid balance (20ml/kg over 24
hr)
 Hyperglycemia (plasma glucose >120) in absence of DM
 Inflammatory Variables:
 Leukocytosis (WBC > 12,000)
 Leukopenia (WBC < 4,000)
 Normal WBC with >10% immature forms (bands)
 Plasma C-Reactive Protein > 2 SD above normal value
 Plasma Procalcitonin > 2 SD above normal value (IL-6)
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 Hemodynamic Variable:
 Arterial Hypotension (SBP < 90mmHg, MAP < 70, or SBP
decreased >40mmHg in adults or < 2SD below normal for age)
 Sv02 > 70%
 CI > 3.5L/min
 Organ Dysfunction Variables:
 Arterial Hypoxemia (Pa02/Fi02 <300)
 Acute Oliguria (UO < 0.5mL/kg/hr)
 Creatinine Increase > 0.5mg/dL
 Coagulation Abnormalities (INR > 1.5 or APT > 60sec)
 Ileus (absent bowel sounds)
 Thrombocytopenia (platelet count < 100,000)
 Hyperbilirubinemia (plasma total bilirubin > 4mg/dL)
 Tissue Perfusion Variables:
 Hyperlactatemia (>1mmol/L)
 Decreased capillary refill or mottling
2. Causes: Infection is the cause of sepsis. The infective agent can be a
bacteria (gram positive or negative), virus or fungi. Once the infection
moves from a local to a systemic problem, sepsis and septic shock can
result.
3. Clinical Presentation:
Although initiated by a localized infection, once the patient is septic they
present with a systemic inflammatory response. This response is a
systemic reaction to the release of endotoxin and biochemical mediators
stimulated by inflammation and inadequate oxygen delivery. The patient
will present with a relative hypovolemia secondary to massive
vasodilation.
 Relative Hypovolemia and Hypoperfusion
 Increased Capillary Permeability and Edema
 Myocardial Depression
 Lactic Acidosis
 Pulmonary Capillary Leak Leading to ARDS
 Activation of Complement System Leading to Microthrombi
 Platelet Abnormalities
 Gluconeogenesis and Insulin Resistance
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4. Therapeutic Goal:
Identify and stop the causative agent. Block the effects of the inflammatory
mediators. Treatment options typically include
1.
Antibiotics
2.
Fluid Resuscitation
3.
Vasopressors
4.
Ventilation and Oxygenation
5.
Restore Hemopoietic Balance.
Distributive Shock
Neurogenic, anaphylactic and septic shock are also known as distributive shock
because of the relative hypovolemia that occurs in each due to massive
vasodilation.
Signs & Symptoms Of Distributive Shock
Signs &
Symptoms
Blood Pressure
Heart Rate
Cardiac Output
Temperature
Skin
Septic
Neurogenic
Anaphylactic
Low
High
High/Low
High
Warm/Cold
Low
Low
Low
Normal
Warm
Low
High
Low
High
Warm
Respiratory Rate
High
High
High
WBC
High
Normal
High
Sympathetic NS
Stimulated
Blocked
Stimulated
Edema
Present
Absent
Present
Bronchospasm
Absent
Absent
Present
Rauen, C., Munro, N. (1998). Shock. In Kinney, M. AACN Clinical Reference for Critical Care Nursing. Pg 1157
106 | P a g e
Initial Hemodynamic Parameters in Shock States
Shock State
HR
BP CO
PAPs
CVP SVR PAOP
Hypovolemic
Cardiogenic
Neurogenic
Anaphylactic
High
High
Low
Low
Low
Low
Low
High
Low
Low
Low
High
Low
Low
High
High
Low
Low
Low
High
Low
Low
Septic
High
Low
Low
Low
Low
C.
High
Low
Low
Low
High/
Low
Low High/
Low
STAGES OF SHOCK
All of the shock states cause hypoperfusion. There is inadequate oxygen
supply to the tissue resulting from hypoperfusion, decreased blood pressure,
and inadequate cardiac output. A supply/demand imbalance develops and
the patient moves into anaerobic metabolism and lactic acidosis. Many
physiologic mechanisms in the body delay this occurrence by compensating
for the perfusion deficit.
Rauen & Munro, 1998
1.
Aerobic vs Anaerobic Metabolism
2.
Stage 1 – Compensatory Stage
As inadequate perfusion persists and significant numbers of cells are
affected, an imbalance of oxygen supply and demand occurs.
Hypoxemia, hypotension, and acidosis activate the body‟s
compensatory mechanisms. The physiological goal of compensation
is to supply or improve oxygenation and perfusion to the cells.
 Neural Response
 Hormonal Response
 Chemical Response
Goal
Improve Cardiac Output and Oxygen Delivery
Mechanisms
Activated Sympathetic Nervous System
Renin/Angiotensin/Aldosterone System
Chemoreceptor Stimulated Respiratory Alkalosis
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3.
Stage 2 – Decompensatory Stage
As shock progresses, the compensatory mechanisms begin to fail.
The progression of shock is evident at the cellular, organ, and system
levels; and extensive physiological dysfunctions occur. The arteriolar
and precapillary sphincters require sufficient energy in the form of
adenosine triphosphate (ATP) to maintain a vasoconstrictive state. As
energy dissipates with the progression of shock, the sphincters relax,
allowing blood to flow into organs and sequester. Sludging of the
blood in these capillary beds occurs, and the microcirculation
becomes blocked. Metabolic waste products, microaggregates of
platelets, white blood cells, and clots accumulate, further enhancing
sludging and contributing to the development of metabolic acidosis.
In response to these events chemical mediators are released that are
harmful to the microciruculation and general system function. This
will be reviewed in more detail in the cellular response to shock
section.
4.
Stage 3 – Irreversible Stage
This is the final stage of shock. It is also referred to as the refractory
phase because the body systems are no longer responsive to treatment.
As each organ system decompensates and requires more and more
support, they reach a point where therapeutic measures are no longer
effective in maintaining function. The term irreversible is appropriate
because it is at this point when several, if not all, of the systems cross
the line from organ dysfunction to organ failure.
D.
Cellular Response to Shock
By definition shock is an imbalance between oxygen supply and demand.
The resultant hypoxia and/or ischemia initiate a cascade of tissue, organ and
cellular responses/reactions. These reactions are intended to assist with
shock compensation and healing but when left unregulated actually become
the source of further chaos.
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Organ Failure Mortality
# FAILED ORGANS MORTALITY RATE
Single Organ Failure
10-40%
Two Organ Failure
41-67%
Three Organ Failure
60-100%
Four Organ Failure
100%
VI. SUMMARY
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Adult CCRN / CCRN-E Certification
Review Course:
Handout
Pulmonary
Presented by:
Suzi Burns, RN, MSN, RRT, CCRN, ACNP, FAAN, FCCM, FAANP
An AACN Critical Care Publication
101 Columbia
Aliso Viejo, CA 92656-1491
2011 American Association of Critical-Care Nurses
©
All rights reserved. AACN grants permission for a single individual to print one copy of
this electronic publication. No additional copies are permitted. No part of this electronic
publication may be reproduced, uploaded, stored in a retrieval system, or transmitted, in
any form or by any means (electronic, photocopying, recording or otherwise) without the
prior written permission of AACN.
110 | P a g e
Objectives
This CCRN pulmonary review session will cover pulmonary diseases/conditions,
pharmacology, and diagnostics common in critical care. Specific content consists
of:
 Basic acid-base abnormalities
 Traditional mechanical ventilation modes and methods
 Pathophysiology and management of selected restrictive and obstructive
pulmonary disease conditions, pulmonary hypertension, pulmonary embolus
and traumatic injuries
Pulmonary Adult Program
 Pulmonary clinical judgment questions make up 18% of the examination.
 Covers diseases/conditions, pharmacology and diagnostics common in critical
care.
 These content areas are covered today.
 Some extra content is included but may not be covered in-depth.
 Good luck!
111 | P a g e
Arterial and Venous Blood Gases
Arterial Norms
 pH: 7.35-7.45
 < 7.35= acid, >7.35= alkaline
 PaCo2: 35-45mm Hg
 < 35= alkaline, > 45= acid
 PaO2: 80-100mm Hg
 < 60=severe, 60-80= moderate hypoxemia
Venous Norms
 Mixed venous O2: 40 mm Hg
 Lower: too much being extracted (i.e. cardiogenic shock)
 Higher: not enough being extracted (e.g. sepsis)
Uncompensated Acid-Base Abnormalities
(In these the pH is abnormal. Look to the respiratory or metabolic component to
determine primary mechanism)
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Compensated Acid-Base Abnormalities
(pH is normal. The primary mechanism –respiratory or metabolic-can be
determined by looking at the DIRECTION of the pH).
Partial compensation is present when the pH is not fully corrected but there is
evidence that the buffering system is at work to compensate.
Base Excess
The base excess indicates the amount of excess or insufficient level of bicarbonate in
the system (A negative base excess indicates a base deficit in the blood).
This is a calculated number and is helpful to determine presence of metabolic acidosis
and degree of acidosis.
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Compensated vs. Uncompensated
 First, interpret the ABG’s
 Second, check the pH - to be fully compensated, the pH must be within normal range (7.357.45)
 Third, check the respiratory and metabolic components to see which is going in the
direction of acidosis or alkalosis. The one that matches the pH direction (acidotic or
alkalotic) is the primary mechanism.
 The body tries to restore a normal pH by altering the buffer system component not involved
in the imbalance - either HCO3 or CO2. The kidneys take longer than the lungs!
 So, you may have a partially compensated picture as well (this is when the pH is not normal
but there is compensation from another system).
A few examples of conditions and associated treatments
 Respiratory Acidosis
o Conditions: Hypoventilation, over-sedation, drug overdose, neuromuscular disease,
inappropriate vent settings.
o Treatments: Narcan, adjust vent settings etc.
 Respiratory Alkalosis
o Conditions: Inappropriate vent settings, pulmonary embolus, pregnancy, hysterical
reaction, anxiety.
o Treatments: Decrease vent rate, decrease Vt, sedation etc.
 Metabolic Acidosis
o Conditions: DKA, Hypoperfusion, aspirin OD, renal failure, shock, sepsis, diarrhea.
o Treatments: Bicarb, increase perfusion, dialysis etc.
 Metabolic Alkalosis
o Conditions: Antacid OD, NGT suctioning, vomiting, K+-wasting diuretics.
o Treatments: Stop offending drugs, Diamox (diuretic which eliminates Bicarb ions
from blood) etc.
Mechanical Ventilation
A brief review of traditional volume and pressure modes…
Volume Modes
 Principle
o Delivers preset volume with every breath
 Disadvantage
o Volume is delivered regardless of the pressure required
 Normal tidal volume (Vt)
o 8-12 ml/kg (6 ml/kg in ARDS). Lower volumes may need to be used in any sick
patient. We’ll come back to this!
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Volume Modes-Monitoring
 Monitor Pressure!
 Pressure changes with changes in compliance (lung and chest wall) and resistance
(airways)
Parameters Volume Ventilation
 Fraction of inspired O2 (FiO2)-21-100%
 Vt: 8-12 (with lung protective strategies a lower volume is used i.e. 6 ml/kg)
 Rate (fx)
o 10-20; adjusted after ABG
 Inspiratory time (Ti)
o Speed (flow rate) of the gas (L/M)
 Average adult Ti time -7-1.0 second
o I:E ratio usually 1:2 or 1:3
 Sensitivity-either pressure or flow setting
 PEEP
Positive End-Expiratory Pressure (PEEP)
 Maintains continuous positive pressure throughout exhalation.
 “Recruits” alveoli and holds them open. Restores FRC.
PEEP
 Restores FRC (used to “recruit” alveoli)
 Redistributes lung water?
 5 cm PEEP “physiologic”?
 Allows for decrease in FiO2 (decreases shunt)
 Increased in 5-10 cm increments in adult
 Weaned slowly (rapid loss of effect)
PEEP
 When set PEEP > 10 cm, avoid breaking the circuit…
 Clinical implications of PEEP
o Hypotension and Barotrauma
What is auto-PEEP?
 Inadequate expiratory time (“waiting to exhale”).
 Common in patients with asthma, COPD, those with high minute ventilation requirements
and those with long inspiratory times. Can also be caused by mechanical factors (i.e., water
in the tubing, small endotracheal tubes).
 Can be measured at bedside. If found…
 Shorten inspiratory time, lower rate, decrease tidal volume, give bronchodilators etc.
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Continuous Positive Airway Pressure (CPAP)
Definition
 PEEP in spontaneously breathing patient, no positive pressure breaths
 Intubated/non-intubated patients
o Weaning method (intubated)
o Nocturnal ventilation in OSA (non-intubated)
 Nasal pillows/nasal mask
 Prevents upper airway obstruction by keeping tongue and soft palate away from posterior
pharyngeal wall
Traditional Volume Modes of Ventilation
How the parameters are configured to deliver breaths to the patient.
Synchronized Intermittent Mandatory Ventilation (SIMV)
 Delivers set number of volume breaths
 Allows patient to breathe spontaneously between set breaths at own volume (in synchrony
with machine breaths)
 Advantages
o “Weaning mode” - gradual decrease in the rate of set breaths
o Often used in conjunction with PSV
SIMV
 Disadvantages
o Risk of increased WOB at low rates, especially if inadequate flow or slow ventilator
response time (this is the main reason we mix PSV with SIMV.
 Parameters set by clinician
 Vt
 Ti
 RR (fx)
 Sensitivity
 FiO2
 PEEP
Assist/Control (A/C) a.k.a. Assist Mandatory
 Delivers mandatory (set) number of volume breaths
 Allows the patient to breathe between set breaths but,
o Upon sensing patient effort, ventilator delivers full preset tidal volume
 Disadvantages
o Excessive patient work if inspiratory time not matched to patient (i.e., inadequate
flow) or not sensitive enough.
o Potential for patient/ventilator dysynchrony
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A/C
 Not for weaning
 Parameters
o Vt
o Ti
o Sensitivity
o RR (fx)
o PEEP
o FiO2
Traditional Pressure Modes
 Principle
o Pre-selected pressure
o Vt varies with each breath
o Decelerating flow pattern may improve gas distribution
 Disadvantages
o Sensitive to changes in patient condition
 Compliance (lung)
 Resistance (airway)
Pressure Modes-Monitoring
 The tidal volume will change with changes in lung or airway.
 Monitor tidal volume!
 In spontaneously breathing patients…must also monitor rate!
Pressure Support (PSV)
 A mode of ventilation that augments or supports a spontaneous inspiration with a
clinician-selected pressure level
 Patient selection
o Stable?
o Reliable ventilatory drive
o Ready to wean
Parameters
 To set
o FiO2
o Inspiratory pressure level (PS level)
o PEEP
o Sensitivity
 To monitor HOURLY
o RR (fx)
o Vt
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PSV
 Advantages
o Patient comfort
 Patient controls Ti, I:E, RR, Vt
 Provides gradual respiratory muscle work
o Endurance
 WOB less than with SIMV (depending on the level of PSV)
 Disadvantages
o RR and Vt dependent on patient condition (lung compliance/airway resistance)
PSV
 High pressure levels provide nearly total ventilatory support!
 PSV may be added to SIMV to offset the WOB on spontaneous breaths.
Pressure Control Ventilation (PCV)
 Purpose
o To lower airway pressures
o To optimize gas exchange
 Application
o ARDS
PCV
 Set parameters
o Pressure limit (IPL)
 Initially set at 25-35 cm H2O or at plateau pressure
 RR
o 20-40
 Initial FiO2 usually 1.00
 Set Ti
PC-Inverse Ratio (PC-IRV)
 Reverses normal I:E
o Start at 1:1; up to 4:1
 Improves oxygenation
o Expands stiff alveoli with longer distending times
 MONITOR FOR AUTO-PEEP
 Sedation/NMBA often required!
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Non-Invasive Ventilation Bi-level Positive Airway Pressure (Bi-PAP )
 Non-invasive via mask
 Two distinct levels of positive pressure
o I-PAP (PSV)
o E-PAP (PEEP)
 Modes names vary with vent manufacturer: spontaneous (PS), Spon/T timed (A/C), timed
(control)
 Patient selection
o Patients with chronic respiratory failure
o ‘Bridging’
o CHF
Bi-Level (Bi-PAP)
 Application
o Set E, then I
o Rate (if a control mode)
o FiO2
o Creativity and mask selection
o Huge time component
 Assessment
o RR and pattern
o Patient comfort
o Skin integrity
o Patient safety
 Emesis
 Secretions
 ABGs
 Abdominal distension
Traditional ventilator settings and relationship to ABG’s
 PaO2 or O2 Saturation: FiO2 and PEEP
 PaCO2: rate and volume (minute ventilation)
 pH: can be affected by ventilation (too much/not enough) or lack of oxygenation (i.e. lactic
acidosis)
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The New Pressure Modes
Application of microprocessor technology has resulted in sophisticated mode options
that are very responsive to patient initiated efforts!
Spontaneous breathing is encouraged. However no data demonstrates that they
improve outcomes!
Many of the new pressure modes are ventilator specific! While many of the modes
are similar, the names differ. Volume Assured Pressure Modes
 Combine pressure supported ventilation with a decelerating flow pattern and a guaranteed
volume
 Settings vary with ventilator
 All require a “selected volume”
 Spontaneous versus control modes determined by selection of fx, Ti etc.
Examples
 VS - Spontaneous mode that adjusts pressure to attain volume
 PRVC - Adjusts pressure to attain volume but other parameters set
Airway Pressure Release and, BiLevel/BiPhasic Positive Airway Pressure
 APRV: Allows spontaneous breathing on a preset CPAP level and which is interrupted by a
short (1s) release for further expiration. Similar to PC/IRV
 BiPAP: Is similar to pressure controlled ventilation, during which unrestricted spontaneous
breathing is possible in each phase of the respiratory cycle.
Patient Selection
 ARDS
 Non-compliant lungs
 Those who otherwise may require muscle relaxants
Weaning from Mechanical Ventilation
 Protocols Work! Use short duration, spontaneous breathing trials-SBTs (CPAP or t-piece)
or decrease ventilatory support (e.g., PSV) over time.
 SBTs range from ½ hour to 2 hours. More than that may tire the patient and longer trials
not associated with better outcomes.
 Assure rest between trials.
 Attention to non-pulmonary factors as well as pulmonary factors (e.g., nutrition, mobility,
psychological support).
 With tracheostomy…more prolonged trials.
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Signs of intolerance (when to stop!)
 Symptoms: Dyspnea, anxiety etc.
 Signs: Tachypnea, chest-abdominal asynchony, drop in sats, tachycardia, BP changes,
diaphoresis etc.
 Trial is terminated with these signs and symptoms.
 Rest is necessary and generally means a return to full ventilation for 12-24 hours.
But prior to wean trials…WAKE THEM UP! Sedation off!
Acute Respiratory Failure
Oxygenation and Ventilation Abnormalities
 PaO2 <60 and/or PaCO2 >50 at rest
Etiology
 Obstructive, restrictive, neuromuscular, V/Q (i.e. PE)
Restrictive Diseases Definition and Concepts
Expansion of the lung is restricted or decreased.
Restrictive Diseases
 Acute respiratory distress syndrome
 Pneumonia
 Atelectasis (volume loss)
 Pulmonary edema
 Others (e.G. Pneumothorax)
Restrictive Disorders
 Lung volumes decreased
 Loss of functional residual capacity
 Compliance decreased
 Increased w.O.B.
 Abnormal v/q (i.e. shunt)
 Oxygenation problems
Functional Residual Capacity
 Volume that remains in the lungs at the end of a resting exhalation
 Helps keep the alveoli open
 Reduces shunt
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Compliance
 How easy the lungs distend
 Takes less pressure to get big volume
Clinical Features
 Dyspnea
 Tachypnea
 Hypoxemia
 Increased w.O.B.
 Weakness and fatigue
Hypoxemia
 Hypoventilation
 Diffusion defect
 Shunt
 V/Q mismatch
Clinical Indices of Oxygenation
 Alveolar-arterial (A-a) gradient: 10-15 on RA, 50-75 on 100%
 a/A ratio: N=0.8 or higher
 PaO2/FiO2 (P/F) ratio:
 < 300 = ALI, <200 =ARDS
 Blood flow shunted/blood flow total (Qs/Qt): 15% or greater is significant in ventilated
patient
Treatment (General)
 Treat precipitating causes
 Support oxygenation and ventilation
 Mechanical ventilation
Acute Respiratory Distress Syndrome ARDS
Pathogenesis: non-cardiogenic pulmonary edema, pulmonary capillary leak, bilateral
diffuse infiltrates, P/F ratio <200.
Etiology is indirect or direct injury. High mortality.
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Pathology
 Increased capillary leak
 V/Q abnormalities
 Decreased lung compliance (and atelectasis)
 Shunt
 Hypoxemia
 Dyspnea
 3 phases (diffuse alveolar damage)
Phases of ARDS
 Exudative: (0- 4 days)
 Proliferative: (3-10 days)
 Fibrotic: (7-14 days)
Clinical Features
 Dyspnea
 Tachypnea
 Hyperventilation (initially)
 Increased work of breathing (respiratory distress)
Diagnosis
 X-RAY
o Bilateral diffuse infiltrates
 ABG’s
o PaO2 low despite FiO2, increased A-a gradient, P/F ratio < 200. “refractory
hypoxemia”
 PCW
o <18 (or other evidence that it is not due to a cardiac condition)
Therapy for ARDS
 Treat Etiology
 Infection, trauma, hypotension etc.
 Supportive
 Oxygenation, ventilation, cardiac output
 Optimize Lung Recovery Prevent volu-press trauma
“Volu-Press” Trauma
 Large Vt’s create high pressures
 Injury to the stiff lung at “distending pressures” > 35 cm H2O for > 72 hours
 Alveolar fractures and edema: non-ARDS, ARDS
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PEEP
 PEEP - Protects against ventilator-induced injury by preventing shear stress injury from
repeated opening/closing of alveoli… protects from tidal stress!
Prevent Lung Injury (a.k.a. volu-trauma)
 Avoid O2 Toxicity (FiO2 < 50-60%)
 Low tidal volumes-6ml/kg (low volumes may result in > CO2 and lower pH—called
permissive hypercarbia)
 Maintain lung recruitment: PEEP
Pneumonia
 Definition
o An inflammatory process (usually due to infection…may be chemical pneumonitis)
 Pathophysiology
o Alveolar filling with exudate (or other), tissue necrosis, ischemia
Classification of Pneumonias
 Community Acquired
 Hospital Acquired (within 3-5 days of being in the hospital, recent hospitalization, nursing
home etc.). Often an aspiration pneumonia
 Ventilator Associated Pneumonia (after 3-5 days of mechanical ventilation)
 Treatment varies: nosocomial organisms include gram negative organisms and are treated
differently
Clinical Presentation
 Symptoms
o Dyspnea, tachypnea, pleuritic chest pain, fever, chills, rigors etc.
 Signs
o Evidence of consolidation, pleural effusions, wheezing, fever, cough (with or without
purulent sputum)
Diagnostic Findings
 Chest x-ray: infiltrates (especially gravity dependent)
 Purulent sputum (or change in quality/quantity)
 Hypoxemia and hypercapnia
 Decreased compliance and/or obstruction to flow
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Sputum Characteristics
Color
 Rust
 Brick Red
 Salmon colored
 Yellow/Green
 Thick purulent, foul
 Frothy
 Watery
 Tenacious, white
 Mucoid, gray
 Brown
 Anchovy chocolate
 Red
 Asthma
 Bronchitis
 Aspergillosis
 Amoebic abscess
 Rifampin
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Organism
 Pneumococcal
 Klebsiella
 Staphylococcus
 Bacterial
 Lung abscess
 Pulmonary edema
 Cold/Allergy
Diagnosis
 Sputum gram stains
 Sputum cultures
 CBC with diff
 Chest x-ray
 Bronchoscopy
Treatment
 Antibiotics
 Fluids
 Oxygen
 Mechanical ventilation
Pulmonary Aspiration
Pathophysiology and Etiology
 Aspiration of particulate or fluid matter causing generalized tissue reaction and/or
airway obstruction. Widespread chemical pneumonitis within 12-36 hrs.
 Compliance is decreased.
Clinical Presentation
 Solid objects
o Cough, dyspnea, wheezing, respiratory distress, cyanosis, aphonia (café
coronary)
 Gastric acid
o Abrupt onset of respiratory distress, hypotension, bronchospasm, increased
secretions, tachypnea, fever, crackles and rhonchi
 Bacterial
o Infection fever
Diagnostic Findings
 Chest x-ray: Infiltrates (especially gravity dependent)
 Purulent sputum (or change in quality/quantity)
 Hypoxemia and Hypercapnia
 Decreased compliance and/or flow
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Therapy/Prevention
 HOB > 30degrees!
 Suctioning and cuff management (CASS-continuous aspiration subglotic suction)
 Oxygenation
 Chest PT
 Bronchoscopic removal
 Antibiotics, oral decontamination
 Ventilatory support
Obstructive Diseases
Definition
A group of diseases including asthma, chronic bronchitis, and emphysema in
which the common denominator is airflow obstruction.
Chronic Bronchitis
 Chronic or recurrent excess mucus production in bronchial tree
 Occurs 3 months in a year for 2 consecutive years
 Common to have repeated respiratory infections (RSV: respiratory syncytial virus,
strep pneumonia, h-flu)
Emphysema
 Abnormal permanent enlargement of airspaces distal to terminal bronchiole
 Accompanied by destruction of the walls
 Centrilobular proximal, most common
Resistance
 How easy, or hard, it is for gases to flow down the airways.
 Affected by small airways (e.g. bronchospasm, small diameter tubes)
 Takes more pressure to maintain flow.
Concepts Obstructive
 Lung volumes are increased (TLC, FRC, RV)
 Expiratory flow rates decreased (FEV1 and peak flow)
 Airways resistance is increased
 Gas trapping common-dynamic hyperinflation and auto-PEEP (if on the ventilator)
 Increased W.O.B
 Increased drive
 Mechanical disadvantage and fatigue
 Precipitating events: infection (and other)
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Clinical Features
 Signs of precipitating event
 Hypoxemia
 Hypercarbia
 Pattern of breathing
Treatment Goals
 Treat cause
 Improve O2 sat!
 Secretion clearance
 Decrease ventilatory demand and load
 Improve respiratory muscle force and endurance
 Correct electrolytes and fluid deficits
 Avoid complications
Therapeutics
 Provide oxygen (check CO2 levels)
 Beta 2 agonists (e.g., albuterol)
 Anticholinergics (e.g. ipratroprium)
 Methylxanthines (e.g., amminophylline)
 Steroids
 Antibiotics
 Hydration
 Nutrition
Mechanical Ventilation
 Provide respiratory muscle rest first 12- 24 hours
 Prevent hyperinflation (small volumes, short inspiratory times, and adequate
exhalation times)…check for auto-PEEP!
Status Asthmaticus
Acute Severe Asthma
Severe acute bronchoconstriction that is intense, unrelenting, and unresponsive
to usual therapy. A clinical emergency!
Asthma Pathophysiology
 Inflammation
 Bronchoconstriction
 Mucus production
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Precipitating Events (“triggers”) Pathophysiology
 Gas exchange
o Predominately high V/Q (dead space ventilation)
 Increased W.O.B.
 Precipitating events
o History is essential!
Clinical Features History
 Recurrent frequent episodes
 Change in pattern of symptoms
 Increased dyspnea
 Cough with sputum
 Change in sputum color
 Refractory to drugs
 Personality changes
Physical Exam
 Mental status
 Anxiety
 Tachypnea and tachycardia
 Accessory muscle use
 Wheezing
 Prolonged expiration
 Pulsus paradox
Laboratory Data
 Flow measurements decreased (peak flow etc.)
 Hypoxemia
 Eucapnia or hypercapnia
 Chest x-ray (hyperinflation)
 Eosinophils in sputum
 Purulent sputum
Therapy (General)
 Bronchodilators
o Beta 2 agonists (1st line)
o Anticholinergics (2nd but often given in combination with beta agonists)
o Methylxanthines, magnesium
 Steroids (always a first line drug)
 Oxygen
 Hydration
 Antibiotics if infection suspected
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Mechanical Ventilation Asthma
 Avoid pressure limiting modes (hard to control volumes with bronchospasm)
 Prevent dynamic hyperinflation (small volumes and low rates)
 May require heavy sedation and paralytics
 Permissive hypercarbia
 Check for auto-PEEP
Acute Pulmonary Embolus
Pathogenesis
 A complication of deep vein thrombosis. Migration of a clot to the pulmonary
vasculature.
Clinical Features DVT
 Pain, increased girth, tenderness, warmth, redness, swelling, edema, venous cord
 Virchows Triad: Hypercoaguability (acquired or congenital-inborn resistance to
activated protein C-genetic mutation in factor V known as "factor V Leyden”), stasis
and injury (most common is hospitalization and lack of prophylaxis)
 More common in left leg (compression of the left common iliac vein by the overlying
right common iliac artery May-Thurner syndrome)
Diagnosis and Therapy DVT
 D-dimer
 Duplex Ultrasonography, due to its high sensitivity, specifity and reproducibility, has
replaced venography as the most widely used test in the evaluation of the disease.
 DVT Prophylaxis: Unfractionated heparin, LMWH, warfarin, SCD’s
Clinical Features PE
 Chest pain, chest wall tenderness, back pain, shoulder pain, upper abdominal pain,
syncope, hemoptysis, shortness of breath, painful respiration, new onset of
wheezing, any new cardiac arrhythmia, or any other unexplained symptom
referable to the thorax–of those who die from PE only 60% have dyspnea.
Clinical Features PE (Cont.)
 Hemodynamic: Increased PA pressures, right ventricular failure
 Pulmonary: V/Q abnormalities, hypoxemia, hyperventilation, atelectasis…infarction
 X-ray: Possible wedge
 ABG’s: Hypoxemia with hyperventilation (at least initially)
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Diagnosis and Therapy PE
 Diagnosis: Estimate risk, search for source, V/Q scan (when CTPA not available),
CTPA, pulmonary angiogram (gold standard… but being replaced with CTPA)
 Therapy: Heparin, thrombolytics, vena cava interruption (filters-removable are
popular now), embolectomy, oxygenation and ventilation
Fat Embolus
 Signs and Symptoms: Otherwise unexplained dyspnea, tachypnea, arterial
hypoxemia with cyanosis and diffuse alveolar infiltrates on chest X-ray, otherwise
unexplained signs of cerebral dysfunction, such as confusion, delirium or coma,
petechiae over the upper half of the body, conjunctive, oral mucosa and retinae.
 Prevention: Prompt surgical stabilization of long bones fractures and correcting or
preventing decreased systemic perfusion, reduce the risk of the syndrome
 Treatment: Supportive (O2, ventilation etc.)
Pulmonary Hypertension
Definition
 Primary pulmonary hypertension (PPH) is a rare disease of unknown etiology.
Occurs in young adults (twice as common in women as in men).
 Known causes
o The use of the appetite suppressant “fen-phen” (dexfenfluramine and
phentermine). chronic liver disease, some rheumatologic disorders,
congenital heart malformations or illicit drug use.
 Symptoms: Often undetected until they get sick with a virus.
 Diagnosis: supported by an abnormal echocardiogram of the heart and confirmed
with right heat catheterization (increased PA pressures).
 Treatment: difficult to treat, although intravenous prostacyclin has proven effective
in many patients. Only cure is lung transplantation.
Pneumothorax
Definition
 Air in the pleural space
Etiology
 Spontaneous, traumatic, tension
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Clinical Features Pneumothorax
 Depends on size
 Symptoms: Dyspnea, pleuritic chest pain
 Signs: Tachycardia, tachypnea, hypotension, decreased respiratory excursion,
elevated chest on affected side, widened costal spaces, absent or reduced breath
sounds, hyper-resonant to percussion, tracheal shift
 ABG’s
o Hypoxemia +/ Hypercapnia
 Ventilator
o Increased peak airway pressure (plateau pressure will increase)
 Cardiac Tamponade!
Diagnosis and Treatment
 Chest x-ray
 Large bore catheter in 2nd intercostal space if unstable
 Chest tube
Other Air-leak Syndromes
 Pneumopericardium
 Pneumomediastinum
 Treatment depends on how it is affecting the patient.
Chest Trauma
Definition
 Penetrating or blunt injury to the chest and/or lungs that interfere with any of the
components of respiration
Clinical Presentation
 Tachypnea, dyspnea, ecchymosis, shock, pain, history of injury
 Pneumothorax, hemothorax and tension pneumothorax
 Flail chest: Unstable chest wall sinks with inspiration (three consecutive ribs)
 Trauma to lung (contusions): Hemoptysis, respiratory distress.
Presentation
Open sucking wounds
 During inspiration the affected lung collapses resulting in ineffective gas exchange.
Patient is dyspneic and sucking sounds on inspiration are noted from wound.
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Hemothorax
 Limited motion of affected side, dull to percussion, absent breath sounds.
Therapies
 ABGs and clinical assessment to follow and intervene
 Pain control, fluids, blood, prepare for surgery
 Flail: Intubation, PEEP and mechanical ventilation
 Emergency decompression of tension pneumo, chest tubes for hemo and other
Thoracic Surgery
 Tracheal perforation and surgery
 Lung reduction
 Pneumonectomy, lobectomy
Practice Exam Questions (13 total)
1. Mr. K. is a patient with diabetes who has been admitted to a medical floor
for management of his glucose which is 500 mg/dL. His ABG is pH=7.24,
PaCo2=36mmHg, Bicarbonate=14 mEq/L, PaO2= 90 mmHg. Interpret Mr. K’s
blood gas.
A. Compensated metabolic acidosis
B. Respiratory acidosis and metabolic alkalosis
C. Uncompensated metabolic acidosis
2. Mrs. C. is admitted to the MICU with the CC of being “short winded”. Her
admission ABG is: pH= 7.3, PaCO2= 84mmHg, Bicarbonate= 30 mEq/L and PaO2
of 48mmHg. Interpret her ABG.
A. Metabolic acidosis and respiratory acidosis with severe hypoxemia.
B. Partially compensated respiratory acidosis with severe hypoxemia
C. Fully compensated respiratory acidosis with moderate hypoxemia.
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3. Ms. Littlepuffin was admitted to the ER following a drug overdose. She is
intubated and ventilated on A/C. Other parameters are as follows: FiO2=
100%, Vt = 500ml, rate (fx) = 15, PEEP=5. Her first ABG, drawn after 20
minutes is: pH= 7.30, PaCO2 =55 mmHg, Bicarb= 22, PaO2 = 300mmHg. What
parameters do you need to adjust?
A. Decrease the ventilator rate to 10, decrease the FiO2 to 90%
B. Increase the ventilator rate to 20, decrease the FiO2 to 60%
C. Increase the PEEP to 10 cmH2O and increase the ventilator rate to 17
breathes/min.
4. Which of the following are true?
A. Research proves that the “new pressure” modes are better than the “traditional”
modes.
B. PC-IRV commonly requires heavy sedation and paralytics whereas APRV does not.
C. The volume assured pressure modes are designed to deliver the breaths as
“pressure breaths” while assuring that the desired Vt is delivered.
5. Billie Boy Blue returned from abdominal surgery to the SICU where he was
placed on SIMV until he woke up. Once awake the nurse practitioner asked
that he be placed on a SBT on CPAP of 5 cm H2O. After 5 minutes of being on a
CPAP of 5, your patient is breathing 40 times/min, he is diaphoretic and
agitated. What will you do for Mr. Blue?
A. Turn the CPAP up to 10 cm H2O
B. Put him back on a control mode and assess reason for intolerance.
C. Put him on a T-piece (he probably just wants you to pull the endotracheal tube
out).
6. A restrictive disease is one that is characterized by:
A. Decreased compliance, hypoxemia and rapid shallow breathing.
B. Increased compliance, hypercarbia and slow deep respirations.
C. Decreased compliance, normal PaO2 and shunting.
7. Your patient has ARDS. His P/F ratio is 90 and he is currently on a ventilator.
The primary goals of ventilatory support are:
A. Prevent lung injury with PEEP and assure that blood gases are normalized.
B. Keep PEEP levels and FiO2 levels low…they both injure the lung.
C. Maintain Vt at 6 ml/kg and assure lung recruitment with PEEP.
134 | P a g e
8. Of the following which is the most appropriate means of preventing
Ventilator Associated Pneumonia?
A. Give prophylactic antibiotics.
B. Keep the HOB > 30 degrees.
C. Decontaminate the room with a bleach mixture.
9.
A.
B.
C.
Obstructive diseases/conditions are characterized by:
Decreased expiratory airflow, increased volumes and low PaCO2.
Increased expiratory airflow, hypoxemia and high PaCO2.
Airflow obstruction, high PaCO2 and hyperinflation.
10. Your patient has COPD. He is currently agitated and s.o.b. His current ABG
is: pH= 7.32, PaCO2= 60mmHg, and PaO2 = 45mmHg on 1 L/min oxygen by
nasal cannula. Essential next step is:
A. Give the patient some sedatives!
B. Don’t give more oxygen. Patients with COPD always have low O2’s and giving more
O2 will eliminate his hypoxic drive.
C. Provide more O2 to attain an oxygen saturation close to 90% (PaO2~60mmHg) and
monitor carefully for an increase in CO2.
11. What is the primary pathophysiologic mechanism in asthma?
A. Bronchoconstriction
B. Mucus plugging
C. Airway inflammation
12. It is July and your ventilated patient just had a subclavian central line placed
by a new intern. Your patient suddenly becomes very short of breath. Peak
airway pressures are > 60cm H2O and alarms are going off. Chest is elevated on
the affected side and BP is dropping. Which are correct?
A. Venogram, V/Q scan, heparin infusion
B. D-dimer, doppler ultrasound of lower extremities, CT-PA, heparin infusion
C. Heparin infusion, SCDs, LMWH, warfarin, SCD’s, filter.
13. Which of the following are true about lung volume reduction surgery
(LVRS)?
A. Those receiving the surgery must receive physical therapy prior to surgery.
B. LVRS works on the premise that by removing an over distended portion of the lung,
the diaphragm will return to a more mechanically efficient position in the thorax.
C. All patients with emphysema qualify for this surgery.
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Practice Exam Answer Key:
1. C
2. B
3. B
4. B&C
5. B
6. A
7. C
8. B
9. C
10. C
11. C
12. B
13. A&B
Selected References
 AACN Protocols for Practice. "Caring for Mechanically Ventilated
Patients", Editor S. Burns. Second edition. 2007 Jones and Bartlett
Publishers
 AACN Essentials of Critical Care Nursing. Chulay M and Burns SM, editors.
Second edition. 2010. McGraw Hill Publishers publications, New York.
 Management of the Mechanically Ventilated Patient. Second edition. Ed:
Lynelle N.B. Pierce. 2007 Saunders / Elsevier
136 | P a g e
Adult CCRN / CCRN-E Certification
Review Course:
Handout
Neurologic
Presented by:
Mary Kay Bader, RN, MSN, CCRN, CNRN, CCNS, FAHA
An AACN Critical Care Publication
101 Columbia
Aliso Viejo, CA 92656-1491
2011 American Association of Critical-Care Nurses
©
All rights reserved. AACN grants permission for a single individual to print one
copy of this electronic publication. No additional copies are permitted. No part of
this electronic publication may be reproduced, uploaded, stored in a retrieval
system, or transmitted, in any form or by any means (electronic, photocopying,
recording or otherwise) without the prior written permission of AACN.
137 | P a g e
Topics
Neuroanatomy
Protective Structures
•
•
Scalp
Skull
Protective Structures
Meninges
•
•
•
Dura Mater
Subarachnoid space
Pia Mater
Central Nervous System
•
•
•
•
Cerebrum
Brainstem
Cerebellum
Spinal Cord
Cerebral Hemispheres
•
Frontal: Voluntary motor function, speech, memory, judgment, affect, learned social
behavior, initiation and higher mental functions
•
•
•
Parietal: Sensory function (left vs. right)
Temporal: Sensory hearing/receptive speech, behavior/emotion
Occipital: Vision
Cerebrum
Corpus Callosum
•
Fibers transfer learned discrimination, sensory, and memory from one hemisphere
to another
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Cerebrum
Basal Ganglia
•
•
•
Regulate/control influences on motor integration
Suppress muscle tone
Extrapyramidal control
Diencephalon Thalamus
Walls of 3rd ventricle
•
•
•
Receive sensory input for general senses, taste, vision, and hearing
Relay station to cerebral cortex
Role in motor function and ascending RAS
Diencephalon Hypothalamus
•
•
Temperature, food/water intake, behavior, and sleep
Autonomic responses: parasympathetic in anterior and sympathetic in posterior
hypothalamus
Brainstem: Motor/sensory pathways
Midbrain
•
Auditory/visual systems
Brainstem and Cerebellum
Motor/sensory pathways
•
•
Midbrain
•
Medulla
Pons
o Respiratory centers
o Respiratory and vasomotor control
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Cerebellum
•
•
Influences muscle tone
Equilibrium, locomotion, posture, and non-stereotyped movements
Blood Supply
•
•
CBF: 20% of cardiac output
Major arteries off aortic arch
o Right side - innonimate
 common carotid
 subclavian-vertebral
o Left side
 carotid
 subclavian-vertebral
Circulation of Brain
•
Anterior Circulation
o Carotid arteries
•
Posterior Circulation
o Vertebral arteries
Ventricle System and CSF
•
•
•
•
Lateral ventricles
Third ventricle
Fourth ventricle
CSF - 500 cc /day
o Choroid plexus
o Arachnoid villi
o 125-150 cc in system
Topics
Consciousness
•
•
Arousable
Awareness
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General Observation
•
•
•
Appearance
•
•
•
•
Flow of speech
Behavior
Mood and affect
o Facial expression
Thought processes
Assessment
Mentation
o Level of consciousness
o Orientation
Talking Points
•
LOC single most important indicator of neuro function
o Just because someone follows commands does not mean their ICP is
normal
o Agitation/restlessness precedes neurologic decline
 Do not sedate for agitation in neuro diagosis
•
Frequent neuro checks for new pathologies
Assessment
•
Mentation
o
o
o
o
o
o
o
Level of consciousness
Orientation
Attention and concentration
Retention and immediate recall
Cognition
Affect and mood
Judgment
Localizing Value of Mental Status Exam
Assessment
•
Language and Communication
o Expressive
o Receptive
•
Special cerebral function
o Gnosia-Agnosia
o Praxia-Apraxia
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Assessment
•
Motor Exam
o Size
o Strength
o Tone
o Coordination
Talking Points
•
Essential Motor strength scored 0-5
o Abnormalities of > 1 on score significant
o Always validate score with oncoming RN
•
Spine Patient
o Motor strength
 Lumbar abnormalities: lower extremity deficit
 Thoracic abnormalities: lower extremity deficit except
sensation
 Cervical abnormalities: upper/lower extremity deficit
Assessment
•
•
Sensory exam
Cranial nerves
o II and III
o III, IV, & VI
o V and VII
o IX and X
o XII
Assessment
•
Vital Signs
o
o
o
o
BP
HR
Respiration
Temperature
Increased Intracranial Pressure Classification
•
•
•
•
•
Increases in tissue volume
Increases in blood volume
Increases in CSF volume
Congenital abnormalities
Metabolic
142 | P a g e
Hydrocephalus Secondary to Infection in Meninges
Hydrocephalus Secondary to Intraventricular Hemorrhage or SAH
Pathophysiology
•
•
Monro-Kellie Doctrine
Compliance
Signs/Symptoms Increased ICP
•
•
Decreased in LOC
•
Cranial Nerves:
o Ipsilateral pupil abnormalities
•
•
Headache and/or vomiting
Motor
o Contralateral motor deficit
Cushing’s Triad
o Bradycardia
o Widening pulse pressure
o Respiratory arrest
ICP Monitoring
•
•
•
Intraparenchymal bolt
Ventriculostomy
ICP Pressure
o Normal:0 – 15 mm Hg
o Elevated: > 20mm Hg
Cerebral Blood Flow
•
CBF = CPP  CVR
o CPP = MAP - ICP
 Injured Brain optimize CPP
 Use target of 50-70 mm Hg
Autoregulation Cerebral Blood Flow
•
Vasomotor control
o Intact: Increase in CPP causes vasoconstriction and decrease in ICP
o Vasomotor reactivity failure: Increase in CPP causes vasodilation and
inc ICP
•
Flow metabolism
o ↑ metabolism ↑ CBF
143 | P a g e
•
Metabolic substances
o PaO2
o PaCO2
o pH i.e., acidosis = vasodilatation
Interventions
•
•
•
•
Head of Bed/Neck positioning
•
Maintain CPP > 50-70 mm Hg
o Maintain euvolemia/vasopressors
•
Normothermia
Quiet environment
Drain CSF
Airway
o PaO2 and PaCO2
 Decrease PaCO2 30-35 if impending herniation
o Suctioning
o Neuromuscular blockade only for ventilation
Secondary Interventions
•
Mannitol
o 0.25-1 gram/kg
o Replace fluids lost to maintain euvolemia
•
Hypertonic Saline
o 3% 200 ml over 20 minutes
o 5% 150 ml over 20 minutes
o 7% 100 ml over 20 minutes
o 23.5% 15-20 ml
Tertiary Interventions
•
Decompressive hemicraniectomy
o Large
o Early
•
Temperature Control
o Hypothermia for refractory Increased ICP
•
Barbiturate Coma
If unable to control Inc ICP: Progression to Brain Death
•
President’s Commission report on guidelines for determination of brain death
culminated in a legal definition and established the Uniform Determination of
Death Act (UDDA)
144 | P a g e
o An individual who has sustained either
 Irreversible cessations of circulatory and respiratory functions
 Irreversible cessation of all functions of the entire brain
If unable to control Inc ICP: Progression to Brain Death
•
Determining Brain Death – 4 steps
o Establish irreversible and proximate cause of coma
 History, Examination, neuroimaging and laboratory
•
Achieve a normal or near-normal core temperature
o Greater than 35 degrees C (as close to 36 degrees C)
 Achieve a normal systolic BP > 100 mm Hg
 Perform one neurologic exam (acceptable in most states)
o Some states require more than 1 exam and some may specify a certain
level of expertise, i.e., Neurologist/neurosurgeon
If unable to control Inc ICP: Progression to Brain Death
•
Determining Brain Death – 4 steps
o Perform one neurologic exam (acceptable in most states)
 Coma: must lack all level of responsiveness (no eye opening, no
eye movement, no motor response to stimuli)
 Absence of brainstem reflexes (fixed pupils, absent dolls eyes/
cold calorics, absent corneal/swallow/gag, & no facial)
 Apnea: absence of spontaneous breathing (Allow PaCO2>60)
 8-10 min support with 100% FIO2 via O2 to ET
o Ancillary tests: EEG, cerebral angio, nuclear scan blood flow
 Not used to confirm brain death and cannot replace the clinical
exam
If unable to control Inc ICP: Progression to Brain Death
•
Determining Brain Death – 4 steps
o Time of brain death is
 Time the PaCO2 reached the target level and absent
spontaneous breathing
 If unable to do apnea, time of ancillary test officially
interpreted
Head Trauma Etiology of Brain Injury
•
Mechanisms of Injury
o Trauma
 Blunt
 Penetrating
 Blast
145 | P a g e
Pathophysiology of Brain Injury
•
Primary Injury
o Trauma
 Skull integrity
 Brain integrity
 Focal injuries
 Diffuse injuries
Classification
•
Secondary Injury r/t event
o Cerebral edema
o Changes in CBF
o Cellular
Types of Primary Injuries
•
•
Scalp
Skull
Primary Injuries
•
Cerebral Injuries
o Diffuse
o Focal
Diffuse Injury: Concussion
Diffuse Axonal Injury Epidural Hematoma
•
Associated with linear skull fracture
o Children may not have skull fx with epidural
o Rare in older adults
•
•
•
•
Location: 75% temporal region
CT: biconvex
Exam
Treatment
Subdural Hematoma
•
•
Associated with high velocity deceleration
Timing and cause
o Acute within 24-48 hours
 Rupture of bridging cortical veins
146 | P a g e
 Increased ICP/contusions
o Subacute 48 hours to 10 days
o Chronic 10 days to 6 weeks
 Rupture of bridging veins across parasagital space
•
•
CT
Clinical presentation
Acute Subdural Hematoma
Subacute Subdural
Chronic Subdural Hematoma
Management Subdural
•
Acute
•
Subacute and chronic
o Burr holes for removal of fluid
o Flat for 1-2 days
o Gradual elevation of head of bed
o Evaluation for deficits
o Acute surgical decompression
o Synchronous with increased ICP management
Cerebral Contusions
•
Types
o
o
o
o
o
o
•
•
•
Fracture
Coup
Countercoup
Herniation
Surface
Gliding (focal hemorrhage in cortex/subjacent white matter found in
DIA
Frequently frontal or temporal regions
Vasogenic edema and central necrosis
Diagnosis: CT and Exam
Focal Injury: Cerebral Contusions
•
Care Priorities
o Manage ICP
o Manage life support systems
o Assessment of deficits
o Education of patient/family
147 | P a g e
Head Injury Assessment
•
•
History of event
•
•
Signs of Increased ICP and evidence of injury
Severity of injury based on GCS
o Mild 13-15
o Moderate 9-12
o Severe 3-8
Diagnostics
Interventions
•
Airway
•
BP and Volume
o 2007 BTF guidelines 50-70
o Fluids/vasopressors
•
•
Mannitol or Hypertonic Saline
o Oxygenation: airway and oxygen
o Ventilation:
 Initial: PaCO2 35-45 mm Hg
 Phase II (days 2-6): PaCO2 may decrease
Positioning
o HOB 30 degrees with neck midline
Interventions
•
•
Draining CSF
•
Medications
o Sedation/Analgesia
o Barbiturate coma
•
•
•
Mild hypothermia
Temperature regulation
o Keep normothermic (36-37 degrees C)
System support
Rehab
Stroke
Ischemic Stroke
•
Etiology
o Thrombotic
o Embolic
148 | P a g e
•
Pathophysiology
o Disturbances in calcium
o Lactic acidosis
o Oxygen free radicals
Ischemic Stroke
•
•
Risk factors
•
Use NIHSS to assess
o Full
o Abbreviated
Signs/symptoms
o FAST:
 Face, Arm, Speech, Time
o Motor weakness
o Asymmetrical smile
o Difficulty speaking
o Numbness
o Visual changes
o Difficulty swallowing
Ischemic Stroke
•
Intervention
o ABC
o BP management
o Monitoring
o IV and labs
o Tests
 CT scan/MRI
 Chest x-ray and 12 lead
Time Window: Patients presenting within 4.5 hours from symptom onset are
candidates for tPA.
Ischemic Stroke
•
Decision Point
o Thrombolysis: up to 6 hours
 IV 3-4.5 hours
 IV/IA 4.5 hours
 IA 6 hours (off label)
o Merci Retrieval/Penumbra device
 Up to 8 hours
o Supportive care
149 | P a g e

Aspirin 325 mg rectally by 48 hours
Ischemic Stroke
•
tPA
•
Supportive care
o Do not drop BP unless
 Systolic BP >220/Diastolic BP > 120
 Treat with Labetalol or Nicardipine
o BP considerations: Tx –
 SBP > 185/DBP >110
o Administration: IV vs. IA
o Post-infusion care: Tx SBP >180 DBP > 105
Ischemic Stroke
•
VS/Neuro checks 1-2 hours
o NIHSS
•
•
•
•
Support Airway/O2/Pulse ox
Cardiac telemetry
Head of bed flat vs. 30 degrees
NPO till swallow assessment
Ischemic Stroke
•
Temperature management:
o Treat temp > 98.6
•
•
•
•
Hydrate/control serum glucose < 180
•
•
Educate family
Observe neuro status
Medications: Statins and Antiplatelet agents
Prevent complications
o Aspiration: NPO till swallow assessment
o DVT
o UTI
Secondary stroke prevention
Hemorrhagic Stroke Intra-cerebral Hemorrhage
•
Usually a result of hypertension
o Releases toxins leads to vasospastic activity
o Local decrease in perfusion
o Global decrease in perfusion
150 | P a g e
o Cellular changes
Subarachnoid Hemorrhage: Aneurysm
•
•
•
•
•
Occur at bifurcation
Defect in artery
Rupture point
Bleeds into SAS, brain tissue or ventricles
Danger
o Re-bleeding
o Vasospasm
Vascular Malformations
•
•
•
Developmental vascular anomalies
•
Symptom onset
o 80% between 20-40 years
o 20% before age 20
Result from error in embryonic vascular network
8.6% of all SAH
o Only 1% of all strokes
o Ratio of AVM to aneurysm 1:10
Pathophysiology: Ruptured AVM
•
Rupture causes hemorrhage, increased ICP, and hemispheric damage
Hemorrhagic Stroke
•
Assessment: ICH
o Headache, altered LOC, and N/V
o Motor weakness and sensory changes
o Cranial nerve deficits
o Signs of increased ICP
Hemorrhagic Stroke
•
Assessment: SAH
o Worst headache of life
o Meningeal: photophobia and nuchal rigidity
o Nausea/vomiting and dizziness
o Focal deficits, i.e., 3rd nerve
Hemorrhagic Stroke
•
Aneurysms – Assessment Grading Hunt and Hess Scale
151 | P a g e
o
o
o
o
o
I: alert, no deficit and minimal HA
II: awake, CN palsy, mild to severe HA
III: drowsy, confusion, mild focal deficit
IV: unresponsive and hemiplegia
V: comatose, moribund, extensor posturing
Hemorrhagic Stroke
•
Diagnostic Work-up
o LP
 Presence of RBCs/WBCs
 Elevated protein
o CT scan
 Presence of SAH
o Angiogram
o Spiral CT angiogram
o MRI/MRA
Hemorrhagic Stroke
•
Management of ICH
o Surgery vs. medical management vs palliative care
o Ventriculostomy
o ABC
 Airway/Ventilation
 BP control: fluids, vasopressors vs. vasodilators
 Circulation: TEDS/compression boots
o ICP control: CSF drainage and mannitol vs HS
o Medications
o System support
Hemorrhagic Stroke
•
Medical Management of SAH
o Pre-op
 BP control
 Hydrocephalus
o Surgical clipping vs. coiling
o Post-op
 Vasospasm
 Intra-arterial verapamil or nicardipine
 Cerebral angioplasty
Hemorrhagic Stroke
•
Team Management of SAH
o Preop
o Post-op
152 | P a g e
 ABC: PaCO2 >35
o ICP control: CSF drainage
o Vasospasm
 BP management and Triple H therapy
 Nimodipine
 Watch for sodium decline/diuresis
o Support Systems
Interventions
•
•
•
•
•
•
NG
IV fluids
Maintain anticonvulsants
Examine pt for injury
Treat hyperthermia
Psychological support
Neurologic Infectious Diseases Meningitis
•
Definition
o Inflammation of the coverings of the brain
•
3 Primary causes - (80% of all cases)
o Bacterial:
 Strep pneumonia
 Neisseria meningitidis
 H flu
o Viral: enteroviruses, arboviruses, and herpes viruses
o Fungal: cryptococcus neoformans
Meningitis
•
Pathophysiology
o Access routes: open wound, mucous membrane, or infected tissue
 Direct
 Penetrating wounds, skull fractures, neuro op
procedures, LPs, ICP, otitis media, sinusitis, or
osteomyelitis
o Hematogenous
 Septicemia/bacteremia, septic emboli, bacterial endocarditis,
URI, pelvic abscess
o CSF leak: rhinorrhea/otorrhea
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Meningitis
•
Pathophysiology
o Bacterial process
 Colonization: invades tissue/gains access to blood
 Crosses B-B barrier
 No host immune defense in CSF
 Rapid replication of bacteria
 Rapid increase in neutrophils
o Lysis of bacteria
 Produces exudate and inflammation of meninges
 Cerebral edema, vasculitis, infarctions, hydrocephalus and
increased ICP
Meningitis
•
Pathophysiology
o Viral transmission: fecal-oral contamination or respiratory droplets
 Virus replicates at site of entry
 Primary viremia is followed by viral replication in blood and
spread to CSF
 Patient is infectious from 3 days after infection to 10 days after
symptoms develop
 Incubation period 3-7 days
o Fungal transmission: similar to bacteria
Meningitis
•
Data Assessment – Neurologic Exam
o Bacterial
 Subjective: headache, stiff neck, photophobia, malaise
 Objective:
 fever, nuchal rigidity, photophobia, headache
 Cranial nerve palsy’s
 Petechial rash: 50% of meningoccal cases have red or
purple pinprick progressing to purple blotches; primary
area located on trunk, lower extremities, mucous
membranes, and conjunctiva
Meningitis
•
Data Assessment – Neurologic Exam
o Viral
 Milder than bacteria
 Resembles influenza
 Headache, fever, photophobia, malaise, and nausea
o Fungal
154 | P a g e

Non-specific: headache, fever, photophobia, malaise and
nausea
Meningitis
•
Data Assessment – Diagnostics
o Cultures, Cells, Glucose, Protein
Complications
•
•
•
•
•
Waterhouse-Friderichsen syndrome (adrenal hemorrhage)
DIC
Brain abscess
Hydrocephalus
Cerebral edema
Meningitis
•
Management
o Bacterial
 Medical – antibiotic therapy
 Strep pneumonia: Pen G, ceftriaxone, cefotaxime
o Resistant to Pen – Vancomycin
 Neisseria: Pen G or ampicillin
 H flu: Cefotaxime or ceftriaxone
o Other therapy
 Steroids, ICP management, Airway control
Meningitis
•
Management
o Nursing
 Institute airborne precautions
 Assess neuro status closely
 Airway/breathing – may be intubated
 Hemodynamic control – may need vasopressor support
 Control ICP
 Monitor lab values
 Administer antipyretics/analgesics/antibiotics,
anticonvulsants
 Administer IV fluids/nutritional support
Meningitis
•
Management
o Viral
 Medical: antiviral therapy (acyclovir)
155 | P a g e
 Nursing: same as bacterial
o Fungal
 Medical: C. neoformans meningitis is treated with
amphotericin B and flucysosine
 Nursing: Same as bacterial
Encephalitis
•
Definition:
o Inflammation of the brain parenchyma caused by virus, bacterium,
fungus, or parasite
•
Etiology
o Virus is most common cause
 Respiratory system: Mumps, measles, varicella virus
 Oral: Enteroviruses/polio
 Oral or genital: herpes simplex
 Bites
 Animal: Rabies
 Insect: Arbovirus (mosquito) Lyme disease (tick)
Encephalitis
•
Pathophysiology
o Virus
 Enters body and colonizes
 Penetrates cell
 Transcribes virus coated proteins and replicates the viral
nucleic acid
 Blood brain barrier prevents virus from entering CNS but can
enter through cerebral capillaries or choroid plexus and/or
along peripheral nerves
 Virus attacks susceptible neurons and causes cell lysis
Encephalitis
•
Pathophysiology
o Herpes virus
 Lies dormant within dorsal ganglia of the trigeminal nerve
 Virus is activated in ganglia then follows the fibers and attacks
frontal/temporal lobes causing bilateral hemorrhagic necrosis
Encephalitis
•
Pathophysiology
o Arbovirus: includes St. Louis/eastern/western equine and West Nile
Virus
 Humans bitten by the vector are asymptomatic or develop
156 | P a g e

vague flu like symptoms
Produces diffuse disintegration of single nerve cells,
inflammation, and necrosis of both white/gray matter (spares
the brainstem)
Encephalitis
•
Data Assessment
o Clinical Presentation
 Herpes simplex: headache, confusion, hallucinations, changes
in LOC, personality changes, behavior problems, aphasia,
hemiparesis, temporal lobe seizures
 Arbovirus: headache, myalgias, malaise, fever, nuchal rigidity,
altered LOC, confusion, N/V, and seizures
 West Nile: swollen lymph nodes, erythematous rash, and
profound muscle weakness with normal sensation and reflexes
Encephalitis
•
Data Assessment
o Diagnostics
 Herpes:
 LP : elevated opening pressure with CSF + lymphocytes,
increase protein, normal glucose, PCR –positive for
HSV-1 antigen in 98% of cases
 CT: gyral enhancement of inferior temporal/frontal
lobes
 MRI: edema/hemorrhage of frontal/temporal areas
 Arbovirus:
 ELISA serological assays for antiviral IgM (early) and
IgG (later)
 West Nile: IgM capture ELISA antibody test
Encephalitis
•
Management
o Medical
 Herpes: Acyclovir for 10-14 days
 Others: Same as meningitis
 Arbovirus: Similar to bacterial meningitis with controlling
impact to body systems
o Nursing
 Same as meningitis
157 | P a g e
Lyme Disease
•
Definition
o Vector-born illness caused by a tick transmitted spirochete affecting
multiple systems
•
Etiology
o Borrelia Burgdorferi, spirochete transmitted by Ixodes dammini
(small tick)
•
Pathophysiology
o Stage 1
 Erythema migrans or a bulls-eyes rash expanding lesion at site
of tick bite
 Flu like symptoms-headache, malaise, fatigue, myalgias
o Stage 2
 Disseminated infection within several weeks
 Meningeal signs including headache, stiff neck, difficulty
concentrating, cranial nerve dysfunction (unilateral or bilateral
facial palsy, radiculopathies, ataxia, cardiac abnormalities such
as AV block, lyme arthritis – joint swelling/pain especially in
knees
o Stage 3
 Lyme encephalopathy with cognitive changes, fatigue, and
polyneuropathy
•
Data Assessment
o Diagnostics
 CSF studies: lymphocyte counts/protein levels increased
 Serology: ELISA positive for IgM followed by elevated IgG
spirochete antibody reaction
 Western Blot analysis positive
•
Treatment
o Medical: Antibiotic
o Nursing:
 Supportive
 Prevention – wear protective clothing and check all skin areas
when out in forrest
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Guillain-Barre Syndrome
•
Definition
o Acute, inflammatory, demyelinating polyneuropathy causing
weakness, sensory loss, and areflexia
•
Etiology
o Immune mediated with precipitating factors of possible infection
(viral 1-2 weeks preceding 70% of all cases)
•
Pathophysiology
o Inflammatory lesions through PNS
o Defect linked to peripheral nerve myelin
 Some cases cause axonal degeneration
o Macrophages attack normal myelin, produce demyelination
•
Data Assessment
o Subjective: rapidly progressing weakness or paresthesias usually
ascending
o Objective:
 Progressive motor weakness which ascends
 Sensory loss may or may not be present
 Loss of DTRs
 Facial, ocular or oropharyngeal muscles affected in 50% of
cases
 Autonomic dysfunction causing ileus, hypotension,
hypertension, and arrhythmias
 Respiratory compromise if ascends to diaphragm
•
Diagnostics
o LP: increased protein
o EMG: slowing of conduction
•
Management - Medical
o Plasma exchange urgent every day for 10-15 days
o IVIG 1-2 mg/kg in divided doses over 3-5 days
 Watch for anaphylaxis, chills, fluid overload
o Pulmonary – may need to be intubated
o Hemodynamic support
o Analgesic support for increased pain
•
Management – Nursing
o Asses VS/Neuro function watching for ascending weakness
o Mechanical ventilation – support respiratory function
o Watch for hemodynamic alteration
 Support BP
o Assess pain and provide analgesia
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Seizures and Epilepsy
•
•
Abnormal firing in the brain
•
Classification
o Partial seizure: onset of synchronous cortical discharges involving a
focal brain region
o Generalized seizure: sudden onset involving both hemispheres
•
Partial Seizures
o Simple partial: focal brain region activity without alteration in
consciousness
 An aura can be SPS
 Motor events such as face twitching/hand jerking
 Somatosensory events such as unusual taste in mouth
 Psychic events – illusions/hallucinations/déjà vu
o Complex partial seizures: brain region affected with alteration in
consciousness
 Often preceded by SPS with progressive impairment in cons
 Automatisms (lip smacking/blinking/picking at clothes)
 Motor phenomena wandering, running, arm jerking
o Partial seizure that secondarily generalize
•
Generalized Seizure – both hemispheres
o Absence seizure: impaired responsiveness, minimal motor
involvement, lasts < 30 seconds
o Myoclonic: sudden shock-like muscle contraction
o Atonic: drop attacks (brief LOC/loss of muscle tone)
o Tonic: increased tone in extensor muscles
o Clonic: start with LOC/sudden hypotonia then limb jerking
o Tonic- Clonic: LOC, increased tone, rhythmic muscle jerks
•
Subjective
o Obtain description of event including time
o Precipitating factors?
o Post-ictal behavior
•
Objective
o
o
o
o
Epileptogenesis occurs during an imbalance between cerebral excitation/inhibition
o Brain cells become abnormally linked together leading to abnormal
electrical firing
o Excitation (glutamate/NMDA) vs Inhibition (GABA – Facilitates
activity of Cl channels/opens K channels or closes Ca channels)
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Assess mental state and cognition
Evidence of trauma/infection
Focal findings
Asymmetries
•
Diagnostics
o Lab tests
o EEG
o CT/MRI to r/o mass lesions
•
Treatment Pharmacologic
o Phenobarbital 60-250 mg/day
15-40
o Dilantin (phenytoin) 300-600 mg/day
o Tegretol (carbamazepine) 600-1200 mg/day
o Mysoline (primidone) 25 mg tid
o Depakote (Valproic Acid) 15-60 mg/kg/day
o Lamictal(lamotrignine)100-300 mg/day
o Neurontin (gabapentin) 900-3600 mg/day
o Keppra (levetiracetam) 1000-3000mg/day
o Vimpat (lacosamide) 10-400 mg/day
10-20
4-12
5-12
50-100
2-4.5
2-20
3-37
3.8-9.3 ng/ml
•
Side effect profile
o Stevens Johnson syndrome: erythema multiforme
o Aplastic anemia
o Allergic dermatitis
o Hepatic failure
o Most common: somnolence, dizziness, memory impairment, cognitive
slowing, ataxia
•
Nursing interventions
o Education
o Explain drug-drug interactions
o Other: Ketogenic diet (high in fat/low carbs/restrict calories); vagal
nerve stimulator; surgery (temporal lobectomy or corpus
callosotomy)
Status Epilepticus Pathophysiology
•
•
•
•
•
Tonic-clonic seizures
Increase cerebral metabolic rate/oxygen use
CBF increases 3-5x normal
Cellular swelling
Systemic metabolic acidosis
Etiology/Precipitating Factors
•
•
•
•
Withdrawal from anticonvulsants, alcohol or drugs
CNS infections
Brain tumors
Metabolic disorders-uremia, hypoglycemia, or hyponatremia
161 | P a g e
•
•
•
Craniocerebral trauma
Cerebral edema
Stroke
Nursing Assessment
•
•
History
Type of seizure activity
o Absence (petit mal)
o Focal
o Tonic-clonic
o Electrical status
o Status
Diagnostics
•
Lab
o
o
o
o
o
o
•
Electrolytes
Hypoglycemia
Hypoxemia
Prolactin level
Myoglobin
Anticonvulsant drug levels
EEG
Interventions
•
Airway and ventilations
o Supplemental oxygen and pulse oximetry
o Intubate if prolonged seizure
o Check Blood glucose
•
Normal Saline IV
o Thiamine 100 mg diluted with 8 ml NS slow IV push over 5 minutes
then
o 50% Dextrose 50ml slow IV push (if bedside Glucose < 70)
•
Stop seizure
o Lorazepam 2 mg IV push q 1 minute up to 8 mg
o Fosphenytoin (Cerebyx) 20 PE mg/kg
•
Protect from injury
Brain Tumors Facts/Stats
•
Incidence
o Primary - 36,000/yr
o Secondary - 18,000/yr
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•
•
•
Males > Females
Age: 40-60 age group
Classification
o Benign: regular cell structure
o Malignant: infiltrates brain tissue, poor boundaries, rapid mitotic
activity, necrosis
o Location: supra vs. infratentorial
o Primary vs. Secondary
o Intra-axial (glial cells) vs. extra-axial (meninges, CN, pituitary, & cysts)
o Histological origin
Intrinsic Tumors
•
Astrocytoma and GBM
o Grades I - IV
•
Oligodendrocytoma
o White matter
o Frontal and parietal lobes
•
Ependymoma
o Ependymal cells in ventricles
•
Medulloblastoma
o Highly malignant in young children
Extrinsic Tumors
•
Meningiomas
o Benign, slow growing
•
Neuromas
o Acoustic tumor (VIII CN)
o Schwannoma
•
Neurofibromatosis
o Type I: café au lait spots
o Type II: bilateral hearing loss
Congenital Tumors
•
Hemangioblastoma
o Slow growing, vascular tumor
o Common in cerebellum
•
Craniopharyngioma
o Embryonic Rathke’s pouch/suprasellar
o Arise from pituitary hypophysis
 Inc ICP, Pituitary/hypothalamic dysfunction
 Visual disturbances
163 | P a g e
Pituitary Tumors
•
Secreting
o ACTH (Cushing) or GH (gigantism)
•
Non-secreting (90% space occupying)
o Compresses pituitary: visual/hypopituitary
Pathophysiology
•
•
•
Increased ICP
Tumor growth
Cerebral edema
o Tissue surrounding the vicinity of tumor
o Endothelial cells of white matter
o Increase permeability of plasma and vasogenic edema
Signs/Symptoms
•
•
•
•
•
•
Headache
Seizures
Vomiting
Alterations in consciousness
Localizing signs
Tumor area
o Frontal: affect, motor, speech, behavior
o Parietal: numbness/sensory
o Temporal: psychomotor seizures/receptive aphasia
o Occipital: vision
o Pituitary: visual, headaches, cushings, acromegaly
o Ventricles: hydrocephalus, HA, changes LOC
o Cerebellum: ataxia, incoordination, dysmetria
o Brainstem: CN defects, vomiting, respiratory
Complications of Tumor Growth
•
•
•
•
•
Edema
Increased ICP
Seizures
Hydrocephalus
Hormonal Changes
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•
Focal Deficits
Treatment
•
•
•
•
•
•
•
Stereotactic therapy
Craniotomy
Gamma Knife
Conventional radiation
Brachytherapy
Chemotherapy
Gene therapy/Virus therapy
Nursing Interventions
•
•
Pre-op: Steroids, anti-convulsants, body image
•
Pituitary Tumors:
o Watch I/O, Na, spec grav
Post-op
o ABC
o Monitor neuro status
o Watch for seizures
 Dilantin: dosing/levels
o System support
o Family/Patient Support
Neurosurgical Approaches to Mass Lesions/Hemorrhage
Reason for Surgery
•
•
•
•
•
Removal of debulking of tumor
Drainage or evacuation of hematoma
Clipping of aneurysm
Removal of an AVM
Removal of seizure focus
Post-Operative Information
•
•
•
•
Reason for surgery
Specific area of involvement
History of pre-op deficits
Pre-existing medical conditions
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•
•
•
Baseline neuro assessment
Type and time of anesthetic/sedative
Fluid status
Objectives of Nursing Management
•
Frequent assessment and monitoring of neuro status for detection of
signs/symptoms
•
•
Control of factors which cause increased ICP
Prevention and early recognition of complications
Supratentorial Craniotomy
•
Focus of exam:
o LOC
o Motor exam
o Sensory exam
o CN II, III, IV, V, VI, and VII
Supratentorial Craniotomy: Complications
•
Cerebral Edema
o Assess: LOC, contralateral motor weakness, and changes in EOM’s and
pupils
o Treat: HOB 30, IVF normovolemic, and ICP monitor (severe cases)
o Inc. ICP: CT scan, mannitol, propofol, and drain CSF
Supratentorial Craniotomy: Complications
•
Intracerebral Hemorrhage
o Occurs in epidural space or within tumor bed
o Assess: decrease in LOC, contralateral motor changes, and
EOM’s/pupil changes
o Treat: mannitol, intubate, propofol and surgery
•
Seizures
o Assess: type of seizure activity
 Grand mal
 Focal involving hand/face
o Intervene: position, suction, assess, oxygen, and medication
o Prophylactic anticonvulsant therapy
•
CSF Leak
o Occurs due to opening in Subarachnoid space
o Sanguenous drainage surrounded by yellow or clear ring
o Treat: serial LPs or lumbar drain and possible surgery
166 | P a g e
•
Diabetes Inspidus
o Seen most frequently in pituitary tumors/ surgery around the
hypothalamus
o Decreased ADH
o Increased U.O. >250cc q1h
o Decreased specific gravity < 1.005
o Rising Na
•
DI -Treatment
o Fluid volume replacement cc/cc or 1-2cc/cc of urine output
o Vasopressin
o DDAVP
Infratentorial Compartment
•
•
Cerebellum
Brain stem
o Midbrain
o Pons
o Medulla oblongata
Infratentorial Craniotomy
•
Focus of Exam
o Level of Consciousness
o Motor and coordination
 Quadraparesis
 Tremors
o Vital sign instability: respiratory arrest, bradycardia, and widening BP
o CN - III, IV, V, VI, VII, VIII, IX, X, XI, and XII
Infratentorial Craniotomy: Complications
•
Posterior Fossa Hemorrhage
o Assess - severe headache, rapid deterioration of LOC, respiratory
ataxia/arrest, quadriparesis, pinpoint pupils, and dysconjugate gaze
o Treat - intubate, mannitol, rapid CT, and stat OR
•
Respiratory Compromise-due to edema of brainstem, aspiration, or neurogenic
pulmonary edema
o Assess - oxygenation/ventilation, respiratory effort and pattern
o Treat - intubate, ventilate, use PEEP if needed, and lasix for NPE
•
Tension pneumocephalus
o Assess - increased lethargy, decreased LOC, and focal/lateral deficits
o Treat - CT scan of brain, evacuate if large, and 100% FIO2 per mask
167 | P a g e
•
Hydrocephalus
o Assess - decrease LOC, Parinaud’s sign, change in pupils and gaze,
unsteady gait, and incontinence
o Treat - place ventriculostomy and possible internal shunt
Complications: Supratentorial and Infratentorial
•
•
•
•
•
Thromboembolism/PE
Gastric ulceration and bleeding
Hypovolemic shock
Meningitis
Cardiac Arrhythmias
Hypoxic Encephalopathy: Causes
•
•
Ischemic hypoxia from decrease in CBF
•
•
Shunt hypoxia from Arteriovenous shunting
•
•
•
Histotoxic hypoxia from toxic agents
Low extractivity hypoxia from low PaO2/low Hgb/Low half saturation tension
(high affinity oxygen)
Dysperfusion hypoxia from increased mean diffusion length of erythrocytes to
mitochondria caused by edema
Uncoupling hypoxia from mitocondrial dysfunction
Hypermetabolic hypoxia from increased demand
Symptoms/Signs: Hypoxic encephalopathy
•
New skill learning and processing of complex information are the most vulnerable
to hypoxia
•
PaO2
o 80 mm Hg: impaired dark adaptation
o 55-45 mm Hg: impaired learning and short term memory
o 40-30 mm Hg: loss of judgment, euphoria, delirium, and muscle
incoordination
o < 25-20 mm Hg: consciousness is rapidly lost
168 | P a g e
Postanoxic Encephalopathy Syndrome
•
•
Myoclonus
•
•
Parkinsonism
Delayed anoxic encephalopathy
o Unexplained phenomenon
o During recovery (1-4 weeks) from an anoxic insult
o Irrritability, confusion, apathy, and agitation/mania
o Serious mental and motor disturbances, diffuse rigidity, spasticity,
weakness, shuffling gait, incontinence, coma and death after 1-2
weeks
Cerebral Palsy
Chronic Neuro Disorders Parkinson’s Disease
•
Neurodegenerative disorder caused by
o Depletion of dopamine producing cells in substantia nigra
o Average onset is age 60, higher in men/causasian
•
Cardinal signs
o Resting tremor, rigidity, bradykinesia, and diminished postural
stability
•
Other
Increased risk of falls
Can have depression/dementia/anxiety/psychosis
Other: apathy, sleep disturbances, impulse control disorders
Autonomic dysfunction: urinary incontinence, sexual dysfunction,
constipation, orthostatic hypotension, impaired thermoregulation,
sensory abnormalities
o Dysphagia/excessive drooling
o
o
o
o
Parkinson’s Treatment
•
Pharmacologic
o L-dopa: Carbidopa plus L-dopa (Sinemet)
o Dopamine agonists: 1st line tx
o Amantadine (Symmetrel): tx dyskinesias
o Catechol-O-methyl transferase (COMT) inhibitors: Used adjunctively
to ldopa to prevent breakdown of dopamine and prolong availability
of L-dopa
169 | P a g e
•
Surgical Interventions
o Deep brain stimulation: Target subthalamic nucleus or globus pallidus
interna
 Permits return of normal or near normal downstream outputs,
allowing normalization of motor and/or limbic function
•
Surgical Interventions
o Deep brain stimulation: Post op
 Observe for changes in neuro exam
 Keep systolic BP < 150 mm hg for first 24 hours
 IV antibiotics 24-48 hours
 Stool softeners / antiembolic devices
 Deep breathing/coughing to reduce pneumonia
o Device turned on 2-3 weeks after placed
Myasthenia Gravis
•
Description: Autoimmune disorder in which normal transmission of nerve impulses
are interrupted at the neuromuscular junction
o Affects voluntary muscle groups including ocular, oropharyngeal,
facial, shoulders, and arms/legs
 Proximal > distal
 Characterized by fluctuating and fatiguable muscle weakness
exacerbated by exercise and improves with rest
o Affects women > men usually 20s/30s
o Etiology
 Acquired autoimmune process rt receptors for Ach @ muscle
surface are reduced by auto-antibodies leads to impaired NM
transmission/weakness
 Thymus abnormalities may be responsible for causing immune
attack on the muscle receptors
Myasthenia Gravis
•
Initial manifestations
o Ptosis/diplopia 80% of cases
o Oropharyngeal weakness – painless/fatigable dysphagia or dysphonia
o Fatigable limb weakness during course of day
•
•
Fluctuate over time/worsens after sustained activity
•
S/S
Exacerbations r/t systemic illness/fever/surgery, menses/pregnancy,
hypothyroidism, heat/stress
o Subjective: muscle weakness, diplopia/ptosis, slurred speech,
dysphagia, or shortness of breath
o Objective: Weakness (more proximal), may have inability to lay flat
(orthopnea), frequent yawning/sighing, difficulty swallowing
170 | P a g e
•
•
EMG
•
Treatment
o Administration of anticolinesterase inhibitors
 Prevents rapid destruction of Ach
 Pyridostigmine (Mestinon) must be given on time with
no missed dose
o Corticosteroids/immunosuppressive agents
o Cyclosporine (Neoral): inhibits tcell immune responses
o Plasma exchange
o IVIG: temporary intervention
o Mycophenolate mofetil (CellCept): immunosuppressive agent reduces
the production of antibodies by attacking the receptor sites of NM
junction
o Surgical intervention: thymectomy
o Nursing: Admin drugs on time/pt education
Edrophoium chloride (Bioniche test): short acting anticholinesterase inhibitor
o Requires IV administration 2 mg/ test for strength 45-60 seconds
later
o Can repeat to 10 mg
o Positive if improvement in strength seen (effect disappears in 5
minutes)
o Use with caution: bradycardia/asystole, excessive salivation,
bronchial secretions
Practice Exam Questions
1. HH, a 45 year old right handed male, presents to the ED with headache,
right arm weakness with right facial droop and difficulty expressing
speech. A CT scan reveals diffuse cerebral edema surrounded by a ringenhancing lesion. The most likely location of the mass is:
A.
B.
C.
D.
Right parietal lobe of cerebral hemisphere
Left temporal lobe of cerebral hemisphere
Right frontal lobe of cerebral hemisphere
Left frontal lobe of cerebral hemisphere
2. BP, a 52 year old female, was admitted to the ICU following rupture of a
cerebral aneurysm and large subarachnoid hemorrhage. Her CT scan of the
brain revealed acute hydrocephalus. The most likely cause of BP’s
hydrocephalus is
Cerebral aneurysm exerting pressure on the choroid plexus in the
ventricles limiting the CSF absorption
171 | P a g e
A. Blood in subarachnoid space mixing with CSF and occluding the arachnoid villi
which helps reabsorb CSF in the brain
B. Overproduction of CSF from the aneurysm rupture
C. Reduced absorption of CSF by the choroid plexus
•
A is incorrect (Cerebral aneurysm exerting pressure on the choroid plexus in the
ventricles limiting the CSF absorption) because the choroid plexus makes CSF. It
does not absorb CSF.
•
C is incorrect (Overproduction of CSF from the aneurysm rupture). Aneurysmal
rupture does not increase CSF production by the choroid plexus.
•
D is incorrect (Reduced absorption of CSF by the choroid plexus) since CSF is
absorbed by the arachnoid villi.
3. LP, a 45 year old male, has a demonstrated right arm weakness 2 out of 5
on the motor scale. Which best defines 2/5 motor strength?
A.
B.
C.
D.
Arm drifts downward and weakens with resistance
Arm demonstrates flicker movement of muscles
Arm can be raised against gravity
Arm moves back and forth but cannot be raised against gravity
•
A is incorrect: Arm drifts downward and weakens with resistance would be rated as
4/5 on the motor strength scale.
•
B is incorrect: Arm demonstrates flicker movement of muscles is indicative of 1/5
motor strength
•
C is incorrect: Arm can be raised against gravity is reflective of 3/5 on motor
strength scale.
4. You are assessing the patient’s pupils and extraocular movements. The
patient left pupil is reactive to light and moves in all directions. When
assessing the right pupil, you notice the pupil is sluggish to light and comes
to rest looking outward toward the ear. Which cranial nerve is affected?
A.
B.
C.
D.
•
Cranial nerve II
Cranial nerve III
Cranial nerve IV
Cranial nerve VI
A is incorrect since Cranial nerve II is responsible for visual acuity and the sensory
limb of the pupillary light reflex
172 | P a g e
•
•
C is incorrect since Cranial nerve IV allows the eye to look downward
D is incorrect since Cranial nerve VI allows the eye to look outward toward the ear.
VI nerve palsy would cause the eye to roll toward the nose at rest.
5. A brain injured patient was admitted 4 hours ago after sustaining a large
subdural hematoma which was evacuated surgically. An ICP monitor with
CSF drainage was placed by the MD. The ICP increases to 24 mm Hg while
the patient’s CPP is 64 mm Hg. After draining CSF, the 1st intervention
would be to lower the ICP by:
A.
B.
C.
D.
Lowering the head of bed
Administer hypertonic saline or mannitol
Institute a pentobarbital coma
Lower the PaCO2 to 28 mm Hg
•
•
A is incorrect: Lowering the head of bed would increase the ICP.
•
D is incorrect since lowering the PaCO2 to 28 mm Hg would decrease CBF and
create ischemia especially on Day 1 of a TBI when cerebral blood flow is often
critically reduced. Lowering PaCO2 < 30 mm Hg should be avoided.
C is incorrect since instituting a pentobarbital coma would be a tertiary
intervention.
6. It is day 4 of FZ’s hospitalization following a severe TBI. He has
experienced an increase in urine output (1000 ml) over the past 3 hours.
His MAP has decreased to 75 mm Hg and his ICP has increased to 30 mm Hg
resulting in a CPP of 45 mm Hg. If FZ has intact autoregulation, the most
appropriate intervention would be to:
A.
B.
C.
D.
Administer 500 ml fluid bolus to increase the MAP and decrease the ICP
Administer 50 grams of mannitol to reduce the ICP
Begin nicardipine to lower the MAP and ICP
Do nothing since the MAP/ICP/CPP is within normal ranges.
•
B is incorrect: Administering 50 grams of mannitol to reduce the ICP may
significantly lower the BP resulting in a further increase in ICP.
•
C is incorrect: Beginning nicardipine to lower the MAP and ICP would actually
increase the ICP.
•
D is incorrect: Do nothing since the MAP/ICP/CPP are within normal ranges. The
ICP is elevated (> 20) and the CPP is not in the ideal range of 50-70 mm Hg.
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7. JR, a 34 year old male, fell from a ladder and sustained a severe TBI. His
GCS on arrival was 1-3-1 with pupils 2 and minimally reactive to light. CT
scan of brain shows multiple punctate hemorrhages along with an acute
epidural hematoma. The neurosurgeon evacuated the bleed and placed an
ICP/Brain oxygen monitor into the brain. Admit to ICU: GCS 1-4-1; MAP 80
ICP 10 CPP 70 PbtO2 12 PaCO2 30 CVP 10.What is your first intervention?
A.
B.
C.
D.
•
•
•
Give 250 ml NS to increase CVP
Administer mannitol 25 grams IVP
Decrease the Tidal volume or rate to increase the PaCO2
Do nothing since the patient’s parameters are within the normal zone
A is incorrect (Give 250 ml NS to increase CVP) since the CVP & CPP are normal
B is incorrect (Administer mannitol 25 grams IVP) since the ICP is normal
D is incorrect (Do nothing since the patient’s parameters are within the normal
zone) since the patients oxygen level is critically low in the brain.
8. EG, an 80 year old male, was previously independent and able to care for
himself. His daughter stated the pt is now unable to walk and is
confused/disoriented. A CT scan of the brain reveals bilateral large chronic
subdural hematomas. The neurosurgeon evacuated both SDH and has
placed a JP to gravity drainage. The patient was extubated post-op. Where
should the head of bed be maintained?
A.
B.
C.
D.
Head of Bed flat for 24-48 hours
Head of bed at 15 degrees for 10 days
Head of bed at 30 degrees to reduce ICP
Head of bed at 45 degrees to reduce ICP
•
B is incorrect (Head of bed at 15 degrees for 10 days) due to the position and length
of time
•
C and D are incorrect (Head of bed at 30 degrees or 45 degrees to reduce ICP) since
ICP is usually normal and the brain needs to re-expand into the space occupied by
the blood clot. Elderly individuals generally sustain significant brain atrophy, thus
have more space in the cranial vault.
9. LL, a 65 yr old female, developed an acute onset of left sided weakness with
neglect to the left side at 1235pm. Her speech became slurred and she
didn’t know where she was. Her son brought LL to the ED where a CT scan
174 | P a g e
of the brain revealed no hemorrhage. A CTA done demonstrated an
occlusion of the right middle cerebral artery. The ED
physician/neurologist has ordered IV tPA. It is 2 hours 50 minutes since
symptom onset. The patient’s last BP was 190/100 mm Hg. Your first
action is:
A. Administer the tPA 0.9 mg/kg IV dose since there is only 10 minutes in the
treatment window.
B. Administer the tPA 0.6 mg/kg IV dose and Labetalol 10 mg IVP at the same time.
C. Start IV nitroprusside to reduce the BP.
D. Administer 10-20 mg of IV labetalol to reduce the BP prior to administering the
tPA.
•
A is incorrect (Administer the tPA 0.9 mg/kg IV dose since there is only 10 minutes
in the treatment window) because controlling the BP must be done prior to
administering tPA
•
B is incorrect (Administer the tPA 0.6 mg/kg IV dose and Labetalol 10 mg IVP at the
same time) because the dose of tPA is incorrect and the BP must be lowered prior to
the administration of tPA
•
C is incorrect (Start IV nitroprusside to reduce the BP). Labetalol and nicardipine
are the first 2 drugs of choice when lowering BP in acute ischemic stroke
10. BP, a 90 year old female, presents with acute onset of aphasia and right
sided hemiparesis. She was last seen normal 12 hours ago. Her BP is
195/105. Which medication do you anticipate the physician team to order
first?
A.
B.
C.
D.
IV labetaolol 10 mg IV to lower the BP
tPA 0.9 mg IV (10% bolus/90% drip over 60 min)
Aspirin 325 mg p.o.
Aspirin 325 mg per rectum
•
A is incorrect (IV labetaolol 10 mg IV to lower the BP) because BP thresholds in the
non-tPA patient is 220/120.
•
B is incorrect (tPA 0.9 mg IV (10% bolus/90% drip over 60 min) since the pt
symptoms are > 3 hours
•
C is incorrect (Aspirin 325 mg p.o.) since the patient may have difficulty swallowing
and needs to have her swallow evaluation prior to receiving any p.o. medications
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11. SS, 50 year old female, presents with the worst headache of her life and
photophobia. Her neuro exam is otherwise normal. CT scan of brain shows
a large subarachnoid hemorrhage from a possible cerebral aneurysm. Her
BP is 170/90. Initially, the physician will want the BP treated if it is greater
than:
A.
B.
C.
D.
Systolic BP >90 mm Hg
Systolic BP > 150 mm Hg
Systolic BP > 180 mm Hg
Systolic BP > 220 mm Hg
•
A is incorrect (Systolic BP >90 mm Hg) A SBP less than 90would not be beneficial to
cerebral perfusion
•
C. and D are incorrect (Systolic BP > 180 mm Hg or Systolic BP > 220 mm Hg). These
ranges are too high and may contribute to re-bleeding of the aneurysm.
12. SS is now 10 days post aneurysm rupture. The aneurysm was surgically
clipped on day 2. SS began c/o of a headache this morning. Her motor exam
has changed in the last 2 hours with her right arm motor strength has
diminished from 5/5 to 3/5. She is having word finding problems with her
speech. The most likely explanation for this change in status is:
A.
B.
C.
D.
Increased ICP
Rebleeding
Ischemic Stroke
Vasospasm
•
A is incorrect (Increased ICP). Although cerebral edema is possible after SAH, a
change in LOC should occur.
•
B is incorrect (Re-bleeding). Since the aneurysm has been surgically repaired, this
complication is unlikely.
•
C is incorrect (Ischemic Stroke). If vasospasm is not treated, the end result could be
an ischemic stroke.
13. SP, a 20 year old college student, presents to the ER with c/o of
photophobia, stiff neck, temp of 103 degrees, malaise, and purple blotches
primary area located on trunk. He is given antibiotics in the ED. He is
176 | P a g e
admitted to the ICU with a BP of 85/50 HR 140 and ventilated. Cultures
have been done but there are no results. SP’s likely infectious illness is:
A.
B.
C.
D.
Lyme Disease
Herpes simplex encephalitis
Neisseria Meningitides
Guillain Barre Syndrome
•
A is incorrect (Lyme Disease) is a viral encephalitis that presents with bull’s eye rash
and malaise. It is not accompanied by purple blotches.
•
B is incorrect (Herpes simplex encephalitis). The pt may experience HA, fever,
malaise but also has strange behavior, personality changes, and seizures.
•
D is incorrect (Guillain Barre Syndrome). Presentation includes ascending weakness
accompanied by sensory loss and cranial nerve dysfunction.
14. Patients sustaining Guillain Barre syndrome are most likely to have
prolonged failure of which organ system?
A.
B.
C.
D.
Cardiac failure
Respiratory failure
Renal failure
Liver failure
•
A is incorrect (Cardiac failure). Although patients may experience autonomic
dysfunction with accompanying BP variation, arrhythmias, ileus, diaphoresis or loss
of sweating, urine retention it is not chronic heart failure.
•
C is incorrect (Renal failure). Patients may experience urinary retention but
generally do not have Acute Renal Failure.
•
D is incorrect (Liver failure). The liver is not generally involved.
15. A 10 year old male is reported by his teacher ignore repeated requests to
answer questions. The student often stares for short periods of time. This
type of seizure is a:
A.
B.
C.
D.
Partial seizure
Complex Partial seizure
Myoclonic seizure
Generalized seizure known as an absence seizure
177 | P a g e
•
A is incorrect (Partial seizure). Partial seizures are localized to one area of the
brain & do not impair consciousness.
•
B is incorrect (Complex Partial seizure). These are manifested by automatisms and
motor phenomena such as wandering, running or arm jerking.
•
C is incorrect (Myoclonic seizure). These are generalized seizures that are sudden
shocklike muscle contractions.
16. A patient in Status epilepticus must receive medication immediately to
halt the seizure activity. The first line medication for status epilepticus is:
A.
B.
C.
D.
Valium 10 mg po
Midazolam 1 mg IV
Phenobarbital 30 mg IV
Lorazepam 2 mg IV
•
A is incorrect (Valium 10 mg po). A patient in status will be unable to take any
medication by mouth.
•
B is incorrect (Midazolam 1 mg IV). Although midazolam is used as a secondary
drug in status, the dose would be much higher, i.e., 10 mg
•
C is incorrect (Phenobarbital 30 mg IV). This drug is considered a second line drug
and the dosing is 20mg/kg IV given slowly 50-100 mg/minute
17. TP, a 53 year old male, has been diagnosed with a brain mass. His
symptoms include: contralateral sensory loss, neglect to the left side, and
inability to draw with loss of spatial orientation. The most likely area of the
brain affected is:
A.
B.
C.
D.
Parietal lobe
Frontal lobe
Temporal lobe
Occipital lobe
•
B is incorrect (Frontal lobe). Tumors in this area affect motor to the opposite side,
speech (if dominant hemisphere), judgment, personality, initiation, and continence.
•
C is incorrect (Temporal lobe). Tumors in this area present with receptive aphasia
(dominant hemisphere only) and some visual field cuts.
•
D is incorrect (Occipital lobe). Tumors in this area affect visual perception and field
of vision.
178 | P a g e
18. TP undergoes a craniotomy for debulking of a large tumor. Post
operatively, he is extubated and is admitted to the ICU. After one hour, TP
sustains a generalized seizure lasting 45 seconds. What is your initial
intervention?
A.
B.
C.
D.
Check the pupillary reaction
Administer IV Midazolam
Assess Airway and Breathing and prepare for possible intubation
Get a stat CT scan of the brain
•
A is incorrect (Check the pupillary reaction). Although the pupils need to be
checked, it would not precede assessing the airway.
•
B is incorrect (Administer IV Midazolam). Airway stabilization is first. Lorazepam
IV would be the preferential drug of choice to reduce recurrence.
•
D is incorrect. (Get a stat CT scan of the brain). This intervention would be done
after C, B, and A.
179 | P a g e
ADULT CCRN REVIEW
CARDIOVASCULAR SYSTEM
Barbara “Bobbi” Leeper, MN, RN, CNS M-S, CCRN, FAHA
Dallas, Texas
BEHAVIORAL OBJECTIVES:
At the end of this session, the participant will be able to:
1.
State the normal values for the following hemodynamic parameters:
a.
Cardiac output
b.
Cardiac index
c.
Pulmonary vascular resistance
d.
Systemic vascular resistance
e.
Stroke Work index (right and left)
2.
List the factors that affect preload, afterload and contractility
3.
Discuss the hemodynamic variables and clinical presentation for
a.
Cardiogenic shock
b.
Hypovolemic shock
4.
Differentiate left and right ventricular failure.
5.
State the indicative changes and appropriate leads associated with the primary sites of
myocardial infarction.
6.
Discuss important aspects of thoracic aneurysms including clinical presentation and acute
management.
CONTENT OUTLINE:
I.
Direct and Derived Hemodynamic Parameters
A.
Cardiac Output:
Normal CO: 4-8 L/min
Cardiac Index: = CO / BSA; 2.8 – 4.2 L/m2
Formula: Stroke Volume (SV) x Heart Rate (HR)
1.
Heart rate
a.
Bradyarrhythmias
b.
Tachyarrhythmias
2.
Stroke Volume
a.
Determinants
1) Preload-end diastolic volume: How to assess:
⇒ RV: CVP / RA Pressure (normal 2 - 6mmHg)
⇒ LV: PAWP / LA Pressure (normal 6 -12mmHg)
180
2) Afterload-pressure the ventricle must generate to open the semilunar valve
and eject its’ contents: How to assess:
• Systemic Vascular Resistance = LV Afterload
⇒ Definition: reflects the overall resistance or impedance to systolic
ejection into the entire systemic circulation. The greatest resistance
to flow lies in the small arteries and arterioles
⇒ Formula: 80 x (MAP - RAP)/CO
⇒ Normal: 800-1200 dynes/sec/cm-5
SVRI: 1970-2390 dynes/sec/cm-5/m2
⇒ Causes of increased SVR
- Volume infusions
- Hypovolemia
- Peripheral vasoconstriction - Vasopressors
- Low cardiac output states
- LV Failure
- Hypothermia
- Alpha-adrenergic agents
- Increased blood viscosity
⇒ Causes of decreased SVR
- Diuretics
- Peripheral vasodilatation
- Vasodilators
- Loss of vasomotor tone
- Hyperdynamic phase of sepsis
• Pulmonary Vascular Resistance = RV Afterload
⇒ Definition: resistance or impedance to right ventricular ejection
into the pulmonary vasculature
⇒ Formula: 80 x (MPAP-PAWP)/CO
⇒ Normal: <250 dynes sec./cm-5
PVRI: 255 – 285 dynes/sec/cm-5/m2
⇒ Causes of increased PVR:
- Hypoxia
- PEEP
- Pulmonary edema
- Pulmonary hypertension
- ARDS
- Sepsis
- Pulmonary emboli
- Valvular heart disease
- Congenital heart defects
⇒ Causes of decreased PVR
- Vasodilator therapy - Prostaglandins
- Correction of hypoxia
3) Contractility: How to assess
⇒ LV Stroke Work / Index:
- LVSWI: SVI (MAP – PAWP) x 0.0136
Normal: 50-62 gms –m/m2/beat
- RVSWI: SVI(MPAP – RAP) x 0.0136
Normal: 5-10 gms-m/m2/beat
181
B.
C.
Pulmonary Artery Pressure
1.
Normal range: 15 - 25/0 - 8mmHg
2.
Clinical significance
a.
High readings
⇒ Primary pulmonary hypertension
⇒ Valvular heart disease
Pulmonary Artery Wedge Pressure
1.
Normal range: 6-12 mmHg
2.
Clinical Significance
a.
High readings
⇒ Left ventricular failure
⇒ Mitral valve disease
⇒ Aortic valve disease
⇒ Cardiac tamponade
b.
Low readings
⇒ Hypovolemia
⇒ Vasodilator therapy
b.
Low Readings
⇒ Hypovolemia
D.
Mean Arterial Pressure
1.
Definition: average pressure in the circuit during systole & diastole
2.
Formula: [SBP + (2 x DBP)] / 3
3.
Normal: 70-105 mmHg
4.
Causes of increased MAP
5.
Causes of decreased MAP
a.
Volume Infusion
a.
Diuretics
b.
Peripheral vasoconstriction
b.
Peripheral vasodilatation
c.
Increased contractility
c.
Inotropic therapy
d.
Hypervolemia
d.
Hypovolemia
e.
Vasopressors
e.
Vasodilators
E.
Mean Pulmonary Artery Pressure
1.
Definition: average pressure in the pulmonary circuit during systole and
diastole
2.
Formula: [SPAP + (2 x DPAP)] / 3
3.
Normal: 10-20 mmHg
4.
Causes of increased MPAP
5.
Causes of decreased MPAP
a.
Volume infusion
a.
Diuretics
b.
Pulmonary vasoconstriction
b.
Pulmonary vasodilatation
c.
Decreased LV contractility
c.
Inotropic therapy
d.
Hypervolemia
d.
Hypovolemia
e.
Hypoxia
f.
COPD
g.
Pulmonary hypertension
182
II.
Manipulating Hemodynamics: Cardiovascular Drugs
Inotropes
1.
Receptor dependent vs
2.
Phosphodiesterase Inhibitors
A.
ATP
Adennal
Cyclase
Hormone
Effect
Cyclic
AMP
Effect
Phosphodiesterase
B.
Types of Receptors
1.
Beta receptors:
a.
β1 receptors are found primarily in the heart. Stimulation produces an  heart rate,
 contractility
a.
β2 receptors are found in the lungs, peripheral arterioles. Stimulation produces
relaxation of the smooth muscle
2.
Alpha receptors:
a.
α1 receptors are found primarily in the lungs, peripheral arterioles. Stimulation
produces constriction of the smooth muscle
b.
α2 receptors are found primarily in the brain.
3.
Dopaminergic receptors:
a.
Found in the renal, mesenteric vascular beds.
b.
Stimulation produces vasodilation.
TISSUE
RECEPTOR
Heart:
SA Node
Atria
Beta
Beta
AV Node
Beta
Ventricles
Beta
Blood Vessels:
Skeletal muscle
Skin, mucosa, GI Tract & Kidney
Renal
Mesentery
Bronchial Smooth Muscle
183
RESPONSE
↑ rate
↑ conduction velocity
↑ contractility
↑ conduction velocity
↓ refractoriness
↑ rate
↑ contractility
Beta
Alpha
Vasodilatation
Vasoconstriction
Dopa, Alpha
Dopa, Alpha
Vasodilatation
Vasodilatation
Beta
Relaxation
C.
Specific Agents
SPECIFIC
INDICATIONS / ACTIONS
AGENTS
Receptor Dependent Inotropes
Shock States: Cardiogenic, Septic; Post-cardiac surgery
Dopamine
Immediate precursor of norepinephrine.
Neurotransmitter in the central and peripheral nervous
system.
Decreases aldosterone secretion in the adrenal cortex.
Inhibits TSH and prolactin release.
Inhibits insulin secretion.
Dobutamine
Synthetic catecholamine which directly stimulates the β1
receptors, β2 receptors and α receptors. It directly increases
myocardial contractility and heart rate while modestly
lowering peripheral vascular resistance. Dobutamine will
lose its effect during prolonged infusions because of down
regulation of beta receptors.
DOSAGES
SIDE EFFECTS / COMMENTS
Titrate the IV infusion to achieve desired
effects:
 0.5 - 2 mcg /Kg/min = ↑ renal perfusion
(dopaminergic)
 5.0 - 10 mcg/Kg/min = ↑ contractility
(beta stimulation)
 > 10.0 mcg/Kg/min = vasoconstriction
(alpha stimulation)
Titrate the infusion to achieve desired effects.
The usual dosage range is 2.5 – 20
mcg/Kg/min.
nausea, emesis
tachyarrhythmias
(ventricular &
supraventricular)
 profound vasoconstriction
 Dysrhythmias
 Half-life: 2.5 - 3 minutes
 Do not administer in
alkaline solutions
Indications: Congestive heart failure;
Shock states: cardiogenic, septic
Epinephrine
Norepinephrine
184
 Cardiac effects are mediated through β receptors:
0.005 - 0.02 mcg/Kg/min = ↑ heart rate;
+ inotropic effect, vasodilation → ↓ SVR
 Vascular effects mediated through α receptors @ high
doses: ↑ SVR, ↑ BP, renal artery vasoconstriction
 β2 stimulation → bronchodilatation
Indications: Low output states; cardiac arrest, shock states,
asthma , anaphylaxis
 0.005 - .02 mcg/Kg/min = beta effects
 alpha effects: 1mg IV push/via ET tube;
Naturally occurring catecholamine with effects that are
dose dependent.
Low doses: beta stimulation
Higher doses: alpha stimulation
Indications: Hypotensive states; Cardiogenic shock (MI);
GI bleeding
Titrate infusion via central line to achieve
desired effect. Weigh cost / benefit ratio.
Dosage / Administration:
Infusion rates 2-4mcg/min are suggested.
Start at .05-.1 mcg/Kg/min and titrate up.
Half life = 2.0 -2.5 min
If infiltration occurs, the drug will cause
sloughing of tissue: use Regitine to block the
intense vasoconstriction.
 half life = 2 minutes
Restlessness, fear
Tachyarrhythmias
Severe hypertension →
CVA, angina
Hypokalemia,
Hypophosphatemia
Contraindicated in
mesenteric and renal
thrombosis
Side effects:
Tachyarrhythmias
Headaches
Tremors
Restlessness
Severe ↑ BP
Phenylephrine
(Neosynephrine)
 Pure α stimulator: effects are primarily vascular causing
vasoconstriction resulting in ↑ SBP and ↑ DBP, ↑ PAP.
The coronary and renal arteries constrict. If the
vasoconstriction is severe, blood flow to the vital organs
could decrease.
 Indirect effect: release of norepinephrine from storage
sites
 At large doses could stimulate β 1 receptors
A reflex bradycardia (from the ↑ BP) has been reported.
This is mediated through vagal stimulation.
 Antidiuretic hormone
 Larger doses: α stimulator causing vasoconstriction. Note
does not have negative effects on myocardium such as
those caused by epineprhine
Phosphodiesterase Inhibitors
Positive inotrope with less peripheral vasodilating effects
Milrinone
than amrinone.
(Primacor)
Indications: Low Cardiac Output states;
Acute CHF; Cardiomyopathy
Vasopressin
(Pitressin)
Vasodilators
Nitroglycerine
185
Systemic and pulmonary venodilation
Decreased left and right ventricular filling pressures
Decreased left ventricular pressure volume relationship
Decreased aortic impedance
Decreased right and left ventricular afterload
Dilation of coronary arteries
Improvement of ischemic zone
Initial dose: 100-180 mcg/min to achieve
desired effect.
Maintenance infusion: 40-60 mcg/min titrated
to maintain BP.
 vasoconstriction
 hypertension
 bradycardia
Pressor effects are immediate and will last 1520 min.
Initial dose (ACLS) : 40 units
Infusion: 0.04units/min
 vasoconstriction
 hypertension
Loading dose: 50 mcg/Kg - slowly over 10
minutes (undiluted)
Infusion: 50/250cc start @ .5mcg/Kg/min.
Increase in increments of .37mcg/Kg/min,
max of .75 mcg/Kg/min
Arrhythmogenic:
SVT, VT
Headaches, tremors
 Thrombocytopenia
Indications:
-Chest pain related to myocardial ischemia
-Preload reduction
-Afterload reduction
Dosage / Administration: continuous
infusion titrated to achieve desired effects. It
is suggested that the infusion rate be started at
10 mcg/min and ↑ in 10 mcg/min increments
until the desired effect is achieved.
Hypotension
Nitrate tolerance
Sodium
Nitroprusside
(Nipride)
Direct vasodilator with balanced effect on the arteriolar
and venous systems.
In 10% of patients can increase pulmonary shunt 6
will see SpO2 and PO2 fall
Can produce coronary steal syndrome
Indications:
-Severe heart failure with ↑ SVR
-Mitral regurgitation to ↓ afterload and improve forward
flow out of the ventricle
-Low cardiac output syndrome with ↑ SVR
-Hypertensive crises
Nesiritide
(Natrecor)
Brain natriuretic peptide – identical to endogenous BNP
 Effects
-Vasodilation
- Natriuresis
 Usual dosages are 0.25 – 10 mcg/Kg/min
 Duration of action: 1 – 5 minutes
 Long term administration of the drug
should be monitored with serum thiocyanate
levels.
Infusion rates of less than 3 mcg/Kg/min are
not associated with toxicity.
Serum thiocyanate levels > 10 mg/dL are
considered to be toxic. (Lab costs $100)
 Poor renal function increases the risk for
thiocyanate toxicity – antidote: sodium
thiosulfate
Usual dosage is:
Bolus: 2 mcg/Kg over 60 seconds
Infusion: 0.01 micrograms/min
Do Not infuse though the same line with other
medications
Nicardipine
(Cardene®)
• Calcium Channel Blocker
• Indicated for: hypertension
Usual dosage is:
Infusion: 0.1mg/mL concentration
Titrate for effect
Note: has been promoted for afterload
reduction similar to sodium nitroprusside
186
CNS effects = nervousness,
twitching, ataxia, headaches
 Cardiac effects =
hypotension, palpitations
 Cyanide poisoning =
impaired tissue oxygenation,
confusion, hyperreflexia,
convulsions
 Contraindications:
use with caution in patients
with hypothyroidism,
hepatic or renal disease as
well as those patients
receiving other
antihypertensive drugs.
 Side effects:
- Hypotension – monitor
BP closely
 Incompatible with:
Enaliprilat  Insulin
 Lasix
 Heparin
 Hydralazine  Bumex
• Side Effects:
- Hypotension
C.
Beta Blockers ( the “lol’s”)
1.
General indications are for
a.
AMI: to prevent sudden death (may alter ventricular remodeling)
b.
Tachycardias (ventricular and supraventricular)
c.
Hypertension
2.
Side effects
a.
AV blocks
b.
Sinus bradycardia
c.
Use with caution in Raynauds, COPD and IDDM
D.
E.
Calcium Channel Blockers (verapamil, diltiazem, nifedipine, etc.
1.
Indications: Hypertension, Supraventricular arrhythmias
2.
Note: Some (nifedipine) are stronger vasodilators, others (verapamil, diltizem)
are stronger AV blockers
ACE Inhibitors
Renin - Angiotensin - Aldosterone System:
Endocrine RAS:
↓ Cardiac Output → ↓ Renal perfusion
↓
Juxtaglomerular cells release renin
↓
Renin combines with Angiotensinogen → Angiotensin I
↓
Angotensin I + Lung converting enzyme → Angiotensin II
Angiotensin II
↓
Adrenal Medulla Cell Growth
↓
Aldosterone
↓
Na+ & H2O retention

Peripheral arterioles
↓
Vasoconstriction
Tissue RAS
a.
b.
Exists in many systems including the cardiac cells
May be responsible for ventricular remodeling process that occurs following
MI or with HF
⇒ ACE INHIBITORS: Block the conversion of Angiotensin I to Angiotensin II
End with “pril” ex: captopril
Major side effects: cough; angiodema; renal insufficiency
⇒ ANGIOTENSIN RECEPTOR BLOCKERS:
Directly block the AII receptors on the cell membrane
Effects equal to ACEIs
187
III.
Shock
A.
Definition: State that develops when there is inadequate tissue perfusion causing the cells to be
deprived of adequate oxygenation, convert to anaerobic metabolism resulting in the production of
lactate and acidosis.
B.
Etiology / Types of Shock
1.
Hypovolemic: blood volume not sufficient to fill the vascular space.
2.
Cardiogenic: Myocardium unable to pump an adequate cardiac output to maintain tissue
perfusion.
3.
Obstructive: physical obstruction to flow (ex: dissecting aortic aneurysm, pulmonary embolus)
4.
Distributive: abnormal distribution of intravascular volume. Includes septic, anaphylactic and
neurogenic shock)
C.
Hemodynamic profiles
Type of Shock
Hypovolemic
Cardiogenic
Obstructive
Distributive:
Neurogenic
Anaphylactic
Septic
Early
Late
1.
Intravascular Volume

----
Preload



Afterload



Cardiac Output



-----






-----No Change or 

No Change, or 


 or NC

Hypovolemic:
a.
Impaired tissue perfusion resulting from severely diminished circulating blood
volume.
b.
Etiology:
⇒ hemorrhage (trauma, surgery, burns, severe dehydration)
⇒ internal, extravascular fluid loss (3rd spacing)
⇒ Adrenal insufficiency
c.
Clinical picture:
⇒ anxious, irritable
⇒ ↓ LOC
⇒ poor capillary refill
⇒ skin pale & gray
⇒ tachycardia
⇒ hypotension
⇒ collapsed neck veins
⇒ tachypnea
⇒ ↓ urine output
d.
Labs:
⇒ ↓ Hct
⇒ abn electrolytes
⇒ respiratory alkalosis, metabolic acidosis
e.
188
Management:
⇒ Volume replacement
⇒ Identify & treat the cause
2.
Cardiogenic:
a.
Definition: Myocardium unable to pump an adequate cardiac output to maintain
tissue perfusion.
b.
Etiology
⇒ Most common is loss of > 40-50% viable myocardial tissue
⇒ Mechanical problems
•Perforated intraventricular septum
•Papillary muscle dysfunction / rupture
•Myocardial rupture
•Valvular heart disease
•Post-op low cardiac output syndrome
⇒ Cardiomyopathies
⇒ Others:
•Hypovolemia
•Metabolic dysfunction
•Vasomotor dysfunction •Microcirculatory dysfunction
c.
Pathophysiology
⇒ Marked decrease in cardiac output: CI = < 1.8 L/m/m2
⇒ Usual compensatory response is an increased peripheral vascular resistance.
If not, MAP will fall → ↓ coronary blood flow worsening the ischemic process.
⇒ If the compensatory mechanisms are working:
↑ SVR and ↑ catecholamine release
↓
↓
↑ afterload
↑ contractility (↑ β stimulation)


↑ myocardial ischemia
d.
189
⇒ LVEDV and LVEDP continue to increase → cavity distention → further ↑ing
afterload
•Limits filling of the endocardial vasculature → endocardial ischemia
• ↑ LVEDP is reflected back into the pulmonary vasculature → ↑
pulmonary pressures → development of pulmonary edema → development
of arterial hypoxemia contributing to cellular acidosis. As pulmonary artery
pressures rise, ischemia and right ventricular failure occur.
Management
⇒ Goals
•Improve oxygen transport
⇒Cardiac Output
⇒Oxygen Content
-Hemoglobin -Arterial oxygen saturation
•Maintain / Improve Nutrition •Decreased Oxygen Demand
•Prevent complications
⇒ Pharmacological
•Inotropes
•Vasodilators
⇒ Mechanical Support
•Intra-aortic balloon
•Intra-pulmonary artery balloon
•Ventricular assist devices
⇒ Surgical
•Revascularization
•Transplant
IV.
Heart Failure
A.
Definition:
1.
Failure of CO to meet metabolic demands of body
2.
Systolic vs diastolic dysfunction
a.
Systolic: problem with contractility
b.
Diastolic: problem with filling
B.
Cardiomyopathies:
1.
Dilated
a.
Causes
• CAD
• Viral
• Chemotherapy
• Pregnancy
• Parasitic – Chaga’s Disease
• Alcohol
2.
Hypertrophic (HOCM)
a.
Causes
• Aortic stenosis
• Congenital - IHSS
b.
Management
3.
Restrictive
a.
Causes
•Infiltrative diseases
b.
Management
C.
Signs & Symptoms
Left Ventricular Failure:
Forward Failure:  CO
Right Ventricular Failure:
 Venous Pressures
190
Backward Failure:  LVEDP
D.
V.
Management: Target Goals
1.
Improve CO/CI
a.
rest
b.
pharmacologic interventions
⇒ inotropes
⇒ vasodilators to reduce afterload / preload
⇒ beta blockers to prevent sudden death
⇒ ACE inhibitors to block ventricular remodeling
⇒ Digitalis
⇒ Diuretics
2.
ECG monitoring (sudden death common - therefore many have ICDs implanted)
3.
Mechanical Assist
a.
IABP
b.
LVAD / RVAD
4.
Prior to d/c: patient & family education
Acute Coronary Syndromes
A.
VI.
Spectrum of coronary artery disease (atherosclerotic process) that includes:
1.
Unstable Angina
2.
Non-ST Elevation MI
3.
ST Elevation MI
Myocardial Infarction: EKG Interpretation: STEMI vs Non STEMI
A.
Current of Ischemia: primary T wave inversion
B.
Current of Injury: ST segment elevation
C.
Current of Necrosis: pathological “q” wave
D.
Primary Sites
PRIMARY SITE
INDICATIVE CHANGES
RECIPROCAL
CHANGES
Inferior
Leads II, III, aVF
Leads I, aVL
Right Coronary
Septal
Lead V1-2
Lead V5-6
Left Anterior Descending
Anterior
Leads V2, 3, 4
Leads II, III, aVF
Left Anterior Descending
Lateral
Leads I,aVL, V5,6
Leads II, III, aVF
Circumflex
Posterior
Leads V8, 9
V1,2
Right Coronary
191
VESSEL INVOLVED
Practice EKG’s:
#1:
193
#2:
194
#3:
195
4.
196
5.
197
F.
G.
H.
I.
J.
K.
Non STEMI: ST segment depression over involved area
1.
Fibrinolytics not effective
2.
ASA and beta blocker should be started within 24 hours of presentation
Acute Management
1.
ASA
2.
Beta blocker
3.
Immediate reperfusion
a.
Fibrinolytic
b.
Primary PCI
Observe for Acute Closure or Extension following intervention
1.
ST segment changes early indicator
2.
Silent ischemia
GPIIbIIIa Inhibitors
1.
Include
a.
Reopro: May be able to reverse with platelets
b.
Integrilin: Dose adjusted for renal insufficiency
2.
Screen as you would for a fibrinolytic
3.
Observe for onset of:
a.
Bleeding
b.
Thrombocytopenia
Discharge Medications
1.
Aspirin
2.
Beta blocker
3.
ACE inhibitor if EF < 40%
Complications
1.
Heart Failure
2.
Cardiogenic Shock
3.
Arrhythmias
4.
Mechanical Complications
a.
Papillary muscle dysfunction / rupture → acute onset mitral regurgitation
⇒ Loud systolic murmur
⇒ Falling BP and CO/CI
⇒ Development of large “v” waves in PAOP waveform
b.
c.
Cardiac tamponade
⇒ Falling BP and CO/CI
⇒ Narrowing pulse pressure
⇒ Sinus tachycardia
⇒ Distended neck veins; ↑ CVP
⇒ Muffled heart tones
⇒ PEA
Perforated ventricular septum
⇒ Falling BP, CO/CI
⇒ Loud holosystolic murmur
⇒ Development of large “v” waves in PAOP tracing
⇒ Insertion of PA catheter: Look for oxygen step-up from RA to RV
L.
199
Valvular Heart Disease
1.
Aortic Valve
a.
Insufficiency: LV volume overload
b.
Stenosis
⇒Dev LVH
⇒Volume dependent
⇒Onset of a fib can be catastrophic r/t loss of atrial kick
⇒PA pressures elevated
2.
M.
N.
O.
VI.
Mitral Valve
a.
Insufficiency
⇒Assoc with large V wave in PAWP waveform
⇒PAP elevated
b.
Stenosis
⇒PAWP not helpful – falsely elevated
⇒PAP elevated
Coronary Bypass Surgery
1.
Approaches:
⇒Minimally invasive
⇒ Sternotomy
2.
Use of cardiopulmonary bypass
⇒On pump
⇒Off pump
Post-Operative Management of the Cardiac Surgery Patient
1.
Assess hemodynamic stability
a.
Hemodynamic assessment
b.
Titrating infusions
c.
IABP
2.
Electrolyte status
a.
Hypokalemia
b.
Hypomagnesemia
3.
Cardiac Arrhythmias
4.
Ventilatory Status
a.
ABG’s
b.
Early extubation (if appropriate) Protocol
5.
Pain control – Can be challenging
a.
Use of local anesthetics & delivery systems
b.
Use of epidurals and PCA pumps
6.
Incisional care
7.
Activity progression
8.
ICU LOS: 1 day …..
Cardiac Surgery Complications - Early
1.
Coagulopathies
2.
Excessive bleeding
3.
Cardiac Tamponade
4.
Electrolytes (K+, Mg+)
5.
Respiratory failure / Atelectasis
6.
Renal Insufficiency / ATN
7.
Cardiogenic shock
8.
Stroke
Aortic Aneurysms
A.
Etiologies
1.
Various diseases
a.
Atherosclerosis
b.
Hypertension
c.
Degeneration of medial layer – cystic medial necrosis
d.
Aortitis
2.
Iatrogenic injury – complication of aortic surgery
3.
Trauma – severe blunt chest trauma
4.
Congenital
a.
Marfan’s Syndrome
b.
Coarctation
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B.
201
Thoracic Aortic Aneurysm
1.
Less common than abdominal aneurysms
2.
Types
a.
True: all layers involved
b.
False: partial or complete disruption of aortic
wall with blood contained in the
adventitial layer.
3.
Described in terms of shape and location
a.
Shape: fusiform vs saccular
b.
Location: ascending, transverse or
descending
4.
Diagnosis
a.
Chest X-ray changes often before s&s
b.
CT scan
c.
Transesophageal Echo
5.
S&S
a.
Ascending Aorta: chest pain; AI; CHF
b.
Transverse Aorta: dyspnea, stridor, hoarseness, cough, chest pain,
JVD (less common)
c.
Descending Aorta: back or chest pain
6.
Significance: Risk for rupture
7.
Medical Management
a.
Goals:
⇒Reduce left ventricular contractility and velocity of blood flow
⇒Reduce systolic blood pressure to lowest possible level
- Combination of beta blockers and vasodilators to lower SBP
- Start beta blocker before vasodilator
- Reduce SBP to 100 -120mmHg or further if patient c/o pain
b.
Type B – medical management first
c.
Relief of pain is the most important clinical sign - Morphine SO4
d.
Vigilant monitoring of the BP - Especially as patient increases activity level
⇒Assess for postural hypotension
e.
Educate patient & family about meds
8.
Surgical Repair:
a.
Type A – surgical emergency
b.
When:
-symptomatic
-size exceeds twice of normal caliber segment - 6cm
c.
Post-op Assessment determined by site of aneurysm
•Ascending aorta: often involves AVR
•Aortic arch: involve flow to brachiocephalic vessels (head, neck and upper
extremities)
•Descending aorta
- Adequacy of peripheral circulation: spinal cord, SMA, renals, etc.
- Adequacy of peripheral neuro status
d.
Routine ICU care
e.
Special emphasis on management of hypertension
f.
Monitor spinal fluid pressures
⇒Goal SP < 8- 10mmHg
⇒ Drain spinal fluid to maintain
g.
Neuro assessments
⇒Central
⇒Peripheral
References:
1.Adams KF, Lindenfeld J, Arnold JMO, et al. HFSA 2006 comprehensive heart practice guideline. Journal of
Cardiac Failuire, 2006;12:e1-e119. Available at www.heartfailureguideline.com/index.cfm?id=73.
2. Alspach JG. Core Curriculum for Critical Care Nursing, ed 6. Philadelphia: WB Saunders, 2006.
3. CarlsonKK, Advanced Critical Care Nursing. Philadelphia: WB Saunders, 2009.
4. Chulay M, Burns SM AACN Essentials of Critical Care Nursing. New York: McGraw Hill Publishing Company,
2010.
5. Conover M. Understanding Electrocardiography, ed 8. St Louis: Mosby , 2003.
6. Daleiden-Burns A. (issue editor) Heart Failure. Critical Care Nursing Quarterly, 2007;30(4).
7. Darovic G. Hemodynamic Monitoring: Invasive and Noninvasive Clinical Application, ed 3. Philadelphia: WB
Saunders, 2002.
8. Fara-Erny A. Heart failure: Challenges and outcomes. Journal of Cardiovascular Nursing 2000;14(4).
9. Fishman WH, Cheng-Lai A, Nawarskas J. Current Cardiovascular Drugs, ed 4. Philadelphia: Current
Medicine, LLC,2005.
10.Hardin S, Hussey L. AACN Synergy model for patient care: Case study of a CHF patient. Critical Care Nurse
2003;23(1):73-76.
11. Hardin SR, Kaplow R. Synergy for Clinical Excellence: The AACN Synergy Model for Clinical Excellence.
Boston: Jones & Barltett Publishers, 2005.
12. Hardin SR, Kaplow R. Cardiac Surgery Essentials for Critical Care Nursing. Boston: Jones and Bartlett Publishers,
2010.
13. Hochman JS. Cardiogenic shock complicating acute myocardial infarction. Circulation. 2003;107:2998.
14. Holmes DR. Cardiogenic shock: A lethal complication of acute myocardial infarction. Review in Cardiovascular
Medicine. 2003;4(3):131135.
15. Jurynec J. Hypertrophic cardiomyopathy: A review of etiology and treatment. Journal of Cardiovascular
Nursing, 2007;22(1):65-73.
16. Kelley DM. Hypovolemic shock: An Overview. Critical Care Nursing Quarterly, 2005;28(1):2-19.
17. Messerli FH. Cardiovascular Drug Therapy, ed 2. Philadelphia: WB Saunders Co., 1996.
18. ----- Synergy Model: Adult Sample Questions. Aliso Viejo, CA: AACN Certification Corporation, 2000.
19. Wagner, GS. Marriott’s Practical Electrocardiography, ed. 10. Baltimore: Williams & Wilkins, 2000.
20. Woods SL, Froelicher ESS, Motzer SA, Bridges E. Cardiac Nursing, ed 6. Philadelphia: Lippincott Williams &
Wilkins, 2009.
21. https//www.certcorp.org
Speaker Contact Information:
Barbara “Bobbi” Leeper, MN, RN, CCRN
Clinical Nurse Specialist, Cardiovascular Services
Baylor University Medical Center
Dallas, Texas
e-mail: [email protected]
202
Self-Assessment Questions:
A patient in cardiogenic shock has the following hemodynamic profile:
BP 90/56
HR 110
CO/CI 1.4 / 0.8
PA 36/20
PAWP 18
SVR 3000
RA 10
The following medications are infusing: dobutamine at 10mcg/Kg/min & epinephrine at 0.02mcg/Kg/min
1.
You would be most concerned about:
a.
BP, CO/CI, PA
b.
CO/CI, SVR
c.
BP, SVR, CO/CI, CVP
d.
All of the above
2.
Which of the following interventions would be appropriate:
a.
Afterload reduction with sodium nitroprusside
b.
Elevate blood pressure with epineprhine
c.
Reduce preload by giving a diuretic
d.
Improve renal blood flow with dopamine at 10 mcg/Kg/min
3.
Indicative changes for acute myocardial infarction include:
a.
tall peaked T wave, ST segment depression
b.
widened QRS duration > 0.12 sec
c.
T wave inversion, ST segment elevation and pathological q wave
d.
Prolonged PR interval
4.
Indicative changes for an inferior MI can be found in:
a.
Leads II, III, aVF
b.
V1 – V2
c.
V2 – V3 – V4
d.
V5 – V6, I, aVL
5.
Which of the following are signs of hypovolemic shock?
a.
↓ intravascular volume; ↓ preload; ↑ afterload, ↑ cardiac output
b.
↓ intravascular volume, ↓ preload; ↓ afterload, ↓ cardiac output
c.
↓ intravascular volume; ↑ preload; ↑ afterload; ↓ cardiac output
d.
↓ intravascular volume; ↓ preload; ↑ afterload; ↓ cardiac output
Answers: 1: b, 2:a, 3:c, 4:a, 5:d
203
Additional Study Resources
Visit the links below to access additional study materials for the Adult
CCRN exam:
AACN Bookstore Publications and Practice Exams
CCRN Self-Assessment Exam (SAE)
How to Prepare for the CCRN Exam
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