Transcript Pain in the Cardiac Surgical ICU Patient

Shana Winchel, BSN, RN-BC
MSN Student
MSN 621-Alverno College
[email protected]
Objectives
Upon completion of this tutorial the learner
will:
Know the definition of pain
Have an increased understanding of the
pathophsyiology of pain
Have a better understanding of why pain is
masked due to hemodynamics
Understand the implications of undertreated
pain and utilize appropriate interventions to
improve patient outcomes
Tutorial Guide
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Definitions
Pain Myths
Pathophysiology
Pharmacology
Genetics
Fifth Vital Sign
Nursing
Considerations
References
What is pain?
Pain means that there is an increase in
vital signs.
True
False
Pain Defined
Margo McCaffery is a registered nurse and
pioneer of the field of pain management
nursing.
She defines pain as “whatever the
experiencing person says it is, existing
whenever and wherever the person say it
does” (McCaffery, 1968, p. 95). This has
become the prevailing conceptualization of
pain for clinicians over the past few
decades.
What are some pain myths?
1. Addiction is common in patients taking pain
medication
2. All people in pain look uncomfortable or
sick
3. If a person can sleep, they are not in pain
4. It is just anxiety, their pain is not that bad
5. People who take narcotics will become so
sedated that they cannot function.
Myths Debunked
1. Addiction to narcotics is rare and
usually occurs in patients who have a
prior history of drug abuse. When
narcotics are properly prescribed and
monitored for pain relief, there should be
little concern about addiction.
Weiner, Peterson, and Keefe (1999)
Myths Debunked
2. Pain is invisible. You will come across
many, many people in your life who are
in pain and look fine. Each person is
different in the way he or she feels and
exhibits pain. A person’s pain is what
they perceive it to be and cannot be
judged by anyone else.
McCaffery and Pasero (1999)
Myths Debunked
3. Prolonged pain can exhaust the body
to the point where sleep occurs, even
though the pain continues.
McCaffery and Pasero (1999)
Myths Debunked
4. Excess anxiety and tension can cause
the experience of heightened anxiety,
increased pain and slower healing
times. Anxiety, which is a stress
response can cause numerous negative
problems.
McCaffery and Pasero (1999)
Myths Debunked
5. When patients start to take a narcotic,
they often feel drowsy. But their bodies
usually will very quickly build up a
resistance to the sedating effects. Some
people, however, become more alert as
they finally achieve pain relief.
McCaffery and Pasero (1999)
What is not a pain myth?
A.
B.
C.
D.
All people in pain look uncomfortable or
sick
If a person can sleep, they are not in
pain
Pain is whatever the patient says it is
It is just anxiety, their pain is not that
bad
Pathophsyiology of Pain
Complex process that is
mediated by multiple
pathways in the spine
and brain
It is a sensory experience
Forms of Pain
1. Nociceptive/Inflammatory
-Normal processing of stimuli that
damages normal tissue or has the potential to
damage tissue if prolonged.
2. Neuropathic
-Stimuli “abnormally” processed by
the central nervous system
McCaffery and Pasero (1999)
Pain Mechanism
1. Transduction: Noxious stimuli causes tissue damage and
initiates the pain mechanism
2. Transmission: Action potential continues from site of
damage and ascends to brain
3. Perception of pain: Conscious experience
4. Modulation: Attempt to inhibit pain experience
Transduction
Cell damage releases sensitizing
substances
-prostaglandin
-bradykinin
-serotinin
-histamine
McCaffery and Pasero (1999)
Transmission
This phase of transmission occurs in the
dorsal horn of the spinal cord
-The signal moves up from the site of
injury or damage to the brain
McCaffery and Pasero (1999)
Perception of pain
The pain experience happens in this
phase
-An individual will be aware of pain at
this point
McCaffery and Pasero (1999)
Modulation
Neurons from the brain stem release
serotinin, norepiphrine and endogenous
opioids
-These are substances our body
releases to fight pain
-An example might be if you burn your
hand, your brain will tell you move it
away from the heat
McCaffery and Pasero (1999)
Used with permission from McCaffery and Pasero (1999)
Pain sensation
Mediators, as previously listed, heighten
nociception and facilitate the
communication of painful sensations to
the spinal cord and the brain.
Porth and Matfin (2009)
What is nociceptive pain?
A.
B.
C.
Stimuli abnormally processed by the
central nervous system
Normal processing of stimuli that
damages normal tissue or has the
potential if prolonged
Processing of pain through the liver
Pain Mediators
Some of the pain mediators:
adrenocorticotropic hormone (ACTH),
glucocorticoids, catecholamines,
substance P, prostaglandins,
leukotrienes, bradykinin, histamine, and
serotonin
Bradykinin
Bradykinin is a molecule produced by
enzymes at the site of an injury and then
binds to receptors to cause pain.
McCaffery and Pasero (1999)
Serotinin
Serotonin also is an important regulator for
pain sensation, and abnormal levels of
serotonin can contribute to painful
events such as migraine headaches.
McCaffery and Pasero (1999)
Substance P
Substance P is a protein found in the brain
and spinal cord, and is associated with
some inflammatory processes.
Its function is to cause pain.
McCaffery and Pasero (1999)
Prostaglandins
Prostaglandin is produced during
inflammatory responses, and it helps to
mediate some of the cardinal features of
inflammation, including pain, edema,
and fever
Stock, Shinjo, Burkhardt, Roach, Taniguchi, Ishikawa, Kim, Flannery, Coffman, McNeish, and Audoly,
(2001).
Histamine
Histamine is released by mast cells.
Substance P is released which causes
mast cells to release histamine, which in
turn stimulates the nociceptors
Overproduction of histamine promotes
inflammation by causing vasodilatation and
increased capillary permeability.
Effects of Mediators
Each of these has one or more effects on
the body. And many of these biochemicals are inflammatory -- that is,
they cause the injury site to swell up.
Inflammation and Pain
Nociceptive stimulation
perpetuates the inflammatory
response.
Inflammation of peripheral tissues
can cause the vicious cycle of
pain
Porth and Matfin (2009)
Inflammation
Some of the chemical mediators that are
released during injury and inflammation:
-Prostaglandins
-Leukotrienes
-Histamine
Inflammation
Inflammation can cause pain with pressure
and tissue damage.
Inflammation causes pain
However, if the inflammation is prolonged
or out of control, it can cause
destruction.
This is what occurs in arthritis, where the
inflammation actually destroys the joints.
Destruction causes pain
Inflammation and Pain
Inflammation can serve to compound
problems by actually causing pain itself.
Stress Response to Pain
Stress causes the Endocrine System to
release excessive amounts of:
-Adrenocorticotrophic Hormone (ACTH)
-Cortisol
-Growth Hormone
-Catecholamines
-Glucagon
Porth and Matfin (2009)
Function of Catecholamines
Click to learn more
Decrease in insulin-which allow more
serum glucose in the blood stream
Increase in glucagon-which increases
serum glucose
Increase in heart rate
Increase in cardiac contractility
Function of ACTH
Click to learn more
Stimulates release of cortisol
ACTH
Adds to the effect of catecholamines
Adds to the effectCortisol
of glucagon-increase in
blood sugar
Stress
Catecholamines and cortisol are released
during the stress response to alert the
individual to a threat or challenge.
What are Catecholamines
NOT responsible for:
a. Decrease in insulin
b. Increase in glucagon
c. Increase in heart rate
d. Increase in cardiac contractility
e. Decrease in heart rate
Pattern developing?
Stress and pain mediators overlap
Inflammation and pain mediators overlap
Inflammation and Stress can increase pain
Pain as the fifth vital
The importance of the adequate
assessment and optimal management of
pain has received a great deal of
attention
Green, Wheeler, and LaPorte (2003)
Pain, “the fifth vital sign” as defined by
Ruth Massaro, an executive vice
president of the Joint Commission on
Accreditation of Healthcare
Organizations (JCAHO)
Hemodynamics and Pain
As nurses we have been educated to look
for hypertension and tachycardia as a
symptom of pain but we now know that
this is not an accurate to way evaluate
pain.
Why…….
Rationale for vitals
Healthy individuals will seek an equilibrium
to return to the stable vital signs despite
severe pain
Some individuals will have medical
conditions that cause bradycardia and
hypotension and severe pain will not
change the vital signs
McCaffery and Pasero (1999)
The Fifth Vital
Using the pain rating as the fifth vital sign
will remind all staff to assess pain
regularly.
This makes pain visible and raises
awareness of the importance of pain
management.
McCaffery and Pasero (1999)
How can I tell if my patient
has pain?
a.
Ask them
b.
Check their vitals
a.
Look for grimacing or other outward
signs
Genetics and pain
Genetics can influence effective pain
management
We all have polymorphisms that can affect
the effectiveness of pain medication
CYP2D6 Polymorphism
The CYP2D6 enzyme is involved in
metabolism of up to 25% of drugs.
About 10% of Caucasians and 3% of
Asian people have this genetic
polymorphism.
Used with permission from P. Jannetto
What does CYP2D6
polymorphism really mean
Polymorphism is a genetic mutation that
changes the rate of the conversion codeine
to morphine.
Of note, Morphine is a metabolite of codeine
that relieves pain
Consequently, some individuals do not
achieve analgesia from codeine
Categories of CYP2D6
Polymorphisms
Super Metabolizers: Clear the drug rapidly
and need higher dose
Intermediate Metabolizers: Slow to obtain
relief and build up effect
Poor Metabolizers: Have no ability to clear
the drug and become toxic easier
Used with permission from P. Jannetto
What is CYP2D6
polymorphism?
a.
A genetic mutation affecting pain
medication effectiveness
About 10% of Caucasians and 3% of
Asian people have this genetic
polymorphism.
c. Polymorphism is a genetic mutation that
makes it impossible for the conversion
codeine to morphine.
d. All of the above
b.
Pharmacology
Analgesics reduce nociception by one of
three mechanisms
1. Inhibition of local pain mediators i.e.
blocking prostaglandins with antiinflammatory drugs
2. Interruption of neural impulse i.e. a
peripheral nerve block
3. Altering the perception of pain in the
central nervous system i.e. opiates
Fentanyl
Opioid
Most rapid onset and shortest duration of
action
Easy to titrate
Low cost
Fentanyl
Has minimal hemodynamic effects
Virtually devoid of histamine-releasing
properties and may therefore be
preferred in presence of hemodynamic
instability or bronchospasm.
Key points of Fentanyl
Bolus Fentanyl prior to initiation of drip to
prevent pain and help reach the “steady
state”
Bolus Fentanyl prior to drip rate increase
to achieve better pain control
Why give Fentanyl with
hemodynamic instability?
a. Most rapid onset and shortest duration
of action
b. Easy to titrate
c. Has minimal hemodynamic effects
d. A, B, and C are correct
e. None of the above
Nursing considerations
If we treat pain only when patients act like
they are in pain, then our patients will be
forced to learn how to act and convince
us that they have pain.
This creates manipulative patients
Seisser and Ward (2002)
Nursing considerations
Accepting and responding to the report of
pain may result in giving analgesics to
patients who may not have pain, it
ensures that everyone who does have
pain receives an attentive pain plan.
McCaffery and Pasero, (1999)
Nursing considerations
Harmful and expensive consequences of
unrelieved pain:
-More likely to have atelectasis
-Longer hospital stay
-Triggers the stress response and release
catecholamines, etc.
-Increased stress may delay healing
What is pain?
Pain means that there is an increase in
vital signs.
True
False
Thank You
Shana Winchel, BSN, RN-BC
MSN Student
MSN 621-Alverno College
[email protected]
All pictures where used courtesy of
Microsoft Office unless otherwise noted
References
Green, C., Wheeler, J., and LaPorte, F. (2003). Clinical decision making in pain
management: Contributions of physician and patient characteristics to variations in
practice. The Journal of Pain, (4)1, 29-39.
http://office.microsoft.com/en-us/tou.aspx
McCaffery, M. (1968). Nursing practice theories related to cognition, bodily pain, and manenvironment interactions. Course syllabus, University of California at Los Angeles
Students’ Store.
McCaffery, M. and Pasero, C. (1999). Pain: Clinical Manual (2nd ed.) St. Louis: Mosby.
Porth, C.M., and Matfin, G. (2009). Pathophysiology: Concepts of Altered Health States. (8th
ed.) Lippincott.
References
Seisser, M. and Ward, S. (2002). Margo McCaffery on quality in pain management. Journal
for Healthcare Quality, (24)6, 19-22.
Stock, J., Shinjo, K., Burkhardt, J., Roach, M., Taniguchi, K., Ishikawa, T., Kim, H.S.,
Flannery, P.J., Coffman, T.M., McNeish, J.D., and Audoly, L.P. (2001). The
prostaglandin E2 EP1 receptor mediates pain perception and regulates blood pressure.
The Journal of Clinical Investigation, 107(3): 325–331.
Weiner, D., Peterson, B., and Keefe, F. (1999). Chronic pain-associated behaviors in the
nursing home: resident versus caregiver perceptions. International association for the
study of pain, 80, 577-588.