UNIT-3

PAIN ASSESSMENT AND MANAGEMENT

BY
Dr.ArunaJothishanmugam,
Assistant professor,
Department of Nursing
University College at Aldair,
Jazan University.
On completion of this chapter, the student
will be able to
1. Define pain.
2. Enlist the types of pain.
3. Describe the four processes of nociception.
4. Explain underlying mechanisms of neuropathic
pain.
5. Identify methods to perform a pain assessment.
6. Explain about Pharmacological and non
pharmacological management of pain
 INTRODUCTION(page no:744)
• Nurses in all settings play a key role in the
management of pain as experts in assessment, drug
administration, and patient education. They are
uniquely positioned to assume this role as the
member of the health care team most consistently at
the patient’s bedside.
• This Unit ,provide complete knowledge and skill
and also preparing students to successfully apply
knowledge and skills in a manner that supports
inter-professional team contributions in providing
quality pain care in the real world .
DEFINITON OF PAIN(page no:745)

• pain as “an unpleasant sensory and emotional

experience associated with actual or potential
tissue damage, or described in terms of such
damage”(American Pain Society (APS) (2008)
Types and Categories of Pain(pageno:745-746)
• Acute pain
• Chronic pain
 Definition of Acute and Chronic
pain (pageno:745-746)
• Acute pain
• which is expected to have a relatively short duration and resolve with
normal healing
• For example, tissue damage as a result of surgery, trauma, or burns
produces acute pain.
• Chronic pain
• Chronic pain is the pain that lasts longer than 6 months and is
constant or recurring with a mild-to-severe intensity
• Chronic pain is subcategorized as being of cancer or noncancer
origin and can be time limited (e.g., may resolve within months) or
persist throughout the course of a person’s life.
• Examples of non cancer pain include peripheral neuropathy from
diabetes, back or neck pain after injury, and osteoarthritis pain from
joint degeneration
Types of pain based on
pathology(page .no:747-748)
1.Nociceptive pain
2.Neuropathic pain
1.Nociceptive (physiologic) pain refers to the normal
functioning of physiologic systems that leads to the
perception of noxious stimuli (tissue injury) as being
painful .
Nociception is also called as “normal” pain
transmission.
2.Neuropathic (pathophysiologic)
pain(Page.NO;753-755)
• 2.Neuropathic (pathophysiologic) pain is
pathologic and results from abnormal
processing of sensory input by the nervous
system as a result of damage to the
peripheral or central nervous system
(CNS) or both.
Nociceptive pain process(page
NO;749-753)
TRANSDUCTION
• Specialized pain receptors or nociceptors can be excited by
mechanical, thermal, or chemical stimuli
• During the transduction phase, harmful stimuli trigger the
release of biochemical mediators, such as prostaglandins,
bradykinin, serotonin, histamine, and substance P, which
sensitize nociceptors.
• Painful stimulation also causes movement of ions across cell
membranes, which excites nociceptors.
 TRANSMISSION
•
• The second process of nociception, transmission of pain,
includes three segments.
1.During the first segment of transmission, the pain impulses
travel from the peripheral nerve fibers to the spinal cord.
• Two types of nocieceptor fibers cause this transmission to the
dorsal horn of the spinal cord:
a.Unmyelinated C fibers, which transmit dull, aching pain,
b.Thin A-delta fibers, which transmit sharp, localized pain.
2.The second segment is transmission of the pain signal through
an ascending pathway in the spinal cord to the brain
3.The third segment involves transmission of information to the
brain where pain perception occurs. Pain control can take place
during this second process of transmission.
PERCEPTION
• The third process, perception, is when the client becomes
conscious of the pain.
• Pain perception is the sum of complex activities in the CNS
that may shape the character and intensity of pain perceived
and give meaning to the pain.
MODULATION
• MODULATION Often described as the “descending system,”
this final process occurs when neurons in the brain send signals
back down to the dorsal horn of the spinal cord.
• These descending fibers release substances such as endogenous
opioids, serotonin, and norepinephrine, which can inhibit or
reduce the ascending painful impulses in the dorsal horn.
• In contrast, excitatory amino acids (e.g., glutamate, N-methyld-
aspartate [NMDA]), can increase these pain signals. The effects
of excitatory amino acids tend to persist, while the effects of the
inhibitory neurotransmitters (endogenous opioids, serotonin, and
norepinephrine) tend to be short lived because they are
reabsorbed into the nerves.
•
2.Neuropathic (pathophysiologic) pain(Page.NO;753-755)-

• Neuropathic pain is sustained by mechanisms that are driven

by damage to, or dysfunction of, the peripheral or central
nervous system and is the
• It may occur in the absence of tissue damage and
inflammation.
Gate control theory
• According to Melzack and Wall’s gate control theory (1965), small
diameter (A-delta or C) peripheral nerve fibers carry signals of noxious
(painful) stimuli to the dorsal horn, where these signals are modified
when they are exposed to the substantia gelatinosa (the milieu in the
CNS), which may be imbalanced in an excitatory or inhibitory direction.
• Ion channels on the pre- and postsynaptic membranes serve as gates that,
when open, permit positively charged ions to rush into the second-order
neuron, sparking an electrical impulse and sending pain signals to the
thalamus.
• Peripherally, large-diameter (A-beta) nerve fibers, which typically send
messages of touch or warm or cold temperatures, have an inhibitory
effect on the substantia gelatinosa, and may activate descending
mechanisms that can lessen the intensity of pain perceived or inhibit the
transmission of those pain impulses—closing the (ion) gates.
HARMFUL EFFECT OF UNRELIVED PAIN(Page
no:746-747)
Pain Assessment(pageNo;755-
763)
Self report
• The pain is highly subjective nature of pain causes challenges
in assessment and management; however, the patient’s self-
report is the undisputed standard for assessing the existence
and intensity of pain
• Self-report is considered the most reliable measure of the
existence and intensity of the patient’s pain.
•
Comprehensive Pain Assessment

• The following are components of a

comprehensive pain assessment
• Location(s) of pain:
• Intensity: Intensity of Pain is assessed by using
following scales
• Numeric Rating Scale (NRS):
• Wong-Baker FACES Pain Rating Scale:
• Faces Pain Scale–Revised (FPS-R):
• Verbal descriptor scale (VDS):
• Visual Analog Scale (VAS):
Numeric Rating Scale
Wong Baker’s Faces
Pain Scale
Faces Pain Scale–Revised (FPS-
R
Verbal Rating Scale
Visual Analog Scale (VAS):
Other information
• Quality: Ask the patient to describe how the pain feels.
• Descriptors such as “sharp,” “shooting,” or “burning” may help
identify the presence of neuropathic pain.
• Onset and duration: Ask the patient when the pain started and
whether it is constant or intermittent.
• Aggravating and relieving factors: Ask the patient what makes
the pain worse and what makes it better.
• Effect of pain on function and quality of life: The effect of
pain on the ability to perform recovery activities should be
regularly evaluated in the patient with acute pain. It is particularly
important to ask patients with persistent pain about how pain has
affected their lives, what could they do before the pain began that
they can no longer do, or what they would like to do but cannot
do because of the pain.
Other information
The patient’s culture,
past pain experiences,
pertinent medical history such as comorbidities,
laboratory tests, and diagnostic studies are considered
when establishing a treatment plan.
Reassessing Pain
Following initiation of the pain management plan, pain is
reassessed and documented on a regular basis to evaluate
the effectiveness of treatment. At a minimum, pain
should be reassessed with each new report of pain and
before and after the administration of analgesic agents.
Key Components-pain
Assessment by nurse in non-
verbale patients
The key components of the hierarchy require the nurse to
• (1) attempt to obtain self-report
• (2) consider underlying pathology or conditions and
procedures that might be painful (e.g., surgery)
• (3) observe behaviors
• (4) evaluate physiologic indicators
• (5) conduct an analgesic trial.
Pain Management(Page
No;763-792)
• Management of Pain

Pain can be managed through:

1. Pharmacological interventions
2. Non pharmacological interventions
3. Invasive/Surgical Interventions
Pharmacological management
Management(Page No;763-795)
• Optimal pain relief is the responsibility of every member of the
health care team and begins with titration of the analgesic
agent, followed by continued prompt assessment and analgesic
agent administration during the course of care to safely achieve
pain intensities that allow patients to meet their functional
goals with relative ease
A multimodal regimen
• Pain is a complex phenomenon involving multiple underlying
mechanisms and as such, requires more than one analgesic
agent to manage it safely and effectively.
• The recommended approach for the treatment of all types of
pain in all age groups is called multimodal analgesia .
• A multimodal regimen combines drugs with different
underlying mechanisms, which allows lower doses of each of
the drugs in the treatment plan, reducing the potential for
each to produce adverse effects.
• Furthermore, multimodal analgesia can result in comparable
or greater pain relief than can be achieved with any single
analgesic agent.
Routes of Administration
• Oral route
• Intravenous (IV) route
• Rectal route
• Topical route
• Transdermal
• Intraspinal analgesia, sometimes referred to as “neuraxial”
analgesia.
• Implanted intrathecal pumps
• Temporary epidural catheters
• . Epidural analgesia
• Patient-controlled epidural analgesia (PCEA).
Dosing Regimen
Two basic principles of providing effective pain management are
• preventing pain
• maintaining a pain intensity that allows the patient to
Accomplish functional or quality of life gals.
• Accomplishment of these goals may require the analgesic
agent to be given on a scheduled around-the-clock (ATC)
basis, rather than PRN (as needed) to maintain stable analgesic
blood levels.
Analgesic Agents
• Analgesic agents are categorized into three main groups:
• (1) Nonopioid analgesic agents, which include
acetaminophen and NSAIDs;
• (2) Opioid analgesic agents, which include, among
others, morphine, hydromorphone, fentanyl, and
oxycodone; and
• (3) adjuvant analgesic agents (sometimes referred to as
coanalgesic agents). The adjuvant analgesic agents
comprise the largest group and include various agents
with unique and widely differing mechanisms of action.
Examples are local anesthetics, some anticonvulsants,
and some antidepressants
Non opioid Analgesic Agents
• Non opioid Analgesic Agents
1. Acetaminophen and
2. 2.NSAIDs(Non steroidal anti Inflammatory drug)
Indication for administration
It is administered for mild to some moderate nociceptive pain
(e.g., from surgery, trauma, or osteoarthritis) and are added to
opioids, local anesthetics, and/or anticonvulsants as part of a
multimodal analgesic regimen for more severe nociceptive pain.
Adverse Effects of Non opioid Analgesic Agents
Hepatotoxicity
Acute kidney injury
Gastric toxicity and ulceration
Opioid Analgesic Agents
• Opioid analgesic agents are divided into two major
groups:
(1)Mu agonist opioids (also called morphine like drugs)
(2)Agonist– antagonist opioids.
1.The mu agonist opioids comprise the larger of the two
groups and include morphine, hydromorphone,
hydrocodone, fentanyl, oxycodone, and methadone, among
others.
2.The agonist–antagonist opioids include buprenorphine
(Buprenex, Butrans), nalbuphine (Nubain), and
butorphanol (Stadol).
Selected Opioid Analgesic
Agents
• Selected Opioid Analgesic Agents
• Morphine.
• Hydromorphone (Dilaudid)
• Oxycodone
• Oxymorphone
common adverse effects of
opioids
• constipation
• nausea, vomiting,
• pruritus
• Hypotension, and sedation .
• Respiratory depression,
• lowers blood pressure by dilating peripheral arterioles
and veins.
• postural hypotension ,
• Sleep disorders,
• Delayed gastric emptying, slowed bowel motility, and
decreased peristalsis
Adjuvant Analgesic Agents
• Adjuvant analgesics use has become increasingly important especially in the
management of mild to moderate pain. Adjuvants act on either the excitatory (e.g.,
substance P, and glutamate), inhibitory neurotransmitters (e.g., GABA), or on
neurotransmitters that modulate pain experience (e.g., serotonin, norepinephrine).
• Examples include:
• Anticonvulsants
• carbamazepine, gabapentin, pregabalin
• Antidepressants
• amitriptyline,[3] duloxetine, venlafaxine
• Antihistamines
• hydroxyzine, promethazine
• Stimulants
• caffeine, cocaine, dextroamphetamine, ephedrine
• carisoprodol
• cyclobenzaprine
• hyoscine (scopolamine)
Local Anesthetics
• Local anesthetics have a long history of safe and effective
use for all types of pain management.
• Local anesthetics are sodium channel blockers that affect
the formation and propagation of action potentials.
• Anticonvulsants
• The anticonvulsants gabapentin (Neurontin) and
pregabalin (Lyrica) are first-line analgesic agents for
neuropathic pain and are increasingly being added to
postoperative pain treatment plans to address the
neuropathic component of surgical pain
Antidepressants
• Antidepressant adjuvant analgesic agents are divided into two
major groups:
• Tricyclic antidepressants (TCAs)
• serotonin Norepinephrine reuptake inhibitors (SNRIs).
Primary adverse effects of TCAs
• Dry mouth, sedation, dizziness, mental clouding, weight gain,
and constipation ,Orthostatic hypotension.
• The most serious adverse effect is cardiotoxicity,
Ketamine
• Ketamine is a dissociative anesthetic with dose-dependent
analgesic, sedative, and amnestic properties
• Ketamine has been used for the treatment of persistent
neuropathic pain.
Non pharmacologic Methods of Pain
Management(page No;794-798)
• Acupuncture,
• Chiropractic manipulation,
• Herbal medicines
• Natural products (e.g., herbs or botanicals, vitamins,
probiotics)
• Mind and body practices
• Massage therapy
• yoga,
• Hot and cold Application

• Meditation
• Distraction

• Imagery

• Non pharmacologic therapies are usually effective alone for

mild to some moderate-intensity pain, and they should
complement, but not replace, pharmacologic therapies for
more severe pain .
• Non pharmacologic methods can facilitate relaxation and
reduce anxiety and stress
Nursing Implications of Pain
Management(page no-799-780)
• The provision of optimal pain management requires a
collaborative approach between patients with pain, their
families, and members of the health care team.
• Everyone involved must share common goals, a common
knowledge base, and a common language with regard to the
analgesics and non pharmacologic methods used to manage
pain.
The “Placebo Effect”
• A placebo is defined as any medication or
procedure, including surgery, that produces an
effect in a patient because of its implicit or
explicit intent and not because of its specific
physical or chemical properties.
Examples
• A saline injection is one example of a placebo.
• Administration of a medication at a known
subtherapeutic dose
Think ??
A 7-year old pediatric patient tells you that he is in pain. The patient rates
the pain as 4 on the Faces Pain Scale of 0-10. His mother, who is in the
room, states that her son is having pain at a level of 8 on the 0-10 scale.
Which is the most accurate assessment of the patient's pain?
A. The patient is the best resource for assessing the pain and should
receive the appropriate pain medication.
B. The patient is the best resource for assessing the pain, but should not
receive any pain medication because his level is only 4 out of 10.
C. The nurse is the best resource for assessing the pediatric patient's
pain level and gives the dose of pain medication that matches the
nurses' judgment.
D. The mother is the best resource for assessing the pain in this case,
and the patient should receive the maximum dose of pain medication
ordered.

Check NCP on Page 799 (chart12-8)

SHOCK
DEFINITON OF SHOCK(PageNo:924)
• Shock can best be defined as a clinical syndrome that results
from inadequate tissue perfusion, creating an imbalance
between the delivery of oxygen and nutrients needed to
support cellular function (Maier, 2015; Moore, Dyson, Singer,
et al., 2015).
• TYPES OF SHOCK
1.Hypovolemic shock,
2.Cardiogenic shock,
3.Obstructive shock,
4.Distributive shock
a. Neurogenic shock
b. Anaphylactic shock
c. Septic shock
PATHOPHYSIOLOGY OF
SHOCK(page No;(926-928)
• Cellular Changes
• Cellular Changes In shock, the cells lack an adequate blood
supply and are deprived of oxygen and nutrients; therefore,
they must produce energy through anaerobic metabolism.
• This results in low-energy yields from nutrients and an acidotic
intracellular environment. Because of these changes, normal
cell function ceases .
• The cell swells and the cell membrane becomes more
permeable, allowing electrolytes and fluids to seep out of and
into the cell.
• The sodium–potassium pump becomes impaired; cell
structures, primarily the mitochondria, are damaged, and death
of the cell results.
Vascular Responses
• Vascular Responses Local regulatory mechanisms, referred to
as autoregulation, stimulate vasodilation or vasoconstriction in
response to biochemical mediators released by the cell,
communicating the need for oxygen and nutrients.
• .
Blood Pressure Regulation
• BP is regulated by baroreceptors (pressure receptors) located
in the carotid sinus and aortic arch.
• These pressure receptors are responsible for monitoring the
circulatory volume and regulating neural and endocrine
activities.
• When BP drops, catecholamines (e.g., epinephrine,
norepinephrine) are released from the adrenal medulla. These
increase heart rate and cause vasoconstriction, restoring BP.
Chemoreceptors, also located in the aortic arch and carotid
arteries, regulate BP and respiratory rate using much the same
mechanism in response to changes in oxygen and carbon
dioxide (CO2) concentrations in the blood.
The kidneys regulate BP
• The kidneys regulate BP by releasing renin, an enzyme needed
for the eventual conversion of angiotensin I to angiotensin II, a
potent vasoconstrictor.
• This stimulation of the renin–angiotensin mechanism and the
resulting vasoconstriction indirectly lead to the release of
aldosterone from the adrenal cortex, which promotes the
retention of sodium and water (i.e., hypernatremia).
• Hypernatremia then stimulates the release of antidiuretic
hormone (ADH) by the pituitary gland. ADH causes the kidneys
to retain water further in an effort to raise blood volume and
BP.
Stages of Shock(page no;929-
944)
• Stage 1.Compensatory
• Stage 2.progressive
• Stage 3.Irreversible
Stage 1.Compensatory Shock(page no;929-936)

In the compensatory stage of shock,

• The BP remains within normal limits.
• Vasoconstriction, increased heart rate, and increased
contractility of the heart contribute to maintaining adequate
cardiac output.
• This results from stimulation of the sympathetic nervous
system and subsequent release of catecholamines (e.g.,
epinephrine, norepinephrine).
• The body shunts blood from organs such as the skin, kidneys,
and gastrointestinal (GI) tract to the brain, heart, and lungs to
ensure adequate blood supply to these vital organs. As a result,
the skin may be cool and pale, bowel sounds are hypoactive,
and urine output decreases in response to the release of
aldosterone and ADH.
Management
• Fluid replacement and medication therapy must be initiated to
maintain an adequate BP and reestablish and maintain
adequate tissue perfusion
• Nursing management
Early interventions include
• Identifying the cause of shock
• Administering intravenous (IV) fluids and oxygen, and
obtaining necessary laboratory tests to rule out and treat
metabolic imbalances or infection
Progressive Stage (Page
Nol936-942)
• In the second stage of shock, the mechanisms that regulate BP
can no longer compensate, and the MAP falls below normal
limits. Patients are clinically hypotensive; this is defined as a
systolic BP of less than 90 mm Hg or a decrease in systolic BP
of 40 mm Hg from baseline. The patient shows signs of
declining mental status
• Although all organ systems suffer from hypo perfusion at this
stage, several events perpetuate the shock syndrome.
•
Clinical manifestation
• Respirations are rapid and shallow. Crackles are heard over
the lung fields.
• Cardiovascular Effects A lack of adequate blood supply leads
to dysrhythmias and ischemia. heart rate is rapid, sometimes
exceeding 150 bpm. The patient may complain of chest pain
and even suffer a myocardial infarction (MI).
• Neurologic Effects As blood flow to the brain becomes
impaired, mental status deteriorates. Changes in mental status
occur with decreased cerebral perfusion and hypoxia. Initially,
the patient may exhibit subtle changes in behavior, become
agitated, confused, or demonstrate signs of delirium.
Subsequently, lethargy increases, and the patient begins to lose
consciousness
• Renal Effects When the MAP falls below 65 mm Hg the
glomerular filtration rate of the kidneys cannot be maintained,
and drastic changes in renal function occur. Acute kidney
injury (AKI) is characterized by an increase in blood urea
nitrogen (BUN).
• Hepatic Effects Decreased blood flow to the liver impairs the
ability of liver cells to perform metabolic and phagocytic
functions.
• Gastrointestinal Effects GI ischemia can cause stress ulcers in
the stomach, putting the patient at risk for GI bleeding. In the
small intestine, the mucosa can become 938 necrotic and
slough off, causing bloody diarrhea.
Hematologic Effects The combination of hypotension, sluggish
blood flow, metabolic acidosis, coagulation system imbalance,
and generalized hypoxemia can interfere with normal hemostatic
mechanisms
In this condition
• Bruises (ecchymoses) and bleeding (petechiae) may appear in
the skin.
• Coagulation times (e.g., prothrombin time, activated partial
thromboplastin time) are prolonged.
• Clotting factors and platelets are consumed and require
replacement therapy to achieve hemostasis.
Medical Management
• Supporting the respiratory system.
• Optimizing intravascular volume
• Supporting the pumping action of the heart
• Early enteral nutritional support,
• Targeted hyperglycemic control with IV insulin and use of
antacids, histamine-2 (H2) blockers, or antipeptic medications
to reduce the risk of GI ulceration and bleeding
Patients in the progressive stage of shock are cared for in the
intensive care setting to facilitate

close monitoring of
• Hemodynamic monitoring,
• Electrocardiographic [ECG] monitoring,
• Arterial blood gases,
• Serum electrolyte levels,
• Physical and mental status changes
• Rapid and frequent administration of various prescribed
medications and fluids; and
• Mechanical ventilation, dialysis (e.g., continuous renal
replacement therapy), and intra-aortic balloon pump.
Preventing Complications
• Monitoring includes evaluating blood levels of medications,
• observing invasive vascular lines for signs of infection, and
• checking neurovascular status if arterial lines are inserted,
especially in the lower extremities.
• Promoting Rest and Comfort Efforts are made to minimize the
cardiac workload by reducing the patient’s physical activity
and treating pain and anxiety.
• Supporting Family Members Because patients in shock receive
intense attention by the health care team. The nurse should
make sure that the family is comfortably situated and kept
informed about the patient’s status.
Irreversible Stage(Page
no:942-944)
• This stage of shock represents the point along the shock
continuum at which organ damage is so severe that the patient
does not respond to treatment and cannot survive. Despite
treatment, BP remains low and leads to renal and liver
dysfunction.
• Later stage ,Multiple organ dysfunction progressing to
complete organ failure has occurred, and death is imminent.
Medical Management
• Medical management during the irreversible
stage of shock is similar to interventions and
treatments used in the progressive stage
Nutritional Support
• Nutritional support is an important aspect of care for critically
ill patients. Increased metabolic rates during shock increase
energy requirements and therefore caloric requirements.
Patients in shock may require more than 3000 calories daily.
• Parenteral or enteral nutritional support should be initiated as
soon as possible. Enteral nutrition is preferred, promoting GI
function through direct exposure to nutrients and limiting
infectious complications associated with parenteral feeding
General Management Strategies in Shock(page
No:944-953)
• Fluid replacement to restore intravascular volume
• The fluids given may include crystalloids and interstitial
spaces), colloids (large-molecule IV solutions), and blood
components (packed red blood cells, fresh frozen plasma, and
platelets).
• Vasoactive medications to restore vasomotor tone and
improve cardiac function

• Nutritional support to address the metabolic requirements

that are often dramatically increased in shock .
• Collaborative care among all members of the health care
team.
• Vasoactive medications are given in all forms of shock to
improve the patient’s hemodynamic stability when fluid
therapy alone cannot maintain adequate MAP.
• When vasoactive medications are given,
• vital signs must be monitored frequently (at least every 15
minutes until stable, or more often if indicated).
• Vasoactive medications should be given through a central
venous line, because infiltration and extravasation of some
vasoactive medications can cause tissue necrosis and
sloughing.
• Dosages are changed to maintain the MAP at a physiologic
level that ensures adequate tissue perfusion (usually greater
than 65 mm Hg).
TYPES OF SHOCK
Hypovolemic Shock(page
no:954-960)
• Hypovolemic Shock, the most common type of shock, is
characterized by decreased intravascular volume
• Pathophysiology Hypovolemic shock can be caused by
external fluid losses, as in traumatic blood loss, or by internal
fluid shifts, as in severe dehydration, severe edema, or ascites .
• Intravascular volume can be reduced by both fluid loss and
fluid shifting between the intravascular and interstitial
compartments.
Medical Management
• To restore intravascular volume to reverse the sequence of
events leading to inadequate tissue perfusion, to redistribute
fluid volume, and to correct the underlying cause of the fluid
loss as quickly as possible.
• Treatment of the Underlying Cause If the patient is
hemorrhaging, efforts are made to stop the bleeding. This may
involve applying pressure to the bleeding site or surgical
interventions to stop internal bleeding.
• If the cause of the hypovolemia is diarrhea or vomiting,
medications to treat diarrhea and vomiting are given while
efforts are made to identify and treat the cause.
• Multiple IV lines allow simultaneous administration of fluid,
medications, and blood component therapy if required.
• A modified Trendelenburg position, also known as passive leg
raising is recommended in hypovolemic shock. Elevation of
the legs promotes the return of venous blood and can be used
as a dynamic assessment of a patient’s fluid responsiveness.
Pharmacologic Therapy

• Medications are also given to reverse the cause of

the dehydration.
• For example,
1. Insulin is given if dehydration is secondary to
hyperglycemia,
2. Desmopressin (DDAVP) is given for diabetes
insipidus
3.Antidiarrheal agents for diarrhea
4. Antiemetic medications for vomiting.
Nursing management

monitoring patients who are at risk for fluid

deficits and assisting with fluid replacement before
intravascular volume is depleted
Cardiogenic Shock(page
No:960-968)
• Definition:
• Cardiogenic shock occurs when the heart’s ability to contract
and to pump blood is impaired and the supply of oxygen is
inadequate for the heart and the tissues.
• The causes of cardiogenic shock are
• 1 coronary or 2. noncoronary.
• 1.Coronary cardiogenic shock is more common and is seen
most often in patients with acute MI resulting in damage to a
significant portion of the left ventricular myocardium
• 2.Noncoronary causes of cardiogenic shock
• severe hypoxemia, acidosis, hypoglycemia, hypocalcemia,
tension pneumothorax, cardiomyopathies, valvular damage,
cardiac tamponade, dysrhythmias)
• Pathophysiology In cardiogenic shock, cardiac output, which
is a function of both stroke volume and heart rate, is
compromised. When stroke volume and heart rate decrease or
become erratic, BP falls and tissue perfusion is reduced.
• Blood supply for tissues and organs and for the heart muscle
itself is inadequate, resulting in impaired tissue perfusion.
Because impaired tissue perfusion weakens the heart and
impairs its ability to pump, the ventricle does not fully eject its
volume of blood during systole.
Clinical Manifestations
• Pain of angina
• Develop dysrhythmias,
• Complain of fatigue,
• Express feelings of doom, and show signs of
hemodynamic instability.
Medical Management
• Administering and increasing oxygen supply to the heart
muscle while reducing oxygen demands.
• . In the case of coronary cardiogenic shock (e.g., acute
coronary syndromes, acute MI),
• The patient may require thrombolytic (fibrinolytics) therapy,
• Percutaneous coronary intervention,
• Coronary artery bypass graft surgery
• Intra-aortic balloon pump therapy
• Ventricular assist device, or some combination of these
treatments
Initiation of First-Line Treatment
• Oxygenation In the early stages of shock, supplemental oxygen
is given by nasal cannula at a rate of 2 to 6 L/min to achieve an
oxygen saturation exceeding 95%.
• Monitoring of arterial blood gas values, pulse oximetry
values, and ventilatory effort (i.e., work of breathing)
• Pain Control If a patient experiences chest pain, IV morphine
is given for pain relief. In addition to relieving pain, morphine
dilates the blood vessels.
• Hemodynamic Monitoring: A multilumen central venous and
pulmonary artery catheter may be inserted to allow
measurement of myocardial filling pressures, pulmonary artery
pressures, cardiac output, and pulmonary and systemic
resistance.
• Laboratory Marker Monitoring
• Fluid Therapy Appropriate fluid administration is also
necessary in the treatment of cardiogenic shock.
• Pharmacologic Therapy
• Vasoactive medication therapy consists of multiple
pharmacologic strategies to restore and maintain adequate
cardiac output.
• Medications commonly combined to treat cardiogenic shock
include dobutamine, nitroglycerin, and dopamine
• Other Vasoactive Medications:
• Additional vasoactive agents that may be used in managing
cardiogenic shock include norepinephrine, epinephrine,
milrinone, vasopressin, and phenylephrine.
• Antiarrhythmic Medications
• Mechanical Assistive Devices If cardiac output does not
improve despite supplemental oxygen, vasoactive medications,
and fluid boluses, mechanical assistive devices are used
temporarily to improve the heart’s ability to pump. Intra-aortic
balloon counter pulsation is one means of providing temporary
circulatory assistance .
• Fluid Therapy Appropriate fluid administration is also
necessary in the treatment of cardiogenic shock.
Administration of fluids must be monitored closely to detect
signs of fluid overload. Incremental IV fluid boluses are
cautiously given to determine optimal filling pressures for
improving cardiac output
Nursing Management
• Preventing Cardiogenic Shock Identifying at-risk patients
early, promoting adequate oxygenation of the heart muscle,
and decreasing cardiac workload can prevent cardiogenic
shock.
• Nursing management includes working with other members of
the health care team to prevent shock from progressing and to
restore adequate cardiac function and tissue perfusion.
• Monitoring Hemodynamic Status.
• Administering Medications and Intravenous Fluids
• Maintaining Intra-Aortic Balloon Counter pulsation
• Enhancing Safety and Comfort
Distributive Shock(page no-
969-970)
• Distributive shock occurs when intravascular volume pools in
peripheral blood vessels.
sub classification of shock into three types:
• Septic shock,
• Neurogenic shock, and
• Anaphylactic shock.
 Sepsis and Septic Shock Septic shock,
(pageno:970-981)

• the most common type of distributive shock, is caused by

widespread infection or sepsis.
• sepsis is “life-threatening organ dysfunction caused by a
dysregulated host response to infection (p. 804),” and septic
shock is “a subset of sepsis in which underlying circulatory
and cellular metabolism abnormalities are profound enough to
substantially increase mortality .
• Hospital-acquired conditions, which may include hospital-
associated infections (i.e., infections not present at the time of
admission to the health care setting) in critically ill patients
that may progress to septic shock most frequently originate in
the bloodstream (bacteremia), lungs (pneumonia), and urinary
tract (urosepsis).
• increased use of invasive procedures and indwelling medical
devices, the increased number of antibiotic-resistant
microorganisms, and the increasingly older population.
Medical management
• Correction of Underlying Causes Current treatment of sepsis
and septic shock involves rapid identification and elimination
of the cause of infection.
• Fluid Replacement Therapy
• Pharmacologic Therapy If the infecting organism is unknown,
broad-spectrum antibiotic agents are started until culture and
sensitivity reports are received
• Nutritional Therapy Aggressive nutritional supplementation
should be initiated within 24 to 48 hours of ICU admission to
address the hypermetabolic state present with septic shock.
Nursing Management
• All invasive procedures must be carried out with aseptic
technique after careful hand hygiene.
• In addition, IV lines, arterial and venous puncture sites,
surgical incisions, traumatic wounds, and urinary catheters
must be monitored for signs of infection.
• Nursing interventions to prevent infection need to be
implemented in the care of all patients.
• Nurses should identify patients who are at particular risk for
sepsis and septic shock adults and immunosuppressed patients
and those with extensive trauma, burns, or diabetes), keeping
in mind that these high-risk patients may not develop typical or
classic signs of infection and sepsis.
• patients in the ICU setting with infection be monitored for the
development of sepsis by using the Sepsis-Related Organ
Failure Assessment Score (also known as the Sequential Organ
Failure Assessment [SOFA] score) .
Neurogenic Shock(page no:982-983)
• In neurogenic shock, vasodilation occurs as a result of a loss of
balance between parasympathetic and sympathetic stimulation.
• Neurogenic shock can be caused by spinal cord injury, spinal
anesthesia, or other nervous system damage.
• It may also result from the depressant action of medications or
from lack of glucose (e.g., insulin reaction)
• Medical Management Treatment of neurogenic shock involves
restoring sympathetic tone, either through the stabilization of
a spinal cord injury or, in the instance of spinal anesthesia, by
positioning the patient properly. Specific treatment depends
on the cause of the shock
• Nursing Management
• It is important to elevate and maintain the head of the bed at
least 30 degrees to prevent neurogenic shock when a patient
receives spinal or epidural anesthesia. Elevation of the head
helps prevent the spread of the anesthetic agent up the spinal
cord. In suspected spinal cord injury, neurogenic shock may be
prevented by carefully immobilizing the patient to prevent
further damage to the spinal cord
Nursing management
• The nurse must check the patient daily for any lower extremity
pain, redness, tenderness, and warmth.
• If the patient complains of pain and objective assessment of the
calf is suspicious, the patient should be evaluated for DVT.
• Passive range of motion of the immobile extremities helps
promote circulation.
• Application of pneumatic compression devices often combined
with antithrombotic agents
 Anaphylactic
Shock(pageno:983-986)
• Anaphylactic shock is caused by a severe allergic reaction when
patients who have already produced antibodies to a foreign
substance (antigen) develop a systemic antigen–antibody reaction;
specifically, an immunoglobulin E (IgE)-mediated response.
• Signs and symptoms of anaphylaxis
• The patient may complain of headache, lightheadedness, nausea,
vomiting, acute abdominal pain or discomfort, pruritus, and
feeling of impending doom. Assessment may reveal diffuse
erythema and generalized flushing, difficulty breathing (laryngeal
edema), bronchospasm, cardiac dysrhythmias, and hypotension.
Characteristics of severe anaphylaxis usually include rapid onset
of hypotension, neurologic compromise, respiratory distress, and
cardiac arrest
Medical Management
• Treatment of anaphylactic shock
• Removing the causative antigen (e.g., discontinuing an antibiotic agent),
• Administering medications that restore vascular tone, and
• providing emergency support of basic life functions.
• Fluid management is critical, as massive fluid shifts can occur within
minutes due to increased vascular permeability.
• Intramuscular epinephrine is given for its vaso constrictive action.
Diphenhydramine (Benadryl) is given intravenously to reverse the effects
of histamine, thereby reducing capillary permeability.
• Nebulized medications, such as albuterol (Proventil), may be given to
reverse histamine-induced bronchospasm.
• If cardiac arrest and respiratory arrest are imminent or have occurred,
cardiopulmonary resuscitation (CPR) is performed.
• Endotracheal intubation may be necessary to establish an airway.
• IV lines are inserted to provide access for administering fluids and
medications.
Nursing Management
• Early recognition of anaphylactic shock.
• The nurse must assess all patients for allergies or previous
reactions to antigens (e.g., medications, blood products, foods,
contrast agents, latex) and communicate the existence of these
allergies or reactions to others.
• When administering any new medication, the nurse observes
all patients for allergic reactions
• A 70 year old patient is malnourished, has a history of type 2
DM, and is admitted from the nursing home with pneumonia
and tachypnea. For which kind of shock should the nurse
closely monitor this patient?

A. septic shock
B. neurogenic shock
C. cardiogenic shock
D. anaphylactic shock
• THANK YOU
Reference:

• Brunner and Suddarth”s, Text book of Medical

Surgical Nursing.14th edition by Dr.Janice L
Hinkle, Keny H. Publized by Wolters kluwer.

• Pain assessment and Management( Page

No:744-795)

• Shock( Page No:923-985)