Critical Care
Created by: Nicole Shafar
RN, BSN
Objectives
 Identify
risk factors for shock and multiple
system organ dysfunction syndrome.
 Compare and contrast the effects of
sepsis, shock, and multiple organ
dysfunction syndrome on the major body
parts.
 Describe the pathophysiology and clinical
manifestations of shock
Objectives continued
 Compare
the collaborative care, drug
therapy, and nursing management of
clients with different types of shock.
 Describe the nursing management of a
client experiencing multiple organ
dysfunction syndrome.
 Select appropriate nursing interventions to
manage common problems and needs of
critically ill clients.
Shock
 Is
widespread abnormal metabolism that
occurs when the human need for
oxygenation and tissue perfusion is not
met to the level needed to maintain cell
function.
 It is a condition, not a disease and
represents the “whole-body” response
that occurs when too little oxygen is
delivered to the tissues.
Shock Continued
 All
organs are affected by shock.
 Any problem that impairs oxygen delivery
to tissues and organs can start the
syndrome of shock and lead to a lifethreatening emergency.
Why does it occur?
 Cardiovascular
problems
 Infections
 Patients
in acute care settings are at a
higher risk.
Types of Shock
 Shock
is classified by the type of
impairment it causes or by the origin of
the problem:

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Cardiogenic
Hypovolemic
Neurogenic
Anaphylactic
Septic
Cardiogenic Shock
 Occurs
when the actual heart muscle is
unhealthy and pumping is directly
impaired.
 This is sometimes referred to as pump
failure.
 Myocardial infarction (MI) is the most
common cause; affecting nearly 15% of
all patients hospitalized with acute MI.
Cardiogenic Shock
 Other
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causes:
Myocardial ischemia
Papillary muscle dysfunction
Cardiomyopathy
Chronic or acute heart failure
Acidosis
Hypovolemic Shock
 Occurs
when too little circulating blood
volume causes a decrease in mean
arterial pressure (MAP), resulting in the
body’s need for oxygen being met.
Pathophysiology



The reduced MAP slows blood flow, resulting
in decreased tissue perfusion.
A decrease in MAP od 5-10mm Hg below the
patient’s baseline is detected by
baroreceptors in the aortic arch and carotid
sinus.
The brain then responds by moving blood into
selected areas and bypassing others. This
“shunting” is what causes the manifestations
of shock
What Happens if it isn’t Fixed?
 When
shock conditions continue for
periods longer than one to two hours
without intervention, the acid-base
imbalance, electrolyte imbalance and
increased metabolites cause so much
damage in vital organs that multiple
organ dysfunction syndrome occurs and
recovery is no longer possible.
Causes of Hypovolemic Shock

Hemorrhage (internal or external)
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GI bleeding, or any condition that reduces
circulation intravascular volume or other body
fluids.
Intestinal obstruction
Peritonitis
Acute pancreatitis
Ascites
Dehydration

From excessive perspiration, severe diarrhea or
protracted vomiting, diabetes insipidus, diuresis,
or inadequate fluid intake.
Stages of shock
 Initial
stage
 Nonprogressive stage
 Progressive stage
 Refractory stage
Initial Stage of Shock




Also known as the early stage; is present when the
patient’s baseline MAP is decreased by less than
10mm Hg.
Compensatory mechanisms return MAP to normal,
oxygen flow to all organs is maintained.
Increased anaerobic metabolism with production
of lactic acid.
A heart and respiratory rate increased from the
patient's baseline level or a slight increase in
diastolic blood pressure may be the only objective
manifestation of this stage.
Nonprogressive Stage of
Shock
 Also
known as compensatory stage;
occurs when MAP decreases by 10-15mm
Hg from baseline.
 Kidney and hormonal adaptive
mechanisms are activated.
 Antidiuretic hormone (ADH), aldosterone,
epinepherine, and norepinepherine are
released.
Nonprogressive Stage
Continued
 Renin
causes a decrease in urine output,
sodium reabsorption, and widespread
blood vessel constriction.
 ADH increases water reabsorption in the
kidney, and blood vessel constriction in
the skin and other nonvital organs.
Nonprogressive Stage
Continued
Manifestations

Tissue hypoxia occurs in
nonvital organs,
acidosis and
hyperkalemia occur.
include:

Subjective

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
Objective


Comparing these
changes with the
values and
manifestations earlier is
critical to identifying
this stage of shock.
Thirst sensation
Anxiety

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Restlessness
Tachycardia
Increased respiratory rate
Decreased urine output
Falling systolic blood
pressure
Rising diastolic blood
pressure
Cool extremities
Narrowing pulse pressure
Decrease in oxygen
saturation
Progressive Stage
 Or
intermediate stage occurs when there
is a sustained decrease in MAP of more
than 20mm Hg from baseline.
 Compensatory mechanisms are working
but no longer sustaining adequate
oxygenation even to the vital organs.
Progressive Stage Continued

Vital organs become hypoxic
and nonvital organs become
anoxic and ischemic.
Manifestations
include:


Tissues have severe cell
damage and die.



This stage is a life threatening
emergency. Vital organs can
only tolerate this for a short
time before becoming
permanently damaged. The
patient’s life can usually be
saved if the conditions
creating shock are corrected
within an hour or less of the
onset of this stage.
Subjective:
Severe thirst and increased
anxiety
Objective:
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Rapid, weak pulse
Low blood pressure
Pallor or cyanosis of mucous
membranes and nail beds
Cool moist skin
Anuria
5-20% decrease in pulse
oximetry
Low pH
Rising lactic acid and
potassium level
Refractory Stage



Or irreversible stage of shock occurs when too
much cell death and tissue damage result
from too little oxygen reaching the tissues.
Vital organs have severe damage, and the
body can no longer respond to interventions
and shock continues.
Therapy is not effective in saving the patient,
even if the cause of shock is corrected and
the MAP returns to normal.
Refractory Stage Continued
 Manifestations

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include:
Rapid loss of consciousness
Non-palpable pulse
Cold, mottled or dusky extremities
Slow shallow respirations
Unmeasurable oxygen saturation
Multisystem Organ Dysfunction
 Assessment
and needs identification
 This is the sequence of cell damage
caused by the massive release of toxic
metabolites and enzymes.
 This causes more cells to die and break
open causing a vicious cycle. Small clots
occur.
 Occurs first in the liver, heart, brain and
kidney.
What to Look For
Later Findings:
Early findings may
include:
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Fever (>101F or 38.3C)
Tachycardia
Narrowed pulse
pressure
Tachypnea
Decreased
pulmonary artery
pressure and
increased cardiac
output

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•
Decreased level of
consciousness
Respiratory depression
Diminished bowel
sounds
Jaundice
Oliguria or anuria
Increased pulmonary
artery pressure and
decreased cardiac output
How do we fix it?
 The
goals of shock management are to
maintain tissue oxygenation, increase
vascular volume to normal range, and
support compensatory mechanisms.
Oxygen therapy, fluid replacement
therapy and drug therapy are all useful
for this problem.
Nursing Interventions


Oxygen therapy
Monitor vital signs
(every 15mins):
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Blood pressure
Pulse pressure
Central venous
pressure
Respiratory rate
Skin and mucosal
color
Oxygen saturation
Mental status
Urine output
 IV
therapy: or fluid
resuscitation
(crystalloids (normal
saline and LR), protein
containing colloids
(whole blood, PRBCs,
plasma, plasma
fractions, and plasma
expanders).
 Inotropics
(dobutamine,
dopamine)
 Adrenergic agonists
(epinephrine,
norepinephrine,
Neo-Synephrine)
 Vasopressors/
vasodilators
Pharmacologic
Management
Inotropics: Dobutamine
(Dobutrex)
 Dosage:
1.0-20mcg/kg/min IV as a
continuous infusion
 Purpose: directly stimulates adrenergic
receptor sites on the heart muscle and
improves heart muscle contraction
 Nursing Intervention: assess for chest pain
(increases myocardial oxygen
consumption and can cause angina or
infarction).
Inotropics: Milrinone
(Primacore)
 Dosage:
50mcg/kg bolus over 10min; 0.30.75mcg/kg/min continuous infusion.
 Purpose: directly stimulates adrenergic
receptor sites on the heart muscle and
improves heart muscle contraction.
 Assess blood pressure every 15mins
(hypertension is a sign of an overdose).
Dopamine (Intropin, Revimine)
 Dosage:
5-20mcg/kg/min IV
 Purpose: Improve blood flow by
increasing peripheral resistance,
increasing venous return to the heart and
improving myocardial contractility.
 Nursing Intervention: assess the patient for
chest pain (drug increases myocardial
oxygen consumption), monitor urine
output hourly (higher doses increase renal
perfusion and urine output).
Adrenergic Agonists:
Epinephrine (Adrenalin)

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Dosage: 0.1-0.25mg every 5-15min; may be
followed by 1-4mcg/min continuous infusion
Purpose: Rapidly stimulates alpha- and betaadrenergic receptors of autonomic nervous
system (alpha: vasoconstriction, beta:
bronchodilation)
Side effects: pallor, tachycardia and
palpitations, nervousness, muscle twitching,
sweating, anxiety, insomnia, hypertension,
headache and hyperglycemia.
Nursing Intervention: Assess lung sounds,
respiratory pattern BP and HR before
administration and at peak.
Adrenergic Agonists:
norepinephrine (Levophed)

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
Dosage: initial: 0.5-1mcg/min IV, to maintain
systolic blood pressure between 90-100mm
Hg.
Purpose: Improve blood flow by increasing
peripheral resistance, increasing venous
return to the heart and improving myocardial
contractility.
Nursing Intervention: assess blood pressure
every 15min (hypertension is a sign of an
overdose), assess the patient for headache (is
an early symptom of drug excess).
Adrenergic Agonists:
Phenylephrine (NeoSynephrine)

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Dosage: 0.1-0.5mg IV every 15min
Purpose: Improve blood flow by increasing
peripheral resistance, increasing venous
return to the heart and improving myocardial
contractility.
Nursing Intervention: Assess every 30min for
extravasation, and check extremities for color
and perfusion (if the drug gets into the tissues
it can cause severe vasoconstriction, tissue
ischemia, and tissue necrosis), Assess for chest
pain (can cause rapid onset of
vasoconstriction in the myocardium and
impair oxygenation).
Vasodilators: Sodium
Nitroprusside (Nitro-press)

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Dosage: 0.25-10mcg/kg/min IV
Purpose: improves blood flow to the
myocardium by dilating the coronary arteries.
This effect is primary and rapid but short.
Nursing Intervention: Protect drug container
from light (light degrades the drug quickly),
assess blood pressure at least every 15mins
(the vasodilating effect can cause systemic
vasodilation and hypotension, especially in
older adults).
Surgical Intervention
 Oxygen,
IV fluids and medications are all
used to stabilize the patient’s
hemodynamic status.
 Once the causative factor has been
identified surgical intervention may be
necessary.
 Surgical interventions may include:
vascular repair or revision, surgical
hemostasis of major wounds, closure of
bleeding ulcers, and chemical scaring
(chemosclerosis) of varicosities.
Neurogenic Shock
 Results
from disruption in the
communication pathways between
upper motor neurons and lower motor
neurons.
 Most commonly in patients with spinal
cord injuries above T6.
 Usually occurs within 24 hours after a
spinal cord injury (SCI).
Neurogenic Shock Continued

Is a type of
hypovolemic shock
causing:

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Severe bradycardia
Warm, dry skin
Severe hypotension
Orthostatic
hypotension and
inability to sweat
below the level of
injury are also
symptoms.
 Notify
the physician
immediately if
these symptoms
occur, because
this problem is an
emergency!
Treatment for Neurogenic
Shock
 This
is done symptomatically by restoring
fluids to the circulating blood volume.
 Positioning: Regardless of the level of SCI,
keep the patient in proper body
alignment to prevent further injury or
irritability.
 Devices such as traction, orthoses, or
collars may be used.
Positioning
 Immobilize
or support the affected body
part, as appropriate.
 Place in the designated therapeutic
position.
 Maintain proper body alignment.
 Position with head and neck in alignment.
 Turn using the log roll technique
 Apply an orthosis collar
Positioning Continued
 Instruct
on orthosis care as needed.
 Apply and maintain a splinting or bracing
device
 Monitor skin integrity under bracing
device
 Instruct on pin site care as needed
 Monitor traction pin insertion site, and
perform care as needed.
 Monitor traction pin device care
Anaphylactic Shock
 Anaphylaxis,
is the most dramatic and lifethreatening example of a type I
hypersensitivity reaction, occurs rapidly
and systemically.
 Anaphylaxis is not common and episodes
can vary in severity.
 It can be fatal!
Common causes
DRUGS/FOREIGN
PROTEINS
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Antibiotics
Adrenocorticotropic hormone
Insulin
Vasopressin
Protamine
Allergen extracts
Muscle relaxants
Hydrocortisone
Vaccines
Local anesthetics
Whole blood
Cryoprecipitate
Immune serum globulin
Radiocontrast media
opiates
Common Causes Continued
FOODS
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Shellfish
Eggs
Legumes, nuts
Grains
Berries
Preservatives
Bananas
Peanuts
Common Causes Continued
INSECTS/ANIMALS

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Hymenopetra: bees,
wasps, hornets
Fire ants
Snake venom
Common Causes Continued
OTHER AGENTS
 Pollens
 Exercise
 Heat/cold
 Latex
 other


This has a rapid
onset and a
potentially fatal
outcome.
Teach the patient
with a history of
allergic reactions
to avoid allergens
whenever
possible, to wear a
medical alert
bracelet and to
alert health care
personnel about
specific allergies.
Health Promotion
Prevention is critical.
Always Be Prepared



Some patient’s must carry an emergency
anaphylaxis kit (bee sting kit with injectable
epinepherine)
The EpiPen is a spring-loaded injector that
delivers 0.3mg of epinepherine per 2mL dose.
Some assembly is required, practice devices
are available. Teach the patient how to use it
and get them to demonstrate in return.
How do you know it’s really an
allergy?
A
patient’s medical record should obtain
ALL allergens.
 If the patient has a known allergy be sure
to document a response.
Anaphylaxis Assessment
 First
reaction is the patient usually reports
feelings of uneasiness, apprehension,
weakness, and impending doom.
 These feelings are usually quickly followed
by generalized itching and urticaria
(hives).
 Erythema and sometimes angioedema
(diffuse swelling), of the eyes, lips or
tongue occur next.
Anaphylaxis Interventions
 Assess
respiratory function FIRST!
 Emergency respiratory management is
critical during an anaphylactic reaction,
because the severity of the reaction
increases with time.
 Call rapid response team
 Keep IV site, but switch out tubing, obtain
a second line if possible.
Septic Shock
A complex type of distributive
shock that usually begins as a
bacterial or fungal infection
and progresses to a dangerous
condition over a period of
days.
Sepsis
 Is
a widespread infection coupled with a
more general inflammatory response,
known as systemic inflammatory response
syndrome (SIRS) that is triggered when an
infection escapes local control.
 the inflammatory response of the body
becomes the enemy leading to extensive
tissue and vascular changes that further
impair oxygenation and tissue perfusion.
Severe Sepsis



Is the progression of sepsis with an amplified
inflammatory response.
All tissues are involved and have some
degree of hypoxia, although some organs are
experiencing cell death and dysfunction at
this time.
Microthrombi formation is widespread, using
too much of the available clotting factors. This
condition is known as disseminated
intravascular coagulation (DIC).
Septic Shock



Is the final stage of sepsis and SIRS when
multiple organ failure is evident and
uncontrolled bleeding occurs.
Even with the appropriate intervention, the
death rate among patients at this stage of
sepsis exceeds 60%.
Severe hypovolemic shock is present. this
results in an inability of the blood to clot
because platelets and clotting factors were
consumed earlier.
What causes it?
A
bacterial infection
that escapes local
control.
 Fungal infections in
immunocompromised
patients.

Gram-negative
bacteria:

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Escherichia coli
Pseudamonas
aeruginosa
Klebsiella
pneumoniae
Gram-positive
bacteria:


Staphylococcus
streptococcus
Prevention is Key
 Early
detection of sepsis before
progression to septic shock is a major
nursing responsibility.
 Teach patients manifestations of local
infections and of early sepsis.
Signs and symptoms
 Manifestations
of sepsis and septic shock
occur over many hours and some change
during the progression.
 No single lab test confirms the presence
of sepsis.
Interventions
 Focus
on identifying the problem as early
as possible and correcting the conditions
causing shock, and preventing
complications.
 Oxygen therapy (same as with
hypovolemic)
 Drug therapy (to enhance cardiac output
and restore vascular volume)
 Blood replacement therapy
Communication and support
to family members
 Develop
effective strategies to manage
issues related to the families of critically ill
clients.
 Assist the critically ill client in reducing
anxiety by addressing such issues as
impaired communication, sensoryperceptual problems, pain, and unfamiliar
environment.
Psychosocial Integrity


The indicator that the patient may be in
the beginning of severe sepsis is often a
change in affect or behavior.
Compare the patient’s current behavior,
verbal responses, and general affect with
those assessed earlier in the day or the
day before. They may just seem slightly
different in their reactions.
Cultural considerations for the
critically ill client
 What
do you do if a patient refuses blood
products?
Educating the critically ill client
and family
 Protecting
patients from infection and
sepsis at home is an important nursing
function.
 Teach about good hygiene, hand
washing, balanced diet, rest, exercise,
skin care, and mouth care, how to take a
temperature.