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
life-threatening 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:

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

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
bodys 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
patients 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 isnt 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)

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
patients 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 1015mm 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

Tissue hypoxia occurs in

nonvital organs, acidosis
and hyperkalemia occur.

Manifestations
include:
Subjective

Comparing these
changes with the values
and manifestations
earlier is critical to
identifying this stage of
shock.

Thirst sensation
Anxiety

Objective

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

organs become hypoxic and
nonvital organs become anoxic
and ischemic.

Manifestations
include:

Vital

have severe cell damage

and die.

Subjective:

Tissues

Objective:

This

stage is a life threatening

emergency. Vital organs can only
tolerate this for a short time before
becoming permanently damaged.
The patients life can usually be
saved if the conditions creating
shock are corrected within an hour
or less of the onset of this stage.

Severe thirst and increased

anxiety

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

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:

Fever (>101F or 38.3C)

Tachycardia
Narrowed pulse
pressure
Tachypnea
Decreased pulmonary
artery pressure and
increased cardiac
output

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):

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;

0.3-0.75mcg/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)
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)
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 (Neo-Synephrine)
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)
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 patients
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:

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

life-threatening 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

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

Shellfish
Eggs
Legumes, nuts
Grains
Berries
Preservatives
Bananas
Peanuts

Common Causes Continued

INSECTS/ANIMA
LS

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

patients 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 its really an

allergy?
A

patients 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:

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 patients 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.