SHOCK

NATURE OF THE PROBLEM

• Shock is a complex physiologic entity representing a diverse
group of life-threatening circulatory conditions

• A condition in which systemic blood pressure is inadequate to

deliver oxygen and nutrients to support vital organs and cellular
functions ( Mikhail, 1999)

• Early recognition of clinical manifestations and initiation of

therapeutic measures may halt the progression of shock and
prevent death
 PHYSIOLOGY
In shock, blood flow to vital organs becomes inadequate or
the cells become unable to extract and use oxygen and
substrates. If left untreated, this functional impairment of
cells, tissues, organs and body systems progresses to
multiple organ dysfunction and death
 Hemodynamic Principles
The circulatory system is composed of the heart, large blood
vessels and microcirculation (peripheral or capillary
circulation). These three components function
interdependently to maintain an adequate cardiac output
and tissue perfusion. Adequate blood flow depends on:
○ Adequate amounts of blood for the heart to pump
○ Effective pumping of the heart
○ Constriction and dilation of blood vessels to
maintain normal blood pressure
 Cardiac Output

01 • The amount of blood the

heart pumps from the
ventricles in 1 minute.
• Stroke Volume is the
amount of blood ejected
by the ventricles with
each heartbeat
 Heart Rate

02 • Influenced by the
autonomic nervous
system
• Sympathetic innervation results in an increase in heart
rate whereas parasympathetic innervation results in a
decrease in heart rate
• Healthy individuals can increase cardiac output up to
three times the normal level for short periods by
increasing the heart rate.
• Increasing heart rate may actually decrease cardiac
output, since myocardial oxygen demand becomes
greater than myocardial oxygen supply
 Preload
03 • The amount of
stretch in the
ventricle at the end
of the diastole.
● It is the function of the volume of blood presented to the
ventricle and compliance of the ventricle at the end of
diastole.
● As blood returns to ventricle, the ventricle distends,
myocardial fibers stretch and the force of contraction
increases.
● Starling’s Law of the heart, states that if the normal left
ventricle accepts increases in volume, it distends and
cardiac output increases until a critical point is reached
 Afterload
04 • Is the ventricular wall
tension or stress during
systolic injection
• Increased afterload
usually results in an
increase in the work of
heart
Conditions that may increase afterload
○ Impede aortic or pulmonary outflow (aortic stenosis
or pulmonary stenosis)
○ Obstruction in the outflow tract (septal hypertrophy)

○ Increased systemic or pulmonary vascular resistance

(vasoconstriction)
 Contractility

05
• The heart’s contractile
force inotropy (from ino,
strength; tropy,
enhancing)

• Represents the innate

ability of the heart
muscle to contract.
• Inotropy can be either positive (stronger contraction) or
negative (weaker contraction)

• Negatively affected by myocardial ischemia and

underlying cardiovascular disease

• It can also be altered by a variety of pharmacologic

agents, especially those mimicking the sympathetic
nervous system ( sympathomimetic, adrenergic)
 Control of Peripheral
Circulation

06 • Intrinsic control of blood

flow mechanism
individual vascular beds
to

occurs through response of

arteriolar muscle to
products of metabolism,
causing either vasodilation
or vasoconstriction.
 Oxygen Transport Principles
● Oxygen Delivery: Depends on blood flow (cardiac output), the
amount of hemoglobin available to carry oxygen, and percentage
of arterial oxygen hemoglobin saturation
● Oxygen Consumptions: Represents the body’s demand for oxygen
and is a reflection of tissue metabolism
● Oxygen consumption and delivery can be measured using a
specialized pulmonary artery catheter.
● Oxygen extraction ratio (VO2/DO2) provides an estimated of the
balance between consumption and delivery.
ETIOLOGY
OF SHOCK
 SHOCK MAY BE CLASSIFIED AS:

Type

HYPOVOLEMIC Occurs due to intravascular fluid volume

It occurs due to systolic or diastolic

CARDIOGENIC
dysfunction

DISTRIBUTIVE neurogenic, anaphylactic & septic

HYPOVOLEMI ● caused by a loss of
whole blood, plasma,
C SHOCK or interstitial fluid in
quantities such that
the body’s metabolic
needs can no longer
be met.
Hypovolemic shock develops from an
absolute or relative hypovolemia.

Absolute hypovolemia results from an

external loss of fluid from the body, as
in hemorrhage.

Relative hypovolemia results from an

internal shift of fluid from the
intravascular space to the
extravascular space.
Reduced intravascular blood volume
leads to a decreased amount of blood
returning to the heart (venous return).

This, in turn, decreases the

amount of blood received by
the ventricles during
diastolic filling (preload) and
decreases the amount of
blood available for ejection
from the ventricle (stroke
volume).
 ETIOLOGIC FACTORS OF
HYPOVOLEMIC SHOCK

INTERNAL
EXTERNAL ● HEMOTHORAX
● RUPTURED AORTIC
ANEURYSM
● TRAUMA ● HEMOPERITONEUM
● GASTROINT ● RETROPERITONEAL
HEMORRHAGE
-ESTINAL ● LOSS OF PLASMA
BLEEDING VOLUME
● BURNS
● SURGERY ● DESQUAMATED-
EXUDATED LESIONS
● LOSS OF OTHER
FLUIDS
 ETIOLOGIC FACTORS OF
HYPOVOLEMIC SHOCK

GASTROINTESTINAL RENAL
● DIABETIC
● SEVERE KETOACIDOSIS
● HYPEROSMOLAR
VOMITTING NONKETOTIC
DIABETES
● SEVERE ● DIABETES
INSIPIDUS
DIARRHEA ● HIGH-OUTPUT
RENAL FAILURE
● ADRENAL
INSUFFICIENCY
● DIURETIC
THERAPY
CLINICAL PRESENTATIONS
 Hypovolemic Shock

Decreased Intravascular Volume

Decreased Preload

Decreased Cardiac Output

Compensatory Shift of
Interstitial fluid Adequate or
Catecholamine
Increased Increased SVR
release
Compensatory renin- Volume
aldosterone, ADH, Increased HR,
splanchnic discharge Adequate or increased Preload, SV
CO
Increased CO
Compensatory
Continued Volume loss mechanisms starts
Decreased CO to fail

Decreased Tissue Perfusion

Impaired cellular
metabolism
 ● A shock response
CARDIOGENIC generated when the
SHOCK heart’s ability to
pump blood becomes
impaired, decreasing
cardiac output.
Cardiogenic shock can be caused by
dysfunction of the left ventricle, right ventricle,
or both.

It may result from

primary ventricular
ischemia, structural
problems, or
dysrhythmias.
Ischemia is a
condition in which ● The most common cause of
the blood flow (and
thus oxygen) is cardiogenic shock is the
restricted or
reduced in a part of
loss of contractile elements
the body. of myocardial muscle
owing to ischemia.
Acute Usually results to ischemia
myocardial
infarction is the related to acute myocardial
medical name infarction (AMI)
for a heart
attack.
Structural problems may cause
cardiogenic shock if forward motion
of blood is disrupted.
Causes include
papillary muscle
rupture and
septal rupture.
 ➔ Regurgitant or stenotic
valve lesions also
interrupt forward flow of
blood through the heart
and may result in abrupt
Doesn’t open
properly properly onset of congestive heart
Doesn’t close

failure progressing to
shock.
Normally open Normally
closed
 Dysrhythmias affecting heart rate can disrupt
pump function and cause cardiogenic shock.

Bradydysrhythmias can lower cardiac output, especially

in patients unable to compensate by increasing stroke
volume.

Conversely, in tachydysrhythmias, as the heart rate

increases, diastolic filling time decreases, reducing
stroke volume because the filling time is too short.
When the left ventricle is unable to
pump blood forward adequately;
three primary problems result.

The amount of blood ejected from the

ventricle with each heartbeat (stroke
volume) decreases.

Cardiac output
Blood pressure
Tissue perfusion
 2. As blood pressure falls, coronary
artery perfusion decreases, which in
turn decreases myocardial muscle
perfusion.

3. The amount of blood remaining in

the left ventricle at the end of systole
increases.
If the primary problem involves the left
ventricle, this increased end-systolic
volume eventually leads to increased
ventricular filling pressure.

Increased filling pressure are

transmitted back to the left atrium and
then to pulmonary circulation.
This increases pulmonary vascular
pressure, causing fluid to move
into the interstitial space and
alveolar spaces, resulting in
pulmonary congestion, hypoxia,
and deteriorating blood gases.
 ETIOLOGIC FACTORS OF
CARDIOGENIC SHOCK

STRUCTURAL
VENTRICULAR
PROBLEMS
ISCHEMIA
● VALVULAR
● MYOCARDIAL DYSFUNCTION
INFARCTION ● SEPTAL RUPTURE
● OPEN HEART ● PAPILLARY
SURGERY MUSCLE
● CARDIAC ARREST
RUPTURE
DYSRHYTHMIAS ● VENTRICULAR
ANEURYSM
● BRADYDYSRHYTHMIAS ● CARDIOMYOPAT
● TACHYDYSRHYTHMIAS HIES
● INTRACARDIAC
TUMORS
 Cardiogenic Shock

Ventricular Structural Dysrhythmias

ischemia problems

Heart becomes an Ineffective ventricular

ineffective pump emptying

Decreased pulmonary
Decreased SV
pressures

Decreased CO
Pulmonary edema

Impaired Impaired tissue

cellular perfusion Decreased Oxygen
metabolism
 ● Results from
inadequate
DISTRIBUTIV vascular tone that
leads to massive
E SHOCK vasodilation.
Subdivided into
three types: Septic,
Neurogenic, and
Anaphylactic.
 ● Is a multisystem
response to infection in
SEPTIC which, unlike other
forms of shock, the fall
SHOCK in blood pressure and
resultant insufficient
perfusion of vital
organs does not
respond to fluid
administration.
Septic shock
generally occurs in
immunocompromise
d patients, infants,
older adults, or
patients undergoing
with risk of
significant bacterial
contamination.
 Septic Shock
Invading
organism

Endothelial Activation of CNS activation

Depressed
damage biochemical, humoral, causing
myocardial
and cellular mediators hypermetabolic
function
state

Microemboli Peripheral Selective

vasodilation vasoconstriction
Increased Increased
capillary cellular
permeability oxygen
demand
Maldistribution of
blood volume

Impaired tissue perfusion

Impaired cellular
metabolism
 ● Is characterized by
massive dilation from
loss or suppression of
sympathetic tone.
NEUROGENI It is a temporary
condition associated with
C SHOCK injury or disease of the
upper spinal cord or
brainstem or with
administration of general
or spinal anesthesia.
Neurogenic shock can be
caused by any condition that
interrupts sympathetic
nerve impulse transmission
or blocks sympathetic
outflow from the vasomotor
center in the brain.
Interruption of sympathetic
activity occurs with trauma to
the spinal cord or medulla,
conditions that disrupt the supply
of oxygen to the medulla, or
conditions that deprive the
medulla of glucose (such as an
insulin reaction).
Other causes of neurogenic shock
include:
● High-level spinal anesthesia
● Ganglionic and adrenergic-
blocking drugs
● Severe emotional stress
● Pain
● Depressive drugs
● Drug overdoses
 Neurogenic Shock
Decreased sympathetic
outflow or Increased
parasympathetic outflow

Decreased arterial tone Decreased venous tone Bradycardia

Decreased systemic vascular Decreased venous return to the

resistance heart Poiklothermic
temperature
Decreased stroke volume regulation
Decreased blood pressure
Decreased cardiac output

Decreased tissue perfusion

Decreased cellular oxygen supply

Impaired cellular
metabolism
 - Also referred to as
anaphylaxis
- Is a sudden, life-
threatening
Anaphylactic hypersensitivity
reaction to an
Shock antigen.
- It is characterized by
massive vasodilation
and increased
capillary permeability.
Anaphylactic reactions
can be either
immunoglobulin E (IgE)
or non-IgE-mediated
responses.
These chemical mediators cause
vasodilation, increased capillary
membrane permeability,
bronchoconstriction, and coronary
capillary permeability.

Shock develops as a consequence of

hypotension from profound
vasodilation and low cardiac output.
Increased capillary permeability
and peripheral pooling of blood
cause the relative fluid volume
deficit.

Death can result because of

severe hypoxemia secondary to
bronchoconstriction or
cardiovascular collapse.
Non-IgE-mediated anaphylactic
reactions occur as a result of direct
activation of mast cells to release
biochemical mediators and are not
due to IgE antibody production. This
type of reaction, called an
anaphylactoid reaction, can occur
with the first exposure to an
antigen.
 Anaphylactic Shock
Antigen introduction
initiating IgE mediated or
non-IgE mediated response

Activation of biochemical
mediators from mast cells and
basophils
Smooth muscle Peripheral vasodilation
constriction Increased capillary membrane Decreased systemic
permeability vascular resistance
Bronchoconstriction
Extravasation of intravascular Decreased cardiac output
Decreased fluids
oxygenation Decreased tissue
edema perfusion
Laryngeal edema
Decreased cellular
oxygen supply

Impaired cellular
metabolism
The earliest signs of systemic
anaphylaxis include feelings
of anxiety and uneasiness,
flushing, diaphoresis,
sneezing, and weakness.

Nausea, dizziness, itching,

and sometimes edema
quickly follow these; and
severe hypotension from
vasodilation and increased
capillary permeability rapidly
develop.
Pathophysiology
Stages
of
Shock
 Compensatory
Stage

01 • An initial decrease in
cardiac output
tissue perfusion
and

• It begin and at least

initially maintain
adequate cardiac output
and tissue perfusion.
● Stimulation of beta-adrenergic receptors in the heart
increases the rate and force of contraction. It causes coronary
artery vasodilation and increased blood flow to myocardium
to meet the heart’s increased oxygen demand.
● Alpha-adrenergic receptor stimulation causes
vasoconstriction. This results in blood being shunted away
from organs, including skeletal muscle, fat and skin.
● The respiratory center in the brain responds by increasing the
rate and depth of respirations, which results in respiratory
alkalosis.
● Decreased cardiac outputs and vasoconstriction in the
kidneys result in decreased renal perfusion.
● Catecholamine stimulation also causes contraction of the
radical muscle of the iris causing pupillary dilation.
● Vasoconstriction of the vessels in the skin and stimulation of
the sweat glands cause the skin to be cool, pale and moist.
● Decreased tissue perfusion in the liver stimulates breakdown
of glycogen stores to increase availability of glucose for
energy production which results in increased blood glucose
levels.
 Progressive
Stage

02 • As shock progresses,
compensatory
mechanisms can no
longer make up for
decreased cardiac
output and fail to
maintain blood pressure
sufficient to perfuse vital
organs.
● Physiologic changes that initially heled shunt blood to vital organs
become ineffective and organs begin to malfunctions.
● Sodium ions accumulate inside the cell causing intracellular swelling
and the function of the organelles deteriorates.
● Bradykinin produces vasodilation, increased capillary permeability,
smooth muscle relaxation, and infiltration of an area with leukocytes.
This may be a factor in the development of associated pulmonary
insufficiency.
● Prolonged hypoperfusion of the liver impairs the organ’s ability to
perform important functions, including metabolism of drugs and
hormones and conjugation of bilirubin. As a result, bilirubin
accumulates in blood and causes jaundice.
● Decreased cerebral blood flow causes further decreases in level of
consciousness.
 Refractory

03
Stage
• Also known as the
irreversible stage, the
final stage of shock.
• The body becomes
refractory to all
therapeutic measures
attempted.
● Multiple organ failure develops and produces signs and
symptoms of cardiac, respiratory, neurologic, hepatic,
gastrointestinal, pancreatic and hematologic failure.
● Intractable circulatory failure develops as blood pressure
and heart rate continue to decrease.
● The shock state is so profound and the degree of cellular
destruction so severe that death is imminent.
COLLABORATIV
E CARE
MANAGEMENT
 Patient Positioning
Trendelenburg’s Position
• Causes fluid to rapidly shift to the
upper thorax, activating baroreceptor
in the aortic arch and carotid arteries.
Supine Position with the
legs slightly elevated above
the level of the heart
• Promotes venous return from the legs to
the heart and improves cardiac output
and organ perfusion.
 Fluid Therapy
• The goal of fluid therapy is to return laboratory and
hemodynamic values to normal baseline levels.
• The major goals in treating hypovolemic shock are to find
and aggressively control the source of blood loss and to
reverse that loss with administration of appropriate fluids to
restore tissue perfusion.
• Benefits of fluid administration include;
-Increase Intravascular Volume
-Increase Venous Return to the Heart (Preload) -
Improved Cardiac Contractility
-Increase Cardiac Output
• Collaborate with the physician regarding the administration of fluid
• Accurately monitor the patient’s intake, output, and daily weights.
• Minimizing fluid loss by limiting blood sampling and applying pressure to
bleeding sites
• A minimum of two large-bore intravenous catheter (no 14 or 16) should be
inserted to the patient to provide routes for immediate and rapid administration of
large volumes of fluids and medications
-Large Peripheral Veins in the Antecubital Fossa
-Multilumen Central Venous Catheter/ Pulmonary Artery Catheter
• Before fluid institution, measure the hemodynamic status (pulmonary end-
diastolic pressure)
• If pressure is less than 18 mmHg and the cardiac index is less than
2.2 L/min, volume replacement should be given
Large Peripheral Veins Intravenous
in the Antecubital Catheters
Fossa
Pulmonary Artery Catheter
 Fluid

01
Challenge
• Dynamic Test of the
Circulation
• Rapid administration of
volume over a particular
period, followed by
assessment of the
response
• The nurse infuses an intravenous fluid
challenge of 2ml to 2L of crystalloid
• Nursing responsibilities include;
obtaining baseline hemodynamic
measurements, administering the fluid
challenge and assessing the patient’s
response
• Carefully monitor the patients
hemodynamic status during such fluid
challenge, especially in patients
suspected of having impaired left
ventricular function
 Fluid

02 fluid
Selection
• The physician’s choice of
or fluids is
determined by the cause
of the volume deficit and
the patient’s clinical status.
Crystalloids Colloids
● Inexpensive and readily ● Improved osmotic pressure holds
available solutions and attracts fluid into vascular
● Electrolyte solutions that compartment.
move freely between the ● Considered to be plasma
intravascular compartments proteins, which are molecules
and the interstitial spaces that are too large to pass through
● Lactated Ringer’s solution capillary membranes.
● Have longer duration of action
closely resembles plasma and
than crystalloids because the
is commonly used to expand
molecules remain within the
intravascular volume, the
intravascular compartment
amount infused usually 3ml
longer.
for each 1ml of blood loss
 Blood
Administration
03 • Whole blood, packed RBC’s,
washed RBC’s, fresh frozen
plasma, and platelets are
administered for treatment of
major blood loss.
• Patients are typed and cross-
matched
• Packed RBC’s increase blood volume and oxygen carrying capacity
without placing the patient at risk of volume overload associated
with whole blood.
• Blood transfusion contains anticoagulant to prevent clotting while
the blood is stored, one unit fresh frozen plasma is administered
to restore coagulation factors and is given for every 4 to 5 units of
blood transfused
• Massive transfusion of cold blood should be warmed before
administration using blood warmer device to avoid hypothermia
which can cause cardiac dysrhythmias.
• Microfilters may be used when massive transfusion (10 units of
whole blood/packed cells less than 24 hours) are given.
• The pH of stored blood is lower than that of normal and the
added anticoagulant makes the blood more acidic
 Blood Substitutes

04 • Perfluorocarbon emulsions
• Cell-free hemoglobin
• Liposome-incapsulated
hemoglobin
● Red cell substitutes do not
require type and cross-matching,
can act potent plasma volume
expanders, and have significant
capacity for oxygen

● These substances do not

transmit viral or bacterial
infection and do not cause
immunosuppression, they offer
considerable promise for the
future.
 Pharmacological
Management

● The major treatment goals are to

enhance the effectiveness of the heart’s
pumping action and to improve tissue
perfusion.

● In coronary cardiogenic shock, the aims

of vasoactive medication therapy are
improved cardiac contractility, decreased
preload and afterload, or stable heart
rate.
 Improving

01 Contractility
• Positively inotropic drugs
are used to increase
contractility, cardiac
output, and tissue
perfusion in cardiogenic
and distributive shock.
● They increase myocardial oxygen demand by
increasing the workload of the heart, therefore,
these agents must be used with caution in patients
with ischemic heart disease or cardiogenic shock
● Drugs such as dopamine, dobutamine, and low
dose of epinephrine stimulate beta-receptor sites in
the heart, causing improved myocardial contractility
and improved cardiac output.
 Altering

02 Preload
• The primary treatment to
improve preload is the
administration of fluids.
• Vasopressor such as epinephrine and
norepinephrine, cause vasoconstriction and
increase venous return to the heart
• Vasodilators such as nitroglycerin and
nitroprusside decrease the heart’s workload by
reducing peripheral vascular resistance, preload
reduction is required in cardiogenic shock.
Continuous blood pressure monitoring is
required during administration either drug.
 Altering Afterload

03 • Afterload reflects the force

the heart must overcome
to eject blood.
• To increase vascular tone and improved venous return to
the heart (preload) , drugs that increase afterload such as
norepinephrine, phenylephrine, or high doses of dopamine
may be required.

• Patients with cardiogenic shock reducing afterload may be

necessary to reduce the heart’s workload, nitroglycerin
and nitroprusside are commonly used as afterload-
reducing agents.
 Mechanical Management

Intraaortic Balloon Ventricular Assist

Counterpulsation Device

Pneumatic Antishock
Garment
 Intraaortic Balloon

01
Counterpulsation

• Indicated for temporary

circulatory assistance to
restore hemodynamic
stability in patients with
cardiogenic shock.
• The physician inserts a polyurethane
balloon percutaneously through the
femoral artery and position it just
distal to the left subclavian artery.
• The overall effects of
counterpulsation are to increase
coronary perfusion and cardiac
output and decrease preload and
afterload.
• The nurse must frequently check the
neurovascular status of the lower
extremities.
 Ventricular Assist

02
Device

• Used to temporarily
support the failing
ventricle not responding to
IABP and pharmacologic
therapy.
• These devices can support the
function of a single ventricle or
the whole heart.
• They divert blood from the
failing ventricle or ventricles and
pump it back into the aorta (left
ventricular assist device, and the
pulmonary artery (right
ventricular assist device), or
both arteries.
 Pneumatic
Antishock
03 •
Garments
Also known as Military Antishock
Trouser, External Counter-
pressure Device and G Suits.
• This can raise blood pressure by
increasing systemic peripheral
resistance and possibly cardiac
output.
• These inflatable garments also put direct pressure on bleeding
sites, helping to control bleeding in pelvic and long-bone fractures
and abdominal and extremely vascular injuries.
• PASG may be beneficial in hypotension resulting from ruptured
abdominal aortic aneurysm, suspected pelvic fracture,
anaphylactic shock unresponsive to standard therapy,
uncontrollable lower extremity hemorrhage and severe traumatic
hypotension.
• Use of PPASG is contraindicated for patients with pulmonary
edema, pregnancy, impaled objects, evisceration of the abdomen,
and thoracic and diaphragmatic trauma.
• When removing PASG abdominal section is deflated first allowing
gradual redistribution of blood volume, followed by the deflation
of the lower extremities.
 Surgical Management
● Percutaneous Transluminal Angioplasty

● Thrombolytic Therapy

● Stent Placement

● Roto-blade Therapy

● Laser Therapy

● Heart Transplantation
● These cardiac procedures are used to attempt early
revascularization of an occluded coronary artery an
AMI complicated by cardiogenic shock.
● Heart transplantation may be an option for a small
percentage of patients with severe myocardial
damage and cardiogenic shock.
 Nursing
Management
 Health History
Assess for:
● Recent illness: history of diabetes mellitus, pancreatitis, or
compromised immune system; recent invasive procedure, surgery,
trauma, or burns
● Hypertension, myocardial infarction, congestive heart failure
● exposure to allergies, including food, drugs latex, venom from insect
bite or sting
● Recent blood transfusion or diagnostic procedure using contrast
media
● Patient response to questions, attention span, mood and behavior
 Physical Examination
Assess for:
● Changes in level of consciousness (restlessness, agitation, lethargy;
mental cloudiness, confusion)
● Heart rate more than 100 to 120 bpm with widened pulse
pressure, thready pulse
● Respiratory rate increased in rate and depth
● Skin cool, moist, pale or cyanotic
● Urinary output less than 0.5 ml/kg/hr
● Capillary refill greater than 3 seconds
Nursing Diagnosis,
Outcomes, and
Interventions
 Nursing
Diagnosis
01 Decreased Cardiac
Output
 Outcomes
Patient will:
● Demonstrate signs of hemodynamic stability as evidenced by the
following values: heart rate less than 100 bpm; systolic blood
pressure greater than 110 mmHg/ within 10 mm Hg of baseline;
cardiac output 4 to 8 L/min, and/or cardiac index greater than
2L/min/m2 ; central venous pressure, 0 to 8 mmHg; systemic
vascular resistance 800 to 1400dynes/sec/cm-5 ; warm
extremities with capillary refill time of less than 3 sec; absence of
dysrhythmias normal sensorium
● Remain free from side effects from medication used to achieve
adequate cardiac output
 Interventions
Hypovolemic Shock
● The nurse should observe the patient for signs and symptoms of fluid loss
● If active external bleeding is resent, the nurse should apply direct,
continuous pressure and elevate the area if possible
● The nurse should insert and maintain two or more large-bore intravenous
lines, a urinary catheter, and setup to monitor central venous pressure.
● The nurse also should monitor the trend of hemodynamic measurements
and urinary output; observe for signs of fluid overload monitor arterial
blood pressure and mean arterial blood pressure via arterial line
● Obtain a complete blood count, blood type and cross-matching, and serum
electrolyte and arterial blood gas values
Cardiogenic Shock
● The nurse should observe for signs and symptoms of poor arterial
perfusion, including tachycardia, hypotension, dysrhythmias, poor
peripheral pulses, oliguria or decreased level of consciousness
● Looks for signs of venous congestion: neck vein distention, lung crackles,
S3 heart sound, and increased liver margin measurement
● Monitor electrocardiogram (ECG) continually for new worsening signs of
ischemia or infarction or significant dysrhythmias
● Assist with insertion of a flow-directed catheter for hemodynamic
pressure monitor
● Inotropic or vasodilators or both may be administered to improve cardiac
output
● Assist with insertion of an intraaortic balloon pump catheter, if used.
Distributive Shock
● The nurse should observe for signs and symptoms of vasogenic shock:
hypotension and decreased systemic vascular resistance and for signs of
specific types of distributive shock
Septic Shock: history of exposure to infectious agent or
immunocompromised state
Neurogenic Shock: history of spinal cord injury, head injury, drug overdose;
normal or increased cardiac output, decreased filling pressure
Anaphylactic Shock: history of allergen exposure, itching, hives, stidor,
wheezing, or angioneurotic edema
● Administers intravenous fluids as ordered and pharmacologic agents
 Nursing
Diagnosis
02 Ineffective Tissue
Perfusion
 Outcomes
Patient will:
● Have increased tissue perfusion as evidenced by signs of
hemodynamic stability; alertness and orientation to time,
place, and person; adequate peripheral tissue perfusion
(skin warm and dry, absence cyanosis and capillary refill
greater than 3 seconds; urinary output of more than 30
ml/hr; no dysrhythmias present; arterial blood gases
within normal limits.
 Nursing Interventions
● The nurse monitors neurologic status, noting subtle changes in
sensorium, which are early signs of decreases circulation and
oxygen to cerebral tissues
● Checks the dorsalis pedis and posterior tibal pulses bilaterally
● Checks capillary refill, which should occur within 3 seconds; and
notes the color and temperature of the skin
 Nursing
Diagnosis
03 Deficient Fluid
Volume
 Outcomes
Patient will:
● Have an intravascular volume within normal limits as
evidenced by stable hemodynamic variables; body weight
within 5% of baseline; balanced fluid intake and output;
urinary output of more than 30 ml/hr; fluid and
electrolyte balance within normal limits as demonstrated
by laboratory data; normal body temperature; adequate
peripheral perfusion
 Nursing Interventions
● The nurse assess the patient to identify factors causing deficient fluid
volume
● Monitors for early signs of hypovolemia
● Monitors intake and output hourly until urinary output averages 30 ml/hr
● Monitor vital signs for decreased pulse pressure, hypertension,
tachycardia, decreased pulse volume and decreased core temperature
● Maintains patent intravenous access and monitors infusion types and
amount
● When ordered, the nurse initiates a fluid challenge of crystalloids and
notes response of vital signs, urinary output and lung sound
 Nursing
Diagnosis
04 Impaired Gas
Exchange
 Outcomes
Patient will:
● Have improved gas exchange and adequate oxygenation
as evidenced by an airway that is patent and clear of
secretions; arterial blood gas values within normal limits
(pH 7.35 to 7.45; PaO2 at least 80 mmHg; PaO2 35 to 45
mmHg; SaO2 at least 95%); respiratory rate of 12 to 20
bpm; breath sounds clear to auscultation; absence of
cyanosis; capillary refill of no more than 3 seconds
 Interventions
● The nurse monitors respiratory rate, depth and effort and observes
the patient’s breathing.
● Monitors client’s mental status for onset of restlessness, agitation,
confusion or lethargy
● Monitors for cyanosis, especially of the tongue and oral mucous
membranes, which is indicative of serious hypoxia
● Administers humidified oxygen through an appropriate device ( nasal
cannula, face mask, endotracheal tube)