Stages of Shock NCLEX Review
What is shock? This condition results from some
type of cause (discussed below) that leads to
decreased tissue perfusion, which causes cell
hypoxia. If the cell hypoxia is severe enough it
will cause organ dysfunction (MODS) and
eventually lead to death.
-The cause of shock depends on what type of
shock is presenting. The types of shock include:
1. Septic shock: occurs due to a severe
infection
2. Hypovolemic shock: occurs due to
severe fluid loss
3. Neurogenic shock: occurs due to severe
damage to the neuro system (example:
spinal injury)
4. Cardiogenic shock: occurs due to a
weak heart
5. Anaphylactic shock: occurs due to an
allergic reaction
Note: Distributive shock includes septic,
anaphylactic, and neurogenic shock.
What are the stages of shock? Initial,
compensatory, progressive, and refractory
a) Initial Stage
-Big Takeaway from this Stage: Cardiac output is
low enough to cause the cells to experience
hypoxia. The cells will SWITCH from AEROBIC to
ANAEROBIC metabolism. Anaerobic metabolism
will create LACTIC ACID, which will accumulate
in the blood and lead to lactic acidosis. Signs
and symptoms of shock in this stage are very
subtle compared to the next stages.
Let’s analyze this stage:
-A type of shock is presenting! Therefore, we
have a cause that has led to DECREASED TISSUE
PERFUSION. Hence, we’re going to have LOW
cardiac output.
-What is cardiac output? It’s the amount of
blood the heart pumps each minute. It is
calculated by taking the heart rate and
multiplying it by the stroke volume and this
equals the cardiac output.
-In this stage, the cardiac output is just low
enough where tissue perfusion is unable to
support the oxygen demands of the cells that
make up the tissues/organs. Remember the
cells that make up our organs and tissues have
to constantly be receiving fresh oxygen and
other nutrients to survive. When they don’t
receive these substances, they start to take
matters into their own hands by…….
-Switching the way they metabolize! The cells
will switch to anaerobic metabolism
(metabolism WITHOUT oxygen ) from aerobic
metabolism (metabolism WITH oxygen).
-Why do they do this? Because they don’t have
any oxygen to use because they aren’t receiving
it…remember tissue perfusion is decreased.
-What’s the downside of anaerobic
metabolism? It produces a waste product called
LACTIC ACID. Normally, our body can deal with
lactic acid via the liver, but the liver is not
functioning at an optimal level because of the
low amount of oxygen its cells are receiving.
-In better circumstances when tissue perfusion
is adequate, the liver takes lactic acid and
convert it to pyruvic acid and then to glucose
via gluconeogenesis. Therefore, lactic acid will
start to accumulate in the blood (especially as
the patient advances to the other stages of
shock).
-The accumulation of lactic acid causes the
blood’s pH level to drop (hence acidosis occurs)
and it further damages the cells.
Important lab values to remember:
-Normal serum lactate level <1 mmol/L
-Abnormal indicating lactic acidosis >4 mmol/L
b) Compensatory Stage
-Big Takeaway from this Stage: The body
systems are coming to the RESCUE!! Hence,
they are going to “try” to compensate by using
the body’s natural built-in survival team: the
hormonal, neural, and biochemical processes in
the body. Be sure to remember what
substances are being released and how they
affect the body during this stage.
-This built-in system will try to fight the results
of anaerobic metabolism. In addition, it will
attempt to increase the cardiac output and
blood pressure via the stimulation of the
sympathetic nervous system (SNS) and renin-
angiotensin system (RAS), which will increase
tissue perfusion (this is what the patient needs
right now so the cells can receive oxygen and
live).
Let’s analyze this stage:
-If the cause of shock is corrected during this
stage (hence a patient with hypovolemic shock
receives fluid replacements that correct the
fluid status of the patient), this stage is
REVERSIBLE and the patient can make a full
recovery. However, if the cause is NOT
corrected the patient will enter the next stage.
-The body will succeed at first with increasing
cardiac output and blood pressure via the
rescue team discussed above. This will result in
an increase in tissue perfusion, BUT the body is
limited on how long it can maintain this rescue
effort.
How does the body provide compensation?
-As the blood pressure drops (hence cardiac
output becomes very low), the body will sense
this and say “Okay, the amount of blood the
heart is pumping per minute it WAY too low,
especially for our vital organs (mainly the heart
and brain), so we must ACT now!”
-One of the structures to sense this drop in
blood pressure is the baroreceptors, specifically
the receptors in the carotid sinus and aortic
arch. This will stimulate the sympathetic
nervous system to release the catecholamines:
epinephrine and norepinephrine.
-What do these catecholamines do? They cause
vasoconstriction! This will result in an increase
in blood pressure and heart rate. When this
occurs there is increased perfusion to the vital
organs. Less blood will go to the non-vital
organs (GI, renal, skin, lungs), while more will go
to the vital organs (heart and brain).
-Furthermore, because there was a drop in
blood pressure (hence arterial pressure), there
will be a decrease in capillary hydrostatic
pressure.
-What does capillary hydrostatic pressure
mean? In a nutshell, it’s the force of pressure
the blood creates around the capillary wall. If
the blood pressure and cardiac output are low,
the force of pressure the blood creates around
the capillary wall is definitely low.
-This will signal to the body to try to increase
venous blood return by shifting fluid from the
interstitial compartment to the intravascular
compartment. Think of it this way: it’s like the
body is trying to give itself a natural IV fluid
bolus. By doing this, the body is attempting to
increase cardiac output and the blood pressure,
which will increase tissue perfusion.
Now let’s talk about how other systems are
affected and how they play a role in the
compensatory stage:
-Kidneys: because blood flow is decreased to
the kidneys they activate the renin-angiotensin
system.
-What this system does? Renin stimulates
angiotensinogen which creates angiotensin I.
Angiotensin I turns into Angiotensin II.
Angiotensin II is a very mighty vasoconstrictor.
This substance will cause vasoconstriction in
both the arterial and venous system.
-The constriction in the venous system will lead
to more blood return to the heart, and the
constriction in the arterial system will increase
blood pressure. All this together will lead to an
increase in tissue perfusion and the cells will
receive more oxygen.
-The presence of angiotensin II will also trigger
the release of ALDOSTERONE.
-What does aldosterone do? It makes the
kidneys KEEP sodium and water. Why does this
matter? It will increase blood volume!
-In addition, because the kidneys are keeping
sodium, it will create the urine to contain a high
amount of sodium, which leads it to have a high
osmolality.
-The high osmolality signals to the posterior
pituitary gland that the body is trying to keep
water for some reason, so it releases ADH
(antidiuretic hormone). What does ADH do? It
prevents water from leaving the kidneys.
Hence, further increases BLOOD VOLUME.
-By increasing blood volume, the cardiac output
by the heart will be increased along with tissue
perfusion.
-Notice that all the systems trying to rescue the
body from shock are trying to release
substances that will increase cardiac output or
increase blood volume because it knows that if
it can do this it will increase tissue perfusion.
-GI: perfusion is decreased to this system so it
slows down. The patient is a risk for paralysis of
the intestines in a condition called paralytic
ileus.
-Skin: perfusion is decreased so blood flow is
low, which leads the skin to be cold and
clammy. Now, this is not the case during this
stage in SEPTIC SHOCK. The patient’s skin will be
hot and flushed due vasodilation presenting.
-Lungs: perfusion is decreased so parts of the
lung may not be perfused. Now, ask yourself
what do the lungs do? They perform gas
exchange. If some parts of the lungs are not
being perfused, gas exchange is not going to
occur in those parts. So, there is a ventilation
and perfusion mismatch and oxygen levels will
become low in the blood. This will lead the
patient to hyperventilate (they are trying to
compensate by increasing the rate and depth of
breathing in an attempt to increase the oxygen
level).
c) Progressive Stage
-Big Takeaway from this Stage: the rescue effort
in the previous stage has FAILED, and the body
can’t compensate anymore. The patient is
progressing to MODS (multiple organ
dysfunction syndrome). There is no more
compensation in this stage. Therefore, cardiac
output is low, tissue perfusion is low, and the
cells are NOT receiving oxygen, which this leads
to cell hypoxic injury. Think of this stage by
body systems and how each system is failing
because of cell hypoxic injury. The cells will start
to swell (the ion pumps are failing) and
CAPILLARY PERMEABILITY is increased.
-The patho in this stage really deals with (which isn’t good because clotting abilities will
capillary permeability. Literally, the flood gates be affected due to liver hypoxia).
have been opened from the intravascular space
-Liver: the decreased perfusion to the liver
to the interstitial space. Fluids and proteins will
causes the cells that make up the liver to die.
be drawn into this space and this will lead to
The liver is a very important organ that plays a
major edema throughout. In addition, this will
role in filtering germs, waste products, and
deplete blood volume (therefore undo
drugs from our body. In addition, it plays a role
everything the body attempted to do in the
with clotting factors. Therefore, when the cells
previous stage). In other words, when the
that do these jobs are malfunctioning there is a
blood volume decreases it decreases the
build-up of toxic waste (bilirubin, ammonia
cardiac output and tissue perfusion.
etc.), risk for infection, and bleeding problems.
Let’s analyze this stage:
-DIC (disseminated intravascular coagulation):
-Brain: cells to the brain are not being perfused. small clots will form in the vessels (further
The mean arterial pressure is < 60 mmHg. This compromising blood flow to organs). This
means the cerebral perfusion pressure (CPP) is depletes the body’s platelets and clotting stores
inadequate to maintain perfusion to the brain’s and leads to massive, uncontrollable bleeding.
cells. When this happens, you will start to see Watch for any type of oozing, especially around
major mental status changes. The patient will IV sites, central lines, blood puncture sites etc.
be very slow in their speech, restless, anxious,
agitated, and not respond to stimulation.
d) Refractory Stage
-Lungs: ARDS (acute respiratory distress
syndrome) will develop. In a nutshell, this -The word “refractory” means unmanageable.
occurs due to increased capillary permeability in Therefore, once a patient enters this stage it
the alveoli sacs (this is where gas exchange cannot be reversed. All organs will shut down
occurs). The alveoli sacs will collapse due to the and fail. What was happening in the previous
fluid surrounding them and the lung will lose its stage is going to be WORSE until the organs
elasticity. The patient will need intubation and quits working. Death is inevitable.
mechanical ventilation to breathe. The patient
will have fluid in the lungs (crackles), increase
respiratory rate, decrease oxygen level, and
respiratory failure.

-Heart: the cells that make up the heart start to

die. This includes the cells that play a role in the
electrical conduction system of the heart and
that help the heart contract/pump. So, cardiac
dysrhythmias occur along with death to
myocardial tissue.

-GI: cells that make up the gut start to die. For

example, the cells that protect the lining of the
gut from its own acid, start to quit working.
Consequently, ulcers can develop which can
turn into massive gastrointestinal bleeding
 1. A patient is in hypovolemic shock. Select
all the stages that a patient can enter when in
shock:*
 A. Proliferative
 B. Compensatory
 C. Exudative
 D. Initial
 E. Progressive
 F. Fibrotic
 G. Refractory
2. During the __________ stage of shock,
the signs and symptoms are very subtle.
However, cells are experiencing _________
due to the lack of tissue perfusion, which
causes the cells to switch from ___________
metabolism to _________ metabolism.*
 A. Proliferative, hyperoxia,
anaerobic, aerobic
 B. Initial, hypoxia, aerobic,
anaerobic
 C. Compensatory, hypoxia,
anaerobic, aerobic
 D. Fibrotic, hypoxia, aerobic,
anaerobic
3. You’re caring for a patient who is
experiencing shock. Which lab result below
demonstrates that the patient’s cells are
using anaerobic metabolism?*
 A. Ammonia 18 µ/dL
 B. Potassium 4.5 mEq/L
 C. Serum Lactate 9 mmol/L
 D. Bicarbonate 23 mEq/L
4. During what stage of shock does the body
attempt to utilize the hormonal, neural, and
biochemical responses of the body?*
 A. Refractory
 B. Initial
 C. Proliferative
 D. Compensatory
5. Which statements are INCORRECT about
the compensatory stage of shock. Select all
that apply:*
 A. This stage is reversible.
 B. During this stage blood is
shunted away from the kidneys, lungs,
skin, and gastrointestinal system to the
brain and heart.
 C. During this stage blood flow to
the kidneys is reduced, which causes
the kidneys to activate the renin-
angiotensin system, and this will lead to
major vasodilation to the arterial and
venous system.
 D. One hallmark sign of this stage is
that there is an increase in capillary
permeability.
 E. A patient is at risk for a paralytic
ileus during this stage.
6. During shock, when a patient experiences
a drop in cardiac output, the body tries to
compensate by stimulating the sympathetic
nervous system, which causes the release of
_________ and ________. This will lead
to?*
 A. acetylcholine and dopamine,
vasodilation
 B. epinephrine and norepinephrine,
vasodilation
 C. dopamine and epinephrine,
vasoconstriction
 D. norepinephrine and epinephrine,
vasoconstriction
7. When the body is attempting to
compensate for shock the adrenal cortex will
release aldosterone due to the presence of
angiotensin II. Select all the effects
aldosterone will have on the body in attempt
to increase cardiac output and maintain
tissue perfusion:*
 A. Increase blood volume
 B. Causes the kidneys to keep
sodium and water
 C. Causes the kidneys to excrete
sodium and water
 D. Cause the urine to have a low
osmolality
8. During what stage of shock is the body
unable to compensate for tissue perfusion
and the body’s cell start to experience
hypoxic injury that result in
__________capillary permeability?*
 A. Refractory, increased
 B. Exudative, decreased
 C. Compensatory, increased
 D. Progressive, increased
9. Select all the complications that can arise
from the progressive stage of shock:*
 A. Acute respiratory distress
syndrome
 B. Extreme edema
 C. Elevated ammonia and lactate
levels
 D. GI bleeding and ulcers
 E. Dysrhythmias
 F. Myocardial infraction
 G. Acute tubular necrosis
 H. Disseminated intravascular
clotting
10. TRUE or FALSE: All types of shock
during the compensatory (early) stage will
cause a patient to experience cold and
clammy (moist or sweaty) skin.*
 True
 False
11. Which stage of shock is irreversible and
unmanageable?*
 A. Progressive
 B. Initial
 C. Exudative
 D. Refractory
12. Based on this scenario, what stage of
shock is this patient most likely
experiencing: A 74-year-old patient is
extremely confused and does not respond to
commands or stimulation. The patient
respiratory rate is 28 and labored, oxygen
saturation 86%, heart rate 120, blood
pressure 70/40, mean arterial pressure is 50
mmHg, and temperature is 97 ‘F. The
patient’s heart rhythm is atrial fibrillation.
The patient’s urinary output is 5 mL/hr. The
patient’s labs: blood pH 7.15, serum lactate
15 mmol/L, BUN 55 mg/dL, Creatinine 6
mg/dL. In addition, the patient is now
 starting to have slight oozing of blood
around puncture sites.*
 A. Initial

 B. Proliferative

 C. Progressive

 D. Compensatory