Shock stages include initial, compensatory, progressive, and refractory stages.

Shock results from a cause of some type that leads to decrease tissue perfusion to
organ/tissue's cells. When the cells are deprived of perfusion they lack oxygen to function and
can suffer hypoxic injury. If this is not corrected, multiple organ dysfunction syndrome can occurs
along with death. Types of shock include the following: -Hypovolemic shock -Cardiogenic shock -
Neurogenic shock -Septic shock -Obstructive shock -Anaphylactic shock During the initial stage
of shock, the cells start to switch from aerobic metabolism to anaerboic. This results in the
accumulation of lactic acid in the body. The signs and symptoms during this stage are not yet
noticeable. During the compensatory stage of shock, the body utilizes it neural, biochemical, and
hormonal faculties in attempt to increase cardiac output and perfusion to the cells. For a while
this works but will eventually fail in the cause of shock is not treated. This stage is reversible and
the patient can recovery is the shock is successfully treated. If the patient is not treated correctly,
they will progress to the progressive stage of shock. During the progressive stage of stock, the
body has failed to compensate and it is progressing to MODS. This stage is highlighted by the
malfunction of all the organs. The patient's neuro status will be impaired due to a severe
decrease of cerebral perfusion. The mean arterial pressure (MAP) will be less than 60 mmHg.
Renal failure will ensure along with GI bleeding, acute respiratory distress syndrome (ARDS), DIC
(disseminated intravascular coagulation) and so forth. The last stage of shock is the refractory
stage. The word refractory means "unmanageable". This stage is irreversible and MODS will
occurs along with death.

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:

 Septic shock: occurs due to a severe infection

 Hypovolemic shock: occurs due to severe fluid loss
 Neurogenic shock: occurs due to severe damage to the neuro system
(example: spinal injury)
 Cardiogenic shock: occurs due to a weak heart
 Anaphylactic shock: occurs due to an allergic reaction
Note: Distributive shock includes septic, anaphylactic, and neurogenic shock.

Stages of Shock
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
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).

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 capillary permeability. Literally, the flood gates have
been opened from the intravascular space to the interstitial space. Fluids and proteins will be
drawn into this space and this will lead to major edema throughout. In addition, this will deplete
blood volume (therefore undo everything the body attempted to do in the previous stage).  In
other words, when the blood volume decreases it decreases the cardiac output and tissue
perfusion.

Let’s analyze this stage:

Brain: cells to the brain are not being perfused. The mean arterial pressure is < 60 mmHg. This
means the cerebral perfusion pressure (CPP) is inadequate to maintain perfusion to the brain’s
cells. When this happens, you will start to see major mental status changes. The patient will be
very slow in their speech, restless, anxious, agitated, and not respond to stimulation.

Lungs: ARDS (acute respiratory distress syndrome) will develop. In a nutshell, this occurs due to
increased capillary permeability in the alveoli sacs (this is where gas exchange occurs). The
alveoli sacs will collapse due to the fluid surrounding them and the lung will lose its elasticity.
The patient will need intubation and 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 (which isn’t good because clotting abilities will be affected due
to liver hypoxia).
Liver: the decreased perfusion to the liver causes the cells that make up the liver to die. The liver
is a very important organ that plays a role in filtering germs, waste products, and drugs from our
body. In addition, it plays a role with clotting factors. Therefore, when the cells that do these jobs
are malfunctioning there is a build-up of toxic waste (bilirubin, ammonia etc.), risk for infection,
and bleeding problems.

DIC (disseminated intravascular coagulation): small clots will form in the vessels (further
compromising blood flow to organs). This depletes the body’s platelets and clotting stores and
leads to massive, uncontrollable bleeding. Watch for any type of oozing, especially around IV
sites, central lines, blood puncture sites etc.

Refractory Stage

The word “refractory” means unmanageable. Therefore, once a patient enters this stage it cannot
be reversed. All organs will shut down and fail. What was happening in the previous stage is
going to be WORSE until the organs quits working. Death is inevitable.

Reference:
Do you know about the life-threatening condition called sepsis?. Retrieved from https://www.cdc.gov/sepsis/index.html

Marieb, E., & Mallatt, J. (2001). Human anatomy-the endocrine system (p. 759). San Francisco: Benjamin Cummings.