7-11 SHIFT.

As a group, develop a chart that compares clinical findings

of the compensatory, progressive, and irreversible stages of shock.
During the initial stage of shock, the cells start to switch from aerobic metabolism
(metabolism WITH oxygen).to anaerobic metabolism (metabolism WITHOUT oxygen). This
results in the accumulation of lactic acid in the body. The signs and symptoms during this
stage are not yet noticeable as clear explaining we have a cause that has led to DECREASED
TISSUE PERFUSION. Hence, we’re going to have LOW cardiac output. And What is cardiac
output? It’s the amount of blood the heart pumps each minute. 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. Which our organs and cells need it to survive. 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

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. 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).
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. hey 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.

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.
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.