Neurogenic Shock NCLEX Review
slow down and this is where the PSNS system would
What’s neurogenic shock?
This type of shock leads to the inability of
the sympathetic nervous system to stimulate nerve
impulses, which causes hemodynamic problems. This
leads to a decrease in tissue perfusion where the cells
that make up our organs and tissue don’t receive enough
oxygen. Hence, signs and symptoms of shock occur.
Neurogenic shock is a type of distributive
shock (anaphylactic and septic shock are the other types
of distributive shock). This means that the vessels that
deliver blood flow to the cells have an issue
with distributing that blood flow.
Neurogenic shock, it’s due to massive vasodilation
because the sympathetic nervous system has lost the
ability to stimulate nerves that control vessel vasomotor
tone (this is the ability to regulate the diameter of the
vessels…discussed in detail below).
What can cause neurogenic shock?
 Spinal cord injuries that are located at the
cervical or upper thoracic locations
(above T6)
 Drugs that affect the autonomic and
sympathetic nervous system
 Spinal anesthesia
Neurogenic shock is sometimes referred to as vasogenic
shock.
Pathophysiology of Neurogenic Shock
Let’s talk about what is occurring in neurogenic shock,
but first, let’s do a quick review of the autonomic
nervous system.
The autonomic nervous system controls the functions
we cannot consciously control like our heart rate,
digestion, rate of breathing, pupil response, etc. It is
divided into two systems called:
Sympathetic Nervous System (SNS)
and Parasympathetic Nervous System (PSNS)
The parasympathetic nervous system is known as the
“rest and digest” system. It helps us relax by decreasing
our heart rate and allows us to digest food, among other
functions.
The sympathetic nervous system is the “keep you alive
or fight or flight” system! It increases the heart rate, and
blood pressure, dilates your pupils for better vision, etc.
Therefore, a HUGE role it plays is that it
controls VASOMOTOR TONE. This means that the SNS
regulates the diameter of our vessels. It will cause our
vessels to constrict or dilate as needed, depending on the
signals it receives from the body.
Now, it’s very important to note that the PSNS and SNS
are always balancing each other out to keep things
regulated in our bodies. For example, if the SNS had to
kick in to save your life, eventually it would have to
help. Therefore, if one system is not working (as in the
case with neurogenic shock…the SNS is
malfunctioning), the other system will be UNOPPOSED
and in a sense take over, which is why many patients
with neurogenic shock will have bradycardia.
How does the sympathetic nervous system regulate the
diameter of our vessels? The nerve fibers of the
sympathetic nervous system branch out and hang out on
the layers of the vessels. When nerve signals are fired, it
will cause the neurotransmitters epinephrine and
norepinephrine to be released. These neurotransmitters
will cause the vessel to constrict (narrow). However, if
there is a low level of nerve firing or NO firing, these
neurotransmitters are NOT released, so the vessel just
relaxes….hence dilates. This is the problem with
neurogenic shock. The nerves are not being
stimulated, so they are relaxed. This causes major
problems!
Why? Dilated vessels affect blood pressure. When the
vasomotor tone is lost, vessel dilation occurs and
this lowers systemic vascular resistance (SVR), which
causes a major decrease in blood pressure (hypotension).
Due to the decreased SVR and low blood pressure, blood
pooling will occur in the vessels. This will DECREASE
the amount of blood draining back to the heart
(remember no pressure/resistance is helping to push it
back so it just hangs out away from the heart).
What does this leave the heart to pump? Hardly anything
at all! This will cause a DECREASE in tissue perfusion.
In addition, this blood pooling will lead to a risk of deep
vein thrombosis (DVT) development and lower the
body’s core temperature (hypothermia).
Why hypothermia? The blood is just sitting in the
extremities cooling down and not returning to the core
body to be warmed. These patients will have
warm/dry extremities but a cold body.
Why does this lead to a decrease in tissue perfusion?
There is venous pooling of blood and not much blood
will be flowing back to the heart because there isn’t any
resistance making it go back.  This will decrease
cardiac preload (the amount the ventricle stretch at the
end of the diastole/filling phase) and cardiac
afterload (resistance the ventricles must overcome to
pump blood out of the heart and this is due to the
decrease in SVR).
Remember we discussed in our lecture on cardiac output
that cardiac preload and afterload play a huge role in
cardiac output because they affect stroke volume (the
amount of blood the ventricle pumps with each BEAT),
which affects the cardiac output. CO is calculated by:
O = Heart Rate (HR) x Stroke Volume (SV)
Cardiac output is the amount of blood the heart pumps
per minute. When CO falls, so does the amount of
blood that is rich in oxygen that flows to the cells that
make up our tissues and organs. If cells don’t receive
enough oxygen they start to die, and the patient starts to
experience the classic signs and symptoms of shock.
Also, hypothermia can occur due to the body’s inability
to regulate the body temperature because of
hypothalamus dysfunction. This is further complicated
by the peripheral vasodilation and pooling of blood in
the extremities (as discussed above). This will lead to
heat loss because the blood isn’t returning to the body to
keep it warm. So, extremities will be warm and dry, but
the body will be cold (poikilothermic: loses the ability to
regular core body temperature).
Bradycardia will occur too! The heart rate is controlled
by both the sympathetic and parasympathetic nervous
systems. SNS increases the heart rate and PSNS works
to decrease the heat rate. Therefore, they are both
balancing out the heart rate. If we lose the function of
the SNS, the PSNS will be unopposed and bradycardia
will occur.
Recap of the pathophysiology and the signs and
symptoms of neurogenic shock:
The major signs and symptoms you will see with
neurogenic shock are…
hypotension, bradycardia, hypothermia, warm/dry
extremities but a cold body
Patho: One major function that is lost in neurogenic
shock is the ability to regulate the diameter of the blood
vessels. Therefore, the vessels are just relaxed (dilated).
This will decrease systemic vascular resistance and
hypotension will occur. Also, since the SNS isn’t
working very well (which helps increase our heart rate)
the parasympathetic system will take over (which
decreases the heart rate)…so bradycardia will occur.
Hypothermia occurs because of hypothalamus
dysfunction and is further complicated by blood pooling
in the extremities (remember this blood is sitting there
and cooling off because it is not going back to the body).
Warm/dry extremities can be found due to dilated
vessels causing the blood to pool in the extremities.
These signs and symptoms are slightly different from the
other types of shock we have covered, especially in the
early stages of shock.
WHY? Remember during the early stages of shock in
the other types of shock, the sympathetic nervous
system kicks into gear to help “save” the body by
causing vasoconstriction with the release of
norepinephrine and epinephrine. This would increase the
heart rate, blood pressure (in hope of increasing CO),
etc. However, in neurogenic shock, this doesn’t occur
because the body has lost the ability to stimulate the
sympathetic nervous system due to this injury.
Neurogenic shock is different from spinal shock because
neurogenic shock causes hemodynamic changes with
hypotension and bradycardia related to its injury.
Whereas, the spinal shock causes changes in sensation,
motor, and reflexes.
Neurogenic Shock Nursing Interventions and
Treatments
Goal: Manage patient’s ABCs (Airway, Breathing,
Circulation & Spine)
Protect the spine: Keep spine immobilized (don’t want to
cause any more damage and decrease perfusion to the
spine) Example: cervical collar, log rolling patient
during transport, using a backboard
May need intubation and mechanical ventilation if the
respiratory failure is present (respiratory issues can
occur depending on the location of the injury)
Maintain tissue perfusion: want MAP to be 85- 90
mmHg. This helps maintain perfusion to organs,
specifically the spine. (Dave and Cho, 2018)
How?
Intravenous fluids: crystalloids (fills the dilated vessels,
increases venous return to the heart which will increase
cardiac preload and cardiac output)
 IFVsFs are used with caution because the
patient usually has a normal blood
volume. Therefore, monitor for fluid
overload.
 Example: dyspnea, crackles, swelling, increased
CVP or PAWP
 If no response with IFVs, then vasopressors may
be used.
Vasopressors: causes vasoconstriction (narrowing of
vessels) which will increase SVR and increase blood
pressure and cardiac output
 Positive
inotropes: Dopamine (vasoconstriction
and increases heart rate)
Bradycardia? Atropine
 blocks the parasympathetic effects on the
heart
 If severe, the patient may need temporary
pacing
Rewarming devices for hypothermia: slowing with
rewarming and monitoring body core temperature
Foley (some patients lose bladder function)…. Want
urinary output 30 cc/hr or higher…this tells us how well
the kidneys are being perfused
Prevent DVT (blood is pooling) apply compression
stockings, ROM (range-of-motion exercises), and
anticoagulants per MD orders
 Avoid crossing the patient legs or placing
a pillow under the patient’s knees because
this further compromises circulation