Shock Talk
Megan Brashear, BS, CVT, VTS (ECC)
Education Manager, DoveLewis Emergency Animal Hospital
Shock is a common syndrome experienced by many patients in many scenarios. Can you recognize it in
your patients? This talk will help you learn to recognize, treat and monitor shock.
Before we begin, it’s important to understand the difference between perfusion and hydration.
 Perfusion: refers to intravascular volume and cardiac output. The volume of fluid that is
circulating through the body and the strength of the cardiac contractions to move the fluid.
 Hydration: refers to interstitial volume and intravascular volume. Strictly speaking of the
amount of fluid within the vessels and in body tissues.
When we talk about shock we are really talking about a deficit of supply and demand. Every cell in the
body requires ATP to protect cell wall integrity and perform cellular functions. ATP has a life span of 3
seconds, so cells are constantly making ATP. The body needs oxygen to create this ATP. Without oxygen
cells begin to die. In a shock situation, because the body is no longer perfusing tissues as it should,
oxygen distribution is interrupted, ATP production decreases and cells die.
The body is set up to try and avoid this cell death, and baroreceptors are the back-up. These receptors
are located in the aorta and kidneys and in times of hypovolemia (for example) sense when blood flow is
low. They tell the heart that blood flow is lacking and compensation kicks in. This compensation shows
up as the clinical signs of shock.
So let's get back to perfusion and hydration. When we collect vital signs and perform serial exams on our
patients we are checking signs of perfusion. We can measure perfusion by looking at the patient’s
mucus membranes/CRT, by assessing pulse quality, and looking at heart rate. Make sure to look at all
three together. A dog may have good pulse quality but if his heart rate has to be elevated to maintain
that quality the dog isn’t normal. The same goes for blood pressure. If the heart rate has to be 200bpm
in order to maintain a ‘normal’ blood pressure then the patient needs help. If perfusion begins to
decrease the body will start to preferentially take care of organs; the heart/lungs/brain being the most
important. Tissues in the periphery will start to get decreased blood and oxygen supply.
To measure hydration we look at skin turgor, mucus membrane moisture, and the patient’s eyeballs.
Eyes that are sunken indicate severe dehydration, as does prolong skin tenting and dry tacky mucus
membranes.
Shock can be divided into the following categories:
 Hypovolemic shock: hypovolemia (low volume) is caused by salt and water loss and/or blood
loss. Most commonly we see this category of shock in patients with severe vomiting and
diarrhea. Blood loss can occur from a bleeding tumor, GI ulcer, etc. Hypovolemic shock is the
result of both poor perfusion and dehydration.
 Traumatic shock: if an animal sustains enough trauma and experiences high amounts of blood
loss they will have an interruption of oxygen supply. Crushing injuries (like patients run over by a
car or mauled by a larger animal) can also suffer from traumatic shock. It is the result of both
hypoperfusion and dehydration.
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Cardiogenic shock: this is challenging to treat, as the lack of oxygen delivery is due to the heart
not being able to adequately pump. Normal treatments for shock cannot be used on a heart that
has poor cardiac output. Cardiogenic shock is the result of hypoperfusion.
Obstructive shock: occurs when there is an obstruction to blood flow. The most common causes
of obstructive shock are GDV, and ATE (arterial thromboembolism). In GDV the distended
stomach puts pressure on the vena cava and prevents venous return of blood back to the heart
decreasing preload and then cardiac output. The same happens with a saddle thrombus in a cat
and the clinical signs of shock are observed in these patients.
Distributive shock: caused by vasodilation usually due to sepsis. In distributive shock the
patient’s volume is often sitting in expanded vessels instead of circulating through the body.
Again it is challenging to treat as it is the result of hypoperfusion and the patient is often well
hydrated.
Now that you understand the causes and compensatory mechanisms next is recognizing the signs of
shock. Early shock is only exhibited by our canine patients. These signs are the result of the body
recognizing an impending problem with perfusion and trying to compensate. The signs are:
 Tachycardia
 Bounding Pulses
 Bright MM/Fast CRT
These patients often have normal mentation. The heart is trying to circulate a smaller volume to all of
the tissues and so it works harder giving us the increased heart rate and bounding pulses.
The next stage of shock, compensatory shock, sees the patient still trying to keep up with losing
perfusion. This stage mimics the pain response in animals, so pain management is important to not only
keep them comfortable, but to rule out this stage of shock. The signs are:
 Tachycardia
 Weak Pulses
 Pale MM
 Decreased Mentation
These patients are still trying to keep up with the elevated heart rate but the body is beginning to focus
inward and only perfuse the major organs (heart lungs and brain). The periphery is less important, and
so we see weak peripheral pulses and can feel cold extremities. The animal’s mentation may also begin
to dull. Cats in this stage will often spiral downward very quickly.
In late or decompensated shock the body begins to shut down and can no longer keep up with oxygen
needs. The heart rate may be decreased, mm color is white or gray, and pulses may be absent. These
patients are often mentally dull.
To treat patients in shock the simplest first treatment is to provide oxygen. Providing flow-by or mask
oxygen is a good way to start providing some of what the body lacks. Next is to provide fluid therapy. As
long as you know the patient is not in cardiogenic shock, IV fluids need to be started quickly and the
patient closely monitored as they begin to respond. A large bore, short length IV catheter needs to be
placed and IV fluids given.
 Crystalloid fluids are replacement electrolyte solutions that will increase circulating intravascular
volume, but only for a short time. High doses are fluids are needed to replace losses and it is
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important to monitor the patient’s response to fluids and titrate the rate. Crystalloids are
administered in a true bolus with the technician responsible for checking vital sign changes
between boluses. USE CARE WITH CATS
Colloids are fluids made of larger molecules that will stay in the intravascular space longer than
crystalloids and will even draw other fluids into the intravascular space. They can be used in
conjunction with crystalloids to manage blood pressure and perfusion. Using colloids can
increase the chance of fluid overload, so use care when administering and monitor your patient
closely.
Hypertonic saline may be administered to facilitate a quick draw of fluids into the intravascular
space. Hypertonic saline has a much higher salt concentration (usually 7% NaCl) as compared to
physiologic saline (0.9% NaCl) drawing fluid into the intravascular space in an attempt to dilute
the salt content. The effects of hypertonic saline are short-lived (30 – 60 minutes), but their
administration will keep the patient alive while they receive a large bolus of crystalloid fluids.
Lactate is normally produced in the body and metabolized. When muscles must work in an absence of
oxygen lactate production increases and overwhelms the liver’s ability to metabolize all of it. Normal
lactate levels are < 2.5mmol/L. Elevated lactate levels will be present in patients experiencing poor
perfusion. As fluid therapy is successful lactate will be picked up and metabolized and levels will fall.
Using serial lactate measurements you can chart the progress of your fluid resuscitation.
It is important to note that cats do not respond to shock the same way dogs do. Cats in shock will
vasodilate (not vasoconstrict like dogs), lose body heat, and their blood pressure drops. This drop is not
necessarily from low circulating volume. As cats warm up their vessels will constrict back to normal size.
Think of their normal vessel size like a drinking straw, and their shock vessel size as a garden hose. If you
fill that garden hose with water (and thus get a great blood pressure!) while the cat is still cold, you’re
going to have too much fluid when the vessel shrinks back to the size of a straw. The unfortunate effect
is that cats will dump the excess fluids into their lungs. It is very important to be careful with fluid
administration on hypothermic cats and focus on warming them as much as providing fluid therapy to
them. While the cat is warming you can give small (20ml) boluses of crystalloids but monitor them
closely. When their body temperature approaches normal and they are still hypotensive you can begin
more aggressive IV fluid therapy.
Shock patients need careful monitoring to chart their progress. Working with the veterinarian, set heart
rate and blood pressure goals for the patient and treatment administered until those goals are met.
Ideally the heart rate will decrease, the blood pressure increase, and mm color improve to pink. The
technician should be monitoring the cardiovascular parameters (heart rate, mm color, CRT, limb
temperature, urine output), respiratory parameters (rate and effort, Sp02), blood pressure, and ECG if
possible. Vitals should be checked multiple times per hour on the critical patients until they remain
normal for a significant period of time.
Patients under anesthesia can experience shock for the same reasons awake animals experience shock.
The signs and treatments are the same, so use care with anesthetized patients and don’t assume
tachycardia means the anesthesia level is too light. Look at blood pressure, mm color and CRT to help
you determine the best course of treatment.
References available upon request