80th Western Veterinary Conference
CSI Critical Care—Hypovolemic Shock 101
Andrew J. Rosenfeld, DVM, ABVP
Veterinary Team Education Courses / HESKA
Scottsdale, AZ, USA
OBJECTIVES OF THE PRESENTATION
The session content reviews the basics of the syndrome of hypovolemic shock (blood loss and
dehydration), its physical characteristics, diagnostic evaluations, and an outline of treatment protocols.
The lecture goal is to enable attendees to understand the concepts of shock, clinical diagnostics of the
emergency shock patient, and treatment.
GENERAL KEY POINTS
Hypovolemic shock refers to an animal that cannot maintain normal blood volume (red blood cells and
fluid) to maintain perfusion needs. Without adequate perfusion, the body cannot oxygenate tissue
properly and the patient begins to decompensate.
Hypovolemic shock can occur in any species, sex and age; and it when there is a rapid loss of red
blood cells or fluid. This loss occurs so acutely the patient cannot recover and their body systems begin to
fail. Possible causes of hypovolemic shock are:
Acute Bleeding: Red blood cell loss.
Severe Life Threatening Anemia: A patient with a disease process that produces massive red blood
destruction or severe chronic anemia can produce hypovolemic shock.
Dehydration: Loss of the fluid portion of the blood form vomiting, diarrhea, heat stroke, burns and
other disease processes.
The decreased blood volume decreases perfusion and oxygenation leading to hypoxia producing
organ and tissue failure.
With concerns of hypovolemic shock, special focus on any possible history of trauma (i.e., hit by
car…) or serious underlying disease should be discussed with client. Specific discussions of
gastrointestinal disease or other disease entities that produce vomiting and diarrhea should be discussed.
Hypovolemic shock is the inability to perfuse blood the tissue due to decreased blood volume. As
the syndrome progresses, the animal cannot adequately oxygenate tissue and becomes weak, collapsed,
nonresponsive and ends in cardiac failure. Common clinical signs of disease are:
o Pulse Rate:
Rapid: Bounding pulse (Canine).
Bradycardia (Feline): Cats tend to be bradycardic in early shock.
o Pulse Character: Pulse deficit: Due to the body’s decreased perfusion, the patient may
also have pulse deficits as the heart cannot produce a pulse for each heart contraction.
o Mentation: In early shock, these pets may be dull to depressed as these patients are
trying to put all their energy into restoring normal control. These patients may also show
o Respiration: Pets may have altered respiratory patterns that alternate between a rapid to
a slow rate. There may also be an abdominal component.
o Body Temperature: Patients may have extreme aberrations in body temperature. Patients
suffering from heat stroke, protracted seizures or severe infectious disease may have
highly elevated body temperature (> 105 degrees Fahrenheit). As the animal becomes
more shocky, body temperature can become subnormal.
o Mucus Membrane Color / Capillary Refill Time: One of the early indicators of shock,
patient’s mucus membrane color can become pale suggesting blood loss or dehydration.
o Capillary Refill Time begins to become prolonged as the body can no longer fill the
smallest peripheral capillaries at a regular rate.
o Bruising: Patients that begin to show spontaneous bruising on the skin, whites of the eye,
gums or other parts of the body can suggest patients with a coagulopathy or DIC. These
patients must be evaluated immediately since they may be acutely decompensating.
o Dehydration: Dependent on the syndrome, pets can start showing early to moderate
o Pupils: Pupils should be even and responsive to light. In some cases, response to a bright
light may be slowed. Further, with head trauma, the pupil size may be different sizes
Severe Shock: As the type of shock worsens, the patient’s signs can be more severe. The time frame
from early to severe shock can sometimes be within minutes. Potential critical care patients must
constantly be re-evaluated until the patient is stabilized. Symptoms of severe shock can be:
o Pulses: As the patient looses their ability to compensate, the cardiovascular system
begins to fail. Pulses become weaker and the heart rate slows. As the patient deteriorates;
pulses and eventually the heart rate stop.
Mentation: Pets become more depressed, non-responsive and even comatose.
o Respiration: Becomes shallower and slower.
o Mucus Membrane Color / Capillary Refill Time: Mucus membrane color and capillary
refill time can worsen and prolong. Changes in mucus membrane color are dependent on
the disease entity producing shock (see above).
o Dehydration: In specific types of shock, as circulation fails, the patient may become more
significantly hypovolemic, decreasing blood flow to the peripheral tissue. This will
decrease normal skin turgor.
o Pupils: become slower to respond to a bright light source. As the patient becomes life
threatened, they may become fixed and non-responsive. Anisocoria is still possible.
o Bruising: Bruising can become more severe and wide spread suggesting whole body
KEY CLINICAL DIAGNOSTIC POINTS
Clinical Diagnostics of Shock
Since shock can affect the entire body, full diagnostics may be required to both outline the cause of shock
and the organs being affected by this syndrome. However, when faced with a patient in some form of
shock, establishing a quick diagnostic baseline (minimal clinical databases) is very important. Some
diagnostic tests may be:
Packed Cell Volume (PCV) / Total Protein (TP): Changes in packed cell volume and protein in
shock situations can help the medical team evaluate significant blood loss, anemia or dehydration.
Glucose: Glucose is a very important factor to monitor in any shocky patient. The patient must have
blood sugar for the central nervous system and muscle. With Blood glucose < 40–50 mg/ dl,
patients can become weak, comatose and seizure.
Electrolytes: Although not as always easily assessed, changes in sodium and potassium can
produce irregular heart rhythms, weakness, muscle fasciculations, collapse, a slowed heart rate and
Clotting Times: Prolonged clotting times represent increased bleeding tendencies, which can both
produce shock and be secondary to the syndrome.
Blood Pressure: Blood pressure becomes a key diagnostic indicator to monitor the patient’s
stability; animals in hypovolemic shock will present with profound hypotension. As the patients is
aggressively treated with fluid therapy, a return of normal systemic blood pressure can help
indicate response to treatment and an indication to decrease shock doses of fluids. This becomes
extremely important in the dehydrated patient, where peripheral skin turgor can take hours to
return to normal elasticity. If not monitored closely, severely dehydrated patients may become
over-hydrated and hypertensive.
KEY THERAPEUTIC POINTS
(See Figure ST-13.1)
The goal to treatment of Hypovolemic shock is to rehydrate the patient and restore normal blood
pressure and perfusion. A treatment protocol may be:
1. Oxygen Therapy: Have an oxygen environment set up (i.e., cage, mask, nasal oxygen catheter) so
that is needed the pet can be placed on oxygen. Oxygen is never contraindicated and by simply
increasing the oxygen concentration in the blood, the patient may become less stressed and shocky.
2. Catheter: Have catheter set up ready and if needed set IV catheter. With a patient in shock, the
ability to set a catheter may change within a very small time range. Having catheter and supplies
readily available, and being able to effectively set a catheter can make the difference in stabilizing
3. Fluids: Shock doses of emergency fluid therapy is recommended. The doses for shock fluid therapy
a. Canine: 40 cc / pound per hour (90 cc/kg/hr)
b. Feline: 20 cc / pound per hour (45 cc/kg/hr)
It is always important that these are only estimates of what an average patient can
tolerate through intravenous fluid bolus before fluids begin to expand beyond the vessels
into the tissue level. Patient should always be closely monitored for signs of fluid
overload while shock doses of fluids are being maintained.
4. Minimal Clinical Databases:
a. PCV / TP
b. Activated Clotting Time
5. Reevaluate: Within 5–10 minutes of fluid administration, reevaluate the patient:
b. Pulse quality
6. Colloids: Synthetic Colloids are large inert sugar molecules (i.e., Hetastarch) that help increase fluid
absorption from the tissue into the vessels producing increased blood pressure.
7. Reevaluate: Within 5–10 minutes of fluid administration, reevaluate the pet. If the patient is not
stabilizing look for other concerns:
a. Internal Abdominal Bleeding: If there is a concern about internal bleeding, aggressive
therapy to slow the process of blood loss may be necessary.
i. Infuse the abdomen with warm sterile fluids: Infusion of a warm sterile
fluid (10 cc/ pound) can help increase intra-abdominal pressure decreasing blood
loss through vessels.
ii. Belly Wrap: After fluids are infused into the abdomen, placement of an
abdominal wrap beginning at the hind limbs working up over the abdomen can
help increase intra-abdominal pressure. Once stabilized, this wrap must be
removed slowly and in phases so as not to produce a rapid hypotension to the
lower body as the bandage is removed.
iii. Transfusion: If PCV / TP continue to decrease and activated clotting
time is abnormal (i.e., > 120 seconds), blood product transfusion is indicated.
The goal would be replace both red blood cells and clotting factors that are in
plasma by either giving whole blood or packed red blood cells or plasma.
b. Worsening Dehydration: In some cases, specific diseases (i.e., Hemorrhagic
Gastroenteritis (HGE)) can produce a worsening dehydration despite aggressive fluid
therapy. Reevaluate PCV/TP and blood pressure will help identify patients with more
severe hydration challenges.
c. Other Causes: Patients may enter the hospital with hypovolemic shock that are
secondary to another underlying entity. If the patient is not stabilizing with fluid and
drug therapy, other causes may need to be evaluated for:
i. Hormonal disease—Addisonian Crisis
ii. Other form of Shock—Sepsis, cardiogenic…
iii. Concussion & coma
iv. Toxin / poison
v. Disseminated Intravascular Coagulopathy (DIC)
Figure 13.1. Algorithm for identifying and treating hypovolemic shock.
KEY PROGNOSTIC POINTS
If hypovolemic shock is not evaluated for, detected and aggressively treated, the patient’s prognosis is
OVERVIEW OF THE ISSUE
This lecture will review the causes and physical symptoms of hypovolemic shock, the clinical diagnostics
which help to identify early signs of the syndrome, and understand treatment protocols.
To successfully stabilize and treat a patient with hypovolemic shock, team members must be able to
identify signs of early and severe shock, understand the clinical diagnostics that help to support the
diagnosis, and understand the treatment protocols.i
i. Image in this text is courtesy of The Veterinary Medical Team Handbook, Rosenfeld, A. Wiley-Blackwell,
Ames, IA, 2007.
Textbooks and on-line programs are recommended as good referral sources for the veterinary team. They
all have strengths in their own field and can be a part of an excellent referral library:
1. Critical care Webinars—www.heska.com—an online interactive continuing education site in clinical pathology
and critical care.
2. CET University (A Virbac Site)—www.cetuniversity.com—an online interactive continuing education site on
3. Dermatology University (A Virbac Site)—www.virbacdermu.com—an online interactive continuing education
site on veterinary Dermatology.
4. Rosenfeld A. The Veterinary Medical Team Handbook, Wiley-Blackwell, Ames, IA, 2007.
5. Tilley Larry and Smith Francis, The Five Minute Manager—Canine and Feline, Blackwell Press.
6. Colville Thomas & Bassert Joanna, Clinical Anatomy and Physiology for Veterinary Technicians, Mosby.