Shock, Hypovolemic

BASIC INFORMATION  ETIOLOGY AND PATHOPHYSIOLOGY  Gastrointestinal accidents (large

• Etiology colon volvulus, gastric rupture)
DEFINITION  Severe hemorrhage (guttural pouch (Figure 1)
mycosis, uterine artery rupture,  Hyperthermia (endurance rides,
A reduction in perfusion that results in
inadequate organ perfusion and tissue trauma) long distance hauling)
oxygenation
 Sepsis (neonatal septicemia, entero- • Pathophysiology
colitis, metritis, pleuritis)  Reduced tissue perfusion caused by

CLINICAL PRESENTATION a decrease in circulating volume

DISEASE FORMS/SUBTYPES
• Hemorrhagic
• Maldistributive (sepsis, endotoxemia)
• Traumatic
HISTORY, CHIEF COMPLAINT
• Ataxia, collapse
• History of observed trauma
• Weak, inappetent foals, often after
dystocia
• History of overt hemorrhage or recent
foaling
• Anorexia, colic, or signs of abdominal
pain
• Increased respiratory rate or labored
breathing
PHYSICAL EXAM FINDINGS  Physical
examination findings may be normal in
early, compensated shock.
• Depression, stupor
• Tachycardia, bright-red mucous mem-
branes (progressing to purple), poor
pulse quality, physiologic murmurs
• Tachypnea, crackles, pleural friction
rubs
• Reduced gastrointestinal borborygmi FIGURE 1  Hyperemic mucous membranes in a horse with a gastric rupture demonstrating
• Hyperthermia or hypothermia hypovolemic shock caused by dehydration, systemic inflammation, and endotoxemia.
Shock, Hypovolemic 525
decreases the delivery of oxygen to
tissues.
 Decreased circulating volume may
result from loss of fluid (hemor-
rhage) or a relative decrease in
volume (sepsis and endothelial dis-
ruption, causing vascular leak
syndrome).
 Local hypoxia results in the conver-
sion to anaerobic metabolism for
energy production, with metabolic
acids (lactate) as a byproduct.
 Severe blood loss (>40% of circulat-
ing volume) or hypovolemia with
severe hypotension (mean pres-
sures, 30–40 mm Hg) may lead to
irreversible shock and death caused
by:
 Cellular dysfunction and death
from free radical production
 Activation of the inflammatory
and coagulation cascades
 Endothelial disruption permitting
endotoxemia and bacterial trans-
location
DIAGNOSIS  ulation factors, fibronectin to
DIFFERENTIAL DIAGNOSIS
• Cardiogenic
• Hypoxic
• Anaphylactic
• Neurogenic
INITIAL DATABASE
Hematocrit and hemoglobin may be
normal in early hemorrhagic conditions.
• Complete blood count
• Packed cell volume (PCV) and total
protein
• Serum chemistry
• Blood pressure
• Colloid oncotic pressure
• Serum lactate
• Coagulation profile
ADVANCED OR CONFIRMATORY
TESTING
• Central venous pressure: Negative
values may indicate hypovolemia (ref-
erence range, 2–15 cm H2O)
• Ultrasonography of the abdomen or
thorax (for specific infections, sus-
pected rupture, or hemorrhage)
• Abdominocentesis or thoracocentesis
to identify free fluid
• Coagulation profiles to monitor for
disseminated intravascular coagulation
(DIC)
• Endoscopy to identify guttural pouch
mycosis
• Cortisol levels and response to an
adrenocorticotropic hormone stimula-
tion test to monitor appropriate endo-
crine response
• Cardiac output monitoring: Lithium
dilution, echocardiography
TREATMENT   Oxyglobin (5–30 mL/kg, <10
THERAPEUTIC GOAL(S)
Restore tissue perfusion and oxygenation
ACUTE GENERAL TREATMENT
• Cardiovascular support
 Volume replacement
 Shock-dose crystalloid fluids
 Hypotensive resuscitation recom-
mended in uncontrolled hemor-
rhage
 Maintains hemostasis at the
site of hemorrhage; does not
dilute coagulation factors
 Administer fluids at a 1 to 2 : 1
ratio to volume of blood lost.
 Maintain a mean blood pres-
sure of 60 mm Hg.
 May also delay fluid admi­
nistration until hemorrhage
stopped if vasopressor support
is provided
 Colloids are recommended to
prolong fluid effects and as
therapy for vascular leakage.
 Plasma (>1 L) may provide coag-
reduce endotoxemia, and antiin-
flammatory protein C.
 Positive ionotropes are recom-
mended if volume resuscitation is
inadequate.
 Central venous pressure should
be 3 to 12 cm H2O in foals and
up to 24 cm H2O in adults
 Dobutamine (2–15 µg/kg/min
IV)
 Dopamine (2–15 µg/kg/min IV)
 Vasopressors only if fluids and ion-
otropes are unsuccessful or for
delayed resuscitation
 Norepinephrine (0.5 µg/kg/min
IV)
 Vasopressin (0.3–1 µg/kg/min
IV): High doses of vasopressors
may reduce splanchnic perfusion
• Oxygen supplementation (5–15 L/
min)
 Indicated with low PaO2 (<70 
mm Hg), PvO2 (<35 mm Hg), and
high lactate (>4 mmol/L)
 Supplementation for low hemo­
globin concentrations may be
detrimental; induces temporary
vasoconstriction
• Control of hemorrhage and PCV
 Surgical hemostasis
 Therapy for DIC
 Hemoglobin replacement: Recom-
mended for hemoglobin concentra-
tion below 7 g/dL, PCV below 15%,
and lactate above 4 mmol/L
 Blood transfusion
 Autotransfusion of blood in body
cavities
 Hemoglobin-based fluids
 
mL/kg/h)
 Side effects include increased
vascular resistance, formation
of free radicals, methemoglo-
binemia, and fluid overload
DRUG INTERACTIONS
Calcium-containing crystalloid solutions
may interfere with citrated blood
transfusions.
POSSIBLE COMPLICATIONS
• Hypovolemia may lead to develop-
ment of the systemic inflammatory
response syndrome and multiorgan
dysfunction (renal, pulmonary, cere-
bral, cardiac or hepatic dysfunction).
• Interstitial edema may result from
overaggressive fluid therapy or endo-
thelial compromise, which may inhibit
oxygen diffusion into tissues.
• Conservative fluid management is
required for congestive heart failure.
• May require earlier transfusions to
support oxygenation.
• Maintain cerebral perfusion pressure
with head trauma without fluid over-
load
 Hypertonic saline
 Mannitol
RECOMMENDED MONITORING
Repeat physical examinations, arterial
blood pressure, central venous pressure,
lactate, arterial and venous blood gas,
urine output, colloid oncotic pressure,
cardiac output
PROGNOSIS AND
OUTCOME 
Depend on the success of treat-
ment of the primary cause and
rapid resolution of hypovolemic shock
through normalization of physical
parameters
PEARLS &
CONSIDERATIONS 
Goal-directed early manage-
ment is key to reducing mortal-
ity from shock with goals of:
• Mean arterial pressure of 60 to
70 mm Hg
• Normal urine production
• Pink mucous membranes with a capil-
lary refill of less than 3 seconds
• Warm extremities
• Normal central venous pressures
• Normalization of arterial and venous
oxygen
• Blood lactate below 2 mmol/L
• Normalization of blood glucose
526 Shock, Hypovolemic Sinoatrial Block and Sinus Arrest

SUGGESTED READING editors: Equine emergencies: treatment acute blood loss in horses. J Am Vet Med
and procedures, St Louis, 2008, Saunders Assoc 229(9):1458–1462, 2006.
Driessen B, Brainard B: Fluid therapy for the
Elsevier, pp 544–552.
traumatized patient. J Vet Emerg Crit Care AUTHOR: AMELIA MUNSTERMAN
Magdesian KG, Fielding CL, Rhodes DM, et al:
16(4):276–299, 2006.
Changes in central venous pressure and EDITORS: R. REID HANSON and AMELIA
Divers TJ: Shock and systemic inflammatory
blood lactate concentration in response to MUNSTERMAN
response syndrome. In Orsini JA, Divers TJ,