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 TREATMENT   Oxyglobin (5–30 mL/kg, <10 

tissues. mL/kg/h)
 Decreased circulating volume may  Side effects include increased
THERAPEUTIC GOAL(S)
result from loss of fluid (hemor- Restore tissue perfusion and oxygenation vascular resistance, formation
rhage) or a relative decrease in of free radicals, methemoglo-
volume (sepsis and endothelial dis- ACUTE GENERAL TREATMENT binemia, and fluid overload
ruption, causing vascular leak • Cardiovascular support
syndrome). DRUG INTERACTIONS
 Volume replacement
 Local hypoxia results in the conver- Calcium-containing crystalloid solutions
 Shock-dose crystalloid fluids
sion to anaerobic metabolism for  Hypotensive resuscitation recom-
may interfere with citrated blood
energy production, with metabolic mended in uncontrolled hemor- transfusions.
acids (lactate) as a byproduct. rhage
 Severe blood loss (>40% of circulat- POSSIBLE COMPLICATIONS
 Maintains hemostasis at the
ing volume) or hypovolemia with site of hemorrhage; does not • Hypovolemia may lead to develop-
severe hypotension (mean pres- dilute coagulation factors ment of the systemic inflammatory
sures, 30–40 mm Hg) may lead to  Administer fluids at a 1 to 2 : 1
response syndrome and multiorgan
irreversible shock and death caused ratio to volume of blood lost. dysfunction (renal, pulmonary, cere-
by:  Maintain a mean blood pres-
bral, cardiac or hepatic dysfunction).
 Cellular dysfunction and death • Interstitial edema may result from
sure of 60 mm Hg.
from free radical production  May also delay fluid admi­ overaggressive fluid therapy or endo-
 Activation of the inflammatory thelial compromise, which may inhibit
nistration until hemorrhage
and coagulation cascades stopped if vasopressor support oxygen diffusion into tissues.
 Endothelial disruption permitting • Conservative fluid management is
is provided
endotoxemia and bacterial trans-  Colloids are recommended to required for congestive heart failure.
location prolong fluid effects and as • May require earlier transfusions to
therapy for vascular leakage. support oxygenation.
 Plasma (>1 L) may provide coag-
• Maintain cerebral perfusion pressure
DIAGNOSIS  ulation factors, fibronectin to with head trauma without fluid over-
reduce endotoxemia, and antiin- load
DIFFERENTIAL DIAGNOSIS flammatory protein C.
 Hypertonic saline

 Mannitol
• Cardiogenic  Positive ionotropes are recom-
• Hypoxic mended if volume resuscitation is
• Anaphylactic RECOMMENDED MONITORING
inadequate.
• Neurogenic  Central venous pressure should
Repeat physical examinations, arterial
be 3 to 12 cm H2O in foals and blood pressure, central venous pressure,
INITIAL DATABASE up to 24 cm H2O in adults lactate, arterial and venous blood gas,
Hematocrit and hemoglobin may be  Dobutamine (2–15 µg/kg/min urine output, colloid oncotic pressure,
normal in early hemorrhagic conditions. IV) cardiac output
• Complete blood count  Dopamine (2–15 µg/kg/min IV)
• Packed cell volume (PCV) and total  Vasopressors only if fluids and ion-
protein otropes are unsuccessful or for
PROGNOSIS AND
• Serum chemistry delayed resuscitation OUTCOME 
• Blood pressure  Norepinephrine (0.5 µg/kg/min
• Colloid oncotic pressure IV) Depend on the success of treat-
• Serum lactate  Vasopressin (0.3–1 µg/kg/min ment of the primary cause and
• Coagulation profile IV): High doses of vasopressors rapid resolution of hypovolemic shock
may reduce splanchnic perfusion through normalization of physical
ADVANCED OR CONFIRMATORY • Oxygen supplementation (5–15 L/ parameters
TESTING min)
• Central venous pressure: Negative  Indicated with low PaO2 (<70 
values may indicate hypovolemia (ref- mm Hg), PvO2 (<35 mm Hg), and PEARLS &
erence range, 2–15 cm H2O) high lactate (>4 mmol/L) CONSIDERATIONS 
• Ultrasonography of the abdomen or  Supplementation for low hemo­
thorax (for specific infections, sus- globin concentrations may be Goal-directed early manage-
pected rupture, or hemorrhage) detrimental; induces temporary ment is key to reducing mortal-
• Abdominocentesis or thoracocentesis vasoconstriction ity from shock with goals of:
to identify free fluid • Control of hemorrhage and PCV • Mean arterial pressure of 60 to
• Coagulation profiles to monitor for  Surgical hemostasis 70 mm Hg
disseminated intravascular coagulation  Therapy for DIC • Normal urine production
(DIC)  Hemoglobin replacement: Recom- • Pink mucous membranes with a capil-
• Endoscopy to identify guttural pouch mended for hemoglobin concentra- lary refill of less than 3 seconds
mycosis tion below 7 g/dL, PCV below 15%, • Warm extremities
• Cortisol levels and response to an and lactate above 4 mmol/L • Normal central venous pressures
adrenocorticotropic hormone stimula-  Blood transfusion • Normalization of arterial and venous
tion test to monitor appropriate endo-  Autotransfusion of blood in body oxygen
crine response cavities • Blood lactate below 2 mmol/L
• Cardiac output monitoring: Lithium  Hemoglobin-based fluids • Normalization of blood glucose
dilution, echocardiography
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,