Equis ISSN 2398-2977

Hypovolemic shock

Contributor(s): Jarred Williams, Gayle Hallowell

Introduction

  • Cause: any condition causing rapid fluid loss leading to inadequate circulating volume, inadequate perfusion, and inadequate oxygen delivery.
  • Signs: tachycardia, tachypnea, cool extremities, delayed capillary refill time, pale pink to white mucous membranes, decreased jugular fill, decreased pulse pressure, altered mentation.
  • Diagnosis: identification of fluid losses, either hemorrhagic or non-hemorrhagic. If hemorrhagic, identify the source of bleeding. If non-hemorrhagic, identify underlying condition, ie colitis, enteritis, extensive burns, etc.
  • Treatment: immediate fluid expansion either with crystalloid, colloid, or whole blood depending on the underlying cause for fluid loss. If hemorrhagic shock, cessation of blood loss is a critical step in treatment and management.
  • Prognosis: depends on underlying cause of fluid loss, volume lost, and organ damage from decreased perfusion. Can range from poor to good.

Pathogenesis

Etiology

  • Hemorrhagic shock:
    • Trauma.
    • Neoplasia.
    • Aneurysm.
    • Penetrating wound.
    • Foreign body.
    • Gastrointestinal ulceration.
    • Large strongyle larvae migration.
  • Non-hemorrhagic shock:
    • Pleuropneumonia (gram-positive and gram-negative organisms).
    • Peritonitis (gram positive and negative organisms).
    • Enteral bacterial infection (Salmonellosis, Clostridium, Enterobacter, Enterococcus).
    • Parasitism.
    • Viral infections (coronavirus, rotavirus).

Predisposing factors

Specific

Pathophysiology

  • Acute fluid shifts out of the intravascular space decreases preload. Preload, afterload, and contractility affect stroke volume, so decreased preload will decrease stroke volume. Cardiac output is the product of heart rate and stroke volume, thus the decrease in stroke volume also decreases cardiac output. Decreases in cardiac output also decrease the delivery of oxygen to tissues leading to tissue dysfunction and ultimately death if prolonged. The end result can be multiple organ dysfunction syndrome (MODS) followed by death.
  • The body compensates by increasing cardiac contractility and heart rate, increasing systemic vascular resistance (in an effort to redirect blood to the brain, heart, and kidneys, and away from the skin, muscle, and GI tract), and increasing blood volume through the actions of aldosterone and antidiuretic hormone (ADH).

Timecourse

  • Acute, depending on hemorrhagic or non-hemorrhagic shock and the rate of fluid loss.
  • Can begin to show signs within 1-6 h.
  • Can present acutely with chronic, slow losses (12-72 h).

Epidemiology

  • When hypovolemic shock is non-hemorrhagic and secondary to fluid losses associated with infectious disease, epidemiologic considerations should be made per the specific infectious disease.
  • There are not population dynamics for hypovolemic shock in general, as it is a product of fluid loss secondary to a primary condition.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Fielding C L & Magdesian KG (2011) A comparison of hypertonic (7.2%) and isotonic (0.9%) saline for fluid resuscitation in horses: A randomized, double-blinded, clinical trial. J Vet Intern Med 25 (5), 1138-1143 PubMed.
  • Nolen-Watson R D (2012) Flow rates of large animal fluid delivery systems used for high-volume crystalloid resuscitation. J Vet Emerg Crit Care 22 (6), 661-665 PubMed.
  • Dugdale A H A, Barron K E, Miller A J & Proudman C J (2015) Effects of preoperative administration of hypertonic saline or pentastarch solution on hematologic variables and long-term survival of surgically managed horses with colic. JAVMA 246 (10), 1104-1111 PubMed.
  • Hallowell G D & Corley K T T (2006) Preoperative administration of hydroxyethyl starch or hyptertonic saline in horses with colic. J Vet Intern Med 20 (4), 980-986 PubMed.

Other sources of information

  • Marino P (2013) Marino’s The ICU Book. 4th edn. Ed: Marino P. Lippincott, Williams, & Wilkins, USA.


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