ISSN 2398-2969      

Shock: hypovolemic

icanis

Synonym(s): Hypovolemic shock


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 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 gastroenteritis, extensive burns, etc.
  • Treatment: fluid expansion either with crystalloid, colloid, or blood products depending on the underlying cause for fluid loss. If hemorrhagic shock, controlling the blood loss is a critical step in treatment and management, if non-hemorrhagic treatment of the underlying cause is an essential step.
  • Prognosis: depends on underlying cause of fluid loss, volume lost, and potential organ damage from decreased perfusion. Can range from guarded to good if rapid treatment and reversal/management of underlying cause.

Pathogenesis

Etiology

Pathophysiology

  • The underlying defect common to all forms of shock Shock is inadequate tissue perfusion resulting in diminished oxygen delivery to cells, altered cellular metabolism, cell death and organ failure.
  • 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 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).
  • Hypovolemic shock is associated with blood loss or excessive loss of other body fluids/severe dehydration that then results in low blood volume. This causes reduced cardiac output due to low venous return, which triggers a sympathetic response → peripheral vasoconstriction, tachycardia, increased cardiac contractility and activation of renin angiotensin aldosterone system (RAAS) → temporary rise in cardiac output and compensatory shock. Ongoing compromise of systemic perfusion leads to failure of compensatory mechanisms causing decompensated shock.
  • Anaerobic metabolism leads to lactic acid accumulation and acidosis resulting in cells taking up water and sodium and losing potassium.
  • Cell injury and death result in activation of vasoactive amines and complement and further circulatory collapse.
  • Most significant effects are seen on kidney, liver and intestine. These have a relatively high demand for blood flow yet are poorly protected in times of shock, whereas blood flow to the brain is well maintained.

Timecourse

  • Minutes to hours, depending on the stage of shock, eg compensated or decompensated.

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.
  • Llewellyn E, Lourenço M, Ambury A (2020) Recognition, Treatment, and Monitoring of Canine Hypovolemic Shock in First Opinion Practice in the United Kingdom. Top Comp Anim Med 39, 100427 doi.org/10.1016/j.tcam.2020.100427.
  • Boyd C J, Claus M A, Raisis Anthea L, Hosgood G, Sharp C R, Smart L (2018) Hypocoagulability and Platelet Dysfunction Are Exacerbated by Synthetic Colloids in a Canine Hemorrhagic Shock Model. Front Vet Sci 5, 279 doi: 10.3389/fvets.2018.00279.
  • Lathan P & Thompson A L (2018) Management of hypoadrenocorticism (Addison's disease) in dogs. Vet Med (Auck) 9, 1-10 doi: 10.2147/VMRR.S125617.
  • Wong C, Borchers A (2018) Severe lactic acidosis and hypoglycemia due to acute metformin intoxication in a dog. J Vet Emerg Crit Care 28, 1479-3261 doi: 10.1111/vec.12711.

Other sources of information

  • De Laforcade A & Silverstein D (2015) Shock. In: Small Animal Critical Care Medicine. 2nd Ed. Philadelphia, pp 26-29.
  • Macintire D K (2000) Hypotension. In: Textbook of Veterinary Internal Medicine. 5th edn. Eds S J Ettinger & E C Feldman. Philadelphia: W B Saunders Co. pp 183-186.

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