Canis ISSN: 2398-2942

Shock

Contributor(s): Kyle Braund, Elisa Mazzaferro, Daniel H Lewis, Neus Elias

Introduction

  • Definition: inadequate cellular energy production; decrease in oxygen delivery in relation to oxygen consumption.
  • Cause: most commonly secondary to loss of intravascular volume (hypovolemic shock), maldistribution of vascular volume (distributive shock) or failure of cardiac pump (cardiogenic shock) that leads to the decrease in oxygen delivery.
  • Signs: poor circulatory function (decreased blood pressure, prolonged capillary refill time, pale mucous membranes, cool extremities, fast but weak pulses).
  • Diagnosis: signs; identification of underlying cause; increased serum lactate levels may be associated with the degree of reduced perfusion/sympathetic response.
  • Treatment: circulatory support; address underlying cause depending on the main cause for the shock.
  • Prognosis: good if appropriate therapy given immediately, depending on whether the underlying cause can be treated: guarded if appropriate treatment delayed or not possible.

Pathogenesis

Pathophysiology

  • The underlying defect common to all forms of shock is inadequate tissue perfusion resulting in diminished oxygen delivery to cells, altered cellular metabolism, cell death and organ failure.
  • Hypovolemic shock: 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 vasconstriction, tachycardia, increased cardiac contractility and activation of RAAS → temporary raise in cardiac output and compensatory shock. Ongoing compromise of systemic perfusion leads to failure of compensatory mechanisms causing decompensated shock.
  • Distributive shock (SIRS Systemic inflammatory response syndrome (SIRS)/sepsis/anaphylaxis, etc): there is no absolute reduction in circulating blood volume, but there is maldistribution of blood that leads to shock, due to the release of vasodilatory cytokines.
  • Cardiogenic shock Shock: cardiogenic: cardiac output is reduced due to cardiac rhythm abnormalities, valvular incompetence or systolic/diastolic dysfunction  → inadequate distribution of oxygen to tissues → cellular hypoxia.
  • Anaerobic metabolism → lactic acid build up → acidosis → cells take up water and sodium and lose potassium.
  • Cell injury and death results in activation of vasoactive amines and complement → 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.
  • Girard C & Higgins R (1999) Staphylococcus intermedius cellulitis and toxic shock in a dogCan Vet J 40 (7), 501-502 PubMed.
  • Shaw N, Burrows C F, King R R (1997) Massive gastric hemorrhage induced by buffered aspirin in a greyhoundJAAHA 33 (3), 215-219 PubMed.

Other sources of information

  • De Laforcade A and 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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