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Shock
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.
Presenting signs
- Decreased mentation.
- Tachycardia or bradycardia.
- Poor peripheral pulse quality and hypotension.
- Pale mucous membranes, except in distributive shock syndromes when inappropriate peripheral vasodilatation leads to bright red ("injected") mucous membranes.
- Hypothermia with cold extremities (pyrexia can be seen, however in septic shock Shock: septic).
- Signs of end organ failure (oliguria, etc).
- Hemorrhagic diarrhea, secondary to hypoperfusion of gastrointestinal tract during shock (especially in dogs).
- Signs of respiratory dysfunction, especially in cats.
Acute presentation
- Acute collapse.
Cost considerations
- Moderate to severe costs incurred in diagnosis and treatment, depending on underlying cause.
Special risks
- Anesthesia and/or surgery which have the potential to further compromise circulatory or respiratory function.
- Secondary end organ damage and multi-organ dysfunction syndrome (MODS) Multiple organ dysfunction syndrome (MODS).
Pathogenesis
Etiology
- Can be classified according to etiology:
- Hypovolemic Shock: hypovolemic, eg fluid loss from burns Fluid therapy: for burns or hemorrhage.
- Severity related to rate and volume of fluid loss.
- Vascular, eg vena caval thrombosis, aortic embolism or vasodilation (often drug related), eg acepromazine.
- Cardiogenic Shock: cardiogenic, eg congestive heart failure Heart: congestive heart failureor arrhythmia.
- Endotoxemic or septic shock Shock: septic.
Pathophysiology
- The underlying defect common to all forms of shock is inadequate tissue perfusion resulting in dimished 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 vasoconstriction, 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 Shock: sepsis/anaphylaxis 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. In contrast, 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.
Other sources of information
- De Laforcade A & Silverstein D (2015) Shock. In: Small Animal Critical Care Medicine. 2nd edn. Philadephia, pp 26-29.