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The pathophysiology of shock in anaphylaxis
1Emergency Medicine Research Unit, The University of Western Australia and Fremantle Hospital, Alma Street, Fremantle, WA 6160, Australia. simon.brown@uwa.edu.au
Immunology and Allergy Clinics of North America
|May 12, 2007
Summary
Anaphylactic shock involves low venous tone and fluid loss, impairing heart function. Aggressive fluids and epinephrine are key, with vasoconstrictors considered if these treatments fail for anaphylaxis management.
Area of Science:
- Anesthesiology
- Immunology
- Critical Care Medicine
Background:
- Anaphylactic shock presents complex pathophysiology.
- Key features include reduced venous tone and fluid extravasation, leading to mixed hypovolemic-distributive shock.
- Myocardial function is often depressed during anaphylaxis.
Purpose of the Study:
- To outline the primary pathophysiologic mechanisms of anaphylactic shock.
- To discuss current treatment strategies for anaphylactic shock.
- To consider adjunctive therapies when standard treatments are insufficient.
Main Methods:
- Review of human observational data.
- Analysis of animal study findings.
- Pathophysiologic considerations for treatment escalation.
Main Results:
- Anaphylactic shock is characterized by decreased venous tone and fluid shifts.
- Reduced venous return and impaired cardiac function are significant consequences.
- Epinephrine administration generally improves vascular tone and cardiac output.
Conclusions:
- Aggressive fluid resuscitation is crucial for managing hypovolemic-distributive shock in anaphylaxis.
- Intravenous epinephrine is a primary treatment to enhance vascular tone and cardiac function.
- Selective vasoconstrictors may be considered as a next step when initial therapies are ineffective.
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