Vasodilation |
Clinical manifestations: Acute, not severe, transient |
Probable mechanisms: Vasodilation and/or connective tissue mast cell degranulation resulting in histamine release |
Management: Administer vasopressors as necessary |
Anaphylaxis |
Clinical manifestations: Signs may include urticaria, wheezing and bronchospasm, or cardiovascular responses (eg, marked vasodilation with profound hypotension) |
Probable mechanisms: Immediate hypersensitivity is IgE-mediated, causing mast cell and basophil activation with subsequent mediator release; IgG formation with complement and neutrophil activation and increased platelet activating factor |
Management: - Stop protamine and administer epinephrine bolus(es) and infusion
- For bronchospasm, treat with albuterol 4 to 8 puffs (or 2.5 mg albuterol in 2.5 mL saline nebulized for administration via the ETT)
- For refractory vasodilatory hypotension that does not respond to epinephrine infusion, administer norepinephrine or vasopressin; also, methylene blue may be administered to treat refractory vasodilation
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Acute (catastrophic) pulmonary vasoconstriction |
Clinical manifestations: - Sudden marked increases in mean PAP and acute RV dilatation
- Shock develops rapidly
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Probable mechanisms: - Rare hypersensitivity reaction that is probably complement-mediated due to antiprotamine IgG antibody interaction and/or protamine-heparin complex development, with C5a-mediated thromboxane formation
- Pulmonary vasoconstriction occurs due to generation of the anaphylotoxin C5a, activation and aggregation of neutrophils that sequester in the pulmonary vasculature, microcirculatory occlusion, and thromboxane release
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Management: - Stop protamine and administer epinephrine bolus(es) and infusion
- Administer inhaled pulmonary vasodilator agents if necessary
- Patients with severe pulmonary vasoconstriction and RV failure and shock may require reinstitution of CPB in cardiac surgical settings
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