Cardiovascular aspects of anaphylaxis: implications for treatment and diagnosis

Purpose of review Anahylactic cardiovascular collapse can be resistant to treatment with epinephrine (adrenaline) and, in some cases, diagnostic uncertainty compromises follow-up care. The purpose of this review is to examine recent studies relevant to the management and diagnosis of this condition. Recent findings Nause, vomiting, incontinence, diaphoresis, dyspnoea, hypoxia, dizziness and collapse are associated with hypothension. Relative bradycardia (falling heart rate despite hypotension) is a consistent feature of hypotensive insect sting anaphylaxis and may represent a non-specific physiological response to severe hypovoaemia in conscious individuals. Upright posture has been found to be associated with death from anaphylaxis. Animal studies have found the intramuscular route for epinephrine is ineffective, intravenous boluses temporarliy effective, but intravenous infusions of epinephrine are able to reverse anaphylactic shoch. In one animal model, antihistamines were found to be harmful. A prospective human study provides evidence for the efficicacy of treatment with intravenous epinephrine infusion and fluid (volume) resuscitation. Case reports support the use of the vasoconstrictors metaraminol, methoxamine and vasopressin if adrenaline is ineffective. Repeated measurements of mast cell tryptase are more sensitive and specific than a single measurement for the diagnosis of anaphylaxis. Summary Current evidence supports use of the supine/Trendelenburg position, epinephrine by intravenous infusion and aggressive volume resuscitation. If these fail, atropine should be considered for sever bradycardia and potent vasoconstrictors may be useful. To confirm the diagnosis of anaphylaxis, serial measurements of mast cell tryptase may be preferable to a single measurement.