Toxin-induced cardiogenic shock is a life-threatening condition characterized by severe hypotension and ineffective tissue perfusion. Many drugs can lead to cardiogenic shock in overdose, for example beta blockers or calcium channel blockers. Given the poor prognosis of these cases AND theoretically-sound reasoning, vasoactive agents make sense as a therapeutic option. A detailed, comprehensive review, just published online in Clinical Toxicology, asks the question “Are vasopressors useful in toxin-induced cardiogenic shock?”
What They Did
The authors’ search identified 130 human case reports and 14 animal studies that met their inclusion criteria.
What They Found
Humans
Surprisingly (at least to me), human case report data showed vasopressors didn’t work more often than they did work. The largest case series, of 48 diltiazem and verapamil overdose patients treated at one center over 25 years, reported good outcomes in almost all patients despite very high vasopressor doses in some cases (Ann Emerg Med 2013). There was no comparison group.
Animals
In the majority of animal studies, vasopressor treatment failed to improve hemodynamic function and resulted in decreased survival.
Application to Clinical Practice
- Don’t throw out vasopressors as an option in these incredibly sick patients, but understand that other therapies, such as insulin, may be more effective.
- Expert consensus recommendations for management of calcium channel blocker poisoning still list norepinephrine and/or epinephrine among their first-line recommendations, though it was assigned 1D level of evidence (same as calcium and insulin) (Crit Care Med 2017).
- Human cases suggest that even though vasopressors are not often effective, they don’t seem to be harmful (unlike in the animal data).
Reference
Skoog CA, Engebretsen KM. Are vasopressors useful in toxin-induced cardiogenic shock? Clin Toxicol. 2017 Feb 3:1-20. Epub ahead of print. PMID 28152638
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