ArticleResuscitation2016
Energy conserving chemical defibrillation of ventricular fibrillation: A randomized two phase controlled blinded trial.
Article in Resuscitation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed, 5 citations in OpenAlex.
- Cardioplegia defibrillation of circulatory and metabolic phase ventricular fibrillation in a swine model.Resuscitation · 2019Article
- Cardioplegic arrest as pharmacological defibrillation; A novel approach for refractory ventricular fibrillation.Annals of cardiac anaesthesiaArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
objectivesPotassium cardioplegia-induced transient asystole may conserve myocardial energy, foster chemical defribrillation, and improve VF arrest outcome. A trial of potassium infusion with or without calcium reversal was conducted to test for improvement in intra-arrest VF waveform and post-ROSC hemodynamics.
methodsEighteen swine were randomized to three treatment arms in two phases. VF was electrically induced and untreated for 4min. The animals then received 6min of mechanical CPR. Blinded investigators infused two study medicines peripherally during this interval. One group received 1.5mEq/kg KCl with CPR initiation followed 3min later by CaCl 10% infusion 0.12cm(3)/kg, the second group received 1.5mEq/kg KCl without CaCl, and the third group received placebo infusions. Ten minutes post VF initiation, defibrillation was performed, as appropriate, followed by ACLS for continued arrest or observation for 30min if ROSC. AMSA change from before to 5min post study drug infusion was compared with nonparametric statistics. MAP post ROSC was compared using mixed linear regression analysis.
resultsAverage normalized AMSA change was -0.15, -0.63, and +0.27 in the KCl, KCl+CaCl, and placebo groups, respectively (p=0.01). Three KCl+CaCl animals developed on organized rhythm chemically without electrical defibrillation. One, 3, and 4 animals in the KCl, KCl+CaCl, and placebo groups, respectively, survived post ROSC. Post ROSC, MAP decreased 1.8mmHg (95% CI -1.4 to 5.1) min(-1) less in the KCl+CaCl group compared to placebo.
conclusionsChemical defibrillation and ROSC are possible post potassium-induced asystole. Potassium followed by calcium reversal, but not potassium alone, led to ROSC and post-ROSC hemodynamics comparable to recommended therapy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.