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Sodium Nitroprusside–Enhanced Cardiopulmonary Resuscitation Improves Blood Flow by Pulmonary Vasodilation Leading to Higher Oxygen Requirements

[Display omitted] •SNPeCPR improves coronary perfusion pressure, tissue perfusion, and carotid blood flow compared to epinephrine-based standard advanced cardiac life support.•In a porcine model of prolonged resuscitation, SNPeCPR was associated with decreased arterial oxygen saturation but improved...

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Bibliographic Details
Published in:JACC. Basic to translational science 2020-02, Vol.5 (2), p.183-192
Main Authors: Ripeckyj, Adrian, Kosmopoulos, Marinos, Shekar, Kadambari, Carlson, Claire, Kalra, Rajat, Rees, Jennifer, Aufderheide, Tom P., Bartos, Jason A., Yannopoulos, Demetris
Format: Article
Language:English
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Summary:[Display omitted] •SNPeCPR improves coronary perfusion pressure, tissue perfusion, and carotid blood flow compared to epinephrine-based standard advanced cardiac life support.•In a porcine model of prolonged resuscitation, SNPeCPR was associated with decreased arterial oxygen saturation but improved tissue oxygen delivery due to improvement in blood flow.•Oxygen supplementation led to alleviation of hypoxemia and maintenance of the SNPeCPR hemodynamic benefits.•Arterial oxygen saturation must be a safety endpoint that will be prospectively assessed in the first SNPeCPR clinical trial in humans. Sodium nitroprusside–enhanced cardiopulmonary resuscitation has shown superior resuscitation rates and neurologic outcomes in large animal models supporting the need for a randomized human clinical trial. This study is the first to show nonselective pulmonary vasodilation as a potential mechanism for the hemodynamic benefits. The pulmonary shunting that is created requires increased oxygen treatment, but the overall improvement in blood flow increases minute oxygen delivery to tissues. In this context, hypoxemia is an important safety endpoint and a 100% oxygen ventilation strategy may be necessary for the first human clinical trial.
ISSN:2452-302X
2452-302X
DOI:10.1016/j.jacbts.2019.11.010