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Background: Recent studies describe an emerging role for percutaneous left ventricular assist devices such as Impella CP® as rescue therapy for refractory cardiac arrest. We hypothesized that the addition of mechanical chest compressions to percutaneous left ventricular assist device assisted CPR would improve hemodynamics by compressing the right ventricle and augmenting pulmonary blood flow and left ventricular filling. We performed a pilot study to test this hypothesis using a swine model of prolonged cardiac arrest. Methods: Eight Yorkshire swine were anesthetized, intubated, and instrumented for hemodynamic monitoring. They were subjected to untreated ventricular fibrillation for 5.75 (SD 2.90) minutes followed by mechanical chest compressions for a mean of 20.0 (SD 5.0) minutes before initiation of percutaneous left ventricular assist device. After percutaneous left ventricular assist device initiation, mechanical chest compressions was stopped (n = 4) or continued (n = 4). Defibrillation was attempted 4, 8 and 12 minutes after initiating percutaneous left ventricular assist device circulatory support. Results: The percutaneous left ventricular assist device + mechanical chest compressions group had significantly higher percutaneous left ventricular assist device flow prior to return of spontaneous heartbeat at four- and twelve-minutes after percutaneous left ventricular assist device initiation, and significantly higher end tidal CO2 at 4-minutes after percutaneous left ventricular assist device initiation, when compared with the percutaneous left ventricular assist device alone group. Carotid artery flow was not significantly different between the two groups. Conclusion: The addition of mechanical chest compressions to percutaneous left ventricular assist device support during cardiac arrest may generate higher percutaneous left ventricular assist device and carotid artery flow prior to return of spontaneous heartbeat compared to percutaneous left ventricular assist device alone. Further studies are needed to determine if this approach improves other hemodynamic parameters or outcomes after prolonged cardiac arrest.

Aim: To evaluate coagulofibrinolytic abnormalities and the effects of ART-123 (recombinant human thrombomodulin alpha) in a porcine model of cardiac arrest and prolonged cardiopulmonary resuscitation (CA/CPR). Methods: Fifteen pigs (n = 5 per group) underwent 8 minutes of no-flow CA followed by 50 minutes of mechanical CPR, while 2 pigs underwent sham arrest. CA/CPR animals were randomized to receive saline or 1 mg/kg ART-123 pre-arrest (5 minutes prior to ventricular fibrillation) or post-arrest (2 minutes after initiation of CPR). Arterial and venous blood samples were drawn at multiple time points for blood gas analysis and measurement of plasma and whole blood markers of coagulation and fibrinolysis. Results: In saline-treated CA/CPR, but not sham animals, robust and persistent activation of coagulation and fibrinolysis was observed throughout resuscitation. After 50 minutes of CPR, plasma tests and thromboelastography indicated a mix of hypercoagulability and consumptive coagulopathy. ART-123 had a robust anticoagulant effect, reducing both thrombin-antithrombin (TAT) complexes and d-dimer (p

The Wolf Creek Conference, initiated in 1975, is a well-established tradition providing a unique forum for robust intellectual exchange between thought leaders and scientists from academia and industry focused on advancing the science and practice of cardiac arrest resuscitation. The Wolf Creek XVII Conference was hosted by the Max Harry Weil Institute for Critical Care Research and Innovation in Ann Arbor, Michigan, USA on June 15–17, 2023. A major focus of the conference proceedings was to identify and prioritize the knowledge gaps, barriers to translation, and research priorities for six major domains in the field of resuscitation: (1) automated cardiac arrest diagnosis, (2) amplifying lay-responder response, (3) mobile AEDs, (4) physiology-guided CPR, (5) extracorporeal support, and (6) neuroprotection. In addition, industry scientists were given the opportunity to present and discuss cutting edge innovations. Finally, building off of the conference’s theme of “The Future of Cardiac Arrest Resuscitation”, the Weil Institute introduced the “Wolf Creek Innovator in Cardiac Arrest and Resuscitation Award” to recognize early career investigators who were challenging current paradigms in resuscitation science. Similar to the early Wolf Creek Conferences, the goal was to fuel active discussion and debate among leading experts to determine where future research efforts should be focused. This manuscript provides an overview of the Wolf Creek XVII conference, and the individual manuscripts within this special edition of Resuscitation Plus describe the conference proceedings and outcomes in more detail. It is our intent that these publications will provide a roadmap for important academic and commercial advances in the field of cardiac arrest resuscitation.

The Wolf Creek Conference is a seminal meeting of resuscitation researchers that has significantly influenced scientific advances and patient care in the field of cardiac arrest resuscitation over nearly half a century. Originating in 1975 at the Wolf Creek Lodge in Georgia, the conference was founded by Drs. James Elam, James Jude, and Peter Safar with the aim of improving clinical practices in cardiopulmonary resuscitation (CPR) by stimulating laboratory and clinical research. Over 17 conferences to date, the scope has broadened to encompass the growing field of resuscitation science, participation has expanded to include thought leaders and scientists from both academia and industry, and the proceedings have catalyzed numerous innovations in field. This narrative review highlights the genesis, objectives, proceedings, and impact of the Wolf Creek Conference from 1975 to the present.

Aim: High-dose valproic acid (VPA) improves the survival and neurologic outcomes after asphyxial cardiac arrest (CA) in rats. We characterized the pharmacokinetics, pharmacodynamics, and safety of high-dose VPA in a swine CA model to advance clinical translation. Methods: After 8 ​min of untreated ventricular fibrillation CA, 20 male Yorkshire swine were resuscitated until return of spontaneous circulation (ROSC). They were block randomized to receive placebo, 75 ​mg/kg, 150 ​mg/kg, or 300 ​mg/kg VPA as 90-min intravenous infusion (n ​= ​5/group) beginning at ROSC. Animals were monitored for 2 additional hours then euthanized. Experimental operators were blinded to treatments. Results: The mean(SD) total CA duration was 14.8(1.2) minutes. 300 ​mg/kg VPA animals required more adrenaline to maintain mean arterial pressure ≥80 ​mmHg and had worse lactic acidosis. There was a strong linear correlation between plasma free VPA Cmax and brain total VPA (r2 ​= ​0.9494; p ​