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Introduction: Failure to restore spontaneous circulation remains a major cause of death for cardiac arrest (CA) patients. Mechanical circulatory support, specifically extracorporeal cardiopulmonary resuscitation (ECPR), has emerged as a feasible and efficacious rescue strategy for selected refractory CA patients. Methods: Mechanical Circulatory Support was one of six focus topics for the Wolf Creek XVII Conference held on June 14-17, 2023 in Ann Arbor, Michigan, USA. Conference invitees included international thought leaders and scientists in the field of CA resuscitation from academia and industry. Participants submitted via online survey knowledge gaps, barriers to translation and research priorities for each focus topic. Expert panels used the survey results and their own perspectives and insights to create and present a preliminary unranked list for each category that was debated, revised and ranked by all attendees to identify the top 5 for each category. Results: Top 5 knowledge gaps included optimal patient selection, pre-ECPR treatments, logistical and programmatic characteristics of ECPR programs, generalizability and effectiveness of ECPR, and prevention of reperfusion injury. Top 5 barriers to translation included cost/resource limitations, technical challenges, collaboration across multiple disciplines, limited patient population, and early identification of eligible patients. Top 5 research priorities focused on comparing the outcomes of prehospital/rapid transport strategies vs in-hospital ECPR initiation, implementation of high-performing ECPR system vs standard care, rapid patient identification tools vs standard clinical judgment, post-cardiac arrest bundled care vs no bundled care, and standardized ECPR clinical protocol vs routine care. Conclusion: This overview can serve as an innovative guide to transform the care and outcome of patients with refractory CA.
RESUMO
OBJECTIVE: To determine the effects of ventricular pacing on the normal contraction sequence of the helical ventricular myocardial band, and its' impact on left ventricular function. METHODS: Ten pigs (25-68 kg) underwent analysis of percent segmental shortening (%SS) by sonomicrometry, with crystals placed along the fiber orientation of the ascending and descending segments, and posterior LV wall of the geometry of the helical heart. Unipolar pacing electrodes stimulated either the right atrium (RA), right ventricular apex (RVA) and outflow tract (RVOT), or posterior LV wall. Systemic hemodynamics, QRS-interval, cardiac index (CI), systolic and diastolic LV function and pressure-dimension (P-D) loops were analyzed and cardiac motion was monitored by video analysis. RESULTS: Normal sinus heart rate (NSR) was elevated from 84+/-15 beats/min to 113+/-22 beats/min by pacing (p<0.05). The variables of NSR were not changed by atrial pacing. Conversely, compared with NSR, ventricular pacing (RVA, RVOT, LV) significantly (p<0.05) prolonged the QRS-interval (94-111 ms vs 52+/-7 ms, p<0.05) decreased mean arterial pressure (46-47 mmHg vs 62+/-11 mmHg), CI (2.7-3.4 L/(min m2) vs 4.9+/-0.9L/(min m2)) and systolic LV pressure (56-61 mmHg vs 92+/-10 mmHg). Furthermore, ventricular pacing decreased peak +dP/dt and -dP/dt (p<0.05) and lowered PRSW to 59-77%, with most profound change after RVA pacing (p<0.05). Each ventricular pacing intervention decreased SS% significantly in the descending, ascending, and posterior LV segments compared with NSR. Disruption of the normal NSR sequence of shortening (progression from descending to posterior to ascending regions) followed each pacing intervention. Changes were characterized by premature stimulation of the segment adjacent to the pacer stimulus, with associated (1) decrease of pressure-dimension loop area, (2) desynchronization of P-D loops and (3) consistent loss of the twisting pattern of visible cardiac motion. CONCLUSIONS: Ventricular pacing disrupts the natural sequence of shortening along the myocardial band, and the resultant dyssynchrony impairs LV function.