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Published on: January 5, 2018
Intra-aortic adrenaline titration during cardiac arrest
James E Manning1, Ed B G Barnard2,3, Jon Barratt4
1Department of Emergency Medicine, CB 7594, University of North Carolina at Chapel Hill School of Medicine, 170 Manning Drive, Chapel Hill, NC, 27599, USA. jmanning@med.unc.edu.
Abstract:
Adrenaline has been the principal vasoactive drug in cardiac arrest for decades. It reliably increases return of spontaneous circulation but has not shown a consistent improvement in long-term survival with favourable neurological outcome. High cumulative doses are associated with poorer neurological outcomes among survivors. Unreliable systemic delivery of intravenous adrenaline during the low-flow state of cardiopulmonary resuscitation (CPR) may be responsible for this disconnect. When return of spontaneous circulation follows multiple doses, abrupt mobilisation of accumulated adrenaline may be deleterious and contribute to post-resuscitation shock. We describe the "Adrenaline Dilemma": patients with the lowest coronary perfusion pressure are most in need of vasoconstriction to improve blood flow, yet they are also those in whom intravenous adrenaline is least likely to circulate promptly; conversely, patients with adequate coronary perfusion pressure may be exposed to excessive dosing. Thoracic aortic catheterisation via femoral arterial access provides rapid systemic arterial drug delivery and real-time haemodynamic feedback. Continuous aortic pressure monitoring allows optimisation of CPR mechanics and rapid titration of intra-aortic adrenaline as small, diluted boluses or continuous infusion targeting an observed physiological endpoint. Preclinical experiments and early prehospital clinical experience have shown favourable results. Haemodynamically guided intra-aortic adrenaline administration during CPR is a plausible, testable endovascular adjunct and warrants prospective evaluation within modern resuscitation pathways.
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