Abstract
BackgroundThe effectiveness of adrenaline during resuscitation continues to be debated despite being recommended in international guidelines. There is evidence that the β-adrenergic receptor (AR) effects of adrenaline are harmful due to increased myocardial oxygen consumption, post-defibrillation ventricular arrhythmias and increased severity of post-arrest myocardial dysfunction. Esmolol may counteract these unfavourable β-AR effects and thus preserve post-arrest myocardial function. We evaluated whether a single dose of esmolol administered prior to adrenaline preserves post-arrest cardiac output among successfully resuscitated animals in a novel, ischaemic cardiac arrest porcine model.MethodsMyocardial infarction was induced in 20 anaesthetized pigs by inflating a percutaneous coronary intervention (PCI) balloon in the circumflex artery 15 min prior to induction of ventricular fibrillation. After 10 min of untreated VF, resuscitation with veno-arterial extracorporeal membrane oxygenation (VA-ECMO) was initiated and the animals were randomized to receive an injection of either 1 mg/kg esmolol or 9 mg/ml NaCl, prior to adrenaline. Investigators were blinded to allocation. Successful defibrillation was followed by a 1-h high-flow VA-ECMO before weaning and an additional 1-h stabilization period. The PCI-balloon was deflated 40 min after inflation. Cardiac function pre- and post-arrest (including cardiac output) was assessed by magnetic resonance imaging (MRI) and invasive pressure measurements. Myocardial injury was estimated with MRI, triphenyl tetrazolium chloride (TTC) staining and serum concentrations of cardiac troponin T.ResultsOnly seven esmolol and five placebo-treated pigs were successfully resuscitated and available for post-arrest measurements (p = 0.7). MRI revealed severe but similar reductions in post-arrest cardiac function with cardiac output 3.5 (3.3, 3.7) and 3.3 (3.2, 3.9) l/min for esmolol and control (placebo) groups, respectively (p = 0.7). The control group had larger left ventricular end-systolic and end-diastolic ventricular volumes compared to the esmolol group (75 (65, 100) vs. 62 (53, 70) ml, p = 0.03 and 103 (86, 124) vs. 87 (72, 91) ml, p = 0.03 for control and esmolol groups, respectively). There were no other significant differences in MRI characteristics, myocardial infarct size or other haemodynamic measurements between the two groups.ConclusionsWe observed similar post-arrest cardiac output with and without a single dose of esmolol prior to adrenaline administration during low-flow VA-ECMO in an ischaemic cardiac arrest pig model.
Highlights
The effectiveness of adrenaline during resuscitation continues to be debated despite being recommended in international guidelines
The esmolol group consisted of six males and four females with average weight 48 kg, and placebo group seven males and three females with average weight 48 kg
Post-arrest cardiac function All animals had significantly reduced cardiac function post-arrest, but there were no significant differences in our primary outcome, cardiac output, between the esmolol and placebo groups (3.5 (3.3, 3.7) vs. 3.3, respectively, p = 0.7)
Summary
The effectiveness of adrenaline during resuscitation continues to be debated despite being recommended in international guidelines. There is evidence that the β-adrenergic receptor (AR) effects of adrenaline are harmful due to increased myocardial oxygen consumption, post-defibrillation ventricular arrhythmias and increased severity of post-arrest myocardial dysfunction. Randomized controlled trials on adrenaline have confirmed the drug’s ability to improve ROSC rates, but have largely failed to translate the large improvements in ROSC into long-term survival with good neurological outcome [7,8,9] It is questioned whether the coveted α-AR effects are negated by unwanted β–AR effects, such as increased myocardial oxygen consumption [10], post-arrest ventricular arrhythmias [11, 12] and post-arrest myocardial dysfunction [13, 14]. Counteracting β–AR stimulation with a β–AR antagonist has been shown to be cardioprotective, anti-arrhythmic and increase ROSC in experimental models where adrenaline has been administered during cardiopulmonary resuscitation (CPR) [15,16,17,18,19,20,21]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
