Sudden cardiac arrest is a leading cause of death in the United States. The neurophysiological mechanism underlying sudden death is not well understood. Previously we have shown that the brain is highly stimulated in dying animals and that asphyxia-induced death could be delayed by blocking the intact brain-heart neuronal connection. These studies suggest that the autonomic nervous system plays an important role in mediating sudden cardiac arrest. In this study, we tested the effectiveness of phentolamine and atenolol, individually or combined, in prolonging functionality of the vital organs in CO2-mediated asphyxic cardiac arrest model. Rats received either saline, phentolamine, atenolol, or phentolamine plus atenolol, 30 min before the onset of asphyxia. Electrocardiogram (ECG) and electroencephalogram (EEG) signals were simultaneously collected from each rat during the entire process and investigated for cardiac and brain functions using a battery of analytic tools. We found that adrenergic blockade significantly suppressed the initial decline of cardiac output, prolonged electrical activities of both brain and heart, asymmetrically altered functional connectivity within the brain, and altered, bi-directionally and asymmetrically, functional, and effective connectivity between the brain and heart. The protective effects of adrenergic blockers paralleled the suppression of brain and heart connectivity, especially in the right hemisphere associated with central regulation of sympathetic function. Collectively, our results demonstrate that blockade of brain-heart connection via alpha- and beta-adrenergic blockers significantly prolonged the detectable activities of both the heart and the brain in asphyxic rat. The beneficial effects of combined alpha and beta blockers may help extend the survival of cardiac arrest patients.
Objective: To investigate whether implementation of a multidisciplinary airway team was associated with improvement in (1) rate of successful airway securement at first attempt; (2) time to secure airway; and (3) overall complication rate in patients with a difficult airway, as compared with usual care. Data Sources: Ovid Medline, Embase, Scopus, Cochrane Central, and CINAHL databases. Review Methods: Systematic review of literature on inpatient multidisciplinary team management of difficult airways, including all studies performed in inpatient settings, excluding studies of ventilator weaning, flight/military medicine, EXIT procedures, and simulation or educational studies. DistillerSR was used for article screening and risk of a bias assessment to evaluate article quality. Data was extracted on study design, airway team composition, patient characteristics, and clinical outcomes including airway securement, complications, and mortality. Results: From 5323 studies screened, 19 studies met inclusion criteria with 4675 patients. Study designs included 12 quality improvement projects, 6 cohort studies, and 1 randomized controlled trial. Four studies evaluated effect of multidisciplinary difficult airway teams on airway securement; all reported higher first attempt success rate with team approach. Three studies reported time to secure the difficult airways, all reporting swifter airway securement with team approach. The most common difficult airway complications were hypoxia, esophageal intubation, hemodynamic instability, and aspiration. Team composition varied, including otolaryngologists, anesthesiologists, intensivists, nurses, and respiratory care practitioners. Conclusion: Multidisciplinary difficult airway teams are associated with improved clinical outcomes compared to unstructured emergency airway management; however, studies have significant heterogeneity in team composition, algorithms for airway securement, and outcomes reported. Further evidence is necessary to define the clinical efficacy, cost-effectiveness, and best practices relating to implementing difficult airway teams in inpatient settings.
Sudden death is an important but underrecognized consequence of stroke. Acute stroke can disturb central control of autonomic function and result in cardiac dysfunction and sudden death. Previous study showed that bilateral common carotid artery ligation (BCCAL) in the spontaneously hypertensive stroke-prone rat strain (SHRSP) is a well-established model for forebrain ischemic sudden death. This study aims to investigate the temporal dynamic changes in electrical activities of the brain and heart and functional interactions between the two vital organs following forebrain ischemia. EEG and ECG signals were simultaneously collected from nine SHRSP and eight Wistar-Kyoto (WKY) rats. RR interval was analyzed to investigate the cardiac response to brain ischemia. EEG power and coherence (CCoh) analysis were conducted to study the cortical response. Corticocardiac coherence (CCCoh) and directional connectivity (CCCon) were analyzed to determine brain-heart connection. Heart rate variability (HRV) was analyzed to evaluate autonomic functionality. BCCAL resulted in 100% mortality in SHRSP within 14 h, whereas no mortality was observed in WKY rats. The functionality of both the brain and the heart were significantly altered in SHRSP compared with WKY rats after BCCAL. SHRSP, but not WKY rats, exhibited intermittent surge of CCCoh, which paralleled the elevated CCCon and reduced HRV, following the onset of ischemia until sudden death. Elevated brain-heart coupling invariably associated with the disruption of the autonomic nervous system and the risk of sudden death. This study may improve our understanding of the mechanism of forebrain ischemia-induced sudden death. NEW & NOTEWORTHY This study demonstrates a marked surge of corticocardiac coupling in rats dying from focal cerebral ischemia, consistent with our earlier data in rats exposed to fatal asphyxia. Since the bidirectional electrical signal coupling (corticocardiac coherence) and communication (corticocardiac connectivity) between the brain and the heart are only identified in dying animals, they could be used as potential biomarkers to predict the risk of sudden death.
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