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1.
J Telemed Telecare ; : 1357633X221124175, 2022 Sep 06.
Artículo en Inglés | MEDLINE | ID: mdl-36066025

RESUMEN

INTRODUCTION: Isolated spaces impair communication and teamwork during tracheal intubation (TI) in suspected coronavirus disease 2019 patients. We thus aimed to evaluate the telemedicine-assisted airway model (TAM) to improve communication and teamwork during the pandemic. METHODS: This two-stage prospective study included adult patients intubated in the emergency department of the National Taiwan University Hospital between 1 August 2020 and 31 July 2021. First, we randomised patients receiving TI in the standard setting into the conventional group (Con-G) and the isolation area into the isolation group (Iso-G). We evaluated the obstacles to communication and teamwork in an isolation scenario. Second, we developed the TAM to facilitate communication and teamwork between staff in separate spaces during TI and assigned patients to the TAM group (TAM-G). Communication and teamwork were evaluated using the Team Emergency Assessment Measure (TEAM). Subjective evaluations were conducted using a questionnaire administered to medical staff. RESULTS: Eighty-nine patients were enrolled: 17, 34, and 38 in the Con-G, Iso-G, and TAM-G, respectively. The communication frequency (CF) of the Con-G and Iso-G was the highest and lowest, respectively. The CF of the TAM-G increased and approached that of the Con-G. The overall TEAM score was the highest in the Con-G and the lowest in the Iso-G, while the overall score in the TAM-G was comparable to that of the Con-G. DISCUSSION: The TAM may improve communication and teamwork for TIs without compromising efficacy during the pandemic. This study was registered at ClinicalTrials.gov; registration numbers: NCT04479332 and NCT04591873.

2.
PLoS One ; 17(2): e0264165, 2022.
Artículo en Inglés | MEDLINE | ID: mdl-35176110

RESUMEN

BACKGROUND: Myocardial dysfunction is a major cause of poor outcomes in the post-cardiac arrest period. Omecamtiv mecarbil (OM) is a selective small molecule activator of cardiac myosin that prolongs myocardial systole and increases stroke volume without apparent effects on myocardial oxygen demand. OM administration is safe and improves cardiac function in patients with acute heart failure. Whether OM improves post-resuscitation myocardial dysfunction remains unclear. This study investigated the effect of OM treatment on post-resuscitation myocardial dysfunction and outcomes. METHODS AND RESULTS: Adult male rats were resuscitated after 9.5 min of asphyxia-induced cardiac arrest. OM and normal saline was continuously intravenously infused after return of spontaneous circulation (ROSC) at 0.25 mg/kg/h for 4 h in the experimental group and control group, respectively (n = 20 in each group). Hemodynamic parameters were measured hourly and monitored for 4 h after cardiac arrest. Recovery of neurological function was evaluated by neurological functioning scores (0-12; favorable: 11-12) for rats 72 h after cardiac arrest. OM treatment prolonged left ventricular ejection time and improved post-resuscitation cardiac output. Post-resuscitation heart rate and left ventricular systolic function (dp/dt40) were not different between groups. Kaplan-Meier analysis showed non-statistically higher 72-h survival in the OM group (72.2% [13/18] and 58.8% [10/17], p = 0.386). The OM group had a higher chance of having favorable neurological outcomes in surviving rats 72 h after cardiac arrest (84.6% [11/13] vs. 40% [4/10], p = 0.026). The percentage of damaged neurons was lower in the OM group in a histology study at 72 h after cardiac arrest (55.5±2.3% vs. 76.2±10.2%, p = 0.004). CONCLUSIONS: OM treatment improved post-resuscitation myocardial dysfunction and neurological outcome in an animal model. These findings support further pre-clinical studies to improve outcomes in post-cardiac arrest care.


Asunto(s)
Reanimación Cardiopulmonar/efectos adversos , Paro Cardíaco/complicaciones , Contracción Miocárdica/efectos de los fármacos , Enfermedades del Sistema Nervioso/prevención & control , Urea/análogos & derivados , Disfunción Ventricular/prevención & control , Función Ventricular Izquierda/efectos de los fármacos , Animales , Masculino , Enfermedades del Sistema Nervioso/etiología , Ratas , Ratas Wistar , Volumen Sistólico , Urea/farmacología , Disfunción Ventricular/etiología
3.
J Am Heart Assoc ; 10(10): e019837, 2021 05 18.
Artículo en Inglés | MEDLINE | ID: mdl-33960200

RESUMEN

Background Steroid use after cardiac arrest has been reported to improve survival and neurological outcome in cardiac arrest survivors. The study aimed to evaluate the effect of post-arrest hydrocortisone use on myocardial damage and cardiac mitochondrial injury in a rat model of ventricular fibrillation cardiac arrest. Methods and Results Ventricular fibrillation cardiac arrest was induced and left untreated for 5 minutes in adult male Wistar rats. Cardiopulmonary resuscitation and electric shocks were then applied to achieve return of spontaneous circulation (ROSC). Successfully resuscitated animals were randomized into 3 groups: control, low-dose hydrocortisone (2 mg/kg), and high-dose hydrocortisone (8 mg/kg). The low-dose hydrocortisone and high-dose hydrocortisone (treatment) groups received intravenous hydrocortisone immediately after ROSC and the control group received saline as placebo. Each group consisted of 15 animals. Within 4 hours of ROSC, both treatment groups showed a higher cardiac output than the control group. At the fourth hour following ROSC, histological examination and transmission electron microscopy demonstrated less myocardial damage and mitochondrial injury in the animals treated with hydrocortisone. In the treatment groups, hydrocortisone mitigated the acceleration of Ca2+-induced mitochondrial swelling and suppression of complex activity observed in the control group. At the 72nd hour after ROSC, a significantly higher proportion of animals treated with hydrocortisone survived and had good neurological recovery compared with those given a placebo. Conclusions Hydrocortisone use after cardiac arrest may mitigate myocardial injury and cardiac mitochondrial damage and thus improve survival, neurological and histological outcomes in a rat model of ventricular fibrillation cardiac arrest.


Asunto(s)
Paro Cardíaco/prevención & control , Hidrocortisona/farmacología , Mitocondrias Cardíacas/efectos de los fármacos , Fibrilación Ventricular/complicaciones , Animales , Antiinflamatorios/farmacología , Modelos Animales de Enfermedad , Paro Cardíaco/etiología , Paro Cardíaco/patología , Masculino , Mitocondrias Cardíacas/metabolismo , Mitocondrias Cardíacas/patología , Ratas , Ratas Wistar , Fibrilación Ventricular/tratamiento farmacológico , Fibrilación Ventricular/patología
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