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Defibrillation is accomplished by the passage of sufficient current through the heart to terminate ventricular fibrillation (VF). Although current-based defibrillation has been shown to be superior to energy-based defibrillation with monophasic waveforms, defibrillators with biphasic waveforms still use energy as a therapeutic dosage. In the present study, we propose a novel framework of current-based, biphasic defibrillation grounded in transthoracic impedance (TTI) measurements: adjusting the charging voltage to deliver the desired current based on the energy setting and measured pre-shock TTI; and adjusting the pulse duration to deliver the desired energy based on the output current and intra-shock TTI. The defibrillation efficacy of current-based defibrillation was compared with that of energy-based defibrillation in a simulated high impedance rabbit model of VF. Cardiac arrest was induced by pacing the right ventricle for 60 s in 24 New Zealand rabbits (10 males). A defibrillatory shock was applied with one of the two defibrillators after 90 s of VF. The defibrillation thresholds (DFTs) at different pathway impedances were determined utilizing a 5-step up-and-down protocol. The procedure was repeated after an interval of 5 min. A total of 30 fibrillation events and defibrillation attempts were investigated for each animal. The pulse duration was significantly shorter, and the waveform tilt was much lower for the current-based defibrillator. Compared with energy-based defibrillation, the energy, peak voltage, and peak current DFT were markedly lower when the pathway impedance was > 120 Ω, but there were no differences in DFT values when the pathway impedance was between 80 and 120 Ω for current-based defibrillation. Additionally, peak voltage and the peak current DFT were significantly lower for current-based defibrillation when the pathway impedance was < 80 Ω. In sum, a framework of adjusting the charging voltage and shock duration to deliver constant energy for low impedance and constant current for high impedance via pre-shock and intra-shock impedance measurements, greatly improved the defibrillation efficacy of high impedance by lowering the energy DFT. [ABSTRACT FROM AUTHOR]

Background. Electroencephalography (EEG) is commonly used to assess the neurological prognosis of comatose patients after cardiac arrest (CA). However, the early prognostic accuracy of EEG may be affected by postresuscitation interventions. Recent animal studies found that hydrogen inhalation after CA greatly improved neurological outcomes by selectively neutralizing highly reactive oxidants, but the effect of hydrogen inhalation on EEG recovery and its prognostication value are still unclear. The present study investigated the effects of hydrogen inhalation on early postresuscitation EEG characteristics in an asphyxial CA rat model. Methods. Cardiopulmonary resuscitation was initiated after 5 min of untreated CA in 40 adult female Sprague-Dawley rats. Animals were randomized for ventilation with 98% oxygen plus 2% hydrogen (H2) or 98% oxygen plus 2% nitrogen (Ctrl) under normothermia for 1 h. EEG characteristics were continuously recorded for 4 h, and the relationships between quantitative EEG characteristics and 96 h neurological outcomes were investigated. Results. No differences in baseline and resuscitation data were observed between groups, but the survival rate was significantly higher in the H2 group than in the Ctrl group (90% vs. 40%, P<0.01). Compared to the Ctrl group, the H2 group showed a shorter burst onset time (21.85 [20.00–23.38] vs. 25.70 [22.48–30.05], P<0.01) and time to normal trace (169.83 [161.63–208.55] vs. 208.39 [186.29–248.80], P<0.01). Additionally, the burst suppression ratio (0.66 ± 0.09 vs. 0.52 ± 0.17, P<0.01) and weighted‐permutation entropy (0.47 ± 0.16 vs. 0.34 ± 0.13, P<0.01) were markedly higher in the H2 group. The areas under the receiver operating characteristic curves for the 4 EEG characteristics in predicting survival were 0.82, 0.84, 0.88, and 0.83, respectively. Conclusions. In this asphyxial CA rat model, the improved postresuscitation EEG characteristics for animals treated with hydrogen are correlated with the better 96 h neurological outcome and predicted survival. [ABSTRACT FROM AUTHOR]

Cardiac arrest leads to sudden cessation of oxygen supply and cerebral hypoxia occurs when there is not sufficient oxygen supplied to the brain. Current Guidelines for adult cardiopulmonary resuscitation (CPR) and emergency cardiovascular care recommend the use of 100% oxygen during resuscitative efforts to maximize the probability of achieving the return of spontaneous circulation (ROSC). However, the optimal strategy for oxygen management after ROSC is still debatable. The aim of the present study was to evaluate the effects of the duration of post-resuscitation hyperoxic ventilation on neurological outcomes in asphyxial cardiac arrest rats treated with targeted temperature management (TTM). Asphyxia was induced by blocking the endotracheal tube in 80 adult male Sprague-Dawley rats. CPR begun after 7 min of untreated cardiac arrest. Animals were randomized to either the normoxic control under normothermia (NNC) group or to one of the 4 experimental groups (n = 16 each) immediately after ROSC: ventilated with 100% oxygen for 0 (O2_0h), 1 (O2_1h), 3 (O2_3h), or 5 (O2_5h) h and ventilated with room air thereafter under TTM. Physiological variables were recorded at baseline and during the 6 h postresuscitation monitoring period. Animals were closely observed for 96 h to assess neurologic recovery and survival. There were no significant differences in baseline measurements between groups, and all animals were successfully resuscitated. There were significant interactions between the duration of 100% oxygen administration and hemodynamics as well as, myocardial and cerebral injuries. Among all the durations of hyperoxic ventilation investigated, significantly lower neurological deficit scores and higher survival rates were observed in the O2_3h group than in the NNC group. In conclusion, postresuscitation hyperoxic ventilation leads to improved PaO2, PaCO2, hemodynamic, myocardial and cerebral recovery in asphyxial cardiac arrest rats treated with TTM. However, the beneficial effects of high concentration-oxygen are duration dependent and ventilation with 100% oxygen during induced hypothermia contributes to improved neurological recovery and survival after 96 h. [ABSTRACT FROM AUTHOR]