3% children had potential over-compression (RICD < 10 mm). 4 cm simulated chest compressions led to 18% (95% CI 13%-24%) of infants with potential over-compression, and this increased to 34% (95% CI 27%-41%) at 4.4 cm (upper limit of "approximately" 4 cm; 4 cm + 10%). 5 cm simulated compressions resulted in 8% (95% CI 4%-12%) of children 1 to 8-years-old with potential over-compression, and this increased to 22% (95% CI 16%-28%) at 5.5 cm (upper limit of "approximately" 5 cm, 5 cm + 10%). In settings whereby chest compression depths can be accurately measured, compressions at the current recommended chest compression of approximately 4 cm (in infants) and 5 cm (in young children) could result in potential for over-compression. In settings whereby chest compression depths can be accurately measured, compressions at the current recommended chest compression of approximately 4 cm (in infants) and 5 cm (in young children) could result in potential for over-compression. Formation of cerebral edema and cardiovascular dysfunction may worsen brain injury following cardiac arrest. We hypothesized that administration of the intermediate calcium-activated potassium (KCa3.1) channel blocker, senicapoc, would reduce cerebral edema and augment mean arterial pressure in the early post-resuscitation period. Male Sprague-Dawley rats, aged 11-15 weeks, were utilized in the study. Rats were exposed to 8 min of asphyxial cardiac arrest. Shortly after resuscitation, rats were randomized to receive either vehicle or senicapoc (10 mg/kg) intravenously. The primary outcome was cerebral wet to dry weight ratio 4 h after resuscitation. Secondary outcomes included mean arterial pressure, cardiac output, norepinephrine dose, inflammatory cytokines and neuron specific enolase levels. Additionally, a sub-study was conducted to validate intravenous administration of senicapoc. The sub-study revealed that senicapoc-treated rats maintained a significantly higher mean arterial pressure during administration of SKA-31 (a KCa3.1 channel opener).The plasma concentration of senicapoc was 1060 ± 303 ng/ml 4 h after administration. Senicapoc did not reduce cerebral edema or augment mean arterial pressure 4 h after resuscitation. Likewise, cardiac function and norepinephrine dose did not vary between groups. Inflammatory cytokines and neuron specific enolase levels increased in both groups after resuscitation with no difference between groups. Senicapoc enhanced the PaO /FiO ratio significantly 4 h after resuscitation. Senicapoc was successfully administered intravenously after resuscitation, but did not reduce cerebral edema or increase mean arterial pressure in the early post-resuscitation period. Senicapoc was successfully administered intravenously after resuscitation, but did not reduce cerebral edema or increase mean arterial pressure in the early post-resuscitation period. Pseudo-pulseless electrical activity (pseudo-PEA) is a global hypotensive ischemic state with retained coordinated myocardial contractile activity and an organized ECG with no clinically detectable pulses. The role of standard external chest compressions (CPR) and its associated intrinsic hemodynamics remains unclear in the setting of pseudo-PEA. We undertook an experimental trial to compare epinephrine alone versus epinephrine with CPR in the treatment of pseudo-PEA. Using a porcine model of hypoxic pseudo-PEA, we randomized 12 Yorkshire male swine to resuscitation with epinephrine only (control) (0.0015 mg/kg) versus epinephrine plus standard CPR (intervention). Animals who achieved return of spontaneous circulation (ROSC) were stabilized, fully recovered to hemodynamic and respiratory baseline, and rearrested up to 6 times. Primary outcome was ROSC defined as a sustained systolic blood pressure (SBP) of 60 mmHg for 2 min. Secondary outcomes included time to ROSC, coronary perfusion pressure (CoPP), and end-tidal carbon dioxide (ETCO ). Among 47 events of pseudo-PEA in 12 animals, we observed significantly higher proportion of ROSC when treatment included CPR (14/21 - 67%) compared to epinephrine alone (4/26 - 15%) (p = 0.0007). CoPP, aortic pressures and ETCO were significantly higher, and right atrial pressures were lower in the intervention group. In a swine model of hypoxia-induced pseudo-PEA, epinephrine plus CPR was associated with improved intra-arrest hemodynamics and higher probability of ROSC. https://www.selleckchem.com/products/abt-199.html Thus, epinephrine plus CPR may be superior to epinephrine alone in the treatment of patients with pseudo-PEA. In a swine model of hypoxia-induced pseudo-PEA, epinephrine plus CPR was associated with improved intra-arrest hemodynamics and higher probability of ROSC. Thus, epinephrine plus CPR may be superior to epinephrine alone in the treatment of patients with pseudo-PEA. Automated real-time feedback devices have been considered a potential tool to improve the quality of cardiopulmonary resuscitation (CPR). Despite previous studies supporting the usefulness of such devices during training, others have conflicting conclusions regarding its efficacy during real-life CPR. This systematic review aimed to assess the effectiveness of automated real-time feedback devices for improving CPR performance during training, simulation and real-life resuscitation attempts in the adult and paediatric population. Articles published between January 2010 and November 2020 were searched from BVS, Cinahl, Cochrane, PubMed and Web of Science, and reviewed according to a pre-defined set of eligibility criteria which included healthcare providers and randomised controlled trial studies. CPR quality was assessed based on guideline compliance for chest compression rate, chest compression depth and residual leaning. The selection strategy led to 19 eligible studies, 16 in training/simulation and three in real-life CPR. Feedback devices during training and/or simulation resulted in improved acquisition of skills and enhanced performance in 15 studies. One study resulted in no significant improvement. During real resuscitation attempts, three studies demonstrated significant improvement with the use of feedback devices in comparison with standard CPR (without feedback device). The use of automated real-time feedback devices enhances skill acquisition and CPR performance during training of healthcare professionals. Further research is needed to better understand the role of feedback devices in clinical setting. The use of automated real-time feedback devices enhances skill acquisition and CPR performance during training of healthcare professionals. Further research is needed to better understand the role of feedback devices in clinical setting.