The purpose of this study was to identify the relationship between the deeper and faster chest compressions suggested by the 2010 cardiopulmonary resuscitation guidelines and complications arising from chest compressions, using multi-detector computed tomography. We performed a retrospective analysis of prospective registry data. This study was conducted with in- and out-of-hospital cardiac arrest patients who underwent successful resuscitation in the emergency departments of two academic tertiary care centres from October 2006 to September 2010 (pre-2010 group) and from October 2011 to September 2015 (post-2010 group). We examined chest injuries related to chest compressions, classified as follows: rib fracture, sternal fracture, and other uncommon complications. We enrolled 185 patients in this study. The most frequent complication to occur in both groups was rib fracture: 27 (62.8%) and 112 (78.9%) patients in the pre-2010 and post-2010 groups, respectively (p = 0.03). However, we observed no statistical differences in sternum fracture, the second most common complication (p = 0.80). Retrosternal and mediastinal haematoma were not reported in the pre-2010 group but 13 patients (9.1%) in the post-2010 group were reported to have haematoma (p = 0.04). Nine serious, life-threatening complications occurred, all in the post-2010 group. Among the younger group (less than 65 years old), 8 (38.1%) patients in the pre-2010 group and 40 (64.5%) in the post-2010 group sustained rib fractures. The deeper and faster chest compressions for enhancing ROSC are associated with increased occurrence of complications. Additional studies are needed to compensate for the limitations of our study design. This study found that the 2010 guidelines, recommending deeper and faster chest compressions, led to an increased proportion of rib fractures and retrosternal and mediastinal haematoma.

Heart failure patients with pulmonary edema presenting to the emergency department (ED) require an effective approach to deliver sufficient oxygen and reduce the rate of intubation and mechanical ventilation in the ED; conventional oxygen therapy has proven ineffective in delivering enough oxygen to the tissues. We aimed to identify whether high-flow nasal cannula (HFNC) therapy over time improved the respiratory rate (RR), lactate clearance, and certain arterial blood gas (ABG) parameters, in comparison with conventional oxygen therapy, in patients with cardiogenic pulmonary edema. This prospective, multi-institutional, and interventional study (clinical trial, reference KCT0004578) conducted between 2016 and 2019 included adult patients diagnosed with heart failure within the previous year and pulmonary edema confirmed at admission. Patients were randomly assigned to the conventional or HFNC group and treated with the goal of maintaining oxygen saturation (SpO₂) ≥ 93. We obtained RR, SpO₂, lactate levels, and ABG parameters at baseline and 30 and 60 min after randomization. All parameters showed greater improvement with HFNC therapy than with conventional therapy. Significant changes in ABG parameters were achieved within 30 min. HFNC therapy could therefore be considered as initial oxygen therapy. Physicians may consider advanced ventilation if there is no significant improvement in ABG parameters within 30 min of HFNC therapy.

Currently, no effective therapy and potential target have been elucidated for preventing myocardial ischemia and reperfusion injury (I/R). We hypothesized that the administration of recombinant klotho (rKL) protein could attenuate the sterile inflammation in peri-infarct regions by inhibiting the extracellular release of high mobility group box-1 (HMGB1). This hypothesis was examined using a rat coronary artery ligation model. Rats were divided into sham, sham+ rKL, I/R, and I/R+ rKL groups (n = 5/group). Administration of rKL protein reduced infarct volume and attenuated extracellular release of HMGB1 from peri-infarct tissue after myocardial I/R injury. The administration of rKL protein inhibited the expression of pro-inflammatory cytokines in the peri-infarct regions and significantly attenuated apoptosis and production of intracellular reactive oxygen species by myocardial I/R injury. Klotho treatment significantly reduced the increase in the levels of circulating HMGB1 in blood at 4 h after myocardial ischemia. rKL regulated the levels of inflammation-related proteins. This is the first study to suggest that exogenous administration of rKL exerts myocardial protection effects after I/R injury and provides new mechanistic insights into rKL that can provide the theoretical basis for clinical application of new adjunctive modality for critical care of acute myocardial infarction.

BACKGROUND AND PURPOSE: The use of invasive cerebral angiography with CTA for active treatment of patients with suspected ischemic strokes has been increasing recently. This study aimed to identify the incidence of postcontrast acute kidney injury using baseline renal function when CTA and cerebral angiography were performed sequentially. MATERIALS AND METHODS: This retrospective observational study evaluated adults (18 years of age or older) with ischemic stroke who underwent CTA and cerebral angiography sequentially between 2010 and 2018. The incidence of postcontrast acute kidney injury was determined using the baseline estimated glomerular filtration rate. The value of the baseline estimated glomerular filtration rate at which the occurrence of postcontrast acute kidney injury increased was also determined. RESULTS: Postcontrast acute kidney injury occurred in 57/601 (9.5%) patients. Those with a baseline estimated glomerular filtration rate of <30 mL/min/1.73 m² showed a higher incidence of acute kidney injury. Age, chronic kidney disease, medication (nonsteroidal anti-inflammatory drugs, angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, β blockers, statins, and insulin) use following contrast media exposure, and serum albumin affected the incidence of postcontrast acute kidney injury. The incidence of postcontrast acute kidney injury increased when the baseline estimated glomerular filtration rate was <43 mL/min/1.73 m². CONCLUSIONS: Patients with low baseline renal function had the highest incidence of postcontrast acute kidney injury after CTA and cerebral angiography, but no fatal adverse effects were documented. Thus, patients suspected of having a stroke should be actively managed with respect to neurovascular function.

Background: The American Heart Association guidelines recommend switching chest compression providers at least every 2 min depending on their fatigue during cardiopulmonary resuscitation (CPR). Although the provider's heart rate is widely used as an objective indicator for detecting fatigue, the accuracy of this measure is debatable. Objectives: This study was designed to determine whether real-time heart rate is a measure of fatigue in compression providers. Study design: A simulation-based prospective interventional study including 110 participants. Methods: Participants performed chest compressions in pairs for four cycles using advanced cardiovascular life support simulation. Each participant's heart rate was measured using wearable healthcare devices, and qualitative variables regarding individual compressions were obtained from computerized devices. The primary outcome was correct depth of chest compressions. The main exposure was the change in heart rate, defined as the difference between the participant's heart rate during individual compressions and that before the simulation was initiated. Results: With a constant compression duration for one cycle, the overall accuracy of compression depth significantly decreased with increasing heart rate. Female participants displayed significantly decreased accuracy of compression depth with increasing heart rate (odds ratio [OR]: 0.97; 95% confidence interval [CI]: 0.95–0.98; P < .001). Conversely, male participants displayed significantly improved accuracy with increasing heart rate (OR: 1.03; 95% CI: 1.02–1.04; P < .001). Conclusion: Increasing heart rate could reflect fatigue in providers performing chest compressions with a constant duration for one cycle. Thus, provider rotation should be considered according to objectively measured fatigue during CPR.

Sudden cardiac arrest leads to a significantly increased risk of severe neurological impairment and higher mortality rates in survivors due to global brain tissue injury caused by prolonged whole-body ischemia and reperfusion. The brain undergoes various deleterious cascading events. Among these damaging mechanisms, neuroinflammation plays an especially crucial role in the exacerbation of brain damage. Clinical guidelines indicate that 33 °C and 36 °C are both beneficial for targeted temperature management (TTM) after cardiac arrest. To clarify the mechanistic relationship between TTM and inflammation in transient global ischemia (TGI) and determine whether 36 °C produces a neuroprotective effect comparable to 33 °C, we performed an experiment using a rat model. We found that TTM at 36 °C and at 33 °C attenuated neuronal cell death and apoptosis, with significant improvements in behavioral function that lasted for up to 72 h. TTM at 33 °C and 36 °C suppressed the propagation of inflammation including the release of high mobility group box 1 from damaged cells, the activation and polarization of the microglia, and the excessive release of activated microglia-induced inflammatory cytokines. There were equal neuroprotective effects for TTM at 36 °C and 33 °C. In addition, hypothermic complications and should be considered safe and effective after cardiac arrest.