Background: It is difficult to predict the return of spontaneous circulation (ROSC) during cardiopulmonary resuscitation (CPR). Cerebral tissue oxygen saturation during CPR, as measured by near-infrared spectroscopy (NIRS), is anticipated to predict ROSC. General markers of cerebral tissue oxygen saturation, such as the tissue oxygenation index (TOI), mainly reflect venous oxygenation, whereas pulse-wave cerebral tissue oxygen saturation (SnO₂), which represents hemoglobin oxygenation in the pulse wave within the cerebral tissue, is an index of arterial and venous oxygenation. Thus, SnO₂ may reflect arterial oxygenation to a greater degree than does TOI. Therefore, we conducted this study to verify our hypothesis that SnO₂ measured during CPR can predict ROSC. Methods: Cardiac arrest patients who presented at the Emergency Department of Yamagata University Hospital in Japan were included in this retrospective, observational study. SnO₂ and TOI were simultaneously measured at the patient’s forehead using an NIRS tissue oxygenation monitor (NIRO 200-NX; Hamamatsu Photonics, Japan). We recorded the initial, mean, and maximum values during CPR. We plotted receiver operating characteristic curves and calculated the area under the curve (AUC) to predict ROSC. Results: Forty-two patients were included. SnO₂ was significantly greater in the ROSC group than in the non-ROSC group in terms of the initial (37.5% vs 24.2%, p = 0.015), mean (44.6% vs 10.8%, p < 0.001), and maximum (79.7% vs 58.4%, p < 0.001) values. Although the initial TOI was not significantly different between the two groups, the mean (45.1% vs 36.8%, p = 0.018) and maximum (71.0% vs 46.3%, p = 0.001) TOIs were greater in the ROSC group than in the non-ROSC group. The AUC was 0.822 for the mean SnO₂ (95% confidence interval [CI]: 0.672–0.973; cut-off: 41.8%), 0.821 for the maximum SnO₂ (95% CI: 0.682–0.960; cut-off: 70.8%), and 0.809 for the maximum TOI (95% CI: 0.667–0.951; cut-off: 49.3%). Conclusion: SnO₂ values measured during CPR, including immediately after arrival at the emergency department, were higher in the ROSC group than in the non-ROSC group.

Hot springs, hot-water bathing, and saunas are widely practiced forms of acute heat exposure and are often perceived as health-promoting. However, emergency clinicians frequently encounter patients in whom these exposures precipitate syncope, hypotension, drowning/aspiration, heat-related illness, and renal or electrolyte disturbances. This narrative review integrates these modalities within a unified “acute heat exposure” framework and summarizes pathophysiology and clinical implications from an emergency medicine perspective. We searched PubMed/MEDLINE from inception to January 2026 using controlled vocabulary and free-text terms related to heat stress, thermoregulation, hot-water immersion, sauna exposure, and acute clinical outcomes; evidence was synthesized qualitatively. Across modalities, acute heat exposure induces shared physiological responses—peripheral vasodilation, relative hypovolemia, circulatory stress, and internal heat storage—that can trigger diverse emergency presentations. We classify acute heat exposure–related illness into four domains: (1) cardiovascular events, including syncope, hypotension, and arrhythmic/ischemic complications in vulnerable individuals; (2) the heat-illness spectrum from exhaustion to heat stroke with organ dysfunction; (3) renal and electrolyte disturbances related to dehydration and hypoperfusion; and (4) neurological and traumatic complications, including falls, drowning, and aspiration. This framework may support risk stratification, evaluation, management, and prevention after hot spring, hot bath, or sauna use.

Introduction: We report a rare survival case of accidental hypothermia (core temperature 20 °C) with cardiac arrest and an initial rhythm of asystole, in which neurological recovery to the point of verbal communication was achieved after extracorporeal cardiopulmonary resuscitation (ECPR) despite prolonged no-perfusion ( ≥ 30 min) and hypoperfusion times ( ≥ 117 min), reviewing the relevant literature. Case Presentation: A 78-year-old woman developed hypothermia while descending a snowy mountain and called emergency services at 13:53. Rescue was delayed and she was found around 18:00; she was handed over in asystole at 18:30. During ambulance transport, the rhythm changed to ventricular fibrillation (VF) and eight defibrillations were delivered. She arrived at the emergency department at 19:01 in cardiac arrest with VF; bladder temperature was 20 °C, with no evidence of trauma. Arterial blood gas analysis revealed mixed acidosis. Active surface rewarming and high-quality cardiopulmonary resuscitation (CPR) with intubation and mechanical ventilation were initiated. Veno-arterial extracorporeal membrane oxygenation (ECMO) was established 56 min after emergency department (ED) arrival. After rewarming to 35 °C, she was defibrillated to sinus rhythm. Targeted temperature management was continued for 48 h. ECMO was weaned on day 5 (62 h after initiation). Computed tomography (CT) on day 5 showed acute pancreatitis without hypoxic–ischemic brain injury. She was extubated on day 11, discontinued oxygen on day 16, and resumed oral intake on day 17. Brain magnetic resonance imaging (MRI) on day 36 demonstrated hypoxic encephalopathy with residual higher brain dysfunction. She was discharged on day 151 with a Cerebral Performance Category of 3. Conclusion: ECPR may be considered for cardiac arrest due to severe accidental hypothermia, even in patients presenting with asystole and prolonged no-perfusion or hypoperfusion times.