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Background: Cardiac arrest remains one of the leading causes of death. After successful resuscitation of patients in cardiac arrest, post-cardiac arrest syndrome develops, part of it being an impaired cerebral blood flow autoregulation. Monitoring cerebral blood flow autoregulation after cardiac arrest is important for optimizing patient care and prognosticating patients' survival, yet remains a challenge. There are still gaps in clinical implications and everyday use. In this article, we present a systematic review of studies with different methods of monitoring cerebral blood flow autoregulation after non-traumatic cardiac arrest. Methods : A comprehensive literature search was performed from 1 June 2024 to 27 June 2024 by using multiple databases: PubMed, Web of Science, and the Cochrane Central Register of Controlled Trials. Inclusion criteria were studies with an included description of the measurement of cerebral blood flow autoregulation in adult patients after non-traumatic cardiac arrest. Results: A total of 16 studies met inclusion criteria. Our data show that the most used methods in the reviewed studies were near-infrared spectroscopy and transcranial Doppler. The most used mathematical methods for calculating cerebral autoregulation were cerebral oximetry index, tissue oxygenation reactivity index, and mean flow index. Conclusions: The use of various monitoring and mathematical methods for calculating cerebral blood flow autoregulation poses a challenge for standardization, validation, and daily use in clinical practice. In the future studies, focus should be considered on clinical validation and transitioning autoregulation monitoring techniques to everyday clinical practice, which could improve the survival outcomes of patients after cardiac arrest.

Background and Objectives : Survival with favorable neurologic outcomes after out-of-hospital cardiac arrest (OHCA) remains elusive. Post-cardiac arrest syndrome (PCAS) involves myocardial and neurological injury, ischemia-reperfusion response, and underlying pathology. Neurologic injury is a crucial determinant of survival and functional outcomes, with damage caused by free radicals among the responsible mechanisms. This study explores the feasibility of adding intravenous vitamin C to the treatment of OHCA survivors, aiming to mitigate PCAS. Vitamin C, a nutrient with antioxidative and free radical-scavenging properties, is often depleted in critically ill patients. Materials and Methods : This randomized, double-blinded trial was conducted at a tertiary-level university hospital with adult OHCA survivors. Participants received either standard care or the addition of 1.5 g of intravenous vitamin C every 12 h for eight consecutive doses. Neurologic injury was assessed using neuron-specific enolase (NSE) levels, with additional clinical and laboratory outcomes, such as enhanced neuroprognostication factors, inflammatory markers, and cardiac parameters. Results : NSE levels were non-significantly higher in patients who received vitamin C compared to the placebo group (55.05 µg/L [95% confidence interval (CI) 26.7-124.0] vs. 39.4 µg/L [95% CI 22.6-61.9], p > 0.05). Similarly, a non-significantly greater proportion of patients in the vitamin C group developed myoclonus in the first 72 h. We also observed a non-significantly shorter duration of mechanical ventilation, fewer arrhythmias, and reduced length of stay in the intensive care unit in the group of patients who received vitamin C ( p = 0.031). However, caution is warranted in interpretation of our results due to the small number of participants. Conclusions : Our findings suggest that intravenous vitamin C should not be used outside of clinical trials for OHCA survivors. Due to the small sample size and conflicting results, further research is needed to determine the potential role of vitamin C in post-cardiac arrest care.

Our core body temperature is held around [Formula: see text]C by an effective internal thermoregulatory system. However, various clinical scenarios have a more favorable outcome under external temperature regulation. Therapeutic hypothermia, for example, was found beneficial for the outcome of resuscitated cardiac arrest patients due to its protection against cerebral ischemia. Nonetheless, practice shows that outcomes of targeted temperature management vary considerably in dependence on individual tissue damage levels and differences in therapeutic strategies and protocols. Here, we address these differences in detail by means of computational modeling. We develop a multi-segment and multi-node thermoregulatory model that takes into account details related to specific post-cardiac arrest-related conditions, such as thermal imbalances due to sedation and anesthesia, increased metabolic rates induced by inflammatory processes, and various external cooling techniques. In our simulations, we track the evolution of the body temperature in patients subjected to post-resuscitation care, with particular emphasis on temperature regulation via an esophageal heat transfer device, on the examination of the alternative gastric cooling with ice slurry, and on how anesthesia and the level of inflammatory response influence thermal behavior. Our research provides a better understanding of the heat transfer processes and therapies used in post-cardiac arrest patients., (© 2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

The purpose of our study was to measure surface body temperatures (SBT) and to determine rewarming patterns after surface cooling in adult comatose survivors of cardiac arrest. We performed a prospective study in two phases from April to May 2016 and from December 2017 to March 2018. In the first phase we measured SBT as soon as possible after admission (t0) and 10 minutes later (t10). In the second phase we measured SBT and changes of SBT after local cooling of different regions in the maintenance phase of targeted temperature management. We included six patients to each phase of the study. In the first phase, we observed lower SBT compared with core body temperature (CBT) at t0 and t10, with nonsignificant differences in head and axillary region at t0 (35.2°C ± 1.3°C vs. 36°C ± 0.6°C, p  = 0.11, and 35.7°C ± 1.4°C vs. 36°C ± 0.6°C, p  = 0.41, respectively) and head at t10 (34.8°C ± 1.6°C vs. 35.9°C ± 0.6°C, p  = 0.13). SBT in all other body regions at t0 and t10 was significantly lower compared with CBT (all p values <0.05). In the second phase, SBT was significantly lower compared with CBT in all regions (all p values <0.05). After local cooling we observed no significant differences in rewarming rate between head (2.1 ± 0.3°C/min), thorax (1.6 ± 0.4°C/min), and abdomen (1.7 ± 0.2°C/min), and a significantly faster rewarming rate when comparing other body regions with legs (0.8 ± 0.4°C/min, all p values <0.03). To conclude, in comatose survivors of cardiac arrest we discovered lower SBT compared with CBT, necessitating CBT measurements as soon as possible, and higher SBT and rewarming rates after local cooling in central (head, thorax, and abdomen) compared with peripheral (upper and lower extremities) regions of the body.

Therapeutic hypothermia was associated with increased mortality in patients with severe bacterial meningitis in a large randomized trial. It still remains a treatment strategy for comatose survivors of cardiac arrest. There are several potential advantages of inhalational anesthetics as long-term sedation agents compared to intravenous sedation, however, uncontrollable increases of intracranial pressure were observed in neurocritical patients. Here we present a patient with severe bacterial meningitis and secondary cardiac arrest where therapeutic hypothermia and inhalational anesthesia were successfully used. A 59-year old female with a history of a vestibular Schwannoma surgery on the left side was admitted with signs of meningitis. Within minutes after admission, she further deteriorated with respiratory arrest, followed by cardiac arrest. She remained comatose after return of spontaneous circulation. The standard treatment of severe meningitis (steroids, antibiotics, insertion of intracranial pressure probe and external ventricular drainage) along with therapeutic hypothermia and inhalational anesthesia were implemented. Intracranial pressure remained stable and daily neurological examination was possible without being confounded by concurrent sedation. She was discharged home without neurological sequelae after 27days. In selected patients with meningitis, therapeutic hypothermia may still present a treatment option, and the long-term use of inhalational anesthetics could be appropriate with concomitant intracranial pressure monitoring., (Copyright © 2016 Elsevier Inc. All rights reserved.)

Background: Temperature management is a recommended part of post-resuscitation care of comatose survivors of cardiac arrest. A number of methods exist for temperature management, all of which have limitations. We aimed to evaluate the performance and ease of use of a new esophageal heat transfer device (EHTD; Advanced Cooling Therapy, Chicago, IL, USA) for temperature management of adult survivors of cardiac arrest., Methods: We performed a prospective study from March to June 2015. Our standard protocol uses servo-controlled water blankets supplemented with ice-cold saline in order to attain goal temperature (32°C-34°C) within 1 hour. We substituted the EHTD for our usual water blankets, then recorded temperature over time and adverse effects., Main Findings: A total of 14 patients were treated, with mean age 65.1±13.7 years, and median weight 75.5 (70; 83) kg. Initial temperature was 35.3±1.2°C. Mean cooling rate during the induction phase was 1.12±0.62°C/h, time to target temperature was 60 (41; 195) min and the volume of iced fluids infused was 1607±858 ml (as compared with 2-2.5L historically). The percentage of time outside target temperature range during the maintenance phase was 6.5% (0.0; 29.0). Rewarming rate was 0.22 (0.18; 0.31)°C/h. No major adverse effects were observed., Conclusion: Using the EHTD, our patient population attained goal temperatures in one hour, the volume of ice-cold saline required to attain this cooling rate was decreased by one-third, and experienced a low percentage of time outside target temperature range and no major adverse effects., (Copyright © 2016 The Authors. Published by Elsevier Inc. All rights reserved.)

In patients with refractory cardiac arrest presumably from acute coronary occlusion, primary percutaneous coronary intervention (PPCI) may provide an opportunity for revascularisation and, subsequently, return of spontaneous circulation. We present our experience from a 24/7 primary percutaneous coronary intervention centre serving a population of approximately 800,000 individuals. A retrospective analysis was performed in patients with cardiac arrest treated from July 2011 to January 2014. Inclusion criteria were cardiac arrest and emergency coronary angiography performed during on-going external cardiopulmonary resuscitation (CPR). Course of treatment was analysed to outline the reasons for poor survival. Eight patients met the inclusion criteria; six (75 %) were male, and the mean age was 63 ± 16 years. Revascularisation under continuous cardiopulmonary resuscitation was achieved in all eight patients. Sustained return of spontaneous circulation was achieved in two patients (25 %). Both patients had poor neurological outcome (cerebral performance category 4), and both died within 3 months. We identified total duration of cardiopulmonary resuscitation (90.5 ± 33.3 min), lack of prehospital mechanical cardiopulmonary resuscitation devices and lack of extra-corporeal life support devices as the most likely reasons contributing to poor survival.

Background Mild induced hypothermia is an established treatment strategy for comatose survivors of cardiac arrest. The goal of the induction phase of mild induced hypothermia is to cool the patient's core body temperature to 32°–34°C. Objective The main goal of this study was to compare temperature changes measured in the esophagus and urinary bladder in survivors of cardiac arrest undergoing mild induced hypothermia using cold saline infusion. Methods We performed a prospective study in a 12-bed adult medical intensive care unit at a tertiary level hospital in comatose adult survivors of nontraumatic cardiac arrest admitted from January to April 2012. Paired temperature readings from bladder and esophageal probes were recorded every 5 min for 95 min (20 readings). Cold fluid infusion was terminated when the measured temperature from either of the probes reached 33.9°C. Factorial repeated-measures analysis of variance was used to determine the effect of time and site of measurement on temperature readings. Results Measurements were performed in 8 patients. Target temperature was achieved in 33 ± 15 min in the esophagus and in 63 ± 15 min in the bladder ( p = 0.006). We discovered a significant interaction effect ( p < 0.001) between time and site of measurement, indicating that temperature changes differently depending on the site of measurement, with esophageal temperatures decreasing faster than temperatures measured in urinary bladder. Conclusions Our results indicate that esophageal temperature measurements show a faster response rate compared to temperature measured in the bladder when cold saline infusion is used to induce mild hypothermia. [ABSTRACT FROM AUTHOR]