Cardiology shock is a syndrome of low cardiac output resulting in end-organ dysfunction. Few interventions have demonstrated meaningful clinical benefit, and cardiogenic shock continues to carry significant morbidity with mortality rates that have plateaued at upwards of 40% over the past decade. Clinicians must rely on clinical, biochemical, and hemodynamic parameters to guide resuscitation. Several features, including physical examination, renal function, serum lactate metabolism, venous oxygen saturation, and hemodynamic markers of right ventricular function, may be useful both as prognostic markers and to guide therapy. This article aims to review these targets, their utility in the care of patients with cardiology shock, and their association with outcomes.

BACKGROUND: Hypoxic-ischemic brain injury is a common cause of mortality after cardiac arrest (CA) and cardiopulmonary resuscitation; however, the specific underlying mechanisms are unclear. This study aimed to explore postresuscitation changes based on multi-omics profiling.
METHODS: A CA swine model was established, and the neurological function was assessed at 24 h after resuscitation, followed by euthanizing animals. Their fecal, blood, and hippocampus samples were collected to analyze gut microbiota, metabolomics, and transcriptomics.
RESULTS: The 16S ribosomal DNA sequencing showed that the microbiota composition and diversity changed after resuscitation, in which the abundance of Akkermansia and Muribaculaceae_unclassified increased while the abundance of Bifidobacterium and Romboutsia decreased. A relationship was observed between CA-related microbes and metabolites via integrated analysis of gut microbiota and metabolomics, in which Escherichia-Shigella was positively correlated with glycine. Combined metabolomics and transcriptomics analysis showed that glycine was positively correlated with genes involved in apoptosis, interleukin-17, mitogen-activated protein kinases, nuclear factor kappa B, and Toll-like receptor signal pathways.
CONCLUSIONS: Our results provided novel insight into the mechanism of hypoxic-ischemic brain injury after resuscitation, which is envisaged to help identify potential diagnostic and therapeutic markers.

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BACKGROUND: Women are known to be disadvantaged compared with men in the early links of the Chain of Survival, receiving fewer bystander interventions. We aimed to describe sex-based disparities in emergency medical service resuscitation quality and processes of care for out-of-hospital cardiac arrest.
RESULTS: We conducted a retrospective analysis of patients who were nontraumatic with out-of-hospital cardiac arrest aged ≥16 years where resuscitation was attempted between March 2019 and June 2023. We investigated 18 routinely captured performance metrics and performed adjusted logistic and quantile regression analyses to assess sex-based differences in these metrics. During the study period, 10 161 patients with out-of-hospital cardiac arrest met the eligibility criteria, of whom 3216 (32%) were women. There were no clinically relevant sex-based differences observed in regard to external cardiac compressions; however, women were 34% less likely to achieve a systolic blood pressure >100 mm Hg on arrival at the hospital (adjusted odds ratio [AOR], 0.66 [95% CI, 0.47-0.92]). Furthermore, women had a longer time to 12-lead ECG acquisition after return of spontaneous circulation (median adjusted difference, 1.00 minute [95% CI, 0.38-1.62]) and 33% reduced odds of being transported to a 24-hour percutaneous coronary intervention-capable facility (AOR, 0.67 [95% CI, 0.49-0.91]). Resuscitation was also terminated sooner for women compared with men (median adjusted difference, -4.82 minutes [95% CI, -6.77 to -2.87]).
CONCLUSIONS: Although external cardiac compression quality did not vary by sex, significant sex-based disparities were seen in emergency medical services processes of care following out-of-hospital cardiac arrest. Further investigation is required to elucidate the underlying causes of these differences and examine their influence on patient outcomes.

This scientific statement presents a conceptual framework for the pathophysiology of post-cardiac arrest brain injury, explores reasons for previous failure to translate preclinical data to clinical practice, and outlines potential paths forward. Post-cardiac arrest brain injury is characterized by 4 distinct but overlapping phases: ischemic depolarization, reperfusion repolarization, dysregulation, and recovery and repair. Previous research has been challenging because of the limitations of laboratory models; heterogeneity in the patient populations enrolled; overoptimistic estimation of treatment effects leading to suboptimal sample sizes; timing and route of intervention delivery; limited or absent evidence that the intervention has engaged the mechanistic target; and heterogeneity in postresuscitation care, prognostication, and withdrawal of life-sustaining treatments. Future trials must tailor their interventions to the subset of patients most likely to benefit and deliver this intervention at the appropriate time, through the appropriate route, and at the appropriate dose. The complexity of post-cardiac arrest brain injury suggests that monotherapies are unlikely to be as successful as multimodal neuroprotective therapies. Biomarkers should be developed to identify patients with the targeted mechanism of injury, to quantify its severity, and to measure the response to therapy. Studies need to be adequately powered to detect effect sizes that are realistic and meaningful to patients, their families, and clinicians. Study designs should be optimized to accelerate the evaluation of the most promising interventions. Multidisciplinary and international collaboration will be essential to realize the goal of developing effective therapies for post-cardiac arrest brain injury.

The novel SARS-CoV-2 introduced several new inflammatory conditions including SARS-CoV-2-associated rhabdomyolysis and viral myositis. We present a 22-year-old man who noted a week of cough followed by myalgias, dark-colored urine, and decreased oral intake. He was found to have acute nontraumatic rhabdomyolysis after an acutely positive SARS-CoV-2 test. Initial creatine kinase (CK) level was above the reference range as were liver enzymes reflective of muscle breakdown. Treatment involved fluid resuscitation and pain control, with close monitoring of kidney, liver, and skeletal markers over five days of hospitalization till there was clinical and symptomatic improvement.

This scientific statement presents a conceptual framework for the pathophysiology of post-cardiac arrest brain injury, explores reasons for previous failure to translate preclinical data to clinical practice, and outlines potential paths forward. Post-cardiac arrest brain injury is characterized by 4 distinct but overlapping phases: ischemic depolarization, reperfusion repolarization, dysregulation, and recovery and repair. Previous research has been challenging because of the limitations of laboratory models; heterogeneity in the patient populations enrolled; overoptimistic estimation of treatment effects leading to suboptimal sample sizes; timing and route of intervention delivery; limited or absent evidence that the intervention has engaged the mechanistic target; and heterogeneity in postresuscitation care, prognostication, and withdrawal of life-sustaining treatments. Future trials must tailor their interventions to the subset of patients most likely to benefit and deliver this intervention at the appropriate time, through the appropriate route, and at the appropriate dose. The complexity of post-cardiac arrest brain injury suggests that monotherapies are unlikely to be as successful as multimodal neuroprotective therapies. Biomarkers should be developed to identify patients with the targeted mechanism of injury, to quantify its severity, and to measure the response to therapy. Studies need to be adequately powered to detect effect sizes that are realistic and meaningful to patients, their families, and clinicians. Study designs should be optimized to accelerate the evaluation of the most promising interventions. Multidisciplinary and international collaboration will be essential to realize the goal of developing effective therapies for post-cardiac arrest brain injury.

Given the high morbidity and mortality associated with cardiopulmonary arrest, there have been multiple trials aimed at better monitoring and augmenting coronary, cerebral, and systemic perfusion. This article aims to elucidate these interventions, first by detailing the physiology of cardiopulmonary resuscitation and the available tools for managing cardiopulmonary arrest, followed by an in-depth examination of the newest advances in the monitoring and delivery of advanced cardiac life support.

BACKGROUND: Approximately 10% of newborns require assistance at delivery, and heart rate (HR) is the primary vital sign providers use to guide resuscitation methods. In 2016, the American Heart Association (AHA) suggested electrocardiogram in the delivery room (DR-ECG) to measure heart rate during resuscitation. This study aimed to compare the frequency of resuscitation methods used before and after implementation of the AHA recommendations.
METHODS: This longitudinal retrospective cohort study compared a pre-implementation (2015) cohort with two post-implementation cohorts (2017, 2021) at our Level IV neonatal intensive care unit.
RESULTS: An initial increase in chest compressions at birth associated with the introduction of DR-ECG monitoring was mitigated by focused educational interventions on effective ventilation. Implementation was accompanied by no changes in neonatal mortality.
CONCLUSIONS: Investigation of neonatal outcomes during the ongoing incorporation of DR-ECG may help our understanding of human and system factors, identify ways to optimize resuscitation team performance, and assess the impact of targeted training initiatives on clinical outcomes.