Background
Given critical care nurses’ high prepandemic levels of moral distress and burnout, the COVID-19 pandemic will most likely have a tremendous influence on intensive care unit (ICU) nurses’ mental health and continuation in the ICU workforce.
Objective
To describe the experiences of ICU nurses during the COVID-19 pandemic in the United States.
Methods
Nurses who worked in ICUs in the United States during the COVID-19 pandemic were recruited to complete a survey from October 2020 through early January 2021 through social media and the American Association of Critical-Care Nurses. Three open-ended questions focused on the experiences of ICU nurses during the pandemic.
Results
Of 498 nurses who completed the survey, 285 answered the open-ended questions. Nurses reported stress related to a lack of evidence-based treatment, poor patient prognosis, and lack of family presence in the ICU. Nurses perceived inadequate leadership support and inequity within the health care team. Lack of consistent community support to slow the spread of COVID-19 or recognition that COVID-19 was real increased nurses’ feelings of isolation. Nurses reported physical and emotional symptoms including exhaustion, anxiety, sleeplessness, and moral distress. Fear of contracting COVID-19 or of infecting family and friends was also prevalent.
Conclusions
Intensive care unit nurses in the United States experienced unprecedented and immense burden during the COVID-19 pandemic. Understanding these experiences provides insights into areas that must be addressed to build and sustain an ICU nurse workforce. Studies are needed to further describe nurses’ experiences during the COVID-19 pandemic and identify effective resources that support ICU nurse well-being.
Posttraumatic stress disorder (PTSD) is a devastating disorder, linked to profound mental, physical, occupational, and functional impairment. In addition, it is a highly complex disorder, characterized by symptom heterogeneity across multiple domains. Nevertheless, emotion dysregulation arising from the exaggerated response to threat or from the inability to regulate negative emotional states plays a defining role in the pathophysiology of PTSD. In order to improve our understanding of how emotion dysregulation manifests in this illness, functional neuroimaging research over the past 20 years provides great insight into underlying neuroanatomy of each component of emotion dysregulation in the context of PTSD. While prior reviews exist on the topic of neuroimaging findings in PTSD, the present review synthesizes that work through the lens of emotion and its regulation. Studies that employed tasks of emotional responding and symptom provocation, implicit regulation (e.g., emotional Stroop and interference), explicit regulation (e.g., cognitive reappraisal), and fear conditioning/extinction were reviewed. Findings demonstrate that emotion dysregulation in PTSD arises from complications within a large neurocircuitry involving the amygdala, insula, hippocampus, anterior cingulate cortex, and prefrontal cortex. Although an exaggerated response in the amygdala and insula to negative emotional triggers is pervasive, PTSD is also marked by deficient appraisal, resolution, and management of negative emotional states subserved by the anterior cingulate cortex and prefrontal cortex during regulation. These findings further support the importance of studying emotion-regulation deficits in tandem with exaggerated symptom provocation in order to better understand the constellation of symptoms present in those with PTSD.
Pharmacotherapy in PBD patients led to differential effort with persistently increased activity in the affective regions and decreased activity in the cognitive regions relative to HC, demonstrating altered mechanisms of affective and cognitive systems of brain function, regardless of symptom response.
Individuals with GAD exhibited over-engagement of amygdala and frontal regions during the viewing of negative images, compared to HCs. Together, these aberrations may indicate that deficits in emotional reactivity rather than regulation contribute to emotion dysregulation in those with GAD.
Objective
The current study examined the impact of risperidone and divalproex on affective and working memory circuitry in patients with pediatric bipolar disorder (PBD).
Method
This was a six-week double blind randomized trial of risperidone plus placebo vs. divalproex plus placebo for patients with mania (n=21; 13.6±2.5 years). The fMRI outcomes were measured using a block design affective N-back task with angry, happy and neutral face stimuli at baseline and at 6-week follow-up. Matched healthy controls (HC; n=15, 14.5±2.8 years) were also scanned twice.
Results
Post hoc analyses on the significant interaction in a 3×2×2 ANOVA which included patient groups and HC revealed that the risperidone group showed greater activation after treatment in response to the angry face condition in the left subgenual anterior cingulate cortex (ACC) and striatum relative to the divalproex group. The divalproex group showed greater activation relative to the risperidone group in left inferior frontal gyrus and right middle temporal gyrus. Over the treatment course, the risperidone group showed greater change in activation in the left ventral striatum than the divalproex group, and the divalproex group showed greater activation change in left inferior frontal gyrus and right middle temporal gyrus than the risperidone group. Furthermore, each patient group showed increased activation relative to HC in fronto-striato-temporal regions over time. The happy face condition was potentially less emotionally challenging in this study and did not elicit notable findings.
Conclusion
When patients performed a working memory task under emotional duress inherent in the paradigm, divalproex enhanced activation in a fronto-temporal circuit while risperidone increased activation in the dopamine (D2) receptor-rich ventral striatum.
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