Exploration of Burnout, Emotional Thriving, and Emotional Recovery in an Academic Medical Center: a Mixed Methods Quality Improvement Project

Introduction: Healthcare provider burnout, an indicator of wellbeing, impacts patient safety, provider distress, and employee turnover. In this mixed methods, multi-site quality improvement study conducted \u3c6 months prior to the start of the COVID-19 pandemic, we assessed employee wellbeing in a large clinical department. Methods: Wellbeing surveys were sent electronically to Department of Medicine clinicians, researchers, administrators, and staff from August-September 2019 assessing perceptions of Burnout, Emotional Thriving (ET), and Emotional Recovery (ER). Qualitative responses were reviewed for themes using mixed inductive-deductive analysis. The initial coding was done by small teams with consensus obtained through large group discussions. This study was IRB-approved as non-human subjects research. Results: Of the 671 respondents, 54% met criteria for burnout (Burnout+), 65% for ER (ER+), and 61% for ET (ET+). ER+ and ET+ were present in nearly half of Burnout+ respondents (53% and 43% respectively). Several themes emerged in the qualitative analysis: workload and expectations; tangible resources; work culture; and salary/benefits, with leadership influencing each of the domains. Conclusion: Burnout, ET, and ER can co-exist within the same individual. Employee wellbeing is not adequately reflected by the binary of whether or not an individual is experiencing burnout. All employees at academic medical centers, including staff, researchers, and clinicians, are vulnerable to the same workplace factors driving burnout. Our findings have been used to target areas of intervention during the COVID-19 pandemic at our institution. We propose that other academic medical centers may have similar workplace stressors that they could assess and target for improvement

Channelopathies in Cav1.1, Cav1.3, and Cav1.4 voltage-gated L-type Ca2+ channels

Voltage-gated Ca2+ channels couple membrane depolarization to Ca2+-dependent intracellular signaling events. This is achieved by mediating Ca2+ ion influx or by direct conformational coupling to intracellular Ca2+ release channels. The family of Cav1 channels, also termed L-type Ca2+ channels (LTCCs), is uniquely sensitive to organic Ca2+ channel blockers and expressed in many electrically excitable tissues. In this review, we summarize the role of LTCCs for human diseases caused by genetic Ca2+ channel defects (channelopathies). LTCC dysfunction can result from structural aberrations within their pore-forming α1 subunits causing hypokalemic periodic paralysis and malignant hyperthermia sensitivity (Cav1.1 α1), incomplete congenital stationary night blindness (CSNB2; Cav1.4 α1), and Timothy syndrome (Cav1.2 α1; reviewed separately in this issue). Cav1.3 α1 mutations have not been reported yet in humans, but channel loss of function would likely affect sinoatrial node function and hearing. Studies in mice revealed that LTCCs indirectly also contribute to neurological symptoms in Ca2+ channelopathies affecting non-LTCCs, such as Cav2.1 α1 in tottering mice. Ca2+ channelopathies provide exciting disease-related molecular detail that led to important novel insight not only into disease pathophysiology but also to mechanisms of channel function