A Rare Case of Sotalol-Induced Respiratory Failure

Introduction: Beta-blockers (BB), a class II antiarrhythmic, are usually associated with respiratory adverse event such as exacerbations of obstructive lung disease, hypersensitivity pneumonitis etc. Sotalol, a BB that has both class II and III antiarrhythmic activities, is commonly used in the treatment and maintenance of atrial fibrillation or atrial flutter. It is generally thought to associate with significantly lower pulmonary side effects. The lower respiratory side effect profile does not eliminate its potential risk, especially in patients who have a history of reactive airway disease. Case: Patient a 71-year-old Caucasian female with a past medical history of atrial fibrillation due to severe mitral regurgitation, Chronic obstructive pulmonary disease, coronary artery disease, breast cancer status post resection and radiation and amiodarone-induced hypothyroidism who initially presented with complaint of shortness of breath, productive cough, and palpitations for 2-day duration that progressively worsened. On presentation, she was found to be in atrial flutter with RVR and started on a Cardizem drip and continued her home Eliquis. Electrophysiology (EP) was consulted and she was started on Sotalol 80mg. A few hours after receiving the first dose of Sotalol, she was found to have agonal respirations with diminished breath sounds, quickly requiring intubation for respiratory distress. Sotalol was promptly discontinued. Approximately 12hrs after intubation she was successfully extubated to BiPAP and eventually weaned to 2-3L of supplemental oxygen without any intervention such as diuresis, cardioversion or COPD treatment. The patient remained in atrial flutter and thus discussions with EP and Pulmonology decision was made to start on amiodarone but was unsuccessful in achieving rate control. Eventually, she underwent 200J direct-current cardioversion with success. The patient remained in sinus rhythm throughout the rest of her hospitalization. Discussion: The case illustrated that the potential risk of acute respiratory failure with use of sotalol is a real concern. Although it is infrequently seen, it is a predictable side effect of sotalol use that physicians should be aware of, especially in patients with a history of reactive airway disease. Sotalol has a rapid onset of action (1-2 hours) and relatively short half-life (12 hours in adult). So, early recognition is crucial to the prompt cessation of Sotalol, prevention of future adverse event and proper intervention to save a patient\u27s life. The case also illustrated that if this adverse event occurs, quick supportive treatments including intubation could be enough to help the patient until the medication went through its duration of action.https://scholarlycommons.henryford.com/merf2020caserpt/1035/thumbnail.jp

Platinum(II) and Palladium(II) Complexes of Pyridine-2-Carbaldehyde Thiosemicarbazone as Alternative Antiherpes Simplex Virus Agents

The cytotoxicity and the antivirus activity of Pd(II) and Pt(II) complexes with pyridine-2-carbaldehyde thiosemicarbazone (HFoTsc) against HSV replication were evaluated on four HSV strains—two wt strains Victoria (HSV-1) and BJA (HSV-2) and two ACVR mutants with different tk gene mutations R-100 (TKA, HSV-1) and PU (TKN, HSV-2). The experiments were performed on continuous MDBK cells and four HSV 1 and HSV 2 strains were used, two sensitive to acyclovir and two resistant mutants. The five complexes of HFoTsc, [Pt(FoTsc)Cl], [Pt(FoTsc)(H2FoTsc)]Cl2, [Pt(FoTsc)2], [Pd(FoTsc)(H2FoTsc)]Cl2, and [Pd(FoTsc)2], were found to be effective inhibitors of HSV replication. The most promising, active, and selective anti-HSV agent was found to be complex [Pt(FoTsc)(H2FoTsc)]Cl2. This complex could be useful in the treatment of HSV infections, since it is resistant to ACV mutants. PCR study of immediate early 300 bp ReIV Us1 region reveals that the complex [Pt(FoTsc)(H2FoTsc)]Cl2 specifically suppressed wt HSV-1 genome 2 hours after the infection, not inducing apoptosis/necrosis on the 8 hours after virus infection. The target was found to be most probably the viral, instead of the host cell DNA

A Socio-Technical and Co-Evolutionary Framework for Reducing Human-Related Risks in Cyber Security and Cybercrime Ecosystems

The focus on cyber security as an interaction between technical elements and humans has typically confined consideration of the latter to practical issues of implementation, conventionally those of `human performance factors' of vigilance etc., 'raising awareness' and/or 'incentivization' of people and organizations to participate and adapt their behavior. But this is far too narrow a view that seriously constrains the ability of cyber security as a whole to adapt and evolve to keep up with adaptive, innovative attackers in a rapidly-changing technological, business and social landscape, in which personal preferences of users are also dynamically evolving. While there is isolated research across different research areas, we noticed the lack of a \emph{holistic} framework combining a range of applicable theoretical concepts (e.g., cultural co-evolution such as technological arms races, opportunity management, behavioral and business models) and technological solutions on reducing human-related risks in the cyber security and cybercrime ecosystems, which involve multiple groups of human actors including offenders, victims, preventers and promoters. This paper reports our ongoing work in developing such a socio-technical framework 1) to allow a more comprehensive understanding of human-related risks within cyber security and cybercrime ecosystems and 2) to support the design of more effective approaches to engaging individuals and organizations in the reduction of such risks. We are in the process of instantiating this framework to encourage behavioral changes in two use cases that capture diverse and complicated socio-technical interactions in cyber-physical systems