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Left ventricular assist device (LVAD) therapy is a lifesaving option for patients with medical therapy-refractory advanced heart failure. Depending on the definition, 5–44% of people supported with an LVAD develop right heart failure (RHF), which is associated with worse outcomes. The mechanisms related to RHF include patient, surgical, and hemodynamic factors. Despite significant progress in understanding the roles of these factors and improvements in surgical techniques and LVAD technology, this complication is still a substantial cause of morbidity and mortality among LVAD patients. Additionally, specific medical therapies for this complication still are lacking, leaving cardiac transplantation or supportive management as the only options for LVAD patients who develop RHF. While significant effort has been made to create algorithms aimed at stratifying risk for RHF in patients undergoing LVAD implantation, the predictive value of these algorithms has been limited, especially when attempts at external validation have been undertaken. Perhaps one of the reasons for poor performance in external validation is related to differing definitions of RHF in external cohorts. Additionally, most research in this field has focused on RHF occurring in the early phase (i.e., ≤1 month) post LVAD implantation. However, there is emerging recognition of late-onset RHF (i.e., > 1 month post-surgery) as a significant cause of morbidity and mortality. Late-onset RHF, which likely has a unique physiology and pathogenic mechanisms, remains poorly characterized. In this review of the literature, we will describe the unique right ventricular physiology and changes elicited by LVADs that might cause both early- and late-onset RHF. Finally, we will analyze the currently available treatments for RHF, including mechanical circulatory support options and medical therapies.

Periprosthetic joint infection is a major complication of total joint arthroplasty (TJA). The intraoperative splash basin has been found to be a potential source of contamination. Although consensus recommendations against the use of splash basin have been made, splash basin use continues to be taught and utilized in practice. This study aims to investigate the effect of dilute betadine addition to the sterile water (SW) contents (0.02% solution) of the splash basin on contamination rates. This intervention could preserve the functionality and preferential use of the splash basin. The primary outcome of this study is the rate of splash basin contamination, with secondary outcomes of prevalence of culture speciation and mean operative times association with the rate of positive cultures.Patients undergoing primary TJA were enrolled in a randomized controlled trial with assignment to either the intervention/betadine group, in which dilute betadine was added to the standard SW splash basin, or the control/standard SW group. For a total cohort of 104 patients, a 120 mL aliquot sample of basin fluid was collected at incision ("preprocedure") and closure ("postprocedure"). Samples were cultured and monitored for 48 hours for growth, with further testing as necessary to identify microbial speciation.Of the final 100 postprocedure samples, 0 (0.0%) were positive in the betadine group, while there were 23 (47.9%) positive samples in the SW group (P.001). Of the positive cultures, the most common species grown were coagulase-negative Staphylococcus, Corynebacterium, and Micrococcus. The mean operative time was an average of 11 minutes longer for cases with positive cultures.In conclusion, treating SW splash basins with dilute povidone-iodine (0.02% solution) eliminates intraoperative contamination of splash basins in TJA procedures. This intervention is simple, low cost, and readily implementable, making it a reasonable addition to TJA protocols.Level 1, Controlled Laboratory Study.