Search

Abstract Right ventricle‐pulmonary artery (RV‐PA) coupling describes the energetic relationship between RV contractility and its afterload. The gold standard for assessment of this relationship requires invasive pressure‐volume (PV) loop measurements. Non‐invasive surrogates of RV‐PA coupling have been developed, such as the echocardiographic tricuspid annular plane systolic excursion to pulmonary artery systolic pressure ratio (TAPSE/PASP), but their performance has not been systematically assessed. We sought to assess performance of TAPSE/PASP ratio compared to PV loop‐defined RV‐PA coupling. A systematic search was conducted. Studies were included if PV loop derived RV‐PA coupling metrics were compared to echocardiographic or magnetic resonance imaging surrogates. We conducted a meta‐analysis of TAPSE/PASP correlation to PV loop‐defined RV‐PA coupling. 1452 studies were identified in the initial search, of which ten met inclusion criteria. Five studies allowed for pooled analysis of TAPSE/PASP to Ees/Ea correlation (r = 0.52, 95% confidence interval 0.36–0.65). There was moderate heterogeneity across the pooled studies. Despite the common use of Non‐invasive surrogates of RV‐PA coupling, there is only moderate correlation with gold standard measurements. These metrics do not inform on the individual components of RV‐PA coupling, limiting their use in the management of patients with RV dysfunction.

Abstract Objective To summarize knowledge and identify gaps in evidence regarding treatment of right ventricular dysfunction (RVD) in acute respiratory distress syndrome (ARDS). Data sources We conducted a comprehensive search of MEDLINE, Embase, CINAHL, Web of Science, and the Cochrane Central Register of Controlled Trials. Study selection Studies were included if they reported effects of treatments on right ventricular function, whether or not the intent was to modify right ventricular function. Data extraction Data extraction was performed independently and in duplicate by two authors. Data items included the study design, patient population, type of intervention, comparison group, and RV-specific outcomes. Data synthesis Of 1,430 studies screened, 51 studies reporting on 1,526 patients were included. By frequency, the included studies examined the following interventions: ventilator settings (29.4%), inhaled medications (33.3%), extracorporeal life support (13.7%), intravenous or oral medications (13.7%), and prone positioning (9.8%). The majority of the studies were non-randomized experimental studies (53%), with the next most common being case reports (16%). Only 5.9% of studies were RCTs. In total, 27% of studies were conducted with the goal of modifying RV function. Conclusions Given the prevalence of RVD in ARDS and its association with mortality, the dearth of research on this topic is concerning. This review highlights the need for prospective trials aimed at treating RV dysfunction in ARDS.

Abstract With an increasing number of left ventricular assist devices (LVADs) being placed every year, emergency clinicians are increasingly likely to encounter them in their practice. Patients may present to the emergency department (ED) with significant hemodynamic perturbations with an LVAD and it is imperative that emergency clinicians are able to assess and treat conditions contributing to low cardiac output states. This review describes the important aspects of the third generation of LVADs and their complications as well as common management approaches for the emergency physician.

Cardiovascular disease remains the leading cause of death in the United States, and cardiopulmonary bypass is a cornerstone in the surgical management of many related disease states. Pathophysiologic changes associated both with extracorporeal circulation and shock can beget a syndrome of low systemic vascular resistance paired with relatively preserved cardiac output, termed vasoplegia. While increased vasopressor requirements accompany vasoplegia, related pathophysiologic mechanisms may also lead to true catecholamine resistance, which is associated with further heightened mortality. The introduction of a second non-catecholamine vasopressor, angiotensin II, and non-specific nitric oxide scavengers offers potential means by which to manage this challenging phenomenon. This narrative review addresses both the definition, risk factors, and pathophysiology of vasoplegia and potential therapeutic interventions.