The SARS-CoV-2 pandemic changed the way intensivists approach extracorporeal membrane oxygenation (ECMO). Patients with COVID-19 acute respiratory distress syndrome (ARDS) placed on ECMO have a high prevalence of right ventricular (RV) failure, which is associated with reduced survival (Maharaj V et al. ASAIO Journal. 2022;68[6]:772). In 2021, our institution supported 51 patients with COVID-19 ARDS with ECMO: 51% developed RV failure, defined as a clinical syndrome (reduced cardiac output) in the presence of RV dysfunction on transthoracic echocardiogram (TTE) (Marra A et al. Chest. 2022;161[2]:535). Total numbers for RV dysfunction and RV dilation on TTE were 78% and 91% respectively, In essence then, TTE signs of RV dysfunction are sensitive but not specific for clinical RV failure.
Rates for survival to decannulation were far lower when RV failure was present (27%) vs. absent (84%). Given these numbers, we felt a reduction in RV failure would be an important target for improving outcomes for patients with COVID-19 ARDS receiving ECMO. Existing studies on RV failure in patients with ARDS receiving ECMO are plagued by scant data, small sample sizes, differences in diagnostic criteria, and heterogenous treatment approaches. Despite these limitations, we felt the need to make changes in our approach to RV management.
Because outcomes once clinical RV-failure occurs are so poor, we focused on prevention. While we’re short on data and evidence-based medicine (EBM) here, we know a lot about the physiology of COVID19, the pulmonary vasculature, and the right side of the heart. There are multiple physiologic and disease-related pathways that converge to produce RV-failure in patients with COVID-19 ARDS on ECMO (Sato R et al. Crit Care. 2021;25:172). Ongoing relative hypoxemia, hypercapnia, acidemia, and microvascular thromboses/immunothromboses can all lead to increased pulmonary vascular resistance (PVR) and an increased workload for the RV (Zochios V et al. ASAIO Journal. 2022; 68[4]:456). ARDS management typically involves high positive end-expiratory pressure (PEEP), which can produce RV-PA uncoupling (Wanner P et al. J Clin Med. 2020;9:432).
We do know that ECMO relieves the stress on the right side of the heart by improving hypoxemia, hypercapnia, and acidemia while allowing for reduction in PEEP (Zochios V et al. ASAIO Journal. 2022; 68[4]:456). In addition to ECMO, proning and pulmonary vasodilators offload RV by further reducing pulmonary pressures (Sato R et al. Crit Care. 2021;25:172). Lastly, a right ventricular assist device (RVAD) can dissipate the work required by the RV and prevent decompensation. Collectively, these therapies can be considered preventive.
Knowing the RV parameters on RV are sensitive but not specific for outcomes though, when should some of these treatments be instituted? It’s clear that once RV failure has developed it’s probably too late, but it’s hard to find data to guide us on when to act. One institution used right ventricular assist devices (RVADs) at the time of ECMO initiation with protocolized care and achieved a survival to discharge rate of 73% (Mustafa AK et al. JAMA Surgery. 2020;155[10]:990). The publication generated enthusiasm for RVAD support with ECMO, but it’s possible the protocolized care drove the high survival rate, at least in part.
At our institution, we developed our own protocol for evaluation of the RV with proactive treatment based on specific targets. We performed daily, bedside TTE and assessed the RV fractional area of change (FAC) and outflow tract velocity time integral (VTI). These parameters provide a quantitative assessment of global RV function, and FAC is directly related to ability to wean from ECMO support (Maharaj V et al. ASAIO Journal. 2022;68[6]:772). We avoided using the tricuspid annular plain systolic excursion (TAPSE) due to its poor sensitivity (Marra AM et al. Chest. 2022;161[2]:535). Patients receiving ECMO with subjective, global mild to moderate RV dysfunction on TTE with worsening clinical data, an FAC of 20%-35%, and a VTI of 10-14 cm were treated with aggressive diuresis, pulmonary vasodilators, and inotropy for 48 hours. If there was no improvement or deterioration, an RVAD was placed. For patients with signs of severe RV dysfunction (FAC < 20% or VTI < 10 cm), we proceeded directly to RVAD. We’re currently collecting data and tracking outcomes.
While data exist on various interventions in RV failure due to COVID-19 ARDS with ECMO, our understanding of this disease is still in its infancy. The optimal timing of interventions to manage and prevent RV failure is not known. We would argue that those who wait for RV failure to occur before instituting protective or supportive therapies are missing the opportunity to impact outcomes. We currently do not have the evidence to support the specific protocol we’ve outlined here and instituted at our hospital. However, we do believe there’s enough literature and experience to support the concept that close monitoring of RV function is critical for patients with COVID19 ARDS receiving ECMO. Failure to anticipate worsening function on the way to failure means reacting to it rather than staving it off. By then, it’s too late.
Dr. Thomas is Maj, USAF, assistant professor, pulmonary/critical care; Dr. O’Neil is Maj, USAF, pediatric and ECMO intensivist, PICU medical director; and Dr. Villalobos is Capt, USAF, assistant professor, pulmonary/critical care, medical ICU director, Brooke Army Medical Center, San Antonio, Tex. The view(s) expressed herein are those of the author(s) and do not reflect the official policy or position of Brooke Army Medical Center, the U.S. Army Medical Department, the U.S. Army Office of the Surgeon General, the Department of the Army, the Department of the Air Force, or the Department of Defense or the U.S. government.