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Summary and Background Data: VV ECMO can be utilized as an advanced therapy in select patients with COVID-19 respiratory failure refractory to traditional critical care management and optimal mechanical ventilation. Anticipating a need for such therapies during the pandemic, our center created a targeted protocol for ECMO therapy in COVID-19 patients that allows us to provide this life-saving therapy to our sickest patients without overburdening already stretched resources or excessively exposing healthcare staff to infection risk. Methods: As a major regional referral program, we used the framework of our well-established ECMO service-line to outline specific team structures, modified patient eligibility criteria, cannulation strategies, and management protocols for the COVID-19 ECMO program. Results: During the first month of the COVID-19 outbreak in Massachusetts, 6 patients were placed on VV ECMO for refractory hypoxemic respiratory failure. The median (interquartile range) age was 47 years (43–53) with most patients being male (83%) and obese (67%). All cannulations were performed at the bedside in the intensive care unit in patients who had undergone a trial of rescue therapies for acute respiratory distress syndrome including lung protective ventilation, paralysis, prone positioning, and inhaled nitric oxide. At the time of this report, 83% (5/6) of the patients are still alive with 1 death on ECMO, attributed to hemorrhagic stroke. 67% of patients (4/6) have been successfully decannulated, including 2 that have been successfully extubated and one who was discharged from the hospital. The median duration of VV ECMO therapy for patients who have been decannulated is 12 days (4–18 days). Conclusions: This is 1 the first case series describing VV ECMO outcomes in COVID-19 patients. Our initial data suggest that VV ECMO can be successfully utilized in appropriately selected COVID-19 patients with advanced respiratory failure.

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Background Myocardial tolerance to ischemia is influenced by age and preoperative cyanosis through unknown mechanisms and significantly affects postoperative outcomes. Cytochrome c oxidase (CcOx), the terminal enzyme of the mitochondrial electron transport chain, may play a role in the susceptibility to ischemic-reperfusion (IR) injury. Our study aimed at investigating changes in human myocardial CcOx activity based on age and preoperative oxygen saturation to understand its role in transition from neonatal to mature myocardium and hypoxic conditions. Methods The right atrial appendage from patients undergoing first time surgical repair/palliation of congenital heart defects was analyzed for steady state CcOx activity by oxidation of ferrocytochrome c via spectrophotometry and steady state CcOx subunit I protein content by protein immunoblotting. Student’s t-test compared CcOx activity and protein levels between patients with preoperative hypoxia and normoxia. Multiple linear regression analysis was used to assess the effects of age and preoperative arterial oxygen saturations (SaO2) on CcOx protein activity and protein content. Results Thirty-two patients with a median (interquartile range) age of 83 days (8–174) and preoperative oxygen saturation 98% (85–100%) were enrolled. Independent of age, preoperative SaO2 ≤90% was associated with significantly greater CcOx steady state activity (p=0.004). Additionally, older age itself was associated with increased CcOx steady state activity (p=0.022); the combination of preoperative SaO2 and age account for 33% of the variation in CcOx steady state activity (R2=0.332). There was no increase in the CcOx subunit I protein content with either age or preoperative hypoxia. Conclusions In patients with congenital heart disease, an increase in CcOx steady state activity is seen with increasing age. Hypoxia leads to upregulation of CcOx steady state activity without an increase in the amount of enzyme protein itself. Higher CcOx activity in older and cyanotic patients may indicate CcOx-dependent reactive oxygen species as the mechanism for IR injury.