Aims Cardiovascular complications, including myocarditis, are observed in coronavirus disease 2019 (COVID‐19). Major cardiac involvement is a potentially lethal feature in severe cases. We sought to describe the underlying pathophysiological mechanism in COVID‐19 lethal cardiogenic shock. Methods and results We report on a 48‐year‐old male COVID‐19 patient with cardiogenic shock; despite extracorporeal life support, dialysis, and massive pharmacological support, this rescue therapy was not successful. Severe acute respiratory syndrome coronavirus 2 RNA was detected at autopsy in the lungs and myocardium. Histopathological examination revealed diffuse alveolar damage, proliferation of type II pneumocytes, lymphocytes in the lung interstitium, and pulmonary microemboli. Moreover, patchy muscular, sometimes perivascular, interstitial mononuclear inflammatory infiltrates, dominated by lymphocytes, were seen in the cardiac tissue. The lymphocytes ‘interlocked’ the myocytes, resulting in myocyte degeneration and necrosis. Predominantly, T‐cell lymphocytes with a CD4:CD8 ratio of 1.7 infiltrated the interstitial myocardium, reflecting true myocarditis. The myocardial tissue was examined for markers of ferroptosis, an iron‐catalysed form of regulated cell death that occurs through excessive peroxidation of polyunsaturated fatty acids. Immunohistochemical staining with E06, a monoclonal antibody binding to oxidized phosphatidylcholine (reflecting lipid peroxidation during ferroptosis), was positive in morphologically degenerating and necrotic cardiomyocytes adjacent to the infiltrate of lymphocytes, near arteries, in the epicardium and myocardium. A similar ferroptosis signature was present in the myocardium of a COVID‐19 subject without myocarditis. In a case of sudden death due to viral myocarditis of unknown aetiology, however, immunohistochemical staining with E06 was negative. The renal proximal tubuli stained positively for E06 and also hydroxynonenal (4‐HNE), a reactive breakdown product of the lipid peroxides that execute ferroptosis. In the case of myocarditis of other aetiology, the renal tissue displayed no positivity for E06 or 4‐HNE. Conclusions The findings in this case are unique as this is the first report on accumulated oxidized phospholipids (or their breakdown products) in myocardial and renal tissue in COVID‐19. This highlights ferroptosis, proposed to detrimentally contribute to some forms of ischaemia–reperfusion injury, as a detrimental factor in COVID‐19 cardiac damage and multiple organ failure.

The COVID-19 pandemic has resulted in an increased need for ventilators. The potential to ventilate more than one patient with a single ventilator, a so-called split ventilator setup, provides an emergency solution. Our hypothesis is that ventilation can be individualized by adding a flow restrictor to limit tidal volumes, add PEEP, titrate FiO 2 and monitor ventilation. This way we could enhance optimization of patient safety and clinical applicability. We performed bench testing to test our hypothesis and identify limitations. We performed a bench testing in two test lungs: (1) determine lung compliance (2) determine volume, plateau pressure and PEEP, (3) illustrate individualization of airway pressures and tidal volume with a flow restrictor, (4a) illustrate that PEEP can be applied and individualized (4b) create and measure intrinsic PEEP (4c and d) determine PEEP as a function of flow restriction, (5) individualization of FiO 2. The lung compliance varied between 13 and 27 mL/cmH 2 O. Set ventilator settings could be applied and measured. Extrinsic PEEP can be applied except for settings with a large expiratory time. Volume and pressure regulation is possible between 70 and 39% flow restrictor valve closure. Flow restriction in the tested circuit had no effect on the other circuit or on intrinsic PEEP. FiO 2 could be modulated individually between 0.21 and 0.8 by gradually adjusting the additional flow, and minimal affecting FiO 2 in the other circuit. Tidal volumes, PEEP and FiO 2 can be individualized and monitored in a bench testing of a split ventilator. In vivo research is needed to further explore the clinical limitations and outcomes, making implementation possible as a last resort ventilation strategy.

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Background- The COVID-19 pandemic has resulted in an increased need for ventilators. The potential to ventilate more than one patient with a single ventilator, a so-called split ventilator setup, provides an emergency solution. Our hypothesis is that ventilation can be individualized by adding a flow restrictor to limit tidal volumes, add PEEP, titrate FiO 2 and monitor ventilation. This way we could ensure optimization of patient safety and clinical applicability. We performed bench testing to test our hypothesis and identify limitations. Methods- We performed a bench testing in two lungs: 1) determine lung compliance 2) determine volume, plateau pressure and PEEP, 3) illustrate individualization of airway pressures and tidal volume with a flow restrictor, 4a) illustrate that PEEP can be applied and individualized 4b) create and measure intrinsic PEEP 4c-d) determine PEEP as a function of flow restriction, 5) individualization of FiO 2 . Results- The lung compliance varied between 13 and 27 mL/cmH 2 O. Set ventilator settings could be applied and measured. Extrinsic PEEP can be applied except for settings with a large expiratory time. Volume and pressure regulation is possible between 70-39% flow restrictor valve closure. Flow restriction in the tested circuit had no effect on the other circuit or on intrinsic PEEP. FiO 2 could be modulated individually between 0.21 and 0.8 by gradually adjusting the additional flow, and minimal affecting FiO 2 in the other circuit. Conclusions- Tidal volumes, PEEP and FiO2 can be individualized and monitored in a bench testing of a split ventilator. In vivo research is needed to further explore the clinical limitations and outcomes, making implementation possible as a last resort ventilation strategy.

Human metapneumovirus (HMPV) is a single negativestranded RNA-enveloped virus in the Paramyxoviridae family [1]. HMPV is known to cause respiratory tract infections. HMPV-induced encephalitis has only sporadically been documented, mostly in children [2]. In adults only three former reports exist [1,3,4].An 78-year-old Caucasian male patient presented at the emergency department because of agitation and confusion. His wife reported myoclonic jerks and urinary incontinence during sleep. Glasgow coma scale was 9/15. He had not taken any psychotropic drugs. Clinical examination showed no lateralisation, plantar reflexes were in flexion. The right eye was red and slightly swollen. Cardiovascular parameters were normal. Temperature was 38.9 °C. Medical history revealed diabetes mellitus type 1, arterial hypertension, hypercholesterolemia, nicotine abuse and glaucoma.Laboratory results showed leucocytosis of 12.600 white blood cells, a normal CRP of 1 mg/l (N < 5), slightly elevated lactate 20.3 mg/dl (N < 19.8) and glucose 161 m/dl (N < 110). Creatinine, electrolytes, enzymes, TSH and carboxy-hemoglobin were within normal limits.EEG showed a generalized slowing of the basal rhythm slightly more pronounced bitemporal, indicative for encephalopathy or encephalitis (Fig. 1). There were no signs of epilepsy. CT scan of the brain was normal. Chest radiography showed accentuated bronchopulmonary markings as seen in viral respiratory infections.Publisher's Note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.