Introduction: In massive pulmonary embolism (PE) with circulatory collapse or with cardiac arrest, treatment can be difficult. Often, the diagnosis is unclear, and the time to treatment is crucial. Our institution has had an out-of-hospital team intended for the treatment of accidental hypothermia with extra corporeal membrane oxygenation (ECMO) since 2004. The team has occasionally been involved in patients suffering massive PE. Methods: We were called to 38 patients with PE, but two were assessed as untreatable. Seventeen were treated with cardiopulmonary resuscitation followed by veno-arterial ECMO. Nineteen were prepared for ECMO with sheaths in the femoral vessels and were intensively observed during diagnosis and treatment. Five of these patients later progressed to ECMO due to cardiac arrest during treatment with thrombolytic medication. Most of the patients were treated with heparin and thrombolytic medication, but if the medications were contraindicated, they were treated with either surgical thrombectomy or only with heparin awaiting spontaneous thrombolysis. Results: Of the 36 patients we intended to treat, 25 (69%) survived one month and 20 survived one year (56%). Of the 22 patients treated with ECMO, 11 survived one month (50%) and 10 survived one year (45%). Discussion: The treatment could have been more uniform. It seems reasonable to build up a PE alert team with ECMO capability to take care of patients with massive PE. Conclusion: The treatment of thrombolytic medications in massive PE is risky, but if the patient is treated or prepared for ECMO, it can be lifesaving.

We hypothesized that apneic oxygenation, using an open lung approach, combined with extracorporeal CO2 removal, would provide adequate gas exchange in acute lung injury. We tested this hypothesis in nine anesthetized and mechanically ventilated pigs (85–95 kg), in which surfactant was depleted from the lungs by repeated lung lavage. After a lung recruitment maneuver, the tracheal tube was connected to 20 cm H2O continuous pressure (100% O2) for oxygenation of the blood. A pumpless membrane ventilator (interventional lung assist by Novalung) was connected in an arteriovenous shunt for CO2 removal. PaO2 and PaCO2 were recorded for 3.5 hours. PaO2 was 464 (403, 502) mm Hg (median and interquartile range) throughout the experiment. The O2 uptake through the lungs was 185 (164, 212) ml/min. PaCO2 increased asymptotic towards 60 mm Hg. The CO2 removal through the membrane ventilator was 180 (150, 180) ml/min. Thus, the method provided adequate gas exchange in this experimental model, suggesting that it might have potential as an alternative treatment modality in acute lung injury.

Acute pulmonary embolism (PE) is the third most common cardiovascular cause of death after acute myocardial infarction and stroke. Patients are, however, often under‐treated due to the risks associated with systemic thrombolysis and surgical embolectomy. Novel pharmacological and catheter‐based treatment strategies show promise, but the data supporting their use in patients are sparse. We therefore aimed to develop an in vivo model of acute PE enabling controlled evaluations of efficacy and safety of novel therapies. Danish Landrace pigs (n = 8) were anaesthetized and mechanically ventilated. Two pre‐formed autologous PEs (PE1, PE2, 20 × 1 cm) were administered consecutively via the right external jugular vein. The intact nature and central location were visualized in situ by magnetic resonance imaging (MRI). The hemodynamic and biochemical responses were evaluated at baseline (BL) and after each PE by invasive pressure measurements, MRI, plus arterial and venous blood analysis. Pulmonary arterial pressure increased after administration of the PEs (BL: 16.3 ± 1.2, PE1: 27.6 ± 2.9, PE2: 31.6 ± 3.1 mmHg, BL vs. PE1: P = 0.0027, PE1 vs. PE2: P = 0.22). Animals showed signs of right ventricular strain evident by increased end systolic volume (BL: 60.9 ± 5.1, PE1: 83.3 ± 5.0, PE2: 99.4 ± 6.5 mL, BL vs. PE1: P = 0.0005, PE1 vs. PE2: P = 0.0045) and increased plasma levels of Troponin T. Ejection fraction decreased (BL: 58.9 ± 2.4, PE1: 46.4 ± 2.9, PE2: 37.3 ± 3.5%, BL vs. PE1: p = 0.0008, PE1 vs. PE2: P = 0.009) with a compensatory increase in heart rate preserving cardiac output and systemic blood pressure. The hemodynamic and biochemical responses were comparable to that of patients suffering from intermediate‐high‐risk PE. This porcine model mirrors the anatomical and physiologic changes seen in human patients with intermediate‐high‐risk PE, and may enable testing of future therapies for this disease.