Patient: Male, 40Final Diagnosis: Patent foramen ovaleSymptoms: Dyspnea exertional • hemoptysis • shortness of breathMedication: —Clinical Procedure: Airway pressure release ventilationSpecialty: Critical Care MedicineObjective:Rare co-existance of disease or pathologyBackground:Patent foramen ovale (PFO) are common, normally resulting in a left to right shunt or no net shunting. Pulmonary embolism (PE) can cause sustained increased pulmonary vascular resistance (PVR) and right atrial pressure. Increasing positive end-expiratory pressure (PEEP) improves oxygenation at the expense of increasing intrathoracic pressures (ITP). Airway pressure release ventilation (APRV) decreases shunt fraction, improves ventilation/perfusion (V/Q) matching, increases cardiac output, and decreases right atrial pressure by facilitating low airway pressure.Case Report:A 40-year-old man presented with dyspnea and hemoptysis. Oxygen saturation (SaO2) 80% on room air with A a gradient of 633 mmHg. Post-intubation SaO2 dropped to 71% on assist control, FiO2 100%, and PEEP of 5 cmH20. Successive PEEP dropped SaO2 to 60–70% and blood pressure plummeted. APRV was initaiated with improvement in SaO2 to 95% and improvement in blood pressure. Hemiparesis developed and CT head showed infarction. CT pulmonary angiogram found a large pulmonary embolism. Transthoracic echocardiogram detected right-to left intracardiac shunt, with large PFO.Conclusions:There should be suspicion for a PFO when severe hypoxemia paradoxically worsens in response to increasing airway pressures. Concomitant venous and arterial thromboemboli should prompt evaluation for intra cardiac shunt. Patients with PFO and hypoxemia should be evaluated for causes of sustained right-to left pressure gradient, such as PE. Management should aim to decrease PVR and optimize V/Q matching by treating the inciting incident (e.g., thrombolytics in PE) and by minimizing ITP. APRV can minimize PVR and maximize V/Q ratios and should be considered in treating patients similar to the one whose case is presented here.

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Introduction: Primary cardiac lymphomas are rare non-Hodgkin lymphomas and account for less than 1% of intrinsic cardiac tumors and extranodal Non-Hodgkin lymphomas. Patients can present with a variety of manifestations including heart failure, chest pain, dyspnea, arrhythmias, and tamponade. Presently, there are no formal established guidelines for treatment of primary cardiac lymphomas. Presentation: This is a case of a 72-year-old white man with past medical history significant for paroxysmal atrial fibrillation and known pulmonary, renal, and cutaneous sarcoidosis who presented with palpitations, dyspnea on exertion and lightheadedness for two-weeks. He was evaluated by his cardiologist who recommended an elective atrial fibrillation radiofrequency ablation (RFA). Prior to the planned procedure a transesophageal echocardiogram was performed which revealed a large tissue density within the pericardial space, adjacent to the free wall of the right ventricle and right atrium, and invading the myocardium with extension through the interatrial septum (Figure 1). The RFA was aborted and the patient was admitted for further evaluation of the new cardiac mass, initially suspected to be cardiac sarcoidosis. Subsequent work up included a cardiac MRI, which displayed a dense 7.5 cm by 3.5 cm mass involving the right ventricle and right atrium, wrapping around the great vessels. Right heart cardiac catheterization with endomyocardial biopsy was performed which revealed clusters of large atypical B lymphoid cells with the following immunophenotype: CD30+, CD79a+, Pax5+, Alk 1-, CD138-, CD 10-, Bcl 2-, Bcl 6-, CD45-, focally CD20+, Ki67: 80-90% (Figure 2). These findings were consistent with diffuse large B cell lymphoma (DLBCL). His PET-CT demonstrated absence of extracardiac lesions, confirming the diagnosis of primary cardiac lymphoma (PCL) (Figure 3). The patient began treatment with a EPOCH-R (rituximab, etoposide, prednisone, vincristine, cyclophosphamide, and doxorubicin) modified chemotherapy based regimen which consisted of a pre-phase treatment with dexamethasone 12 mg once daily for four days, a cumulative dose of cyclophosphamide 600 mg/m2 over five days and etoposide 50 mg/m2 for three days. Doses of cyclophosphamide and etoposide were initiated at lower doses and titrated upward to reach the target dose. This strategy was invoked based upon prior experiences and studies that suggest that a modest pre-phase cytoreduction reduces the risk of cardiac perforation. Rituximab was given on day six. He was also given granulocyte colony stimulating factor (GCSF). Our patient was observed closely in the cardiac intensive care unit throughout the duration of chemotherapy due to the high risk of fatal arrhythmia, tamponade, perforation and heart failure. Interim restaging, confirmed complete remission of the intracardiac mass. His post chemotherapy TTE demonstrated a slight reduction in ejection fraction (Figure 1). He received a total of three cycles of EPOCH-R and remained hemodynamically stable within the hospital. No further chemotherapy was given due to a decline in the patient's performance status. Conclusion: This is the first documented case of primary cardiac diffuse large B cell lymphoma successfully treated with EPOCH-R consisting of a modest pre-phase cytoreduction with steroids, cyclophosphamide and etoposide. The high area under the curve of doxorubicin in this setting is far less cardiotoxic. This regimen reduces the risk of cardiac perforation in patients with relatively normal ejection fractions. Disclosures O'Connor: Mundipharma: Membership on an entity's Board of Directors or advisory committees; Seattle Genetics: Research Funding; TG Therapeutics: Research Funding; Bristol Myers Squibb: Research Funding; Spectrum: Research Funding; Celgene: Research Funding; Bristol Myers Squibb: Research Funding; Celgene: Research Funding; TG Therapeutics: Research Funding.