High Hemoglobin Level As a Limiting Factor for Extracorporeal Membrane Oxygenation.

We report the case of a 47 year old male who developed acute respiratory distress syndrome after bariatric surgery, requiring a venovenous extracorporeal membrane oxygenation. An inadequate extracorporeal membrane oxygenation output flow was observed, possibly because of severe polycythemia and hyperviscosity. Management with acute normovolemic hemodilution corrected both the biologic and hemodynamic parameters. To our knowledge, this is the first reported case of acute normovolemic hemodilution to improve extracorporeal membrane oxygenation outflow. Clinicians should be aware that polycythemia and hyperviscosity may impair extracorporeal membrane oxygenation support and that acute normovolemic hemodilution may be a safe and efficient procedure to address such matter. The optimal hemoglobin level on extracorporeal membrane oxygenation deserves further investigation.

Right over left ventricular end-diastolic area relevance to predict hemodynamic intolerance of high-frequency oscillatory ventilation in patients with severe ARDS.

BACKGROUND: High-frequency oscillatory ventilation (HFOV) does not improve the prognosis of ARDS patients despite an improvement in oxygenation. This paradox may partly be explained by HFOV hemodynamic side-effects on right ventricular function. Our goal was to study the link between HFOV and hemodynamic effects and to test if the pre-HFOV right over left ventricular end-diastolic area (RVEDA/LVEDA) ratio, as a simple parameter of afterload-related RV dysfunction, could be used to predict HFOV hemodynamic intolerance in patients with severe ARDS. METHODS: Twenty-four patients were studied just before and within 3 h of HFOV using transthoracic echocardiography and transpulmonary thermodilution. RESULTS: Before HFOV, the mean PaO2/FiO2 ratio was 89 ± 23. The number of patients with a RVEDA/LVEDA ratio >0.6 significantly increased after HFOV [11 (46 %) vs. 17 (71 %)]. Although HFOV did not significantly decrease the arterial pressure (systolic, diastolic, mean and pulse pressure), it significantly decreased the cardiac index (CI) by 13 ± 18 % and significantly increased the RVEDA/LVEDA ratio by 14 ± 11 %. A significant correlation was observed between pre-HFOV RVEDA/LVEDA ratio and CI diminution after HFOV (r = 0.78; p < 0.0001). A RVEDA/LVEDA ratio superior to 0.6 resulted in a CI decrease >15 % during HFOV with a sensitivity of 80 % (95 % confidence interval 44-98 %) and a specificity of 79 % (confidence interval 49-95 %). CONCLUSION: The RVEDA/LVEDA ratio measured just before HFOV predicts the hemodynamic intolerance of this technique in patients with severe ARDS. A high ratio under CMV raises questions about the use of HFOV in such patients. TRIAL REGISTRATION: ClinicalTrials.gov: NCT01167621.

Cardiac tamponade related to a coronary injury by a pericardial calcification: an unusual complication.

BACKGROUND: Cardiac tamponade is a rare but severe complication of pericardial effusion with a poor prognosis. Prompt diagnosis using transthoracic echocardiography allows guiding initial therapeutic management. Although etiologies are numerous, cardiac tamponade is more often due to a hemopericardium. Rarely, a coronary injury may result in such a hemopericardium with cardiac tamponade. Coronary artery aneurysm are the main etiologies but blunt, open chest trauma or complication of endovascular procedures have also been described. CASE PRESENTATION: A 83-year-old hypertensive man presented for dizziness and hypotension. The patient had oliguria and mottled skin. Transthoracic echocardiography disclosed a circumferential pericardial effusion with a compressed right atrium, confirmed by contrast-enhanced thoracic CT scan. A pig-tail catheter allowed to withdraw 500 mL of blood, resulting in a transient improvement of hemodynamics. Rapidly, recurrent hypotension prompted a reoperation. An active bleeding was identified at the level of the retroventricular coronary artery. The pericardium was thickened with several "sharping" calcified plaques in the vicinity of the bleeding areas. On day 2, vasopressors were stopped and the patient was successfully extubated. Final diagnosis was a spontaneous cardiac tamponade secondary to a coronary artery injury attributed to a "sharping"calcified pericardial plaque. CONCLUSION: Cardiac tamponade secondary to the development of a hemopericardium may develop as the result of a myocardial and coronary artery injury induced by a calcified pericardial plaque.