The Role of Focused 2-Dimensional Echocardiography in Managing Left Ventricular Outflow Tract Obstruction Mimicking Cardiogenic Shock.

Left ventricular outflow tract obstruction (LVOTO) is a common cardiogenic shock (CS) mimic. We present 3 cases of patients presenting with CS following myocardial infarction, exhibiting a poor response to conventional treatment with inotropy and mechanical circulatory support. This triggered echocardiographic assessment by critical care physicians using focused 2-dimensional (2D) echocardiography. This timely assessment identified anterior mitral valve leaflet entrainment into the left ventricular outflow tract (LVOT), causing LVOTO as the underlying shock mechanism. Echocardiographic findings have led to significant changes in management. The patients underwent fluid administration, weaning from inotropy, and mechanical circulatory support explantation, leading to relief of LVOTO and improved hemodynamics. Critical care basic 2D echocardiography accreditations focus on myocardial function and pericardial effusions. Relevant societies administering these accreditations should consider adding LVOT assessment to enable timely diagnosis of this life-threatening CS mimic.

FUSIC HD. Comprehensive haemodynamic assessment with ultrasound.

FUSIC haemodynamics (HD) - the latest Focused Ultrasound in Intensive Care (FUSIC) module created by the Intensive Care Society (ICS) - describes a complete haemodynamic assessment with ultrasound based on ten key clinical questions: 1. Is stroke volume abnormal? 2. Is stroke volume responsive to fluid, vasopressors or inotropes? 3. Is the aorta abnormal? 4. Is the aortic valve, mitral valve or tricuspid valve severely abnormal? 5. Is there systolic anterior motion of the mitral valve? 6. Is there a regional wall motion abnormality? 7. Are there features of raised left atrial pressure? 8. Are there features of right ventricular impairment or raised pulmonary artery pressure? 9. Are there features of tamponade? 10. Is there venous congestion? FUSIC HD is the first system of its kind to interrogate major cardiac, arterial and venous structures to direct time-critical interventions in acutely unwell patients. This article explains the rationale for this accreditation, outlines the training pathway and summarises the ten clinical questions. Further details are included in an online supplementary appendix.

Lund University Cardiac Assist System Induced Liver Laceration and Anterior Cord Infarction After Cardiac Arrest: A Case Report.

We describe a hepatic laceration and subsequent anterior spinal artery syndrome in a 21-year-old man, secondary to prolonged cardiopulmonary resuscitation with a Lund University Cardiac Assist System (LUCAS2) mechanical cardiac compression device. We briefly review the current literature pertaining to hepatic injury from trauma due to cardiopulmonary resuscitation. The etiology of the anterior spinal artery syndrome in this patient is discussed. This case highlights that intra-abdominal causes of hypotension should be considered in patients after a prolonged resuscitation attempt. Extending focused cardiac ultrasound to exclude intra-abdominal free fluid should be routinely considered in these patients.

Extracorporeal support for patients with acute and acute on chronic liver failure.

The number of patients developing liver failure; acute on chronic liver failure and acute liver failure continues to increase, along with the demand for donor livers for transplantation. As such there is a clinical need to develop effective extracorporeal devices to support patients with acute liver failure or acute-on-chronic liver failure to allow time for hepatocyte regeneration, and so avoiding the need for liver transplantation, or to bridge the patient to liver transplantation, and also potentially to provide symptomatic relief for patients with cirrhosis not suitable for transplantation. Currently devices can be divided into those designed to remove toxins, including plasma exchange, high permeability dialyzers and adsorption columns or membranes, coupled with replacement of plasma proteins; albumin dialysis systems; and bioartificial devices which may provide some of the biological functions of the liver. In the future we expect combinations of these devices in clinical practice, due to the developments in bioartificial scaffolds.

Photodrive of magnetic bubbles via magnetoelastic waves.

Precise control of magnetic domain walls continues to be a central topic in the field of spintronics to boost infotech, logic, and memory applications. One way is to drive the domain wall by current in metals. In insulators, the incoherent flow of phonons and magnons induced by the temperature gradient can carry the spins, i.e., spin Seebeck effect, but the spatial and time dependence is difficult to control. Here, we report that coherent phonons hybridized with spin waves, magnetoelastic waves, can drive magnetic bubble domains, or curved domain walls, in an iron garnet, which are excited by ultrafast laser pulses at a nonabsorbing photon energy. These magnetoelastic waves were imaged by time-resolved Faraday microscopy, and the resultant spin transfer force was evaluated to be larger for domain walls with steeper curvature. This will pave a path for the rapid spatiotemporal control of magnetic textures in insulating magnets.

The immunobiology of primary sclerosing cholangitis.

Primary sclerosing cholangitis (PSC) is a chronic cholestatic liver disease histologically characterized by the presence of intrahepatic and/or extrahepatic biliary duct concentric, obliterative fibrosis, eventually leading to cirrhosis. Approximately 75% of patients with PSC have inflammatory bowel disease. The male predominance of PSC, the lack of a defined, pathogenic autoantigen, and the potential role of the innate immune system suggest that it may be due to dysregulation of immunity rather than a classic autoimmune disease. However, PSC is associated with several classic autoimmune diseases, and the strongest genetic link to PSC identified to date is with the human leukocyte antigen DRB01*03 haplotype. The precise immunopathogenesis of PSC is largely unknown but likely involves activation of the innate immune system by bacterial components delivered to the liver via the portal vein. Induction of adhesion molecules and chemokines leads to the recruitment of intestinal lymphocytes. Bile duct injury results from the sustained inflammation and production of inflammatory cytokines. Biliary strictures may cause further damage as a result of bile stasis and recurrent secondary bacterial cholangitis. Currently, there is no effective therapy for PSC and developing a rational therapeutic strategy demands a better understanding of the disease.