Describing and Classifying Shock: Recent Insights

Cardiogenic shock continues to present a daunting challenge to clinicians, despite an increasing array of percutaneous mechanical circulatory support devices. Mortality for cardiogenic shock has not changed meaningfully in more than 20 years. There have been many attempts to generate risk scores or frameworks to evaluate cardiogenic shock and optimize the use of resources and assist with prognostication. These include the Intra-Aortic Balloon Pump in Cardiogenic Shock (IABP-SHOCK) II risk score, the CardShock score and the new CLIP biomarker score. This article reviews the Society for Cardiac Angiography and Interventions (SCAI) classification of cardiogenic shock and subsequent validation studies. The SCAI classification is simple for clinicians to use as it is based on readily available information and can be adapted depending on the data set that can be accessed. The authors consider the future of the field. Underlying all these efforts is the hope that a better understanding and classification of shock will lead to meaningful improvements in mortality rates

Efficacy of Manual Hemostasis for Percutaneous Axillary Artery Intra-Aortic Balloon Pump Removal

Background. The prevalence of peripheral vascular disease has led to the re-emergence of percutaneous axillary vascular access as a suitable alternative access site to femoral artery. We sought to investigate the efficacy and safety of manual hemostasis in the axillary artery. Methods. Data were collected from a prospective internal registry of patients who had a Maquet® (Rastatt, Germany) Mega 50 cc intra-aortic balloon pumps (IABP) placed in the axillary artery position. They were anticoagulated with weight-based intravenous heparin to maintain an activated partial thromboplastin time (aPTT) of 50-80 seconds. Anticoagulation was discontinued 2 hours prior to the device explantation. Manual compression was used to achieve the hemostasis of the axillary artery. Vascular and bleeding complications attributable to manual hemostasis were classified based on the Valve Academic Research Consortium-2 (VARC-2) and Bleeding Academic Research Consortium-2 (BARC-2) classifications, respectively. Results. 29 of 46 patients (63%) achieved axillary artery homeostasis via manual compression. The median duration of IABP implantation was 12 days (range 1-54 days). Median compression time was 20 minutes (range 5-60 minutes). There were no major vascular or bleeding complications as defined by the VARC-2 and BARC-2 criteria, respectively. Conclusion. Manual compression of the axillary artery appears to be an effective and safe method for achieving hemostasis. Large prospective randomized control trials may be needed to corroborate these findings

Assessment of a numerical model to reproduce event-scale erosion and deposition distributions in a braided river

Becky Goodsell and Eric Scott are thanked for field assistance. Antony Smith assisted with figure production. The field campaign wa funded by NERC Grant NE/G005427/1 and NERC Geophysical Equipment Facility Loan 892. Richard Williams was funded by NERC Grant NE/G005427/1during fieldwork and by a British Hydrological Society Travel Grant whilst visiting NIW

Negative Autoregulation by Fas Stabilizes Adult Erythropoiesis and Accelerates Its Stress Response

Erythropoiesis maintains a stable hematocrit and tissue oxygenation in the basal state, while mounting a stress response that accelerates red cell production in anemia, blood loss or high altitude. Thus, tissue hypoxia increases secretion of the hormone erythropoietin (Epo), stimulating an increase in erythroid progenitors and erythropoietic rate. Several cell divisions must elapse, however, before Epo-responsive progenitors mature into red cells. This inherent delay is expected to reduce the stability of erythropoiesis and to slow its response to stress. Here we identify a mechanism that helps to offset these effects. We recently showed that splenic early erythroblasts, ‘EryA’, negatively regulate their own survival by co-expressing the death receptor Fas, and its ligand, FasL. Here we studied mice mutant for either Fas or FasL, bred onto an immune-deficient background, in order to avoid an autoimmune syndrome associated with Fas deficiency. Mutant mice had a higher hematocrit, lower serum Epo, and an increased number of splenic erythroid progenitors, suggesting that Fas negatively regulates erythropoiesis at the level of the whole animal. In addition, Fas-mediated autoregulation stabilizes the size of the splenic early erythroblast pool, since mutant mice had a significantly more variable EryA pool than matched control mice. Unexpectedly, in spite of the loss of a negative regulator, the expansion of EryA and ProE progenitors in response to high Epo in vivo, as well as the increase in erythropoietic rate in mice injected with Epo or placed in a hypoxic environment, lagged significantly in the mutant mice. This suggests that Fas-mediated autoregulation accelerates the erythropoietic response to stress. Therefore, Fas-mediated negative autoregulation within splenic erythropoietic tissue optimizes key dynamic features in the operation of the erythropoietic network as a whole, helping to maintain erythroid homeostasis in the basal state, while accelerating the stress response

SCAI Clinical Expert Consensus Statement on the Classification of Cardiogenic Shock: This Document was Endorsed by the American College of Cardiology (ACC), the American Heart Association (AHA), the Society of Critical Care Medicine (SCCM), and the Society of Thoracic Surgeons (STS) in April 2019

BACKGROUND: The outcome of cardiogenic shock complicating myocardial infarction has not appreciably changed in the last 30 years despite the development of various percutaneous mechanical circulatory support options. It is clear that there are varying degrees of cardiogenic shock but there is no robust classification scheme to categorize this disease state. METHODS: A multidisciplinary group of experts convened by the Society for Cardiovascular Angiography and Interventions was assembled to derive a proposed classification schema for cardiogenic shock. Representatives from cardiology (interventional, advanced heart failure, noninvasive), emergency medicine, critical care, and cardiac nursing all collaborated to develop the proposed schema. RESULTS: A system describing stages of cardiogenic shock from A to E was developed. Stage A is at risk for cardiogenic shock, stage B is beginning shock, stage C is classic cardiogenic shock, stage D is deteriorating , and E is extremis . The difference between stages B and C is the presence of hypoperfusion which is present in stages C and higher. Stage D implies that the initial set of interventions chosen have not restored stability and adequate perfusion despite at least 30 minutes of observation and stage E is the patient in extremis, highly unstable, often with cardiovascular collapse. CONCLUSION: This proposed classification system is simple, clinically applicable across the care spectrum from pre-hospital providers to intensive care staff but will require future validation studies to assess its utility and potential prognostic implications

SCAI clinical expert consensus statement on the classification of cardiogenic shock: This document was endorsed by the American College of Cardiology (ACC), the American Heart Association (AHA), the Society of Critical Care Medicine (SCCM), and the Society of Thoracic Surgeons (STS) in April 2019

BACKGROUND: The outcome of cardiogenic shock complicating myocardial infarction has not appreciably changed in the last 30 years despite the development of various percutaneous mechanical circulatory support options. It is clear that there are varying degrees of cardiogenic shock but there is no robust classification scheme to categorize this disease state. METHODS: A multidisciplinary group of experts convened by the Society for Cardiovascular Angiography and Interventions was assembled to derive a proposed classification schema for cardiogenic shock. Representatives from cardiology (interventional, advanced heart failure, noninvasive), emergency medicine, critical care, and cardiac nursing all collaborated to develop the proposed schema. RESULTS: A system describing stages of cardiogenic shock from A to E was developed. Stage A is at risk for cardiogenic shock, stage B is beginning shock, stage C is classic cardiogenic shock, stage D is deteriorating , and E is extremis . The difference between stages B and C is the presence of hypoperfusion which is present in stages C and higher. Stage D implies that the initial set of interventions chosen have not restored stability and adequate perfusion despite at least 30 minutes of observation and stage E is the patient in extremis, highly unstable, often with cardiovascular collapse. CONCLUSION: This proposed classification system is simple, clinically applicable across the care spectrum from pre-hospital providers to intensive care staff but will require future validation studies to assess its utility and potential prognostic implications