Adult advanced life support: Section 3 of the European Resuscitation Council Guidelines for Resuscitation 2015

Erweiterte lebensrettende Maßnahmen für Erwachsene („advanced life support“, ALS) kommen zum Einsatz, nachdem Basismaßnahmen zur Wiederbelebung („basic life support“, BLS) begonnen und, wenn sinnvoll, ein automatisierter externer Defibrillator (AED) verwendet wurde. Die Basismaßnahmen zur Wiederbelebung eines Erwachsenen und der Einsatz von AEDs wird in Kap. 2 ausgeführt. Basis- und erweiterte Maßnahmen sollen nahtlos ineinander übergehen, da erstere fortgeführt werden und sich mit den erweiterten überschneiden. Dieses Kapitel über die erweiterten Maßnahmen beinhaltet die Vermeidung des Kreislaufstillstands, spezielle Aspekte des außerklinischen ALS, den Start der innerklinischen Reanimation, den ALS-Algorithmus, die manuelle Defibrillation, das Atemwegsmanagement während der Reanimaton, Medikamente und ihre Anwendung während der Reanimation sowie die Behandlung von Periarrest-Arrhythmien. Es gibt zwei Änderungen in der äußeren Form dieser Leitlinien des Europäischen Rats für Wiederbelebung seit den Leitlinien von 2010: [1] Das Kapitel „Elektrotherapie“ [2] ist nicht mehr eigenständig, sondern Teil dieses Kapitels; und die Leitlinien zur Behandlung nach Reanimation sind in ein neues Kapitel ausgegliedert, welches die Bedeutung dieses letzten Glieds der Überlebenskette unterstreicht [3]. Diese Leitlinien basieren auf den International Liaison Committee on Resuscitation (ILCOR) Consensus on Science and Treatment Recommendations (CoSTR) für ALS von 2015 [4]. Die Überprüfung der ILCOR-Empfehlungen von 2015 konzentrierte sich auf 42 Themen, entsprechend der zeitlichen Abfolge der erweiterten Maßnahmen: Defibrillation, Atemwege, Oxygenierung und Ventilation, Kreislaufunterstützung und Überwachung und Einsatz von Medikamenten während der Reanimation. Für diese Leitlinien wurden die ILCOR-Empfehlungen durch ein gezieltes Literatur-Review ergänzt, welches von der ERC-ALS-Leitlinien Autorengruppe zu den Themen die nicht in den ILCOR-CoSTR-Empfehlungen von 2015 überarbeitet wurden erstellt wurde. Die Leitlinien wurden ausgearbeitet, von den ALS-Verfassern geprüft und abschließend von der ERC-Vollversammlung und dem ERC-Vorstand abgesegnet

Pre-hospital body surface potential mapping improves early diagnosis of acute coronary artery occlusion in patients with ventricular fibrillation and cardiac arrest

Aims: To determine whether 80-lead body surface potential mapping (BSPM) improves detection of acute coronary artery occlusion in patients presenting with out-of-hospital cardiac arrest (OHCA) due to ventricular fibrillation (VF) and who survived to reach hospital. Methods and results: Of 645 consecutive patients with OHCA who were attended by the mobile coronary care unit, VF was the initial rhythm in 168 patients. Eighty patients survived initial resuscitation, 59 of these having had BSPM and 12-lead ECG post-return of spontaneous circulation (ROSC) and in 35 patients (age 69±13 yrs; 60% male) coronary angiography performed within 24. h post-ROSC. Of these, 26 (74%) patients had an acutely occluded coronary artery (TIMI flow grade [TFG] 0/1) at angiography. Twelve-lead ECG criteria showed ST-segment elevation (STE) myocardial infarction (STEMI) using Minnesota 9-2 criteria - sensitivity 19%, specificity 100%; ST-segment depression (STD) =0.05. mV in =2 contiguous leads - sensitivity 23%, specificity 89%; and, combination of STEMI or STD criteria - sensitivity 46%, specificity 100%. BSPM STE occurred in 23 (66%) patients. For the diagnosis of TFG 0/1 in a main coronary artery, BSPM STE had sensitivity 88% and specificity 100% (c-statistic 0.94), with STE occurring most commonly in either the posterior, right ventricular or high right anterior territories. Conclusion: Among OHCA patients presenting with VF and who survived resuscitation to reach hospital, post-resuscitation BSPM STE identifies acute coronary occlusion with sensitivity 88% and specificity 100% (c-statistic 0.94). © 2012 Elsevier Ireland Ltd

On the mechanisms governing gas penetration into a tokamak plasma during a massive gas injection

A new 1D radial fluid code, IMAGINE, is used to simulate the penetration of gas into a tokamak plasma during a massive gas injection (MGI). The main result is that the gas is in general strongly braked as it reaches the plasma, due to mechanisms related to charge exchange and (to a smaller extent) recombination. As a result, only a fraction of the gas penetrates into the plasma. Also, a shock wave is created in the gas which propagates away from the plasma, braking and compressing the incoming gas. Simulation results are quantitatively consistent, at least in terms of orders of magnitude, with experimental data for a D 2 MGI into a JET Ohmic plasma. Simulations of MGI into the background plasma surrounding a runaway electron beam show that if the background electron density is too high, the gas may not penetrate, suggesting a possible explanation for the recent results of Reux et al in JET (2015 Nucl. Fusion 55 093013)

SARS-CoV-2-specific nasal IgA wanes 9 months after hospitalisation with COVID-19 and is not induced by subsequent vaccination

BACKGROUND: Most studies of immunity to SARS-CoV-2 focus on circulating antibody, giving limited insights into mucosal defences that prevent viral replication and onward transmission. We studied nasal and plasma antibody responses one year after hospitalisation for COVID-19, including a period when SARS-CoV-2 vaccination was introduced. METHODS: In this follow up study, plasma and nasosorption samples were prospectively collected from 446 adults hospitalised for COVID-19 between February 2020 and March 2021 via the ISARIC4C and PHOSP-COVID consortia. IgA and IgG responses to NP and S of ancestral SARS-CoV-2, Delta and Omicron (BA.1) variants were measured by electrochemiluminescence and compared with plasma neutralisation data. FINDINGS: Strong and consistent nasal anti-NP and anti-S IgA responses were demonstrated, which remained elevated for nine months (p < 0.0001). Nasal and plasma anti-S IgG remained elevated for at least 12 months (p < 0.0001) with plasma neutralising titres that were raised against all variants compared to controls (p < 0.0001). Of 323 with complete data, 307 were vaccinated between 6 and 12 months; coinciding with rises in nasal and plasma IgA and IgG anti-S titres for all SARS-CoV-2 variants, although the change in nasal IgA was minimal (1.46-fold change after 10 months, p = 0.011) and the median remained below the positive threshold determined by pre-pandemic controls. Samples 12 months after admission showed no association between nasal IgA and plasma IgG anti-S responses (R = 0.05, p = 0.18), indicating that nasal IgA responses are distinct from those in plasma and minimally boosted by vaccination. INTERPRETATION: The decline in nasal IgA responses 9 months after infection and minimal impact of subsequent vaccination may explain the lack of long-lasting nasal defence against reinfection and the limited effects of vaccination on transmission. These findings highlight the need to develop vaccines that enhance nasal immunity. FUNDING: This study has been supported by ISARIC4C and PHOSP-COVID consortia. ISARIC4C is supported by grants from the National Institute for Health and Care Research and the Medical Research Council. Liverpool Experimental Cancer Medicine Centre provided infrastructure support for this research. The PHOSP-COVD study is jointly funded by UK Research and Innovation and National Institute of Health and Care Research. The funders were not involved in the study design, interpretation of data or the writing of this manuscript

Large-scale phenotyping of patients with long COVID post-hospitalization reveals mechanistic subtypes of disease

One in ten severe acute respiratory syndrome coronavirus 2 infections result in prolonged symptoms termed long coronavirus disease (COVID), yet disease phenotypes and mechanisms are poorly understood1. Here we profiled 368 plasma proteins in 657 participants ≥3 months following hospitalization. Of these, 426 had at least one long COVID symptom and 233 had fully recovered. Elevated markers of myeloid inflammation and complement activation were associated with long COVID. IL-1R2, MATN2 and COLEC12 were associated with cardiorespiratory symptoms, fatigue and anxiety/depression; MATN2, CSF3 and C1QA were elevated in gastrointestinal symptoms and C1QA was elevated in cognitive impairment. Additional markers of alterations in nerve tissue repair (SPON-1 and NFASC) were elevated in those with cognitive impairment and SCG3, suggestive of brain–gut axis disturbance, was elevated in gastrointestinal symptoms. Severe acute respiratory syndrome coronavirus 2-specific immunoglobulin G (IgG) was persistently elevated in some individuals with long COVID, but virus was not detected in sputum. Analysis of inflammatory markers in nasal fluids showed no association with symptoms. Our study aimed to understand inflammatory processes that underlie long COVID and was not designed for biomarker discovery. Our findings suggest that specific inflammatory pathways related to tissue damage are implicated in subtypes of long COVID, which might be targeted in future therapeutic trials

Pharmacological vasodilatation improves efficiency of rewarming from hypothermic cardiopulmonary bypass

An afterdrop in core temperature after hypothermic cardiopulmonary bypass (CPB) is related to inadequate peripheral rewarming. We proposed that pharmacological vasodilatation during rewarming on bypass would improve peripheral rewarming and reduce the degree of afterdrop. Fifty-nine of 120 patients were randomized to receive a sodium nitroprusside (SNP) infusion during the rewarming stage of hypothermic CPB. Mean systemic vascular resistance (SVR) during the rewarming phase of CPB was 1129 dyne s-1 cm-5 in the control group and 768 dyne s-1 m-5 in the SNP group (P &lt; or = 0.001). Patients receiving SNP rewarmed to 37.0 degrees C faster (299 min vs 376 min; P = 0.003) and were extubated earlier (490 min vs 621 min; P = 0.001). Patients receiving SNP had a warmer mean peripheral temperature (MPT) (32.9 degrees C vs 32.4 degrees C; P = 0.05) on termination of CPB. Postoperative core temperature fell less in the SNP group (35.6 degrees C vs 35.2 degrees C; P = 0.01) as did MPT (31.8 degrees C vs 31.2 degrees C; P = 0.004). SNP-induced vasodilatation during rewarming from hypothermic CPB improves peripheral rewarming, reduces the degree of postoperative core and peripheral hypothermia and reduces time to extubation

Are European Resuscitation Council recommendations for paddle force achievable during defibrillation?

Transthoracic impedance (TTI) is an important determinant of success in defibrillation. Low TTI increases transmyocardial current and therefore increases the chance of depolarising a critical mass of myocardium. A major component of TTI occurs at the paddle-skin interface and is minimised by pressure applied to the defibrillation paddles. The International Liaison Committee on Resuscitation (ILCOR) 2000 guidelines recommend that 'firm force' should be applied to both paddles, whereas previous European Resuscitation Council (ERC) 1992 guidelines were more precise, recommending that 12 kg of force should to be applied. We assessed whether defibrillator operators are capable of achieving 12 kg paddle force. Fifty advanced life support-trained doctors and nurses attempted to achieve 12 kg paddle force while simulating defibrillation on a resuscitation doll. The median value of the maximum pressures obtainable was 10.1 (max 16.0; min 5.0) kg force. Only 14% could achieve &gt; or =12 kg force on both paddles for defibrillation. Men achieved more force than women (10.7 vs. 8.1 kg force; P&lt;0.01), and there was a correlation between maximum force achieved and operator height (r2=0.27) and dominant hand-grip strength (r2=0.34). The ERC recommendation of 12 kg paddle force is not achievable by the majority of defibrillator operators

Effects of changes in packed cell volume on the specific heat capacity of blood: implications for studies measuring heat exchange in extracorporeal circuits

Extracorporeal circuits such as cardiopulmonary bypass (CPB) and renal dialysis machines cause active and/or passive loss of body heat. Attempts to quantify this heat loss are generally based on the Fick principle which requires knowledge of the specific heat capacity (SHC) of blood. As changes in packed cell volume are common, we investigated the effect of these changes on the SHC of blood over a range of packed cell volumes (PCV) from whole blood at 43.1% (3594 J kg-1 degrees C-1) to pure Hartmann's solution (4153 J kg-1 degrees C-1). The SHC of other fluids used during CPB was also measured and found to be 4139 J kg-1 degrees C-1 and 4082 J kg-1 degrees C-1 for normal saline and Gelofusine, respectively. The maximum variability in SHC over the range of PCV values encountered during CPB was calculated to be small (5.5%). We conclude that use of a constant value of SHC for calculation of thermal energy transfer is currently justified