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Author(s): V. Chhor [sup.1] [sup.2], A. Follin [sup.1], J. Joachim [sup.1], B. Champigneulle [sup.1], J. Chatelon [sup.1], G. Favé [sup.1], A. Neuschwander [sup.1], J. Mantz [sup.1], Romain Pirracchio [sup.1] [sup.3] [...]

Objective Brain injury is well established as a cause of early mortality after out-of-hospital cardiac arrest (OHCA), but postresuscitation shock also contributes to these deaths. This study aims to describe the respective incidence, risk factors, and relation to mortality of post-cardiac arrest (CA) shock and brain injury. Design Retrospective analysis of an observational cohort. Setting 24-bed medical intensive care unit (ICU) in a French university hospital. Patients All consecutive patients admitted following OHCA were considered for analysis. Post-CA shock was defined as a need for infusion of vasoactive drugs after resuscitation. Death related to brain injury included brain death and care withdrawal for poor neurological evolution. Intervention None. Measurements and main results Between 2000 and 2009, 1,152 patients were admitted after OHCA. Post-CA shock occurred in 789 (68 %) patients. Independent factors associated with its onset were high blood lactate and creatinine levels at ICU admission. During the ICU stay, 269 (34.8 %) patients died from post-CA shock and 499 (65.2 %) from neurological injury. Age, raised blood lactate and creatinine values, and time from collapse to restoration of spontaneous circulation increased the risk of ICU mortality from both shock and brain injury, whereas a shockable rhythm was associated with reduced risk of death from these causes. Finally, bystander cardiopulmonary resuscitation (CPR) decreased the risk of death from neurological injury. Conclusions Brain injury accounts for the majority of deaths, but post-CA shock affects more than two-thirds of OHCA patients. Mortality from post-CA shock and brain injury share similar risk factors, which are related to the quality of the rescue process., Author(s): Virginie Lemiale [sup.1] [sup.5] [sup.7], Florence Dumas [sup.2] [sup.6], Nicolas Mongardon [sup.1] [sup.5], Olivier Giovanetti [sup.6], Julien Charpentier [sup.1] [sup.5], Jean-Daniel Chiche [sup.1] [sup.5], Pierre Carli [sup.4] [sup.5], Jean-Paul [...]

Byline: Brendan G. Carr (1,2,4,5), Munish Goyal (2,3), Roger A. Band (2), David F. Gaieski (2,3), Benjamin S. Abella (2,3), Raina M. Merchant (1,2,3,4), Charles C. Branas (5), Lance B. Becker (2,3), Robert W. Neumar (2,3) Abstract: Purpose We sought to generate national estimates for post-cardiac arrest mortality, to assess trends, and to identify hospital factors associated with survival. Methods We used a national sample of US hospitals to identify patients resuscitated after cardiac arrest from 2000 to 2004 to describe the association between hospital factors (teaching status, location, size) and mortality, length of stay, and hospital charges. Analyses were performed using logistic regression. Results A total of 109,739 patients were identified. In-hospital mortality was 70.6%. A 2% decrease in unadjusted mortality from 71.6% in 2000 to 69.6% in 2004 (OR 0.96, P < 0.001) was observed. Mortality was lower at teaching hospitals (OR 0.58, P = 0.001), urban hospitals (OR 0.63, P = 0.004), and large hospitals (OR 0.55, P < 0.001). Conclusion Mortality after in-hospital cardiac arrest decreased over 5 years. Mortality was lower at urban, teaching, and large hospitals. There are implications for dissemination of best practices or regionalization of post-cardiac arrest care. Author Affiliation: (1) The Robert Wood Johnson Clinical Scholars Program, University of Pennsylvania School of Medicine, 932 Blockley Hall, 423 Guardian Drive, Philadelphia, PA, 19104-6021, USA (2) Department of Emergency Medicine, University of Pennsylvania School of Medicine, Philadelphia, USA (3) Center for Resuscitation Science, University of Pennsylvania School of Medicine, Philadelphia, USA (4) The Leonard Davis Institute of Health Economics, University of Pennsylvania, Philadelphia, USA (5) Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania School of Medicine, Philadelphia, USA Article History: Registration Date: 08/10/2008 Received Date: 28/04/2008 Accepted Date: 26/09/2008 Online Date: 21/10/2008

Byline: Roberto Imberti (1), Guido Bellinzona (1), Francesca Riccardi (1), Michele Pagani (1), Martin Langer (1) Keywords: Cardiac arrest Cardiopulmonary resuscitation Brain tissue partial pressure of oxygen Intracranial pressure Cerebral perfusion pressure Cerebral oxygen metabolism Abstract: Objective: To report on the effects of cardiopulmonary resuscitation (CPR) instituted immediately after a cardiac arrest on cerebral perfusion pressure (CPP) and cerebral tissue oxygen tension (PbrO.sub.2). Design: Case report. Setting: ICU of a university hospital. Patient: A head-injured 17-year-old man submitted to multimodal neurological monitoring underwent sudden cardiac arrest and successful CPR. Interventions: External chest compression, 100% oxygen ventilation, volume expansion and standard ACLS protocols. Measurements and results: Heart rate, ECG, mean arterial blood pressure (MABP), ETCO.sub.2,PaO.sub.2, intracranial pressure (ICP), CPP and PbrO.sub.2 were continuously monitored during CPR and data recorded at 15-s intervals by a dedicated personal computer. At the onset of the cardiac arrest, PbrO.sub.2 decreased to zero. The institution of CPR resulted in a progressive increase of MABP, CPP and PbrO.sub.2. Assuming, on the basis of previous experimental and clinical reports, 8 mmHg PbrO.sub.2 as a possible ischaemic/hypoxic threshold value, during the first 6.5 min of CPR, PbrO.sub.2 values were below this threshold (range 0--7 mmHg) and CPP values were 25 mmHg for 77.3% of the time. These values were associated with a PbrO.sub.2 >8 mmHg (range 8--28 mmHg) at all times. Conclusions: In the clinical setting of a witnessed cardiac arrest, immediate institution of CPR can be effective in generating PbrO.sub.2 values above a supposed ischaemic/hypoxic threshold when CPP is >25 mmHg. PbrO.sub.2 monitoring by the Licox system is sensitive and reliable, even at low values, and can be suitable for evaluating cerebral oxygenation during experimental CPR. Author Affiliation: (1) Servizio di Anestesia e Rianimazione II, IRCCS Policlinico S. Matteo, 27100, Pavia, Italy Article History: Received Date: 29/10/2002 Accepted Date: 18/02/2003 Article note: Electronic Publication

Byline: D. Scherr (1), G. Brunner (1), P. Kaufmann (1), P. Lercher (1), A. Lueger (1), B. Rotman (1), K. Smolle (1), G. Stark (1), W. Klein (1), G. Krejs (1) Keywords: Ajmaline Arrhythmia Brugada syndrome Ventricular fibrillation ST segment elevation Sudden death Abstract: We report a 37-year-old man with documented aborted sudden death. After resuscitation, the patient showed no structural heart disease but the ECG showed a right bundle-branch block with a descending ST segment elevation in leads V.sub.1 and V.sub.2. After transient normalization of the ECG, the administration of ajmaline led to spontaneous development of the distinct descending ST segment elevation in the right precordial leads and therefore to the diagnosis of Brugada syndrome. The incidence of sudden cardiac death among these patients is high. The only treatment is an implantable cardioverter-defibrillator (ICD). The Brugada syndrome should therefore be borne in mind in the differential diagnosis of sudden death. Author Affiliation: (1) Department of Internal Medicine, Karl-Franzens-University Hospital, Auenbruggerplatz 15, 8036 Graz, Austria Article History: Received Date: 14/08/2001 Accepted Date: 12/03/2002 Article note: Electronic Publication

Byline: Andreas Bur (1), Harald Kittler (2), Fritz Sterz (1), Michael Holzer (1), Philip Eisenburger (1), Elisabeth Oschatz (1), Julia Kofler (1), Anton N. Laggner (1) Keywords: Basic life support Cardiopulmonary resuscitation Defibrillation Heart arrest Hospital costs Intubation Outcome assessment Ventricular fibrillation Abstract: Objective: To evaluate the effects of basic life support, time to first defibrillation and emergency medical service arrival time on neurologic outcome and expenses for hospital care in patients after cardiac arrest. Setting: Large urban emergency medical services system and emergency department in a 2000-bed university hospital. Design: Outcome and cost benefit analysis of patients admitted to the hospital after witnessed, out-of-hospital, ventricular fibrillation cardiac arrest from October 1, 1991, until December 31, 1997. Patients: Out of 1054 patients with out-of-hospital cardiac arrest, 276 were eligible. Measurements and results: The effects of basic and advanced life support measures on neurologic outcome and hospital expenses were evaluated. In contrast to intubation (odds ratio 1.08 95% CI: 0.51--2.31 p=0.84), basic life support (odds ratio 0.44 95% CI: 0.24--0.77 p=0.004) and time to first defibrillation (odds ratio 1.08 95% CI: 1.03--1.13 p=0.001) were significantly correlated with good neurologic outcome. Among the patients who did not receive basic life support, the average cost per patient with good neurologic outcome significantly increased with the delay of the first defibrillation (p Author Affiliation: (1) University Clinic of Emergency Medicine, Allgemeines Krankenhaus der Stadt Wien, Wahringer Gurtel 18--20/6/D, 1090 Vienna, Austria (2) Department of Dermatology, Allgemeines Krankenhaus der Stadt Wien, Wahringer Gurtel 18--20/6/D, 1090 Vienna, Austria Article History: Received Date: 12/10/2000 Accepted Date: 27/06/2001 Article note: Final revision received: 26 June 2001 Electronic Publication

Byline: M. Oppert (1), C. H. Gleiter (3), C. Muller (2), A. Reinicke (1), N. von Ahsen (1), U. Frei (1), K.-U. Eckardt (1) Keywords: Key words Hypoxia; Ischemia; Acute phase proteins; Cardiac arrest; Infections Abstract: Objective: Inflammation and hypoxia are frequently associated, but their interaction is poorly understood. In vitro studies have shown that hypoxia stimulates the genes of acute phase proteins (APP) and cytokines known to induce APP. We decided to determine kinetics and potential determinants of an acute phase response after cardiac arrest and to assess whether isolated moderate hypoxia can induce APP in humans in vivo. Design: Prospective, observational study in patients and human experiment. Setting: Tertiary care university hospital. Patients and participants: 22 patients after primarily successful cardiopulmonary resuscitation (CPR) and 7 healthy volunteers. Interventions: None in patients exposure of volunteers to simulated altitude (460 torr/6 h). Results: Following CPR, type-1 APP (C-reactive protein, [alpha].sub.1-acidglycoprotein, serum amyloid A) and type-2 APP (haptoglobin, [alpha].sub.1-antitrypsin) increased consistently within 1--2 days and the 'negative' APP transferrin was downregulated. This APP response occurred irrespective of the cause of arrest, the estimated time of anoxia, clinical course or patient outcome and was not different in patients with and without infectious complications. Exposure of healthy volunteers to less severe but more prolonged hypoxia did not induce APP, although a time dependent increase of serum erythropoietin (EPO) was measurable under these conditions, indicating the activation of oxygen dependent gene expression. Conclusions: (i) A marked acute phase response occurs regularly after cardiac arrest, but within the complexity of this situation the severity of hypoxia is not a predominant determinant of this response. (ii) Despite in vitro evidence for similarities in the oxygen dependent regulation of APP and EPO production, the oxygen sensitivity of these proteins in vivo is different. (iii) Measurements of APP are not revealing regarding infectious complications in the early phase after CPR. Author Affiliation: (1) Department of Nephrology and Medical Intensive Care, Campus Virchow Klinikum, Charite, Humboldt University, Augustenburger Platz 1, 13 353 Berlin, Germany e-mail: kai-uwe.eckardt@charite.de Tel.: + 49(30)45 05 31 32 Fax: + 49(30)45 05 39 09, DE (2) Department of Clinical Chemistry, Campus Virchow-Klinikum, Charite, Humboldt University, Berlin, Germany, DE (3) Department of Clinical Pharmacology, University of Gottingen, Germany, DE Article note: Received: 28 March 1999 Final revision received: 10 June 1999 Accepted: 1 September 1999

Byline: S. Gando (1), M. Igarashi (2), T. Kameue (2), S. Nanzaki (2) Keywords: Key words Human; Cardiac arrest; Cardiopulmonary resuscitation; Ionized calcium; Lactate Abstract: Objective: To determine the relationship between ionized calcium concentrations and blood lactate levels during cardiac arrest and cardiopulmonary resuscitation (CPR). Design: A prospective cohort study. Setting: Emergency department (ED) and general intensive care unit in a city hospital (tertiary care center). Patients and participants: 32 patients with out-of-hospital cardiac arrest 14 of the patients had a return of spontaneous circulation (ROSC) and 18 of the patients died. Interventions: Basic and advanced life support. Measurements and results: Concentrations of ionized and total calcium, bicarbonate, lactate, and pyruvate and pH were simultaneously determined immediately upon arrival at the ED, and at 30 and 60 min. Upon arrival at the ED, all patients had ionized hypocalcemia (1.09 +- 0.02 mmol/l). Ionized and total calcium concentrations progressively decreased during and after CPR, but pH and bicarbonate concentrations did not show any significant changes. In patients who had ROSC, a significant, but perhaps not clinically relevant, relationship was observed between the ionized calcium concentrations and pH (r .sup.2 = 0.152, p = 0.0117). In the patients who died, there were significant correlations between ionized calcium and pH (r .sup.2 = 0.382, p = 0.0001) and bicarbonate concentrations (r .sup.2 = 0.298, p = 0.0006). No definite correlations were demonstrated when comparing ionized calcium concentrations with lactate and pyruvate concentrations. Conclusions: Ionized hypocalcemia during out-of-hospital cardiac arrest and CPR is not due to binding by both lactate and pyruvate, but may be partly due to complexing by bicarbonate, with some modifications due to variations in pH. Author Affiliation: (1) Department of Anesthesiology and Intensive Care, Hokkaido University School of Medicine, N15, W7, Kita-ku, Sapporo, 060 Japan FAX: +81 (11) 716-9666, JP (2) Department of Emergency and Critical Care Medicine, Sapporo City General Hospital, Sapporo, Japan, JP Article note: Received: 20 January 1997 Accepted: 18 October 1997

Left ventricular hypertrophy, small vessel disease and premature coronary artery atherosclerosis, with or without lumen thrombosis, are frequent findings that may account for myocardial ischaemia and risk of cardiac arrest [...]