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Description / Table of Contents: Abstract A paper published in various US journals on Emergency Medicine in 1997 [9], has raised considerable concerns. The authors [9] question if it is justified to continue to recommend initial ventilation as part of basic CPR when performed by lay-bystanders. A few aspects need to be discussed and some questions have to be answered before any changes in the current recommendations may even be considered: e.g. 1. How convincing does the available evidence support the following hypotheses: 1.1. Lay CPR without mouth-to-mouth-ventilation provides better outcome after cardiac arrest than lay CPR with mouth-to-mouth-ventilation. 1.2. Endotracheal intubation may be detrimental in patients suffering from hemodynamic compromises, particularly from VF [46]. 2. Is it scientifically and ethically acceptable to design and perform prospective randomized controlled trials(RCTs) to evaluate the efficacy of those components of BCLS and ACLS which have in accordance with AHA-, ERC Guidlines and ILCOR Statements in the past been applied in millions of cardiac arrest victims and have obviously enabled the patients to lead a meaningsful life after survival; under conditions of the proposed study design patients of the study group would be left without the treatment option ventilation, thus diminishing their chances of survival. Ad 1: The arguments presented by the authors are hardly convincing. The authors themselves state elsewhere that reluctance to perform mouth-to-mouth-ventilation should not represent a major problem because most cardiac arrests of cardiac etiology occur at home and in the presence of a relative or friend. Moreover, unreliable recommendations for mouth-to-mouth-ventilation(AHA) [4], lack of training, retention of skills and knowledge, and a deficit in motivation include the main causes of the disappointingly low figures of bystander CPR worldwide. This situation cannot be improved simply by eliminating a lifesaving component of CPR-ventilation. Instead, the proposal to abandon the administration of unreasonably high ventilation volumens (800–1200 ml/breath) from the present guidlines and to recommend volumes ranging from 400–500 ml/breath recently made by the ERC should be given serious consideration. Furthermore, equipment and training manikins need to be adapted to these more reasonable volumes. Independently of the mechanisms of slow decreases in SaO2 after cardiac arrest (provided no compressions are performed) independently of gasping,ventilatory effects of standard compression or ACD-HCPR in the absence of mouth-to-mouth-ventilation, it is essential to realise that the patient’s airways need to be maintained open at all times (this is unlike animal experiments where the airways are primarily kept open by the respective tissue structures): The minimum requirement of First Responder CPR is the guarantee that open airways are maintained. It may possibly be discussed if the present sequence of ABC might be changed to CAB, a practice adopted in the Netherlands many years ago, however, outcome trials an CAB have not been published to date. In addition, greater demands should be made of training requirements in BLS, attendance of refresher courses should be required, and other groups of the population should be included into these programmes than only relatives or friends of patients at risk of a cardiac arrest. The programmes need to be made mandatory for greater variety of groups and individuals to increase the efficacy and efficiency of bystander resuscitation. The hypotheses made by the above-mentioned authors are neither scientifically nor ethically acceptable. Ad 2: Pepe’s argument [46] regarding the efficacy of endotracheal intubation (ETI)in VF-patients has not been scientifically proven and lacks conclusive evidence. ETI serves to protect the airways and lungs against aspiration of regurgitated material and to facilitate artificial ventilation including PEEP, both under anaesthesia and resuscitation. The efficacy of ETI in the OR has long been proven in RCTs. There is therefore no reason to believe that the protective capabilities of ETI are in any way different for anaesthesia or CPR. There is thus no need to require RCTs which would place one group of patients at a gtreater risk of mortality from aspiration (under conditions which do not permit intubation) than any other group just because somebody is interested in finding out if there is a higher mortality rate in one group of VF patients which is due to a greater percentage of patients dying from aspiration than from VF. Based on these considerations it follows that the RCTs postulated by Becker e.a. are neither scientifically nor economically or ethically justified apart from the fact that in the German speaking countries not a single ethics committee would agree to a study design similar to that described by Becker e.a.

Description / Table of Contents: Abstract Neurogenic pulmonary edema (NPE) is a rare but always life-threatening complication in patients with central nervous system lesions. NPE is evident if patients shortly after cerebral lesions suddenly develop pulmonary edema and other causes of the symptoms, such as aspiration of gastric content, congestive heart failiure and direct toxic exposure, are ruled out. Methods: The current body of literature, partially obtained by computer-guided search (Winspirs) regarding epidemiology, pathophysiology and therapy of NPE was reviewed. Additionally, the case of a patient who developed a sudden pulmonary edema after an episode of tonic-clonic seizures is analyzed. We first provide information about history, definition, incidence and mortality of NPE. Second, a case report of a postictal NPE is presented to illustrate the clinical picture of NPE, and the applied therapeutic strategies are discussed. Third, recent pathophysiologic concepts about symptoms and possible therapeutic principles are reviewed. Fourth, a rational therapeutic plan for the prehospital emergency therapy of NPE is outlined. Results: The different ethiologies all have one characteristic feature: an acute emergency which causes increased intracerebral pressure (ICP). NPE is known in patients after cerebral trauma, intracranial hemorrhage, stroke, intracranial tumor or seizures. The incidence is estimated at around 1% after cerebral trauma, at 71% after cerebral hemorrhage and at 2% after seizures. Mortality is appraised to lie between 60 and 100%, independent of etiology. There is a definite pathophysiologic sequence leading to NPE: a central nervous system lesion causes a sudden increase in ICP which triggers an upregulation of sympathetic signal transduction to assure brain perfusion. Increased tonus of venous and arterial vessels and of myocardial function are the immediate consequences. However, if systemic vascular resistance (SVR) increases excessively, left ventricular failure and finally pulmonary edema (NPE) may result. Additionally, the protein-rich edema fluid points to an increased endothelial permeability within the pulmonary circuit. This is thought to be caused by the acute pressure increase and by neurohumoral mechanisms, possibly similar to those described for the systemic inflammatory response syndrome (SIRS). The most important central nervous system structures involved in NPE are the medulla oblongata and the hypothalamus. Conclusion: NPE is always a life-threatening symptom after increased ICP, where immediate therapeutic interventions are imperative. A rational therapeutic approach needs to be focused on decreasing ICP as primary goal. Additionally, attempts should be made to optimize body oxygenation, decrease pre- and afterload and increase myocardial contractility. Postictal patients suspicious for incipient ventilation problems must be admitted to hospital for further evaluation.