Resuscitation
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In November 1992 the European Resuscitation Council issued new guidelines which included the description of a modified recovery position. Anecdotal reports have suggested that this 'new' position may result in obstructed venous return in the dependent arm. The findings of a small study to evaluate the 'new' recovery position are reported here. ⋯ In the 'new' position 67% of the study group developed signs of venous or venous and arterial obstruction; no such complication was encountered when the same individuals were placed in the semi-prone recovery position. The need to position unconscious persons in some form of recovery position is emphasised, however, the suggestion that the semi-prone position be re-adopted is offered for discussion. Alternatively, adequate monitoring of perfusion and venous drainage in the dependent limb must be undertaken if the 'new' recovery position is chosen.
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Anaesthetic residents used bag valve mask (BVM) or mouth mask (MM) ventilation, both with an O2 flow of 15 l min-1 to ventilate 30 ASA I or II anaesthetised patients for 4 min prior to endotracheal intubation. Mean nasopharyngeal O2 was higher with BVM (BVM 95% (S. D. 3%) MM 54% (S. ⋯ Gastric insufflation was detected in two MM and two BVM patients. This tended to be more severe with MM ventilation. Although MM ventilation has some important disadvantages it can be used effectively by resuscitators with little or no experience in its use.
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Defibrillation of patients with primary ventricular fibrillation (VF) results in a variety of rhythm changes. We analysed these changes in rhythm in 200 patients, using the American Heart Association's recommendation of two defibrillations prior to drug therapy. Sixty-three (31.5%) patients were immediate survivors with 38 (19%) being discharged from hospital alive. ⋯ Seventeen percent (34) of patients were defibrillated to sinus rhythm after the first defibrillation and 14% (19) after the second, with similar hospital discharge rates (62% and 58%, respectively). Sixty percent (32) of patients in sinus rhythm, after two defibrillations, were discharged alive, compared to only 4% (6) of those patients not in sinus rhythm after two defibrillations. Our data provide new information on rhythm changes during resuscitation and supports the need for the earliest possible initiation of basic life support and defibrillation to improve survival from cardiac arrest due to ventricular fibrillation.
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The exact impact of the 'interval between cardiac arrest (CA) and the start of basic cardiopulmonary resuscitation (CPR) performed by bystanders' on outcome is not fully established. We retrospectively evaluated data with regard to response intervals of 1195 out-of-hospital CA interventions where bystander CPR was performed and continued by the eight mobile intensive care units (MICUs) participating in the Belgian Cerebral Resuscitation Registry between 1982 and 1990. Partial correlations between time elapsed from CALL to CPR by lay public and outcome were determined when the effect of response times of 1st and 2nd tier were removed. ⋯ The partial correlation coefficient between prolonged survival and time passed between CALL and bystander CPR was negative for all types of CA, yet significance was reached only in the non-witnessed group. Using ROSC as the endpoint significance is achieved in all groups except the VF patients, where the intervention times were shorter. In our population, prolonged survival was independently and negatively influenced by a delay between CALL and any CPR in the non-witnessed CA group (n = 421).
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Tumor necrosis factor (TNF) is a key mediator involved in many physiologic processes including immunity, inflammation, and metabolism. A relationship between TNF and hemorrhagic shock has not been clearly demonstrated. To help understand the role of TNF in hemorrhagic shock we developed a hemorrhagic shock model to measure TNF and monocyte levels during hemorrhage and resuscitation. ⋯ Blood levels of TNF were initially undetectable but rose within 10 min after hemorrhage, peaked at 30 min after hemorrhage, and then became undetectable during resuscitation. In this model, macrophages and TNF are released into the circulation after hemorrhagic shock. TNF may play a role as a mediator in the pathophysiology of hemorrhagic shock.