Resuscitation
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We have assessed the deleterious effects of methylmethacrylate (MMA) on cardiac function and metabolism in the isolated heart-lung preparation with or without volatile anesthetics. Wistar rats were prepared for the heart-lung model. They were randomly divided into 5 groups as follows. (1) Control (C) group. (2) Cement (M) group; they received MMA. (3) Halothane (H) group; they received MMA and 1% halothane. (4) Isoflurane (I) group; they received MMA and 1.5% isoflurane. (5) Sevoflurane (S) group; they received MMA and 2.5% sevoflurane. ⋯ MMA 1000 micrograms/ml is much higher than the blood level (0.05-31.89 micrograms/ml) which was reported in clinical patients who had femoral prosthesis. Therefore, the direct contribution of MMA itself to cardiac depression may be less than the other factors such as embolism in clinical situations. Volatile anesthetics did not influence the deleterious effects of MMA on cardiac function and metabolism.
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Randomized Controlled Trial Comparative Study Clinical Trial
High dose and standard dose adrenaline do not alter survival, compared with placebo, in cardiac arrest.
This trial compared blinded 10 mg aliquots of adrenaline with placebo in 194 cardiac arrest patients treated in hospital using American Heart Association guidelines. In-hospital and out-of-hospital arrests were included. Of the 339 eligible patients a large proportion (145 (45%)) were not randomised and received open 1 mg aliquots of adrenaline. ⋯ No significant differences in immediate survival (IS) or hospital discharge (HD) exists between open 1 mg adrenaline (IS 14 (9.7%), HD 3 (2%)) or the 10 mg adrenaline (IS 9 (9.6%), HD 0) vs. placebo (IS 7 (7%), HD 0) trial arms. Patients reaching the point of use of adrenaline have a uniformly poor immediate survival (8.8%) and hospital discharge rate (0.9%). Dosing with 10 mg or 1 mg adrenaline does not influence outcome compared with placebo.
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Active compression-decompression cardiopulmonary resuscitation (ACD-CPR) has been evaluated in animal cardiac arrest models and in human outcome studies. Blood flow to the brain and heart is significantly increased during ACD-CPR compared to standard CPR. Transoesophageal Doppler analysis indicates that ACD-CPR increases left ventricular blood volume, velocity of blood flow through the mitral valve (82-140%), and stroke volume (85%). ⋯ There is no evidence that ACD-CPR is worse than standard CPR. Appropriate ACD-CPR training using a standardized curriculum must preceed its implementation. Long-term neurologic outcome studies are needed.
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One of the arguments put forward in support of a relatively fast rate of chest compression during CPR, is that it facilitates the achievement of a high compression:relaxation ratio. This has been shown to increase blood flow. In this study a group of volunteers carried out chest compression at the rate that each felt was correct and comfortable. ⋯ In a second study volunteers carried out chest compression on a manikin at rates of 40/min; 60/min; 80/min and 100/min. There was no significant rate related difference in the compression:relaxation ratios recorded. The ability to achieve a high compression duration is not related to compression rate, and should not be a consideration when guidelines on CPR are revised.