Resuscitation
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We have demonstrated recently that therapeutic moderate hypothermia of 32-33 degrees C, induced by surface cooling under the administration of narcotics, sedatives and muscle relaxant, suppresses cytokine production after traumatic brain injury. We present here the first documented case report of augmented cytokine production in two accidental hypothermia patients, unconscious 84- (acute immersion) and 87- (non-immersion) year-old women, whose rectal temperatures were below 28 degrees C. The victims were artificially ventilated after sedation with midazolam and buprenorphine in accordance with our protocol. ⋯ Since the mechanisms for developing accidental hypothermia were different, simple comparisons between the two cases should be limited. But, these findings may suggest a need for testing a hypothesis whether cytokine modulation could be a therapeutic approach worthy of consideration. The results presented here also suggest that in hypothermia, changes in cytokine release may vary depending on procedures such as the anesthetic drugs used, the duration of the therapy, or the rate of rewarming from hypothermia.
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Clinical Trial
Quality assessment of defribrillation and advanced life support using data from the medical control module of the defibrillator.
What actually occurred during the two last links in the 'chain of survival': defibrillation and advanced life support (ALS), was studied in 156 patients with cardiac arrest of cardiac aetiology using the computer recording of the defibrillator and the Utstein-style data record. Ten patients (6%) survived. The ECG artefacts caused by chest compressions enabled a detailed analysis of compression rates (median 108 min(-1)) and duration of important compression free periods. ⋯ An isoelectric period followed 38% of the shocks, and in 27% this lasted more than 20 s, with five patients obtaining electrical activity with a pulse after more than 30 s of isoelectric ECG. Thoracic impedance did not affect the shock efficacy. The method of analysing resuscitation we describe may be useful for quality improvement.
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Meta Analysis Comparative Study
Effect of active compression-decompression resuscitation (ACD-CPR) on survival: a combined analysis using individual patient data.
Active compression decompression resuscitation (ACD-CPR) has been developed as an alternative to standard cardiopulmonary resuscitation (S-CPR). To determine the effect of ACD-CPR on survival and neurologic outcome in patients with out-of-hospital cardiac arrest, this combined analysis involved individual patient data from 2866 patients from seven separate randomized prospective prehospital studies who had received ACD-CPR or S-CPR after out-of-hospital cardiac arrest in seven international sites. Significant improvement in 1-h survival (odds ratio (OR) = 0.83; confidence interval (CI): 0.695-0.99; P < 0.05) was found with ACD-CPR (n = 1410) versus S-CPR (n = 1456). ⋯ This improvement was largely due to the influence of results from one study site. Neurological outcome and complication rates were comparable between groups. Further study is needed to determine which emergency medical services systems may benefit from out-of-hospital use of ACD-CPR.
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Comparative Study Clinical Trial
Prognostic significance of the difference between mixed venous and jugular bulb oxygen saturation in comatose patients resuscitated from a cardiac arrest.
To determine the prognostic significance of the difference between mixed venous and jugular bulb oxygen saturation in survivors and non-survivors of a cardiac arrest, we studied 30 comatose patients (21 non-survivors and 9 survivors) resuscitated from a cardiac arrest. We measured mixed venous oxygen saturation (SmvO2) and jugular bulb oxygen saturation (SjO2) immediately after haemodynamic stabilisation (always within 6 h after cardiac arrest) and 6, 12 and 24 h later. In all patients the SjO2 was about 10% lower than the SmvO2 in the first measurement. ⋯ Sensitivity and specificity are 65 and 89%, respectively. In a previous study we concluded that early jugular bulb oximetry (within 4 h after cardiac arrest) cannot predict cerebral outcome in comatose patients after cardiac arrest. More studies are needed to clarify the role of prolonged monitoring in the prediction of cerebral outcome after cardiac arrest.