Survival was significantly higher in the hypothermia group (56 % versus 36 % ), whereas no significant difference was observed in severity between the two periods. Only age, time from return to spontaneous circulation <20 min, and therapeutic hypothermia were independently associated with survival. Therapeutic hypothermia was well tolerated and was associated with a significant improvement in neurological outcome. Whereas only 23 % of patients actually reached the target temperature in 2003, 100 % did in 2005.
Therapeutic hypothermia is efficient in significantly improving survival and neurological outcome of out-of-hospital cardiac arrest with ventricular fibrillation. By using a simple method, it can be implemented easily and quickly, without side effects.
jrn_nsub.gif"" alt=""You are not entitled to access the full text of this document"" title=""You are not entitled to access the full text of this document"" width=12 height=14""> Pressor drugs in the treatment of cardiac arrest Cardiology Clinics, Volume 20, Issue 1, February 2002, Pages 61-78 Norman A. Paradis, Volker Wenzel, John Southall |
End tidal CO2 is reduced during hypotension and cardiac... Resuscitation |
jrn_nsub.gif"" alt=""You are not entitled to access the full text of this document"" title=""You are not entitled to access the full text of this document"" width=12 height=14""> End tidal CO2 is reduced during hypotension and cardiac arrest in a rat model of massive pulmonary embolism Resuscitation, Volume 53, Issue 1, April 2002, Pages 83-91 D. Mark Courtney, John A. Watts, Jeffrey A. Kline Abstract Background: We investigated the effect of massive pulmonary embolism (MPE) on end tidal CO2 (etCO2) and tested two hypotheses: (1) that etCO2 can distinguish massive PE from hemorrhagic shock and (2) that PE with cardiac arrest reduces etCO2 during resuscitation to a greater extent than arrhythmic cardiac arrest. Methods: Anesthetized, mechanically ventilated rats (N=10 per group), were subjected to either graded PE (latex microspheres), or graded hemorrhagic shock to produce a final mean arterial blood pressure, (MAP) of 40 mmHg; a third group was subjected to surgical/anesthetic control conditions. Cardiac arrest was induced by the following methods: intravenous injection of a large bolus of microspheres in the PE group, aortic puncture in the hemorrhage group, and intravenous tetrodotoxin (TTX) to produce arrhythmic cardiac arrest in the control group. Results: At a MAP of 40 mmHg, etCO2 was significantly decreased in the PE group (18.3±1.9 torr) compared with both the hemorrhage (24.3±1.3) and the control group (35.0±1.3 torr; ANOVA P<0.001). The decreased etCO2 occurred coincident with an increase in alveolar dead space fraction in the PE group. In the first minute of ventilation after cardiac arrest, the etCO2 was significantly decreased in the PE group (6.5±0.9) versus both hemorrhage (16.5±1.1) and TTX (34.2±2.4 torr). Conclusions: Massive PE with shock decreases the etCO2 and increases the dead space fraction to a greater extent than hemorrhagic shock at the same MAP. Cardiac arrest from PE is associated with extremely low etCO2 readings during CPR. Purchase PDF (159 K) |
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