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    Moderate hypothermia for severe cardiogenic shock (COOL Shock Study I & II)

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    Aim of the study: Hypothermia exerts profound protection from neurological damage and death after resuscitation from circulatory arrest. Its application during concomitant cardiogenic shock has been discussed controversially, and still hypothermia is used with reserve when haemodynamic parameters are impaired. On the other hand hypothermia improves force development in isolated human myocardium. Thus, we hypothesized that hypothermia could beneficially affect cardiac function in patients during cardiogenic shock. Methods: 14 Patients, admitted to Intensive Care Unit for cardiogenic shock under inotropic support, were enrolled and moderate hypothermia (33 degrees C) was induced for either one (n = 5, short-term) or twenty-four (n = 9, mid-term) hours. Results: 12 patients suffered from ischaemic cardiomyopathy, 2 were female, and 6 were included after cardiac arrest and resuscitation. Body temperature was controlled by an intravascular cooling device. Short-term hypothermia consistently decreased heart rate, and increased stroke volume, cardiac index and cardiac power output. Metabolic and electrocardiographic parameters remained constant during cooling. Improved cardiac function persisted during mid-term hypothermia, but was reversed during re-warming. No severe or persistent adverse effects of hypothermia were observed. Conclusion: Moderate Hypothermia is safe and feasable in patients during cardiogenic shock. Moreover, hypothermia improved parameters of cardiac function, suggesting that hypothermia might be considered as a positive inotropic intervention rather than a risk for patients during cardiogenic shock. (C) 2012 Elsevier Ireland Ltd. All rights reserved

    Effects of large volume, ice-cold intravenous fluid infusion on respiratory function in cardiac arrest survivors

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    International guidelines for cardiopulmonary resuscitation recommend mild hypothermia (32-34 degrees C) for 12-24 h in comatose survivors of cardiac arrest. To induce therapeutic hypothermia a variety of external and intravascular cooling devices are available. A cheap and effective method for inducing hypothermia is the infusion of large volume, ice-cold intravenous fluid. There are concerns regarding the effects of rapid infusion of large volumes of fluid on respiratory function in cardiac arrest survivors. We have retrospectively studied the effects of high volume cold fluid infusion on respiratory function in 52 resuscitated cardiac arrest patients. The target temperature of 32-34 degrees C was achieved after 4.1 +/- 0.5 h (cooling rate 0.48 degrees C/h). During this period 3427 +/- 210 mL ice-cold fluid was infused. Despite significantly reduced LV-function (EF 35.8 +/- 2.2%) the respiratory status of these patients did not deteriorate significantly. On intensive care unit admission the mean PaO(2). was 231.4 +/- 20.6 mmHg at a F(i)O(2) of 0.82 +/- 0.03 (PaO(2)/F(i)O(2) = 290.0 +/- 24.1) and a PEEP level of 7.14 +/- 0.31 mbar. Until reaching the target temperature of <= 34 degrees C the F(i)O(2) could be significantly reduced to 0.63 +/- 0.03 with unchanged PEEP level (7.23 +/- 0.36 mbar). Under these conditions the PaO(2)/F(i)O(2) ratio slightly decreased to 247.5 +/- 18.5 (P = 0.0893). Continuing the saline infusion to achieve a body temperature of 33 degrees C, the F(i)O(2) Could be further reduced with unchanged PEEP. The infusion of large volume, ice-cold fluid is an effective and inexpensive method for inducing therapeutic hypothermia. Resuscitation from cardiac arrest is associated with a deterioration in respiratory function. The infusion of large Volumes of cold fluid does not cause a statistically significant further deterioration in respiratory function. A larger, randomized and prospective study is required to assess the efficacy and safety of ice-cold fluid infusion for the induction of therapeutic hypothermia. (C) 2009 Elsevier Ireland Ltd. All rights reserved
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