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REFERENCES 1. Dellinger RP, Levy MM, Rhodes A, et al; Surviving Sepsis Campaign Guidelines Committee including the Pédiatrie Subgroup: Surviving sepsis campaign: International guidelines for management of severe sepsis and septic shock: 2012. Crit Care Med 2013; 41:580-637 2. Mahambrey T, Pendry K, Nee A, et al: Critical care in emergency department: Massive haemorrhage in trauma. Emerg Med J 2013; 30:9-14 3. Ince C: The microcirculation is the motor of sepsis. Crit Care 2005; 9(Suppl 4):S13-S19 4. Sakr Y, Dubois MJ, De Backer D, et al: Persistent microcirculatory alterations are associated with organ failure and death in patients with septic shock. Crit Care Med 2004; 32:1825-1 831 5. den Uil CA, Lagrand WK, van der Ent M, et al: Impaired microcirculation predicts poor outcome of patients with acute myocardial infarction complicated by cardiogenic shock. Eur Heart J 2010; 31:3032-3039 6. van Genderen ME, Klijn E, Lima A, et al: Microvascular Perfusion as a Target for Fluid Resuscitation in Experimental Circulatory Shock. Crit Care Med 2014; 42:e96-e105

7. Shoemaker WG, Appel PL, Kram HB, et al: Prospective trial of supranormal values of survivors as therapeutic goals in high-risk surgical patients. Chest 1988; 94:1176-1186 8. Hayes MA, Timmins AC, Yau EH, et al: Elevation of systemic oxygen delivery in the treatment of critically ill patients. N Engi J Med 1994; 330:1717-1722 9. Gattinoni L, Brazzi L, Pelosi P, et al: A trial of goal-oriented hemodynamic therapy in critically ill patients. SvO^ Collaborative Group. N Engi J Med 1995; 333:1025-1032 10. Rivers E, Nguyen B, Havstad S, et al; Early Goal-Directed Therapy Collaborative Group: Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engi J Med 2001 ; 345:1 368-1377 11. Kern JW, Shoemaker WC: Meta-analysis of hemodynamic optimization in high-risk patients. Crit Care Med 2002; 30:1686-1692 1 2. Knotzer H, Pajk W, Dünser MW, et al: Regional microvascular function and vascular reactivity in patients with different degrees of multiple organ dysfunction syndrome. Anesth Anaig 2006; 102:1187-1193 13. Knotzer H, Hasibeder WR: Microcirculatory function monitoring at the bedside-A view from the intensive care. Physioi Meas 2007; 28:R65-R86

In Comatose Postcardiac Arrest Patients Treated With Therapeutic Hypothermia: What Is the Optimal Rate of Rewarming?* Michael A. Kuiper, MD, PhD, FCCM Department of Intensive Care Medical Center Leeuwarden Leeuwarden, Friesland The Netherlands The temperature's rising, it isn't surprising—Irving Berlin

O

ne of the most important recent additions to the armamentarium of the critical care specialist is therapeutic hypothermia (TH) for treatment of patients in coma after cardiac arrest (1,2). Although we now know that in postcardiac patients we should make use of TH, many issues remain. To start with: which patients should we treat? All comatose postcardiac arrest patients? Or just those that were included in the original studies, which were out-of-hospital cardiac arrest (OHCA) patients, with a witnessed arrest and ventricular fibrillation or pulseless VT as first presenting rhythm and having received basic life support? And should not just OHCA patients

*See also p. el06. Key Words: cardiac arrest; resuscitation; rewarming; therapeutic hypothermia The author has disclosed that he does not have any potential conflicts of interest. Copyright © 2013 by the Society of Critical Care Medicine and Lippincott Williams & Wilkins

DOI: 10.1097/01.ccm.0000435682.98929.73

Critical Care Medicine

be treated with TH but also in-hospital cardiac arrest patients who are admitted to the ICU for postcardiac arrest treatment? Should patients with nonshockable rhythms undergo treatment with TH? Although the International Liaison Committee on Resuscitation advises to use TH in both shockable and nonshockable rhythms, a recent Finish study suggests that there is no support for the use of TH in comatose OHCA patients with nonshockable rhythms (3). This study, however, seems underpowered to answer this question definitively, and other studies are underway to provide additional data (4). We also do not know when to start hypothermia. It seems logical, based on the presumed mechanisms of hypothermia, that we should start as early as we can, and many Emergency Medical teams have adopted strategies to apply hypothermia before hospital admission. There are presently, however, no data on survival or neurologic outcome supporting this. Spontaneous hypothermia on admission in patients after cardiac arrest is a marker for poor outcome (5), which may be a confounder in studies looking for an effect of early TH. The optimal temperature for TH is also not known, and a large randomized controlled trial has recently been completed that has compared 33°C and 36°C (4). Same goes for the optimal duration of TH, use of sedative and analgesic drugs, use of drugs (including muscle relaxants) to prevent or diminish muscle shivering, hemodynamic monitoring and support thereof, and optimal ventilator settings for both ventilation (optimal PcOj and pH) and optimal oxygénation (preventing both hypoxia and hyperoxia). We also need to establish the effects of prognostication on outcome, and we need to consider www.ccmjournal.org

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the effects of withdrawal of life sustain treatment, which has been applied to a high percentage of patients in studies on outcome after cardiac arrest, as well (6). In this issue of Critical Care Medicine, a study by Lu et al (7) is published that aims at answering the question of what the rate of postresuscitation rewarming following TH after cardiac arrest should be. Theirs is a prospective randomized controlled animal study in which four groups of Sprague-Dawley rats looked for the optimal rewarming rate after TH. The groups were randomized as a normothermia group acting as controls; a second group that underwent a rewarming rate at 2°C/hr; a third group that was rewarmed at a rate of TC/hr; and a last group that was more slowly rewarmed at a rate of 0.5°C/hr. Their study shows first that TH was beneficial for both myocardial and neurologic outcome. The main outcome of their experiment is that a slow rewarming rate at 0.5-l°C/hr was needed to not lose the beneficial eftects of TH. The rats that underwent TH and fhereafter were more rapidly rewarmed, at a rate of 2°C/hr, lost the protective effects of hypothermia. This result suggests that we should be careful during the rewarming phase of TH. There are some remarks that need to be made before we may conclude that we know the optimal rate of rewarming in humans. First, the negative effect of rewarming at 2°C/hr, compared with the 0.5°C/hr and l°C/hr groups, may be due to the rewarming rate; it may, however, also been due to the longer duration of TH in the groups with slower rewarming. The group of rats that was rewarmed at 0.5°C/hr has had a temperature below 34°C which was 90 minutes longer than the duration in the group that had been rewarmed at 2°C/hr (360 vs 270 min). However, in rats, prolonging the duration of TH over 4 hours does not seem to improve outcome. Although there are no sufficiently reliable data on rewarming human victims of cardiac arrest, one observational study showed neither an effect of the rewarming rate nor the use of

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active rewarming versus passive rewarming (8). A very recent study from Copenhagen showed a negative effect of the occurrence of fever in the postrewarming phase of TH, suggesting that fever should be avoided after TH in comatose patients after cardiac arrest (9). Although the study by Lu et al (7) is a step that should urge us to be careful and patient during the rewarming process after TH, ultimately human studies need to be performed to answer the question of what the optimal rate of rewarming will be.

REFERENCES 1. Hypothermia after Cardiac Arrest Study Group: Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N EngI J Med 2002; 346:549-556 2. Bernard SA, Gray TW, Buist MD, et al: Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. N EngI J Med 2002; 346:557-563 3. Vaahersalo J, Hiltunen P, Tiainen M, et al: Therapeutic hypothermia after out-of-hospital cardiac arrest in Finnish intensive care units: The FINNRESUSCI study. Intensive Care Med 2013; 39:826-837 4. Nielsen N, Wetterslev J, al-Subaie N, et al: Target temperature management after out-of-hospital cardiac arrest-a randomized, parallelgroup, assessor-blinded clinical trial-rationale and design. Am Heart Í2012; 163:541-548 5. den Hartog AW, de Pont AC, Robillard LB, et al: Spontaneous hypothermia on intensive care unit admission is a predictor of unfavorable neurological outcome in patients after resuscitation: An observational cohort study. Cr/i Care 2010; 14:R121 6. Cronberg T, Horn J, Kuiper MA, et al: A structured approach to neurologic prognostication in clinical cardiac arrest trials. Seand J Trauma Resuse Emerg Med 2013; 21:45 7. Lu X, Ma L, Sun S, et al: The Effects of the Rate of Postresuscitation Rewarming Following Hypothermia on Cutcomes of Cardiopulmonary Resuscitation in a Rat Model. Crit Care Med 2014; 42:e106 - e l 13 8. Bouwes A, Robillard LB, Binnekade JM, et al: The influence of rewarming after therapeutic hypothermia on outcome after cardiac arrest. Resuseitation 201 2; 83:996-1 000 9. Bro-Jeppesen J, Hassager C, Wanscher M, et al: Post-hypothermia fever is associated with increased mortality after out-of-hospital cardiac arrest. Resuseitation 2013; 84:1734-1740

February 2014 • Volume 42 • Number 2

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In comatose postcardiac arrest patients treated with therapeutic hypothermia: what is the optimal rate of rewarming?

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