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Aim: Hypothermia is recommended by international guidelines for treatment of unconscious survivors of cardiac arrest to improve neurologic outcomes. However, temperature management is often underutilized because it may be difficult to implement. The present study evaluated the efficacy of pharmacologically induced hypothermia on survival and neurological outcome in rats resuscitated from cardiac arrest., Methods: Cardiac arrest was induced for 10 min in 120 rats. Sixty-one rats were resuscitated and randomized to normothermia, physical cooling or pharmacological hypothermia 5 min after resuscitation. Pharmacological hypothermia rats received a combination of ethanol, vasopressin and lidocaine (HBN-1). Physical hypothermia rats were cooled with intravenous iced saline and cooling pads. Rats in the pharmacological hypothermia group received HBN-1 at ambient temperature (20 °C). Normothermic rats were maintained at 37.3 ± 0.2 °C., Results: HBN-1 (p < 0.0001) shortened the time (85 ± 71 min) to target temperature (33.5 °C) versus physical hypothermia (247 ± 142 min). The duration of hypothermia was 17.0 ± 6.8h in the HBN-1 group and 17.3 ± 7.5h in the physical hypothermia group (p = 0.918). Survival (p = 0.034), neurological deficit scores (p < 0.0001) and Morris Water Maze performance after resuscitation (p = 0.041) was improved in the HBN-1 versus the normothermic group. HBN-1 improved survival and early neurological outcome compared to the physical hypothermia group while there was no significant difference in performance in the Morris water maze., Conclusion: HBN-1 induced rapid and prolonged hypothermia improved survival with good neurological outcomes after cardiac arrest suggesting that pharmacologically induced regulated hypothermia may provide a practical alternative to physical cooling., (Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.)

Therapeutic hypothermia (TH) and targeted temperature management improve neurologic recovery, and survival for patients resuscitated from witnessed out-of-hospital ventricular tachycardia (VT) and ventricular fibrillation (VF) cardiac arrest. The American Heart Association recently gave a class IIb recommendation for the use of TH for non-VT/VF and unwitnessed arrests. We explored changes in baseline characteristics, resource use, and outcomes after expanding indications for TH at our institution based on these guidelines. Fifty-six consecutive patients treated with TH for out-of-hospital cardiac arrest were retrospectively evaluated based on whether they received treatment before (protocol 1) or after (protocol 2) broadening inclusion criteria. In protocol 1, TH was indicated after a witnessed VT/VF arrest. In protocol 2, TH was indicated for unwitnessed arrests, pulseless electrical activity, or asystole. Both populations undergoing TH had similarly extensive medical comorbidities and consumed considerable hospital resources. Overall, 64% of the patients from both protocols died in the hospital, although nominally lower mortality was seen in patients treated under protocol 1 compared with protocol 2 (59% vs. 67%, P = 0.57). Lower mortality was observed after VT/VF than after pulseless electrical activity or asystole (47% vs. 93% vs. 56%, P = 0.017). No patient survived following an unwitnessed arrest, and age (odds ratio per 10 years = 2.59; 95% confidence interval, 1.34-4.81) was independently associated with increased mortality. In an evolving field where best practice is still poorly defined, these data, along with future prospective studies in larger populations, should help to enhance care delivery and optimize cost-effectiveness strategies.

Hypothermia during brain ischemia can improve neurological outcome. This study tested whether local cranial cooling during the low-flow state of cardiopulmonary resuscitation (CPR) could produce clinically significant cerebral cooling. Ice was applied to the heads and necks of subjects (hypothermia group) with out-of-hospital cardiac arrest (OOHCA) during CPR. Nasopharyngeal and tympanic temperatures were measured as surrogates for cerebral temperature. The rate of cranial cooling in the hypothermia group (-0.06 +/- 0.06 degrees C/min) was not significantly increased compared with a control group without ice (-0.04 +/- 0.07 degrees C/min), although older age was associated with more rapid cranial cooling. Of note, many subjects with OOHCA are already mildly hypothermic (mean cranial temperature= 35.0 +/- 1.2 degrees C) when they are first encountered in the field. This study suggests that brief cranial cooling is ineffective for rapidly lowering brain temperature. However, most cardiac arrest victims are spontaneously mildly hypothermic and preventing rewarming may provide some of the desired benefits of cerebral hypothermia.

Abstract: Background: Vasoconstriction, an inherent property of Hemoglobin Based Oxygen Carriers (HBOC) potentially due to nitric oxide (NO) scavenging, may increase cardiovascular complications in HBOC resuscitated trauma patients. The purpose of this study was to determine if co-administration of a weak NO donor, intravenous nitroglycerin (NTG), with HBOC-201 during resuscitation from hemorrhagic shock could safely attenuate HBOC-201 vasoconstriction. Methods and results: Hemorrhagic shock was induced in 44 swine randomized to receive fluid resuscitation with HBOC, HBOC+NTG10mcg/kg/min, HBOC+NTG20mcg/kg/min, HBOC+NTG40mcg/kg/min, Hetastarch (HES), HES+NTG20mcg/kg/min, NTG20mcg/kg/min and Lactated Ringers (LR). HBOC resuscitation from hemorrhagic shock increased mean arterial pressure (MAP=94±33mmHg), mean pulmonary artery pressure (MPAP=29±11mmHg) and systemic vascular resistance (SVR=2684±871dyns/cm5) in comparison to HES. Co-administration of NTG during HBOC resuscitation attenuated vasoconstriction with HBOC+40mcg/kg/min demonstrating the most robust reduction in vasoconstriction (MAP=59±23mmHg, MPAP=18±7mmHg, and SVR=1827±511dyns/cm5), although the effects were transient. Co-administration of NTG with HBOC did not alter base deficit, lactate, methemoglobin levels, nor cause profound hypotension during resuscitation. Conclusion: Nitroglycerin attenuates vasoconstrictive properties of HBOC when co-administered during resuscitation in this swine model of hemorrhagic shock. Translational survival studies are required to determine if this strategy of attenuation of the vasoconstriction of HBOC-201 reduces cardiovascular complications and improves outcome with HBOC fluid resuscitation for hemorrhagic shock. [Copyright &y& Elsevier]

Hypothermia during brain ischemia can improve neurological outcome. This study tested whether local cranial cooling during the low-flow state of cardiopulmonary resuscitation (CPR) could produce clinically significant cerebral cooling. Ice was applied to the heads and necks of subjects (hypothermia group) with out-of-hospital cardiac arrest (OOHCA) during CPR. Nasopharyngeal and tympanic temperatures were measured as surrogates for cerebral temperature. The rate of cranial cooling in the hypothermia group (−0.06±0.06 °C/min) was not significantly increased compared with a control group without ice (−0.04±0.07 °C/min), although older age was associated with more rapid cranial cooling. Of note, many subjects with OOHCA are already mildly hypothermic (mean cranial temperature=35.0±1.2 °C) when they are first encountered in the field. This study suggests that brief cranial cooling is ineffective for rapidly lowering brain temperature. However, most cardiac arrest victims are spontaneously mildly hypothermic and preventing rewarming may provide some of the desired benefits of cerebral hypothermia. [Copyright &y& Elsevier]