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- Negative inotropic effects of epinephrine in the presence of increased β-adrenoceptor sensitivity during hypothermia in a rat model. [JOURNAL ARTICLE]
- Cryobiology 2014 Nov 13.
Animal studies show reduced inotropic effects of cardiac β-adrenoceptor agonists like epinephrine (Epi) during hypothermia and rewarming, while drugs targeting other pharmacological mechanisms have positive effects. This study therefore aimed to determine β-adrenoceptor sensitivity in isolated cardiomyocytes and investigate hemodynamic effects of Epi and its ability to stimulate cardiac β-adrenoceptors at different temperatures in vivo.Isolated rat myocardial cells were incubated with the radioactive β-adrenoceptor ligand [(3)H]-CGP12177 and propranolol, used as a displacer. Cells were subjected to normothermia (37°C) or hypothermia (15°C). After incubation, radioactivity was measured to estimate β-adrenoceptor affinity for propranolol (IC50), as a measure of β-adrenoceptor sensitivity. In separate in vivo experiments, Epi (1.25μg/min) was administered the last 5min of experiments in normothermic (37°C, 5h), hypothermic (4h at 15°C) and rewarmed rats (4h at 15°C, and subsequently rewarmed to 37°C). Hemodynamic parameters were monitored during infusion. Hearts were thereafter freeze-clamped and tissue cAMP was measured.In vitro measurements of IC50 for propranolol showed a hypothermia-induced increase in β-adrenoceptor sensitivity at 15°C. Corresponding in vivo experiments at 15°C showed decreased cardiac output and stroke volume, whereas total peripheral resistance (TPR) increased during Epi infusion, simultaneous with a 4-fold cAMP increase.This experiment shows a hypothermia-induced in vivo and in vitro increase of cardiac β-adrenoceptor sensitivity, and simultaneous lack of inotropic effects of Epi in the presence of increased TPR. Our findings therefore indicate that hypothermia-induced reduction in inotropic effects of Epi is due to substantial elevation of TPR, rather than β-adrenoceptor dysfunction.
- Wilderness Medical Society Practice Guidelines for the Out-of-Hospital Evaluation and Treatment of Accidental Hypothermia. [JOURNAL ARTICLE]
- Wilderness Environ Med 2014 Oct 31.
To provide guidance to clinicians, the Wilderness Medical Society (WMS) convened an expert panel to develop evidence-based guidelines for the out-of-hospital evaluation and treatment of victims of accidental hypothermia. The guidelines present the main diagnostic and therapeutic modalities and provide recommendations for the management of hypothermic patients. The panel graded the recommendations based on the quality of supporting evidence and the balance between benefits and risks/burdens according the criteria published by the American College of Chest Physicians. The guidelines also provide suggested general approaches to the evaluation and treatment of accidental hypothermia that incorporate specific recommendations.
- Prognostication in comatose survivors of cardiac arrest: An advisory statement from the European Resuscitation Council and the European Society of Intensive Care Medicine. [JOURNAL ARTICLE]
- Resuscitation 2014 Nov 25.:1779-1789.
To review and update the evidence on predictors of poor outcome (death, persistent vegetative state or severe neurological disability) in adult comatose survivors of cardiac arrest, either treated or not treated with controlled temperature, to identify knowledge gaps and to suggest a reliable prognostication strategy.GRADE-based systematic review followed by expert consensus achieved using Web-based Delphi methodology, conference calls and face-to-face meetings. Predictors based on clinical examination, electrophysiology, biomarkers and imaging were included.Evidence from a total of 73 studies was reviewed. The quality of evidence was low or very low for almost all studies. In patients who are comatose with absent or extensor motor response at ?72h from arrest, either treated or not treated with controlled temperature, bilateral absence of either pupillary and corneal reflexes or N20 wave of short-latency somatosensory evoked potentials were identified as the most robust predictors. Early status myoclonus, elevated values of neuron specific enolase at 48-72h from arrest, unreactive malignant EEG patterns after rewarming, and presence of diffuse signs of postanoxic injury on either computed tomography or magnetic resonance imaging were identified as useful but less robust predictors. Prolonged observation and repeated assessments should be considered when results of initial assessment are inconclusive. Although no specific combination of predictors is sufficiently supported by available evidence, a multimodal prognostication approach is recommended in all patients.
- Thermoregulatory capacities and torpor in the South American marsupial, Dromiciops gliroides. [Journal Article]
- J Therm Biol 2014 Oct.:1-8.
During periods of adverse conditions small endotherms depend on a continuous supply of food and energy to maintain body temperature. Thus, rapid and reversible phenotypic modifications at different organizational levels are key for an efficient use of resources and survival. In this study, we provide a quantitative description of thermoregulatory capacities and energy-saving strategies in the Chilean marsupial Dromiciops gliroides. In particular, we evaluated the effect of thermal acclimation on basal metabolic rate (BMR), thermal conductance (C) and torpor patterns, as well as the presence of non-shivering thermogenesis (NST) as a rewarming mechanism in this marsupial. Non-significant effects of thermal acclimation were observed in BMR, C and body mass, but cold-acclimated individuals exhibited significantly longer torpor bouts. Also, minimum body temperature during torpor, inter-bout body temperature and arousal rewarming rate were lower in cold-acclimated animals. Furthermore, we found that D. gliroides did not display NST in response to Norepinephrine. Hence, despite the high regulation of torpor of other species, D. gliroides shows low flexibility in the ability to adjust energy expenditure and insulation properties, and (as in other marsupials) NST do not seems to be important as thermoregulatory mechanism.
- Hypothermia modulates cytokine responses after neonatal rat hypoxic-ischemic injury and reduces brain damage. [Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't]
- ASN Neuro 2014; 6(6)
While hypothermia (HT) is the standard-of-care for neonates with hypoxic ischemic injury (HII), the mechanisms underlying its neuroprotective effect are poorly understood. We examined ischemic core/penumbra and cytokine/chemokine evolution in a 10-day-old rat pup model of HII. Pups were treated for 24 hr after HII with HT (32℃; n = 18) or normothermia (NT, 35℃; n = 15). Outcomes included magnetic resonance imaging (MRI), neurobehavioral testing, and brain cytokine/chemokine profiling (0, 24, 48, and 72 hr post-HII). Lesion volumes (24 hr) were reduced in HT pups (total 74%, p < .05; penumbra 68%, p < .05; core 85%, p = .19). Lesion volumes rebounded at 72 hr (48 hr post-HT) with no significant differences between NT and HT pups. HT reduced interleukin-1β (IL-1β) at all time points (p < .05); monocyte chemoattractant protein-1 (MCP-1) trended toward being decreased in HT pups (p = .09). The stem cell signaling molecule, stromal cell-derived factor-1 (SDF-1) was not altered by HT. Our data demonstrate that HT reduces total and penumbral lesion volumes (at 24 and 48 hr), potentially by decreasing IL-1β without affecting SDF-1. Disassociation between the increasing trend in HII volumes from 48 to 72 hr post-HII when IL-1β levels remained low suggests that after rewarming, mechanisms unrelated to IL-1β expression are likely to contribute to this delayed increase in injury. Additional studies should be considered to determine what these mechanisms might be and also to explore whether extending the duration or degree of HT might ameliorate this delayed increase in injury.
- From therapeutic hypothermia towards targeted temperature management: a decade of evolution. [JOURNAL ARTICLE]
- Anaesthesiol Intensive Ther 2014 Nov 25.
More than a decade after the first randomised controlled trials with targeted temperature management (TTM), it remains the only treatment with proven favourable effect on postanoxemic brain damage after out-of-hospital cardiac arrest. Other well-known indications include neurotrauma, subarachnoidal haemorrhage, and intracranial hypertension. When possible pitfalls are taken into consideration when implementing TTM, the side effects are manageable. After the recent TTM trials, it seems that classic TTM (32-34°C) is as effective and safe as TTM at 36°C. This supports the belief that fever prevention is one of the pivotal mechanisms that account for the success of TTM. Uncertainty remains concerning cooling method, timing, speed of cooling and rewarming. New data indicates that TTM is safe and feasible in cardiogenic shock, one of its classic contra-indications. Moreover, there are limited indications that TTM might be considered as a therapy for cardiogenic shock per se.
- Interventions for treating inadvertent postoperative hypothermia. [Journal Article, Research Support, Non-U.S. Gov't]
- Cochrane Database Syst Rev 2014.:CD009892.
Inadvertent postoperative hypothermia (a drop in core body temperature to below 36°C) occurs as an effect of surgery when anaesthetic drugs and exposure of the skin for long periods of time during surgery result in interference with normal temperature regulation. Once hypothermia has occurred, it is important that patients are rewarmed promptly to minimise potential complications. Several different interventions are available for rewarming patients.To estimate the effectiveness of treating inadvertent perioperative hypothermia through postoperative interventions to decrease heat loss and apply passive and active warming systems in adult patients who have undergone surgery.We searched the Cochrane Central Register of Controlled Trials (CENTRAL) (2014, Issue 2), MEDLINE (Ovid SP) (1956 to 21 February 2014), EMBASE (Ovid SP) (1982 to 21 February 2014), the Institute for Scientific Information (ISI) Web of Science (1950 to 21 February 2014) and the Cumulative Index to Nursing and Allied Health Literature (CINAHL), EBSCO host (1980 to 21 February 2014), as well as reference lists of articles. We also searched www.controlled-trials.com and www.clincialtrials.gov.Randomized controlled trials of postoperative warming interventions aiming to reverse hypothermia compared with control or with each other.Three review authors identified studies for inclusion in this review. One review author extracted data and completed risk of bias assessments; two review authors checked the details. Meta-analysis was conducted when appropriate by using standard methodological procedures as expected by The Cochrane Collaboration.We included 11 trials with 699 participants. Ten trials provided data for analysis. Trials varied in the numbers and types of participants included and in the types of surgery performed. Most trials were at high or unclear risk of bias because of inappropriate or unclear randomization procedures, and because blinding of assessors and participants generally was not possible. This may have influenced results, but it is unclear how the results may have been influenced. Active warming was found to reduce the mean time taken to achieve normothermia by about 30 minutes in comparison with use of warmed cotton blankets (mean difference (MD) -32.13 minutes, 95% confidence interval (CI) -42.55 to -21.71; moderate-quality evidence), but no significant difference in shivering was noted. Active warming was found to reduce mean time taken to achieve normothermia by almost an hour and a half in comparison with use of unwarmed cotton blankets (MD -88.86 minutes, 95% CI -123.49 to -54.23; moderate-quality evidence), and people in the active warming group were less likely to shiver than those in the unwarmed cotton blanket group (Relative Risk=0.61 95% CI= 0.42 to 0.86; low quality evidence). There was no effect on mean temperature difference in degrees celsius at 60 minutes (MD=0.18°C, 95% CI=-0.10 to 0.46; moderate quality evidence), and no data were available in relation to major cardiovascular complications. Forced air warming was found to reduce time taken to achieve normothermia by about one hour in comparison to circulating hot water devices (MD=-54.21 minutes 95% CI= -94.95, -13.47). There was no statistically significant difference between thermal insulation and cotton blankets on mean time to achieve normothermia (MD =-0.29 minutes, 95% CI=-25.47 to 24.89; moderate quality evidence) or shivering (Relative Risk=1.36 95% CI= 0.69 to 2.67; moderate quality evidence), and no data were available for mean temperature difference or major cardiovascular complications. Insufficient evidence was available about other comparisons, adverse effects or any other secondary outcomes.Active warming, particularly forced air warming, appears to offer a clinically important reduction in mean time taken to achieve normothermia (normal body temperature between 36°C and 37.5°C) in patients with postoperative hypothermia. However, high-quality evidence on other important clinical outcomes is lacking; therefore it is unclear whether active warming offers other benefits and harms. High-quality evidence on other warming methods is also lacking; therefore it is unclear whether other rewarming methods are effective in reversing postoperative hypothermia.
- Passive rewarming from torpor in hibernating bats: minimizing metabolic costs and cardiac demands. [JOURNAL ARTICLE]
- Am J Physiol Regul Integr Comp Physiol 2014 Nov 19.:ajpregu.00341.2014.
Endothermic arousal from torpor is an energetically costly process and imposes enormous demands on the cardiovascular system, particularly during early stage arousal from low body temperature (Tb). To minimize these costs many bats and other heterothermic endotherms rewarm passively from torpor using solar radiation or fluctuating ambient temperature (Ta). Because the heart plays a critical role in the arousal process in terms of blood distribution and as a source of heat production it is desirable to understand how the function of this organ responds to passive rewarming and how this relates to changes in metabolism and Tb. We investigated heart rate (HR) in hibernating long-eared bats (Nyctophilus gouldi) and its relationship to oxygen consumption (V̇O2) and subcutaneous temperature (Tsub) during exposure to increasing Ta in comparison to endogenous arousals at constant low Ta. During passive rewarming, HR and V̇O2 remained low over a large Tsub range and increased concurrently with increasing Ta (Q10 2.4 and 2.5, respectively). Absolute values were higher than during steady-state torpor, but below those measured during torpor entry. During active arousals, mean HR and V̇O2 were substantially higher than during passive rewarming at corresponding Tsub. In addition, partial passive rewarming reduced the cost of arousal from torpor by 53% compared to entirely active arousal. Our data show that passive rewarming considerably reduces arousal costs and arousal time; we suggest this may also contribute to minimizing exposure to oxidative stresses as well as demands on the cardiovascular system.
- [The use of intravascular hypothermia to correct intracranial hypertension in patients with severe traumatic brain injury]. [English Abstract, Journal Article]
- Zh Vopr Neirokhir Im N N Burdenko 2014; 78(5):41-7; discussion 47-8.
Assess to impact hypothermia on ABP, CPP, ICP and cerebral autoregulation. Material and methods. 14 patients with TBI (GOS<9) underwent hypothermia by Thermogard system within 32-35 °C (Zoll, USA). ICP was measured intraparenchymal by Codman sensor. Cerebral autoregulation was estimated by correlation coefficient Prx (Soft ICM Plus, Cambridge, UK). Temperature was measured in urinary bladder. There were selected five time periods: 1 - phase of initial state, 2 - phase of induction hypothermia, 3 - phase of hypothermia, 4 - phase of rewarming, 5 - phase after finishing hypothermia. All data preset as Mediana (min; max). Stat analysis was perfomed using Soft Statistica 10.0. Results. Phase 1 lasted nearly 7 (2; 12) h, ABP 94 (81; 102), CPP - 73 (52; 87), ICP 27 (16; 45) mm Hg, Prx 0,25 (-0,15; 0,7), temperature 38,2 °C (37; 39,8). Phase 2: 5 (2; 12) h, ABP 95 (85; 114), CPP 80 (65; 96), ICP 18 (10; 22) mm Hg, Prx -0,055 (-0,15; 0,7), temperature 35,2 °C (34,5; 35,5). Phase 3: 55 (20; 100) h, there were not significant changed ABP, CPP, Prx, ICP 15 (10; 18) mm Hg, temperature was 33,5 °C (32; 34,7). Phase 4: 17 (8; 24) h, ABP 90 (70; 100), CPP 77 (55; 85), ICP 15 (9; 27) mm Hg and Prx 0,2 (-0,2; 0,32). Temperature 36,9 °C (35,9; 38,5). Phase 5: 20 (6; 240) h, ABP 87(53; 110), CPP 72 (47; 107), ICP 17 (10; 32) mm Hg and Prx 0,2 (-0,2; 0,6). Temperature 37,7 °C (36,7; 39,0). Conclusion. Hypothermia is an effective method for correction of intracranial hypertension. Hypothermia can use as a additional option of intensive care during refractory intracranial hypertension. Rewarming phase is the most dangerous time on the re-development of intracranial hypertension and disruption of autoregulation.
- Out in the cold: the hypothermic heart response. [Journal Article]
- BMJ Case Rep 2014.
We present an interesting case of a 49-year-old woman with hypothermia and associated Osborn waves (also called J waves) on ECG. She was found on the floor of her home and difficult to arouse. On arrival to the emergency department (ED), her rectal temperature was 87.5°F. ECG showed Osborn waves in diffuse leads. She was intubated in the ED and was started on vasopressor support for hypotension refractory to intravenous fluid boluses. She was transferred to the critical care unit for continued respiratory and cardiovascular support. With active external rewarming her core body temperature continued to improve. Blood pressure also improved and vasopressor was tapered off. She was extubated and was transferred to the medical floor for continued supportive care. Osborn waves on ECG resolved within 12 h of achieving normal range body temperature. The patient was eventually discharged home with medical follow-up.