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Robert W. Neumar - One of the best experts on this subject based on the ideXlab platform.
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abstract 15971 neuroprotective mechanisms of intra arrest hypothermic Targeted Temperature Management
Circulation, 2017Co-Authors: Tulasi R Jinka, Xiaodan Ren, Robert W. NeumarAbstract:Objective: Mechanistic optimization of inta-arrest hypothermic-Targeted Temperature Management (HTTM) is necessary for successful translation to clinical practice. Our study evaluates the potential neuroprotective mechanisms of brain cooling initiated during cardiopulmonary resuscitation (CPR) in a rat model of asphyxial cardiac arrest. Methods: Twenty nine male Long Evens rats were subjected to 10 minute asphyxial cardiac arrest followed by CPR. Brain Temperature was monitored through intracranial Temperature probes. Rats were block randomized to normothermic Targeted Temperature Management (NTTM; n=8), or hypothermic TTM at 34 o C (HTTM-34; n=8) or 32 o C (HTTM-32; n=7). HTTM was initiated at the onset of CPR using nasopharyngeal cold saline infusion to reach target Temperatures within 10 minutes of 34 o C (flow rate 100 ml/kg/min) or 32 o C (flow rate 200 ml/kg/min). Rats were maintained at target Temperature for one hour after return of spontaneous circulation (ROSC) and then euthanized; brains collected for subcellular fractionation, mitochondrial isolation and analysis of post-ischemic injury and survival pathways. Sham rats subjected to anesthesia and instrumentation but not cardiac arrest or cooling were used as uninjured controls (n=6). Results: Brain target Temperature was achieved 5.8 ± 0.8 min in HTTM-34 group and 8.2 ± 1.3 min in HTTM-32 group after initiation of cooling. There was no statistical difference in ROSC rate between groups. Oxidative injury as measured by mitochondrial protein carbonylation was increased 40-fold in the NTTM group compared to sham controls (p Conclusion: Intra-arrest HTTM with target Temperature achieved within 10 minutes of CPR onset significantly reduces brain mitochondrial oxidative injury and may increase early survival signaling . These treatment effects was similar with 32°C and 34°C hypothermic target Temperatures.
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abstract 15971 neuroprotective mechanisms of intra arrest hypothermic Targeted Temperature Management
Circulation, 2017Co-Authors: Tulasi R Jinka, Xiaodan Ren, Robert W. NeumarAbstract:Objective: Mechanistic optimization of inta-arrest hypothermic-Targeted Temperature Management (HTTM) is necessary for successful translation to clinical practice. Our study evaluates the potential...
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Valproic Acid Combined With Postcardiac Arrest Hypothermic-Targeted Temperature Management Prevents Delayed Seizures and Improves Survival in a Rat Cardiac Arrest Model:
Critical Care Medicine, 2017Co-Authors: Jinka Tulasi, Ren Xiaodan, William C. Stacey, Robert W. NeumarAbstract:OBJECTIVES High-dose valproic acid in combination with hypothermic-Targeted Temperature Management has been reported to synergistically improve neurologic outcomes after cardiac arrest. This study investigated the potential synergistic mechanisms. DESIGN Prospective, randomized, experimental study. SETTING University research institution. SUBJECTS Male Long Evans rats. INTERVENTION Rats resuscitated from asphyxial cardiac arrest were randomized to one of the three groups: normothermic-Targeted Temperature Management (37°C ± 1°C), hypothermic-Targeted Temperature Management (33° ± 1° × 24 hr + placebo infusion), hypothermic-Targeted Temperature Management plus high-dose valproic acid (300 mg/kg IV × 1 initiated 5 min post return of spontaneous circulation and infused over 20 min) (hypothermic-Targeted Temperature Management + valproic acid). MEASUREMENTS AND MAIN RESULTS Seventy-two-hour survival was significantly greater with hypothermic-Targeted Temperature Management + valproic acid, compared to hypothermic-Targeted Temperature Management and normothermic-Targeted Temperature Management (p < 0.05). Survival with good neurologic function, neurodegeneration, expression of HSP70, phosphorylation of Akt and Erk1/2 were not significantly different between hypothermic-Targeted Temperature Management and hypothermic-Targeted Temperature Management + valproic acid. The prevalence of seizures during the first 72-hour postcardiac arrest was significantly lower with hypothermic-Targeted Temperature Management + valproic acid compared to hypothermic-Targeted Temperature Management and normothermic-Targeted Temperature Management (p = 0.01). CONCLUSIONS High-dose valproic acid combined with hypothermic-Targeted Temperature Management prevents postcardiac arrest seizures and improves survival. It remains to be determined if the mechanism of seizure prevention is through the antiepileptic effect of valproic acid or direct neuroprotection. Overall, the combination of high-dose valproic acid and hypothermic-Targeted Temperature Management remains a promising strategy to improve cardiac arrest outcomes.
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Clinical Applications of Targeted Temperature Management
Chest, 2014Co-Authors: Sarah M. Perman, Robert W. Neumar, Munish Goyal, Alexis A. Topjian, David F. GaieskiAbstract:Targeted Temperature Management (TTM) has been investigated experimentally and used clinically for over 100 years. The initial rationale for the clinical application of TTM, historically referred to as therapeutic hypothermia, was to decrease the metabolic rate, allowing the injured brain time to heal. Subsequent research demonstrated the Temperature dependence of diverse cellular mechanisms including endothelial dysfunction, production of reactive oxygen species, and apoptosis. Consequently, modern use of TTM centers on neuroprotection following focal or global neurologic injury. Despite a solid basic science rationale for applying TTM in a variety of disease processes, including cardiac arrest, traumatic brain injury, ischemic stroke, neonatal ischemic encephalopathy, sepsis-induced encephalopathy, and hepatic encephalopathy, human efficacy data are limited and vary greatly from disease to disease. Ten years ago, two landmark investigations yielded high-quality data supporting the application of TTM in comatose survivors of out-of-hospital cardiac arrest. Additionally, TTM has been demonstrated to improve outcomes for neonatal patients with anoxic brain injury secondary to hypoxic ischemic encephalopathy. Trials are currently under way, or have yielded conflicting results in, examining the utility of TTM for the treatment of ischemic stroke, traumatic brain injury, and acute myocardial infarction. In this review, we place TTM in historic context, discuss the pathophysiologic rationale for its use, review the general concept of a TTM protocol for the Management of brain injury, address some of the common side effects encountered when lowering human body Temperature, and examine the data for its use in diverse disease conditions with in-depth examination of TTM for postarrest care and pediatric applications.
Niklas Nielsen - One of the best experts on this subject based on the ideXlab platform.
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repolarization and ventricular arrhythmia during Targeted Temperature Management post cardiac arrest
Resuscitation, 2021Co-Authors: Jakob Hartvig Thomsen, Niklas Nielsen, Christian Hassager, Steen Pehrson, Johannes Grand, John Brojeppesen, Claus Graff, David Erlinge, Matias Greve Lindholm, Lars KøberAbstract:Abstract Background Targeted Temperature Management (TTM) following out-of-hospital cardiac arrest (OHCA) prolongs the QT-interval but our knowledge of different Temperatures and risk of arrhythmia is incomplete. Objective To assess whether the QTc, QT-peak (QTp) and T-peak to T-end interval (TpTe) may be useful markers of ventricular arrhythmia in contemporary post cardiac arrest treatment. Methods An ECG-substudy of the TTM-trial (TTM at 33 °C vs. 36 °C) with serial ECGs from 680 (94%) patients. Bazett’s (B) and Fridericia’s (F) formula were used for heart rate correction of the QT, QTp and TpTe. Ventricular arrhythmia (VT/VF) were registered during the first three days of post cardiac arrest care. Results The QT, QTc and QTp intervals were prolonged more at 33 °C compared to 36 °C and restored to similar and lower levels after rewarming. The TpTe-interval remained between 92–100 ms throughout TTM in both groups. The QTc intervals were associated with ventricular arrhythmia, but not after adjustment for cardiac arrest characteristics. The QTp-interval was not associated with risk of ventricular arrhythmia. Heart rate corrected TpTe-intervals were associated with higher risk of arrhythmia (Odds ratio (OR): TpTe(B): 1.12 (1.02–1.23, p = 0.01 TpTe(F): 1.12 (1.02–1.23, p = 0.02) per 20 ms). Further a prolonged TpTe-interval ≥ 90 ms was consistently associated with higher risk (ORadjusted: TpTe(B): 2.05 (1.25–3.37), p Conclusions TTM prolongs the QT-interval by prolongation of the QTp-interval without association to increased risk. The TpTe-interval is not significantly affected by core Temperature, but heart rate corrected TpTe intervals are robustly associated with risk of ventricular arrhythmia. Trial registration The TTM-trial is registered and accessible at ClinicalTrials.gov (Identifier: NCT01020916).
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meta analysis of Targeted Temperature Management in animal models of cardiac arrest
Intensive Care Medicine Experimental, 2020Co-Authors: Hilmer Olai, Niklas Nielsen, Hans Friberg, Tobias Cronberg, Gustav Thorneus, Hannah Watson, Malcolm R Macleod, Jonathan Rhodes, Tomas DeierborgAbstract:Targeted Temperature Management (TTM) of 32 to 34 °C has been the standard treatment for out-of-hospital cardiac arrest since clinical trials in 2002 indicated benefit on survival and neurological outcome. In 2013, a clinical trial showed no difference in outcome between TTM of 33 °C and TTM of 36 °C. In this meta-analysis, we investigate the evidence for TTM in animal models of cardiac arrest. We searched PubMed and EMBASE for adult animal studies using TTM as a treatment in different models of cardiac arrest or global brain ischemia which reported neurobehavioural outcome, brain histology or mortality. We used a random effects model to calculate estimates of efficacy and assessed risk of bias using an adapted eight-item version of the Collaborative Approach to Meta-Analysis and Review of Animal Data from Experimental Studies (CAMARADES) quality checklist. We also used a scoring system based on the recommendations of the Stroke Treatment Academic Industry Roundtable (STAIR), to assess the scope of testing in the field. Included studies which investigated a post-ischemic induction of TTM had their treatment regimens characterized with regard to depth, duration and time to treatment and scored against the modified STAIR criteria. The initial and updated search generated 17809 studies after duplicate removal. One hundred eighty-one studies met the inclusion criteria, including data from 1,787, 6,495 and 2,945 animals for neurobehavioural, histological and mortality outcomes, respectively. TTM was favoured compared to control for all outcomes. TTM was beneficial using short and prolonged cooling, deep and moderate Temperature reduction, and early and delayed time to treatment. Median [IQR] study quality was 4 [3 to 6]. Eighteen studies checked seven or more of the eight CAMARADES quality items. There was no clear correlation between study quality and efficacy for any outcome. STAIR analysis identified 102 studies investigating post-ischemic induction of TTM, comprising 147 different treatment regimens of TTM. Only 2 and 8 out of 147 regimens investigated comorbid and gyrencephalic animals, respectively. TTM is beneficial under most experimental conditions in animal models of cardiac arrest or global brain ischemia. However, research on gyrencephalic species and especially comorbid animals is uncommon and a possible translational gap. Also, low study quality suggests risk of bias within studies. Future animal research should focus on mimicking the clinical scenario and employ similar rigour in trial design to that of modern clinical trials.
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arterial blood pressure during Targeted Temperature Management after out of hospital cardiac arrest and association with brain injury and long term cognitive function
European heart journal. Acute cardiovascular care, 2019Co-Authors: Johannes Grand, Niklas Nielsen, Michael Wanscher, Jesper Kjaergaard, Hans Friberg, Gisela Lilja, John Brojeppesen, Tobias Cronberg, Christian HassagerAbstract:Objectives:During Targeted Temperature Management after out-of-hospital cardiac arrest infusion of vasoactive drugs is often needed to ensure cerebral perfusion pressure. This study investigated me...
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mean arterial pressure during Targeted Temperature Management and renal function after out of hospital cardiac arrest
Journal of Critical Care, 2019Co-Authors: Johannes Grand, Niklas Nielsen, Christian Hassager, Hans Friberg, Matt P Wise, M Wintherjensen, Malin Rundgren, Janneke Horn, Michael A Kuiper, Sebastian WibergAbstract:Purpose: This study investigates the association between mean arterial pressure (MAP) and renal function after out-of-hospital cardiac arrest (OHCA). Materials and methods: Post-hoc analysis of 851 comatose OHCA-patients surviving >48 h included in the Targeted Temperature Management (TTM)-trial. Results: Patients were stratified by mean MAP during TTM in the following groups; 80 mmHg (35%). Median (interquartile range) eGFR (ml/min/1.73 m2) 48 h after OHCA was inversely associated with MAP-group (70 (47–102), 84 (56–113), 94 (61–124), p 80-group respectively). After adjusting for potential confounders, in a mixed model including eGFR after 1, 2 and 3 days this association remained significant (pgroup_adjusted = 0.0002). Higher mean MAP was independently associated with lower odds of renal replacement therapy (odds ratioadjusted = 0.77 [95% confidence interval, 0.65–0.91] per 5 mmHg increase; p =.002]). Conclusions: Low mean MAP during TTM was independently associated with decreased renal function and need of renal replacement therapy in a large cohort of comatose OHCA-patients. Increasing MAP above the recommended 65 mmHg could potentially be renal-protective. This hypothesis should be investigated in prospective trials.
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protocol driven neurological prognostication and withdrawal of life sustaining therapy after cardiac arrest and Targeted Temperature Management
Resuscitation, 2017Co-Authors: Irina Dragancea, Tommaso Pellis, Hans Friberg, G Glover, Nawaf Alsubaie, Jules Cranshaw, Andrew Walden, Matt P Wise, Rebecca Rylance, Niklas NielsenAbstract:Abstract Background Brain injury is reportedly the main cause of death for patients resuscitated after out-of-hospital cardiac arrest (OHCA). However, the majority may actually die following withdrawal of life-sustaining therapy (WLST) with a presumption of poor neurological recovery. We investigated how the protocol for neurological prognostication was used and how related treatment recommendations might have affected WLST decision-making and outcome after OHCA in the Targeted Temperature Management (TTM) trial. Methods Analyses of prospectively recorded data: details of neurological prognostication; recommended level-of-care; WLST decisions; presumed cause of death; and cerebral performance category (CPC) 6 months following randomization. Results Of 939 patients, 452 (48%) woke and 139 (15%) died, mostly for non-neurological reasons, before a scheduled time point for neurological prognostication (72 h after the end of TTM). Three hundred and thirteen (33%) unconscious patients underwent prognostication at a median 117 (IQR 93–137) hours after arrest. Thirty-three (3%) unconscious patients were not neurologically prognosticated and for 2 patients (1%) data were missing. Related care recommendations were: continue in 117 (37%); not escalate in 55 (18%); and withdraw in 141 (45%). WLST eventually occurred in 196 (63%) at median day 6 (IQR 5–8). At 6 months, only 2 patients with WLST were alive and 248 (79%) of prognosticated patients had died. There were significant differences in time to WLST and death after the different recommendations (log rank Conclusion Delayed prognostication was relevant for a minority of patients and related to subsequent decisions on level-of-care with effects on ICU length-of-stay, survival time and outcome.
Tulasi R Jinka - One of the best experts on this subject based on the ideXlab platform.
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abstract 15971 neuroprotective mechanisms of intra arrest hypothermic Targeted Temperature Management
Circulation, 2017Co-Authors: Tulasi R Jinka, Xiaodan Ren, Robert W. NeumarAbstract:Objective: Mechanistic optimization of inta-arrest hypothermic-Targeted Temperature Management (HTTM) is necessary for successful translation to clinical practice. Our study evaluates the potential neuroprotective mechanisms of brain cooling initiated during cardiopulmonary resuscitation (CPR) in a rat model of asphyxial cardiac arrest. Methods: Twenty nine male Long Evens rats were subjected to 10 minute asphyxial cardiac arrest followed by CPR. Brain Temperature was monitored through intracranial Temperature probes. Rats were block randomized to normothermic Targeted Temperature Management (NTTM; n=8), or hypothermic TTM at 34 o C (HTTM-34; n=8) or 32 o C (HTTM-32; n=7). HTTM was initiated at the onset of CPR using nasopharyngeal cold saline infusion to reach target Temperatures within 10 minutes of 34 o C (flow rate 100 ml/kg/min) or 32 o C (flow rate 200 ml/kg/min). Rats were maintained at target Temperature for one hour after return of spontaneous circulation (ROSC) and then euthanized; brains collected for subcellular fractionation, mitochondrial isolation and analysis of post-ischemic injury and survival pathways. Sham rats subjected to anesthesia and instrumentation but not cardiac arrest or cooling were used as uninjured controls (n=6). Results: Brain target Temperature was achieved 5.8 ± 0.8 min in HTTM-34 group and 8.2 ± 1.3 min in HTTM-32 group after initiation of cooling. There was no statistical difference in ROSC rate between groups. Oxidative injury as measured by mitochondrial protein carbonylation was increased 40-fold in the NTTM group compared to sham controls (p Conclusion: Intra-arrest HTTM with target Temperature achieved within 10 minutes of CPR onset significantly reduces brain mitochondrial oxidative injury and may increase early survival signaling . These treatment effects was similar with 32°C and 34°C hypothermic target Temperatures.
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abstract 15971 neuroprotective mechanisms of intra arrest hypothermic Targeted Temperature Management
Circulation, 2017Co-Authors: Tulasi R Jinka, Xiaodan Ren, Robert W. NeumarAbstract:Objective: Mechanistic optimization of inta-arrest hypothermic-Targeted Temperature Management (HTTM) is necessary for successful translation to clinical practice. Our study evaluates the potential...
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combined intra and post cardiac arrest hypothermic Targeted Temperature Management in a rat model of asphyxial cardiac arrest improves survival and neurologic outcome compared to either strategy alone
Resuscitation, 2016Co-Authors: Ren Xiaodan, Tulasi R Jinka, Taeyun Kim, Michael G Paine, He Meng, Jacob Cohen, Huiyong Zheng, James A CranfordAbstract:Abstract Aim Post-cardiac arrest hypothermic-Targeted Temperature Management (HTTM) improves outcomes in preclinical cardiac arrest studies. However, inadequate understanding of the mechanisms and therapeutic windows remains a barrier to optimization. We tested the hypothesis that combined intra- and post-cardiac arrest HTTM provides a synergistic outcome benefit compared to either strategy alone. Methods Rats subjected to 8-min asphyxial cardiac arrest were block randomized to 4 treatment groups ( n =12/group): NTTM) normothermic-Targeted Temperature Management; 1-24 HTTM) HTTM initiated 1h post-ROSC and maintained for 24h; Intra-1 HTTM) HTTM initiated at CPR onset and maintained for 1h; and Intra-24 HTTM) HTTM initiated at CPR onset and maintained for 24h. HTTM was induced by nasopharyngeal cooling and maintained using an automated Temperature regulation system. Target Temperature range was 36.5–37.5°C for NTTM and 32.0–34.0°C for HTTM. Post-arrest neurologic function score (NFS) was measured daily, and rats surviving 72h were euthanized for histological analysis of neurodegeneration. Results Target brain Temperature was achieved 7.8±3.3min after initiating intra-arrest cooling. The survival rate was 42%, 50%, 50%, and 92% in the NTTM, 1-24 HTTM, Intra-1 HTTM, and Intra-24 HTTM groups, respectively ( p p p Conclusion Combined intra- and post-cardiac arrest HTTM has greater outcome benefits than either strategy alone.
David Carlbom - One of the best experts on this subject based on the ideXlab platform.
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energy expenditure and shivering severity during Targeted Temperature Management at 36 c after cardiac arrest a case series
Critical care nursing quarterly, 2020Co-Authors: Makayla Cordoza, David Carlbom, Elizabeth Bridges, Lingtak Neander Chan, Hilaire J ThompsonAbstract:Patients undergoing Targeted Temperature Management (TTM) after cardiac arrest are at risk for shivering, which increases energy expenditure (EE) and may attenuate TTM benefits. This article reports patterns of EE for patients with and without shivering who received TTM at 36°C after cardiac arrest. Based on 96 case assessments, there were 14 occasions when more than one 15-minute interval period was required to appropriately modify the Bedside Shivering Assessment Scale (BSAS) score. Investigators noted that although higher EE was related to higher BSAS scores, there may be opportunities for earlier detection of shivering.
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association between target Temperature variability and neurologic outcomes for patients receiving Targeted Temperature Management at 36 c after cardiac arrest a retrospective cohort study
Therapeutic hypothermia and temperature management, 2020Co-Authors: Makayla Cordoza, Hilaire J Thompson, Elizabeth Bridges, Robert L Burr, David CarlbomAbstract:Maintaining strict Temperature control during the maintenance phase of Targeted Temperature Management (TTM) after cardiac arrest may be an important component of clinical care. Temperature variabi...
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Targeted Temperature Management at 33 Versus 36 Degrees: A Retrospective Cohort Study.
Critical Care Medicine, 2020Co-Authors: Nicholas J. Johnson, Kyle R. Danielson, Catherine R. Counts, Katelyn Ruark, Sue Scruggs, Catherine L. Hough, Charles Maynard, Michael R. Sayre, David CarlbomAbstract:Objectives:To determine the association between Targeted Temperature Management goal Temperature of 33°C versus 36°C and neurologic outcome after out-of-hospital cardiac arrest.Design:This was a retrospective, before-and-after, cohort study.Setting:Urban, academic, level 1 trauma center from 2010 to
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Abstract 30: Targeted Temperature Management at 33 versus 36 Degrees: Outcomes After Real-World Implementation
Circulation, 2019Co-Authors: Nicholas J. Johnson, Catherine R. Counts, Katelyn Ruark, Sue Scruggs, Catherine L. Hough, Charles Maynard, Michael R. Sayre, Kyle Danielson, David CarlbomAbstract:Objective: To determine the association between Targeted Temperature Management (TTM) goal Temperature of 33 versus 36°C and neurologic outcome after out-of-hospital cardiac arrest (OHCA). Methods:...
Benjamin S. Abella - One of the best experts on this subject based on the ideXlab platform.
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practical considerations for postarrest Targeted Temperature Management
Turkish journal of emergency medicine, 2020Co-Authors: Isabelle Mullen, Benjamin S. AbellaAbstract:Out-of-hospital cardiac arrest remains a major challenge worldwide, with survival to discharge rates of <20% in the great majority of countries. Advancements in prehospital care, including increasing deployment of automated external defibrillators and improvements in bystander cardiopulmonary resuscitation, have led to more victims achieving return of spontaneous circulation (ROSC), yet the majority of patients with ROSC suffer in-hospital mortality or significant neurologic injuries that persist after discharge. This postarrest morbidity and mortality is largely due to a complex syndrome of mitochondrial dysfunction, inflammatory cascades and cellular injuries known as the postcardiac arrest syndrome (PCAS). The Management of PCAS represents a formidable task for emergency and critical care providers. A cornerstone of PCAS treatment is the use of aggressive core body Temperature control using thermostatically controlled devices, known as Targeted Temperature Management (TTM). This therapy, demonstrated to be effective in improving both survival and neurologic recovery by several randomized controlled trials nearly 20 years ago, remains a major topic of clinical investigation. Important practical questions about TTM remain: How soon must providers initiate the therapy? What TTM goal Temperature maximizes benefit while limiting potential adverse effects? How long should TTM therapy be continued in patients following resuscitation? In this review, we will address these issues and summarize clinical research over the past decade that has added to our fund of knowledge surrounding this important treatment of patients following cardiac arrest.
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abstract 17084 timing of onset of pyrexia and cardiac arrest outcomes by duration of Targeted Temperature Management
Circulation, 2016Co-Authors: Anne V. Grossestreuer, Michael W Donnino, Benjamin S. Abella, Douglas J Wiebe, David F. GaieskiAbstract:Introduction: Post-arrest pyrexia (≥38°C) has been associated with poor outcomes in recent clinical studies. Optimal duration and degree of Targeted Temperature Management (TTM) remain unclear. It is unknown to what extent the association of timing of post-TTM pyrexia with clinical outcomes is affected by duration of TTM maintenance. Hypothesis: We hypothesized that duration of TTM would modify the relationship between timing of onset of pyrexia and outcomes. Methods: We included post-arrest data from a US multicenter registry. We tested for effect modification in univariate analysis using Mantel-Hanszel tests and in multivariate logistic regression using interaction terms. Our primary outcome was neurologic status (Cerebral Performance Category (CPC) score dichotomized into “good” (1-2) and “poor” (3-5)); secondary outcome was survival to hospital discharge. We reported the distribution of patient and arrest factors by duration of TTM to explore whether these affected the relationship. We repeated this with two different calculations regarding timing: 1) time from induction of TTM to pyrexia onset; 2) time from normothermia to pyrexia onset. Results: Of 502 TTM-treated patients at 14 hospitals between 2005-2015 with serial Temperatures in the time frame of interest, 466 patients had data on time between arrest and onset of pyrexia; 195 (42%) had a pyrexic Temperature. Mean age was 59±16 years, 58% male, 41% had initial VF/VT, 47% survived and 36% had CPC 1-2 at hospital discharge. In unadjusted and adjusted analyses, the relationship between time to onset of pyrexia and outcomes were significantly modified by duration of TTM; early fever was beneficial for patients with long TTM and late fever beneficial for those with short (Figure 1). Patients differed significantly by group of TTM duration in terms of arrest duration and time to target Temperature. Conclusions: Duration of TTM may modify the relationship between timing of post-arrest pyrexia and outcomes.
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variability in postarrest Targeted Temperature Management practice implications of the 2015 guidelines
Therapeutic hypothermia and temperature management, 2015Co-Authors: Marion Leary, Gail Delfin, Audrey L. Blewer, Benjamin S. AbellaAbstract:In 2002 postarrest care was significantly altered when multiple randomized controlled trials found that therapeutic hypothermia at a goal Temperature of 32–34°C significantly improved survival and neurologic outcomes. In 2013, Targeted Temperature Management (TTM) was reexamined via a randomized controlled trial between 33°C and 36°C in post-cardiac arrest patients and found similar outcomes in both cohorts. Before the release of the 2015 American Heart Association (AHA) Guidelines, our group found that across hospitals in the United States, and even within the same institution, TTM protocol variability existed. After the 2013 TTM trial, it was anticipated that the 2015 Guidelines would clarify which target Temperature should be used during postarrest care. The AHA released their updates for post-cardiac arrest TTM recently and, based on the literature available, have recommended the use of TTM at a goal Temperature between 32°C and 36°C. Whether this variability has an effect on TTM implementation or pat...
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shorter time to target Temperature is associated with poor neurologic outcome in post arrest patients treated with Targeted Temperature Management
Resuscitation, 2015Co-Authors: Sarah M. Perman, Anne V. Grossestreuer, Marion Leary, Benjamin S. Abella, David F. Gaieski, Jonas H Ellenberg, Brendan G CarrAbstract:Introduction Time to achieve target Temperature varies substantially for patients who undergo Targeted Temperature Management (TTM) after cardiac arrest. The association between arrival at target Temperature and neurologic outcome is poorly understood. We hypothesized that shorter time from initiation of cooling to target Temperature (“induction”) will be associated with worse neurologic outcome, reflecting more profound underlying brain injury and impaired thermoregulatory control.
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Variability in Postarrest Targeted Temperature Management Practice: Implications of the 2015 Guidelines
Therapeutic hypothermia and temperature management, 2015Co-Authors: Marion Leary, Gail Delfin, Audrey L. Blewer, Benjamin S. AbellaAbstract:In 2002 postarrest care was significantly altered when multiple randomized controlled trials found that therapeutic hypothermia at a goal Temperature of 32-34°C significantly improved survival and neurologic outcomes. In 2013, Targeted Temperature Management (TTM) was reexamined via a randomized controlled trial between 33°C and 36°C in post-cardiac arrest patients and found similar outcomes in both cohorts. Before the release of the 2015 American Heart Association (AHA) Guidelines, our group found that across hospitals in the United States, and even within the same institution, TTM protocol variability existed. After the 2013 TTM trial, it was anticipated that the 2015 Guidelines would clarify which target Temperature should be used during postarrest care. The AHA released their updates for post-cardiac arrest TTM recently and, based on the literature available, have recommended the use of TTM at a goal Temperature between 32°C and 36°C. Whether this variability has an effect on TTM implementation or patient outcomes is unknown.
