scholarly journals Our experiences with therapeutic hypothermia

2007 ◽  
Vol 60 (9-10) ◽  
pp. 431-435 ◽  
Author(s):  
Milovan Petrovic ◽  
Ilija Srdanovic ◽  
Gordana Panic ◽  
Tibor Canji ◽  
Tihomir Miljevic
Keyword(s):  
Cardiac Arrest ◽  
Therapeutic Hypothermia ◽  
Neurological Outcome ◽  
Mild Hypothermia ◽  
Acute Myocarditis ◽  
Neuroprotective Effect ◽  
Sudden Cardiac Arrest ◽  
Neurological Recovery ◽  
Global Cerebral Ischemia ◽  
Resuscitation Guidelines

Introduction. The single most important clinically relevant cause of global cerebral ischemia is cardiac arrest. The estimated rate of sudden cardiac arrest is between 40 and 130 cases per 100.000 people per year. Almost 80% of patients initially resuscitated from cardiac arrest remain comatose for more than one hour. One year after cardiac arrest only 10-30% of these patients survive with good neurological outcome. The ability to survive anoxic no-flow states is dramatically increased with protective and preservative hypothermia. The results of clinical studies show a marked neuroprotective effect of mild hypothermia in resuscitation. Material and Methods. In our clinic, 12 patients were treated with therapeutic hypothermia. A combination of intravascular and external method of cooling was used according to the ILCOR (International Liaison Committee on Resuscitation) guidelines. The target temperature was 33oC, while the duration of cooling was 24 hours. After that, passive rewarming was allowed. All patients also received other necessary therapy. Results. Six patients (50%) had a complete neurological recovery. Two patients (16.6%) had partial neurological recovery. Four patients (33.3%) remained comatose. Five patients (41.66%) survived, while 7 (58.33%) patients died. The main cause of cardiac arrest was acute myocardial infarction (91.6%). One patient had acute myocarditis. Conclusion. Mild resuscitative hypothermia after cardiac arrest improves neurological outcome and reduces mortality in comatose survivors. .

scholarly journals Therapeutic hypothermia and neurological outcome after cardiac arrest

2011 ◽  
Vol 68 (6) ◽  
pp. 495-499 ◽  
Author(s):  
Milovan Petrovic ◽  
Gordana Panic ◽  
Aleksandra Jovelic ◽  
Tibor Canji ◽  
Ilija Srdanovic ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Therapeutic Hypothermia ◽  
Neurological Outcome ◽  
Mild Hypothermia ◽  
Spontaneous Circulation ◽  
Neurologic Outcome ◽  
Return Of Spontaneous Circulation ◽  
Significant Difference ◽  
Normothermic Group ◽  
The Impact

Introduction/Aim. The most important clinically relevant cause of global cerebral ischemia is cardiac arrest. Clinical studies showed a marked neuroprotective effect of mild hypothermia in resuscitation. The aim of this study was to evaluate the impact of mild hypothermia on neurological outcome and survival of the patients in coma, after cardiac arrest and return of spontaneous circulation. Methods. The prospective study was conducted on consecutive comatose patients admitted to our clinic after cardiac arrest and return of spontaneous circulation, between February 2005 and May 2009. The patients were divided into two groups: the patients treated with mild hypothermia and the patients treated conservatively. The intravascular in combination with external method of cooling or only external cooling was used during the first 24 hours, after which spontaneous rewarming started. The endpoints were survival rate and neurological outcome. The neurological outcome was observed with Cerebral Performance Category Scale (CPC). Follow-up was 30 days. Results. The study was conducted on 82 patients: 45 patients (age 57.93 ? 14.08 years, 77.8% male) were treated with hypothermia, and 37 patients (age 62.00 ? 9.60 years, 67.6% male) were treated conservatively. In the group treated with therapeutic hypothermia protocol, 21 (46.7%) patients had full neurological restitution (CPC 1), 3 (6.7%) patients had good neurologic outcome (CPC 2), 1 (2.2%) patient remained in coma and 20 (44.4%) patients finally died (CPC 5). In the normothermic group 7 (18.9%) patients had full neurological restitution (CPC 1), and 30 (81.1%) patients remained in coma and finally died (CPC 5). Between the two therapeutic groups there was statistically significant difference in frequencies of different neurologic outcome (p = 0.006), specially between the patients with CPC 1 and CPC 5 outcome (p = 0.003). In the group treated with mild hypothermia 23 (51.1%) patients survived, and in the normothermic group 30 (81.1%) patients died, while in the group of survived patients 23 (76.7%) were treated with mild hypothermia (p = 0.003). Conclusion. Mild therapeutic hypothermia applied after cardiac arrest improved neurological outcome and reduced mortality in the studied group of comatose survivors.

Abstract 14258: Modulation of Kynurenine Pathway to Prevent Brain Injury After Cardiac Arrest and Cardiopulmonary Resuscitation in Mice

Circulation ◽  
2021 ◽  
Vol 144 (Suppl_2) ◽  
Author(s):  
Aurora Magliocca ◽  
Carlo Perego ◽  
Francesca Motta ◽  
Giulia Merigo ◽  
Francesca M Fumagalli ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Neurological Outcome ◽  
Diffusion Tensor ◽  
Neuroprotective Effect ◽  
Brain Mri ◽  
Brain Magnetic Resonance Imaging ◽  
Kynurenine Pathway ◽  
Baseline Heart Rate ◽  
Brain White Matter ◽  
Fluoro Jade B

Introduction: Kynurenine pathway (KP) is emerging as one of the potential components affecting cardiac arrest (CA) outcomes. The aim of this study is to evaluate the effects of KP inhibition through genetic deletion of the rate-limiting enzyme of the KP, indoleamine-2,3-dyoxygenase (IDO) on survival and neurological outcome after CA. Methods and Results: Sixteen adult male wild-type (WT) and IDO-deleted (IDO -/- ) mice were subjected to 8 min untreated CA followed by resuscitation. At baseline heart rate and mean arterial pressure (MAP) did not differ among groups. At the time of return of spontaneous circulation, 30 and 60 min later, MAP was higher in the IDO -/- group compared to the WT one (p=0.0005). IDO -/- mice showed higher survival compared to WT at 7 days after CA (68.5% in IDO -/- vs 37.5% in WT; log rank p=0.036). Neurological function was higher in IDO -/- than in WT mice during the 7 days following CA (p=0.0124). IDO -/- mice also showed an improved locomotor function compared to WT mice (p=0.037). Brain magnetic resonance imaging (MRI) with diffusion tensor imaging (DTI) sequences showed a reduction in fractional anisotropy in the external capsule of the corpus callosum in WT mice compared to IDO -/- mice at 7 days after resuscitation (p=0.015). We then treated additional IDO -/- mice with L-kyn 15 min before CA, to revert the IDO -/- phenotype. Brain MRI with diffusion-weighted imaging (DWI) sequences and histological analysis were performed 24h after CA in WT, IDO -/- , and IDO -/- +L-Kyn mice. Brain MRI revealed restriction of water diffusivity 24h after CA in WT mice. IDO-deletion reduced water diffusion abnormalities while the beneficial effect was reverted in the L-kyn group (p=0.01). Degenerating neurons in the frontal cortex, represented as Fluoro-Jade B positive cells, were more numerous in WT compared to IDO -/- mice; L-kyn halted this IDO deletion-induced reduction in degenerating cells (p=0.05). Conclusion: KP inhibition improves survival and neurological outcome after CA. The neuroprotective effect of IDO-deletion was associated with preservation of brain white matter microintegrity and with reduction of cerebral cytotoxic edema. Reversal of these beneficial effects by L-kyn administration in IDO -/- mice further confirm the KP role in CA outcome.

Early Prognostic Evaluation After Mild Therapeutic Hypothermia in Sudden Cardiac Arrest Survivors

2015 ◽  
Vol 68 (2) ◽  
pp. 155-157
Author(s):  
José C. Sánchez-Salado ◽  
Albert Ariza-Solé ◽  
Victòria Lorente-Tordera ◽  
Remedios Sánchez-Prieto ◽  
Guillem Muntané-Carol ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Therapeutic Hypothermia ◽  
Sudden Cardiac Arrest ◽  
Mild Therapeutic Hypothermia ◽  
Prognostic Evaluation

THERAPEUTIC HYPOTERMIA IN THE COMPLEX TREATMENT OF POST-RESUSCITATION DISEASE

2021 ◽  
Vol 22 (1) ◽  
pp. 76-80
Author(s):  
V. Niković ◽  
R. Bulajić ◽  
D. Kojić ◽  
S. Vujaćić ◽  
D. Zogović ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Cardiopulmonary Resuscitation ◽  
Therapeutic Hypothermia ◽  
Clinical Management ◽  
Neurological Outcome ◽  
Current Evidence ◽  
Complex Treatment ◽  
Current State ◽  
The Subject

This article is about of two cases of successful cardiopulmonary resuscitation (CPR) and using therapeutic hypothermia as a important part of treatment of post-resuscitation disease. Current evidence supports that induction of therapeutic hypothermia in selected patients after cardiac arrest can improve neurological outcome. It is hoped that by summarizing the current state of knowledge on the subject and highlighting issues on clinical management will enable more patients to benefit from the therapy. 

Abstract 173: The Neuroprotective Effect Of JZL184 is Comparable With Therapeutic Hypothermia in a Rat Model of Cardiac Arrest

Circulation ◽  
2019 ◽  
Vol 140 (Suppl_2) ◽  
Author(s):  
Jing Xu ◽  
Guanghui Zheng ◽  
Juntao Hu ◽  
Weiwei Ge ◽  
Jennifer Bradley ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Therapeutic Hypothermia ◽  
Rat Model ◽  
Neuroprotective Effect ◽  
Experimental Studies ◽  
Flow Index ◽  
Protective Effects ◽  
Cerebral Microcirculation ◽  
Sprague Dawley ◽  
Neuroprotective Effects

Introduction: JZL184 is a synthetic monoacylglycerol lipase inhibitor that reduces brain edema, infarct size and alleviates inflammation following cerebral ischemia in experimental studies. In this study, we compared its cerebral protective effects with therapeutic hypothermia following cardiopulmonary resuscitation (CPR) in a rat model. Hypothesis: JZL184 will have similar neuroprotective effects to therapeutic hypothermia after cardiac arrest (CA) by reducing brain and blood brain barrier (BBB) injury and preserving cerebral microcirculation following CPR. Methods: Thirty six male Sprague-Dawley rats weighing between 450-550 g were randomized: 1) control 2) hypothermia 3) JZL184. Ventricular fibrillation was induced and untreated for 6 min for all rats. Resuscitation was attempted with a 4 Joule defibrillation after 8 min of CPR. Immediately following resuscitation, either hypothermia (33+0.5 o C) or JZL184 (16 mg/k, IP) was administered. Cerebral microcirculation, S-100β, NSE and Evan’s Blue (EB) concentrations were analyzed at 6hrs after resuscitation. Results: NSE and S-100β levels were higher in control compared to hypothermia and JZL18 at 6hr post ROSC (p < 0.001) (Fig. 1). Compared with control, there was a significant decrease in brain permeability to EB in Hypothermia and JZL184 after 6hr post ROSC (p<0.001) (Fig. 2). Microvascular flow index (MFI) was reduced in control compared with hypothermia and JZL184 6hr post ROSC (p <0.01). Conclusions: JZL184 administered following resuscitation reduced brain and BBB injury and preserved cerebral microcirculation at 6 hr post arrest to the same extent as hypothermia in a rat model of cardiac arrest.

Abstract 246: Therapeutic Hypothermia Mimicking Peptide Administration During Cardiopulmonary Resuscitation Improved Cardiac Arrest Survival in Swine

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_4) ◽  
Author(s):  
Matt Oberdier ◽  
Jing Li ◽  
Dan Ambinder ◽  
Xiangdong Zhu ◽  
Sarah Fink ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Therapeutic Hypothermia ◽  
Venous Blood ◽  
Plasma Concentrations ◽  
Sudden Cardiac Arrest ◽  
The United States ◽  
Rapid Onset ◽  
Spontaneous Circulation ◽  
Control Group ◽  
Swine Model

Background: Out-of-hospital sudden cardiac arrest is a leading cause of death in the United States, affecting over 350,000 people per year with an overall survival rate around 10%. CPR, defibrillation, and therapeutic hypothermia are common resuscitation strategies, but hypothermia is difficult to implement timely to achieve survival benefit. A cell-permeable peptide TAT-PHLPP9c has been shown to alter metabolic pathways similar to hypothermia, and decreases the release of two biomarkers, taurine and glutamate, during the high osmotic stress of heart stunning and brain injury in a mouse arrest model. Hypothesis: TAT-PHLPP9c, given during CPR, enhances 24-hour survival in a swine ventricular fibrillation (VF) model. Methods: In 14 (8 controls and 6 treated) sedated, intubated, and mechanically ventilated swine, after 5 min of VF, ACLS with vest CPR and periodic defibrillations was performed. Venous blood samples were collected at baseline, after 2 min of CPR, and at 2 and 30 min after return of spontaneous circulation (ROSC). The animals were survived up to 24 hrs and plasma samples were analyzed for glutamate and taurine in 2 controls and 1 animal given peptide. Results: Three of the control animals had ROSC, but none survived for 24 hrs, while 4 of 6 treated animals achieved neurologically intact survival at 24 hrs (p < 0.02). Compared to baseline, both taurine and glutamate plasma concentrations increased in the control group, but the increase was reduced substantially by the peptide treatment at 30 min after ROSC (Figure). Conclusion: The use of the cooling mimicking peptide TAT-PHLPP9c administered during CPR significantly improved 24-hour survival in this swine model of cardiac arrest. It reduced the increase of cerebral and myocardial metabolic biomarkers, which encourages utilizing a strategy of cell-permeable peptides for intravenous administration for more rapid onset of hypothermia-like salutary effects than are possible with current CPR cooling devices.

Targeted temperature management: beneficial or not?

2020 ◽  
Vol 12 (6) ◽  
pp. 235-241 ◽  
Author(s):  
Kelley Ricketts ◽  
Bridie Jones
Keyword(s):  
Cardiac Arrest ◽  
Therapeutic Hypothermia ◽  
Survival Rates ◽  
Treatment Strategies ◽  
Targeted Temperature Management ◽  
Prehospital Setting ◽  
Neurological Recovery ◽  
Temperature Management ◽  
Potential Treatment ◽  
Potential Benefits

Targeted temperature management (TTM), formerly known as therapeutic hypothermia, has been shown to improve survival and neurological recovery in patients following cardiac arrest. Following successes with its in-hospital implementation, many guidelines now advocate its use in the prehospital domain for all out-of-hospital cardiac arrests (OHCAs). It has been suggested that patients presenting with shockable rhythms who receive early initiation of TTM have better survival rates. TTM can be initiated in the prehospital setting with minimal equipment. This article discusses and explores the potential benefits and pitfalls of targeted temperature management when initiated in the prehospital environment. Particular focus is given to potential treatment strategies that can be used by paramedics to adequately manage OHCA. It is proposed that prehospital TTM is advantageous to all patients in cardiac arrest and can be efficacious in a variety of prehospital environments, with its implementation requiring only minimal equipment.

P1706Neurological outcome in patients with out-of-hospital cardiac arrest undergoing a standardised protocol including therapeutic hypothermia and routine coronary angiography

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
M Akin ◽  
V Garcheva ◽  
J T Sieweke ◽  
J Tongers ◽  
L C Napp ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Coronary Angiography ◽  
Therapeutic Hypothermia ◽  
Neurological Outcome ◽  
Life Support ◽  
Neuron Specific Enolase ◽  
Good Neurological Outcome ◽  
Male Predominance ◽  
S 100 ◽  
Hospital Cardiac Arrest

Abstract Purpose To establish cut-offs for neuromarkers such as neuron-specific enolase (NSE) and S-100 predicting good neurological outcome for patients treated with therapeutic hypothermia with out-of-hospital cardiac arrest (OHCA) and return of spontaneous circulation (ROSC) as current cut-offs had been derived from normothermic cohorts. Methods Consecutive data of all patients with OHCA admitted to our institution between 01/2011 and 12/2016 were collected in a database. Patient received standard intensive care according to the Hannover Cardiac Resuscitation Algorithm (HaCRA) including mandatory hypothermia. Neurological markers such as neuron-specific enolase (NSE) and S-100 have been used to assess neurological damage following OHCA. Results Mean age of overall patient population (n=302) was 63±14 [54–74] years with a male predominance (77%). Cardiac arrest was witnessed in 81% and bystander cardiopulmonal resuscitation (CPR) was performed in 67%. Initial rhythm was ventricular fibrillation in 69%. ROSC had been achieved after 24±17 minutes. Hypothermia was applied in all patients. In 95% percutaneous coronary angiography and in 57% of them coronary intervention was performed. After ROSC, STEMI was present in 44%. Mechanical support was required in 19%. 30 day mortality was 44% in the total cohort. Mean NSE was 27±69 μg/l, mean NSE with good neurological outcome was 20±8.7 μg/l, highest NSE with good neurological outcome was 46 μg/l. Mean S-100 was 0.114±2.037μg/l, mean S-100 with good neurological outcome was 0.068±0.067 μg/l, highest S-100 with good neurological outcome was 0.360 μg/l. Conclusion Even when using a strict protocol for OHCA patients and routinely applying therapeutic hypothermia, the cut-offs for NSE and S-100 regarding good neurological outcome are similar to those reported before without therapeutic hypothermia, but they must not be used solitary to withdraw life support as even very high markers can be associated with goof neurological outcome in individual patients.

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