To clarify the clinical characteristics of hyperthermia at an early stage after resuscitation from cardiac arrest (CA).
We reviewed the medical records of 43 adult patients with non-traumatic out-of-hospital CA, who survived for longer than 24 h after admission to our intensive care unit (ICU) between January, 1995, and December, 1998. The patients were divided into two groups: a clinical brain death (CBD) group (n=23) and a non-CBD group (n=20), and various factors relating to hyperthermia were compared between the two groups.
The mean value of peak axillary temperatures within 72 h of admission was 39.8+/-0.9 degrees C for the CBD group, which was significantly greater than 38.3+/-0.6 degrees C for the non-CBD group (P<0.0001). The time of occurrence of the peak axillary temperature was at 19+/-16 h of admission in the CBD group and 20+/-18 h in the non-CBD group (not significantly different). There were no significant differences in risk factors relating to the occurrence of hyperthermia between the two groups, except for the number of patients who received epinephrine at ICU. In 23 patients with a peak axillary temperature of > or =39 degrees C during the first 72 h of hospitalization, brain death was diagnosed in 20 patients, whereas only 3 of 20 patients having a peak axillary temperature of <39 degrees C developed brain death (odds ratio, 37.8; 95% confidence interval, 6.72-212.2).
Hyperthermia at an early stage after resuscitation from CA may be associated with the outcome of brain death.
"The use of mild therapeutic HT in the treatment of cardiac arrest survivors has recently been questioned due to a low level of evidence of its benefits [7,8]; in addition, spontaneous hyperthermia that may have occurred in the control patients in published clinical trials seems to be a significant risk factor [10,11]. However, to date, there have been few publications directly comparing mild therapeutic HT with controlled NT after cardiac arrest. "
[Show abstract][Hide abstract] ABSTRACT: Background
Mild therapeutic hypothermia (HT) has been implemented in the management of post cardiac arrest (CA) syndrome after the publication of clinical trials comparing HT with common practice (ie, usually hyperthermia). Current evidence on the comparison between therapeutic HT and controlled normothermia (NT) in CA survivors, however, remains insufficient.
Eight female swine (sus scrofa domestica; body weight 45 kg) were randomly assigned to receive either mild therapeutic HT or controlled NT, with four animals per group. Veno-arterial extracorporeal membrane oxygenation (ECMO) was established and at minimal ECMO flow (0.5 L/min) ventricular fibrillation was induced by rapid ventricular pacing. After 20 min of CA, circulation was restored by increasing the ECMO flow to 4.5 L/min; 90 min of reperfusion followed. Target core temperatures (HT: 33°C; NT: 36.8°C) were maintained using the heat exchanger on the oxygenator. Invasive blood pressure was measured in the aortic arch, and cerebral oxygenation was assessed using near-infrared spectroscopy. After 60 min of reperfusion, up to three defibrillation attempts were performed. After 90 min of reperfusion, blood samples were drawn for the measurement of troponin I (TnI), myoglobin (MGB), creatine-phosphokinase (CPK), alanin-aminotransferase (ALT), neuron-specific enolase (NSE) and cystatin C (CysC) levels. Reactive oxygen metabolite (ROM) levels and biological antioxidant potential (BAP) were also measured.
Significantly higher blood pressure and cerebral oxygenation values were observed in the HT group (P<0.05). Sinus rhythm was restored in all of the HT animals and in one from the NT group. The levels of TnI, MGB, CPK, ALT, and ROM were significantly lower in the HT group (P<0.05); levels of NSE, CysC, and BAP were comparable in both groups.
Our results from animal model of cardiac arrest indicate that HT may be superior to NT for the maintenance of blood pressure, cerebral oxygenation, organ protection and oxidative stress suppression following CA.
Journal of Translational Medicine 05/2013; 11(1):124. DOI:10.1186/1479-5876-11-124 · 3.93 Impact Factor
"It is possible that hyperbaric oxygen or hyperbaric treatment itself may trigger more protective mechanisms and the maintenance of brain temperature might be one of them. Previous studies show that hyperthermia is frequently observed in the first 72 h after resuscitation from cardiac arrest and were associated with poor outcome (Takasu et al. 2001). Similarly, ischemic stroke is usually followed by hyperthermia, resulting from both a stroke-induced inflammatory reaction and disturbances in cell metabolism (Zaremba 2004). "
[Show abstract][Hide abstract] ABSTRACT: Anoxic brain injury resulting from cardiac arrest is responsible for approximately two-thirds of deaths. Recent evidence suggests that increased oxygen delivered to the brain after cardiac arrest may be an important factor in preventing neuronal damage, resulting in an interest in hyperbaric oxygen (HBO) therapy. Interestingly, increased oxygen supply may be also reached by application of normobaric oxygen (NBO) or hyperbaric air (HBA). However, previous research also showed that the beneficial effect of hyperbaric treatment may not directly result from increased oxygen supply, leading to the conclusion that the mechanism of hyperbaric prevention of brain damage is not well understood. The aim of our study was to compare the effects of HBO, HBA and NBO treatment on gerbil brain condition after transient forebrain ischemia, serving as a model of cardiac arrest. Thereby, we investigated the effects of repetitive HBO, HBA and NBO treatment on hippocampal CA1 neuronal survival, brain temperature and gerbils behavior (the nest building), depending on the time of initiation of the therapy (1, 3 and 6 h after ischemia). HBO and HBA applied 1, 3 and 6 h after ischemia significantly increased neuronal survival and behavioral performance and abolished the ischemia-evoked brain temperature increase. NBO treatment was most effective when applied 1 h after ischemia; later application had a weak or no protective effect. The results show that HBO and HBA applied between 1 and 6 h after ischemia prevent ischemia-evoked neuronal damage, which may be due to the inhibition of brain temperature increase, as a result of the applied rise in ambient pressure, and just not due to the oxygen per se. This perspective is supported by the finding that NBO treatment was less effective than HBO or HBA therapy. The results presented in this paper may pave the way for future experimental studies dealing with pressure and temperature regulation.
Experimental Brain Research 01/2013; 224(1):1-14. DOI:10.1007/s00221-012-3283-5 · 2.04 Impact Factor
"Increased body temperature after cardiac arrest is associated with worse outcome and brain death . In a study of 40 patients, all 20 patients who had a peak axillary temperature above 39 within the first 72 hours after cardiac arrest became brain dead versus only 3 of 20 patients who had a peak temperature less than 39 C . Considerations related to the cause of temperature elevation may have contributed significantly to the poor outcome, but with recent evidence that hypothermia is beneficial, the prevention of hyperthermia with routine antipyretics and cooling measures are important clinical interventions . "
[Show abstract][Hide abstract] ABSTRACT: Less than 3% of all patients who have out-of-hospital cardiac arrests have return of spontaneous circulation (ROSC), survive the hospitalization, and have a reasonable functional recovery. The fact that many patients who have ROSC ultimately die or fail to have favorable neurologic recovery suggests that processes that occur after hospitalization, especially in the ICU, have an impact on survival and neurologic recovery. This article addresses the acute care, with emphasis on the cardiac and neurologic aspects,that patients who have post cardiac arrest are provided in the cardiac ICU.
Neurologic Clinics 03/2006; 24(1):41-59, vi. DOI:10.1016/j.ncl.2005.11.002 · 1.40 Impact Factor
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