Nevroprotektiv effekt av hypotermi

Dietrichs, Erik Sveberg; Dietrichs, Espen

doi:10.4045/tidsskr.14.1250

Cited by 18 publications

(17 citation statements)

References 102 publications

(52 reference statements)

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“…Hypothermia is also used as a therapeutic measure. Comatose survivors of cardiac arrest are often cooled to temperatures between 32–36 °C for cerebral protection [73]. More than 50% of this patient group are in need of inotropic support to facilitate adequate circulation [74].…”

Section: Resultsmentioning

confidence: 99%

“…More than 50% of this patient group are in need of inotropic support to facilitate adequate circulation [74]. Cooling and rewarming of patients down to, and occasionally below 20 °C is also used for cerebral protection during procedures like aortic arch surgery [73]. Providing optimal pharmacological, cardiovascular support in hypothermic patients therefore seems essential, both in therapeutic hypothermia, and when aiming to improve a high mortality rate associated with accidental hypothermia [2].…”

Section: Resultsmentioning

confidence: 99%

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Altered pharmacological effects of adrenergic agonists during hypothermia

Dietrichs

Sager

Tveita

2016

Scand J Trauma Resusc Emerg Med

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Rewarming from accidental hypothermia is often complicated by hypothermia-induced cardiac dysfunction, calling for immediate pharmacologic intervention. Studies show that although cardiac pharmacologic support is applied when rewarming these patients, a lack of updated treatment recommendations exist. Mainly due to lack of clinical and experimental data, neither of the international guidelines includes information about pharmacologic cardiac support at temperatures below 30 °C. However, core temperature of accidental hypothermia patients is often reduced below 30 °C. Few human studies exploring effects of adrenergic drugs during hypothermia have been published, and therefore prevailing information is collected from pre-clinical studies. The most prominent finding in these studies is an apparent depressive effect of adrenaline on cardiac function when used in doses which elevate cardiac output during normothermia. Also noradrenaline and isoprenaline largely lacked positive cardiac effects during hypothermia, while dopamine is a more promising drug for supporting cardiac function during rewarming. Data and information from these studies are in support of the prevailing notion; not to use adrenergic drugs at core temperatures below 30 °C.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Altered pharmacological effects of adrenergic agonists during hypothermia

Dietrichs

Sager

Tveita

2016

Scand J Trauma Resusc Emerg Med

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“…Current advice is to apply targeted temperature management (36 − 32 °C) for neuroprotection in these patients [1]. During surgical procedures like reconstructive cardiac surgery, the neuroprotective effect of cooling is evident and core temperature is occasionally reduced to below 20 °C [2]. Similar neuroprotection is obvious in in victims of accidental hypothermia, where survival after several hours of cardiac arrest is reported after core-temperature reduction down to 13.7 °C [3].…”

Section: Introductionmentioning

confidence: 99%

Resistance to ventricular fibrillation predicted by the QRS/QTc - ratio in an intact rat model of hypothermia/rewarming

Dietrichs¹,

Kondratiev²,

McGlynn

et al. 2020

Preprint

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Background Accidental hypothermia is associated with increased risk for arrhythmias, including ventricular fibrillation and cardiac arrest. Recently QRS/QTc was proposed as an ECG-marker, where decreasing QRS/QTc ratio could predict ventricular arrhythmias in such patients. If reliable it should also predict nonappearance of arrhythmias, observed in species like rat that regularly tolerate prolonged hypothermia, during sustained sinus rhythm. Methods A rat model designed for studying cardiovascular function during cooling, 4 h experimental hypothermia (15 °C core temperature) and subsequent rewarming was used, and ECG recorded throughout the experimental protocol. Results No ventricular arrhythmias occured and there was no sign of a hypothermia-induced reduction of QRS/QTc values during moderate hypothermia. The ratio steadily increased throughout the entire cooling period and remained above normothermic baseline until rewarmed. Conclusion Different from the high incidence of hypothermia-induced ventricular arrhythmias in accidental hypothermia patients, where QRS/QTc ratio is decreased in moderate hypothermia, hypothermia and rewarming of rats is not associated with increased risk for ventricular fibrillation. This resistance to lethal hypothermia-induced arrhythmias was predicted by the QRS/QTc ratio.

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“…In the course of ischaemic brain injury, necrotic cell death or apoptosis can ensue in the brain cells [7]. More specifically, there are three phases of brain injury in patients with CA [8,9].…”

Section: Cardiac Arrest Cell Death and Ttmmentioning

confidence: 99%

“…In addition, certain cold shock proteins can augment cell survival by inhibiting apoptosis specifically during cooling [12]. The accumulation and release of glutamate are decreased, and thus effects on glutamate receptors can reduce hazards of calcium influx into cells [7]. Hypothermia can inhibit inflammatory responses to ischaemia, such that formation of oxygen free radicals, reactive nitrogen compounds, cytokines and matrix metalloproteases [21,22].…”

Section: Introductionmentioning

confidence: 99%