Hypokalemia during the cooling phase of therapeutic hypothermia and its impact on arrhythmogenesis

Mirzoyev, Sultan A.; McLeod, Christopher J.; Bunch, T. Jared; Bell, Malcolm R.; White, Roger D.

doi:10.1016/j.resuscitation.2010.08.007

Cited by 59 publications

(55 citation statements)

References 21 publications

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“…In addition, it is known that moderate hypothermia causes reductions in potassium levels (Clifton et al, 1992;Mirzoyev et al, 2010). Because posttraumatic hypothermia may delay or prevent energy depletion and subsequent neuronal depolarization after brain injury (Prieto et al, 2011;Welsh et al, 1990), the effect of moderate hypothermia on the metabolic status of the posttraumatic brain may be one reason for the described effects on P2X7 receptor protein levels reported in our study.…”

Section: Discussionsupporting

confidence: 52%

Effects of Therapeutic Hypothermia on Inflammasome Signaling after Traumatic Brain Injury

Tomura

Vaccari

Keane

et al. 2012

J Cereb Blood Flow Metab

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Traumatic brain injury (TBI) activates the NALP1/NLRP1 inflammasome, which is an important component of the early innate inflammatory response to injury. We investigated the influence of therapeutic hypothermia on inflammasome activation after TBI. Adult male Sprague-Dawley rats were subjected to moderate fluid percussion brain injury. Temperature manipulation (331C or 371C) was initiated 30 minutes after TBI and maintained for 4 hours. At 4 or 24 hours after TBI, traumatized cortex and hippocampus were prepared for immunoblot or immunohistochemical analysis. In the normothermic groups, caspase-1, caspase-11 and expression of the purinergic receptor P2X7 increased at 24 hours after TBI. Posttraumatic hypothermia lead to decreased expression of these proteins at 24 hours compared with normothermic levels. Immunocytochemical studies showed that posttraumatic hypothermia also decreased caspase-1 staining in cerebral cortical neurons compared with normothermic TBI. Cultured cortical neurons subjected to stretch injury demonstrated significant secretion of caspase-1 into the culture medium and caspase-3 activation, both results reduced by hypothermic treatment. Posttraumatic hypothermia decreases inflammasome signaling in neurons and reduces the innate immune response to TBI at 24 hours after injury. Therapeutic hypothermia may protect the injured central nervous system by targeting the detrimental consequences of the innate immune response to injury.

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Section: Discussionsupporting

confidence: 52%

Effects of Therapeutic Hypothermia on Inflammasome Signaling after Traumatic Brain Injury

Tomura

Vaccari

Keane

et al. 2012

J Cereb Blood Flow Metab

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show abstract

“…The focus of this study is the impact of potassium changes on the risk of arrhythmia. A few studies have shown that serum potassium decreases during hypothermia and that subsequent rewarming causes a rebound increase in potassium (Koht et al, 1983;Sprung et al, 1992;Mirzoyev et al, 2010). Our current knowledge of the potassium changes during TH and its effects on physiology remain sparse.…”

Section: Introductionmentioning

confidence: 99%

“…Our current knowledge of the potassium changes during TH and its effects on physiology remain sparse. It is known that high or low levels of potassium increase the risk of adverse arrhythmia (Podrid 1990;Cohn et al, 2000;Mirzoyev et al, 2010). Patients with cardiac ischemia and heart failure are at greater risk of arrhythmias due to myocardial ischemia, increased endogenous level of catecholamines, and treatment with diuretics and arrhythmogenic drugs (Leier et al, 1994;Cohn et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

Serum Potassium Changes During Therapeutic Hypothermia After Out-of-Hospital Cardiac Arrest—Should It Be Treated?

Soeholm

Kirkegaard

2012

Therapeutic Hypothermia and Temperature Management

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Serum potassium decreases significantly during the induction of TH (p=0.005). Potassium levels were not found to be different in patients with and without VF/VT in this study, perhaps due to the low number of patients, as a difference has been seen in other studies. It is recommended that an infusion of supplementary potassium be initiated during the early cooling phase in order to avoid severe hypokalemia (serum potassium <3.0 mmol/L) and terminated in due time before normothermia is reached during rewarming in order to avoid severe hyperkalemia (serum potassium >5.5 mmol/L), as serum potassium increases during rewarming.

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“…Electrolyte disorders are common during cooling, especially in the induction phase during which magnesium and potassium levels are reduced (Polderman, 2009;Tokutomi et al, 2004), although no change have been reported for serum sodium concentrations (Yanamoto et al, 1999). Hypokalemia is associated with the development of polymorphic ventricular tachycardia (Mirzoyev et al, 2010), while low magnesium can aggravate brain injury (Polderman, 2009). Myocardial sensitivity to potassium is increased by hypothermia, which can offset the effects of hypokalemia and have an overall protective role (Tokutomi et al, 2004).…”

Section: Other Complicationsmentioning

confidence: 99%

“…Myocardial sensitivity to potassium is increased by hypothermia, which can offset the effects of hypokalemia and have an overall protective role (Tokutomi et al, 2004). Although maintaining normal electrolyte levels through supplementation is both safe and effective, caution must be applied since rebound hyperkalemia has been reported in patients who undergo rapid rewarming (Mirzoyev et al, 2010;Tokutomi et al, 2004).…”

Section: Other Complicationsmentioning

confidence: 99%

Therapeutic hypothermia for stroke: Where to go?

Han

Liu

Luo

et al. 2015

Experimental Neurology

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Hypokalemia during the cooling phase of therapeutic hypothermia and its impact on arrhythmogenesis

Cited by 59 publications

References 21 publications

Effects of Therapeutic Hypothermia on Inflammasome Signaling after Traumatic Brain Injury

Effects of Therapeutic Hypothermia on Inflammasome Signaling after Traumatic Brain Injury

Serum Potassium Changes During Therapeutic Hypothermia After Out-of-Hospital Cardiac Arrest—Should It Be Treated?

Therapeutic hypothermia for stroke: Where to go?

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