Resuscitative hypothermia

D, Marion; Leonov, Yuval; Ginsberg, Myron D.; Katz, Laura M.; Pm, Kochanek; Lechleuthner, A.; Nemoto, E. M.; Obrist, Walter D.; Šafář, Peter; Sterz, Fritz; Tisherman, S.; Rj, White; Xiao, Feng; Zar, Harvey

doi:10.1016/0300-9572(96)84731-9

Cited by 35 publications

(36 citation statements)

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“…37,41,[43][44][45] Hypothermia is thought to play a neuroprotective role after ROSC by decreasing metabolic demand, 46,47 decreasing the release of excitatory neurotransmitters, 16 and decreasing inflammation. 48 Animal studies since the 1980s [49][50][51][52][53][54][55][56][57] have suggested that mild induced hypothermia may be beneficial as a neuroprotectant after cardiac arrest. In addition, human literature describes a beneficial effect of mild induced hypothermia in resuscitated post cardiac arrest patients.…”

Section: Discussionmentioning

confidence: 99%

Systematic review of randomized controlled trials of therapeutic hypothermia as a neuroprotectant in post cardiac arrest patients

Cheung

Green

Magee

2006

CJEM

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Objective: Several randomized controlled trials have suggested that mild induced hypothermia may improve neurologic outcome in comatose cardiac arrest survivors. This systematic review of randomized controlled trials was designed to determine if mild induced hypothermia improves neurologic outcome, decreases mortality, or is associated with an increased incidence of adverse events. Science (1989 to November 2005. For each included study, references were reviewed and the primary author contacted to identify any additional studies. Study selection: Studies that met inclusion criteria were randomized controlled trials of adult patients (>18 years of age) with primary cardiac arrest who remained comatose after return of spontaneous circulation. Patients had to be randomized to mild induced hypothermia (32°C-34°C) or normothermia within 24 hours of presentation. Only studies reporting pre-determined outcomes including discharge neurologic outcome, mortality or significant treatment-related adverse events were included. There were no language or publication restrictions. Data synthesis: Four studies involving 436 patients, with 232 cooled to a core temperature of 32°C-34°C met inclusion criteria. Pooled data demonstrated that mild hypothermia decreased inhospital mortality (relative ratio [RR] 0.75; 95% confidence interval [CI], 0.62-0.92) and reduced the incidence of poor neurologic outcome (RR 0.74; 95% CI, 0.62-0.84). Numbers needed to treat were 7 patients to save 1 life, and 5 patients to improve neurologic outcome. There was no evidence of treatment-limiting side effects. Conclusions: Therapeutically induced mild hypothermia decreases in-hospital mortality and improves neurologic outcome in comatose cardiac arrest survivors. The possibility of treatment-limiting side effects cannot be excluded. RÉSUMÉObjectif : Plusieurs essais comparatifs randomisés ont suggéré qu'une légère hypothermie provoquée peut améliorer le résultat clinique chez les victimes d'arrêt cardiaque dans le coma. La

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Section: Discussionmentioning

confidence: 99%

Systematic review of randomized controlled trials of therapeutic hypothermia as a neuroprotectant in post cardiac arrest patients

Cheung

Green

Magee

2006

CJEM

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“…SUCCESSFUL USE OF THERAPEUTIC hypothermia after cardiac arrest in humans was described in the late 1950s as a procedure to improve the clinical outcomes but then almost abandoned because of uncertain benefits and difficulties with its use (17). It was demonstrated in 2002 by two prospective randomized trials that the induction of therapeutic hypothermia in patients, who had been resuscitated after cardiac arrest due to ventricular fibrillation (VF), increased neurological recovery and reduced mortality (2, 12a).…”

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confidence: 99%

Moderate hypothermia increases the chance of spiral wave collision in favor of self-termination of ventricular tachycardia/fibrillation

Harada

Honjo

Yamazaki

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

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I. Moderate hypothermia increases the chance of spiral wave collision in favor of self-termination of ventricular tachycardia/fibrillation. Am J Physiol Heart Circ Physiol 294: H1896-H1905, 2008. First published February 29, 2008 doi:10.1152/ajpheart.00986.2007.-In cardiac arrest due to ventricular fibrillation (VF), moderate hypothermia (MH, 33°C) has been shown to improve defibrillation success compared with normothermia (NR, 37°C) and severe hypothermia (SH, 30°C). The underlying mechanisms remain unclear. We hypothesized that MH might prevent reentrant excitations rotating around functional obstacles (rotors) that are responsible for the genesis of VF. In two-dimensional Langendorff-perfused rabbit hearts prepared by cryoablation (n ϭ 13), action potential signals were recorded by a high-resolution optical mapping system. During basic stimulation (2.5-5.0 Hz), MH and SH caused significant prolongation of action potential duration and significant reduction of conduction velocity. Wavelength was unchanged at MH, whereas it was shortened significantly at SH at higher stimulation frequencies (4.0 -5.0 Hz). The duration of direct current stimulation-induced ventricular tachycardia (VT)/VF was reduced dramatically at MH compared with NR and SH. The spiral wave (SW) excitations documented during VT at NR were by and large organized, whereas those during VT/VF at MH and SH were characterized by disorganization with frequent breakup. Phase maps during VT/VF at MH showed a higher incidence of SW collision (mutual annihilation or exit from the anatomical boundaries), which caused a temporal disappearance of phase singularity points (PS-0), compared with that at NR and SH. There was an inverse relation between PS-0 period in the observation area and VT/VF duration. MH data points were located in a longer PS-0 period and a shorter VT/VF duration zone compared with SH. MH causes a modification of SW dynamics, leading to an increase in the chance of SW collision in favor of self-termination of VT/VF. optical mapping; ventricular fibrillation SUCCESSFUL USE OF THERAPEUTIC hypothermia after cardiac arrest in humans was described in the late 1950s as a procedure to improve the clinical outcomes but then almost abandoned because of uncertain benefits and difficulties with its use (17). It was demonstrated in 2002 by two prospective randomized trials that the induction of therapeutic hypothermia in patients, who had been resuscitated after cardiac arrest due to ventricular fibrillation (VF), increased neurological recovery and reduced mortality (2, 12a). This has led to recent guideline recommendations that all unconscious adult patients with spontaneous circulation after out-of-hospital cardiac arrest should be cooled to 32-34°C for 12-24 h when the initial rhythm was VF (1). In experiments using swines with induced VF, Boddicker et al. (3) demonstrated that defibrillation success of electrical shocks and resuscitation outcomes were significantly improved under moderate hypothermia (MH, 33°C) compared with normothermia (NR, 3...

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“…Successful use of therapeutic hypothermia after cardiac arrest in humans was also described in the late 1950s [1][2][3] but was subsequently abandoned because of uncertain benefit and difficulties with its use. 4 Since then, induction of hypothermia after return of spontaneous circulation (ROSC) has been associated with improved functional recovery and reduced cerebral histological deficits in various animal models of cardiac arrest. [5][6][7][8] Additional promising preliminary human studies have been completed.…”

Section: Introductionmentioning

confidence: 99%