Time to loss of brain function and activity during circulatory arrest

Pana, Raluca; Hornby, Laura; Shemie, Sam D.; Dhanani, Sonny; Teitelbaum, Jeanne

doi:10.1016/j.jcrc.2016.04.001

Cited by 57 publications

(44 citation statements)

References 48 publications

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“…Loss of neurologic function has been demonstrated by isoelectric electroencephalography in observational studies [16]. Pana et al identified human studies demonstrating isoelectric electroencephalography rhythms within 15 seconds and 30 seconds of asystole and ventricular fibrillation, respectively [16]. These findings are corroborated by animal studies establishing a similar timeline of 10 to 30 seconds from the onset of cerebral ischemia to isoelectric electroencephalography [18].…”

Section: Primary Injurymentioning

confidence: 96%

“…Historically, Rossen et al demonstrated that cessation of cerebral blood flow (CBF) by neck cuff insufflation to 600 mmHg in humans precipitated acute decreased level of consciousness within 10 seconds [16]. Decreased level of consciousness after CA occurs within 20 seconds after onset of ventricular fibrillation [17].…”

Section: Primary Injurymentioning

confidence: 99%

“…Decreased level of consciousness after CA occurs within 20 seconds after onset of ventricular fibrillation [17]. Loss of neurologic function has been demonstrated by isoelectric electroencephalography in observational studies [16]. Pana et al identified human studies demonstrating isoelectric electroencephalography rhythms within 15 seconds and 30 seconds of asystole and ventricular fibrillation, respectively [16].…”

Section: Primary Injurymentioning

confidence: 99%

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Clinical pathophysiology of hypoxic ischemic brain injury after cardiac arrest: a “two-hit” model

2017

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Hypoxic ischemic brain injury (HIBI) after cardiac arrest (CA) is a leading cause of mortality and long-term neurologic disability in survivors. The pathophysiology of HIBI encompasses a heterogeneous cascade that culminates in secondary brain injury and neuronal cell death. This begins with primary injury to the brain caused by the immediate cessation of cerebral blood flow following CA. Thereafter, the secondary injury of HIBI takes place in the hours and days following the initial CA and reperfusion. Among factors that may be implicated in this secondary injury include reperfusion injury, microcirculatory dysfunction, impaired cerebral autoregulation, hypoxemia, hyperoxia, hyperthermia, fluctuations in arterial carbon dioxide, and concomitant anemia.Clarifying the underlying pathophysiology of HIBI is imperative and has been the focus of considerable research to identify therapeutic targets. Most notably, targeted temperature management has been studied rigorously in preventing secondary injury after HIBI and is associated with improved outcome compared with hyperthermia. Recent advances point to important roles of anemia, carbon dioxide perturbations, hypoxemia, hyperoxia, and cerebral edema as contributing to secondary injury after HIBI and adverse outcomes. Furthermore, breakthroughs in the individualization of perfusion targets for patients with HIBI using cerebral autoregulation monitoring represent an attractive area of future work with therapeutic implications.We provide an in-depth review of the pathophysiology of HIBI to critically evaluate current approaches for the early treatment of HIBI secondary to CA. Potential therapeutic targets and future research directions are summarized.

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Section: Primary Injurymentioning

confidence: 96%

Section: Primary Injurymentioning

confidence: 99%

Section: Primary Injurymentioning

confidence: 99%

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Clinical pathophysiology of hypoxic ischemic brain injury after cardiac arrest: a “two-hit” model

2017

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“…2 The timing of cardiopulmonary resuscitation is critical and of paramount importance as asphyxia triggers neuronal damage beyond two minutes of cardiac arrests. 3 Cardiovascular diseases cause 30% of global mortality amounting to 17 million deaths every year. In the developing countries, the mortality is double in numbers as that of the deaths caused by HIV, malaria and tuberculosis putting together.…”

Section: Introductionmentioning

confidence: 99%

Knowledge of basic life support among the students of Jazan University, Saudi Arabia: Is it adequate to save a life?

Ahmad

Akhter

Mandal

et al. 2018

Alexandria Journal of Medicine

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Background: Basic Life Support [BLS; including cardiopulmonary resuscitation (CPR)] is a part of medical skills utilized in case of an emergency medical care to save human lives. It is well established that the young students can become major healthcare supportive workforce for a community including the cases of emergency. Therefore, adequate knowledge of BLS is necessary for all the university attending students. This study evaluated the awareness of BLS knowledge and attitude towards BLS training among the students of Jazan University, Saudi Arabia. Methods: A self-administered survey questionnaire using cross-sectional design was employed. Results: Out of 360 participants, the majority were male students (84.2%). The participants have mediocre knowledge of BLS, and their mean score was 7.83 out of 14. The knowledge score, i.e., correct response of male and female students was almost similar. Not a single student answered all the questions correctly. About 28% participants had received BLS training previously during their study course and showed better BLS knowledge (mean score 10.41) in comparison with the other participants. In contrast with the students of health science related courses, the highest mean knowledge score (11.5) was opted by the students of emergency medical services, whereas the lowest score (6.58) was opted by the students of nursing background. Conclusions: Overall, a majority of the students of Jazan University did not have complete knowledge of BLS (CPR). The outcomes of this study will be helpful for education and healthcare service providers of the Saudi kingdom as a whole and for Jazan region.

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“…12,13 Hypoxic-Ischemic Brain Injury Upon cessation of cerebral circulation due to a cardiac arrest, energy depletion will lead to unconsciousness and cessation of cortical electric activity on the electrocardiogram (EEG) within seconds. 16 Further energy depletion will lead to anoxic depolarization with loss of membrane potentials, the release of excitatory glutamate, loss of ion gradients, and the influx of water and calcium ions, triggering further intracellular pathological processes. 17 While the brain stem neurons are more resistant to injury from circulatory arrest, particularly vulnerable neurons are found in the hippocampus, cerebellum, and neocortex.…”

Section: Death After Successful Resuscitationmentioning

confidence: 99%

Neuroprognostication of Cardiac Arrest Patients: Outcomes of Importance

Cronberg

2017

Semin Respir Crit Care Med

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During the last two decades, survival rates after cardiac arrest have increased while the fraction of patients surviving with a severe neurological disability or vegetative state has decreased in many countries. While improved survival is due to improvements in the whole "chain of survival," improved methods for prognostication of neurological outcome may be of major importance for the lower disability rates. Patients who are resuscitated and treated in intensive care will die mainly from the withdrawal of life-sustaining (WLST) therapy due to presumed poor chances of meaningful neurological recovery. To ensure high-quality decision-making and to reduce the risk of premature withdrawal of care, implementation of local protocols is crucial and should be guided by international recommendations. Despite rigorous neurological prognostication, cognitive impairment and related psychological distress and reduced participation in society will still be relevant concerns for cardiac arrest survivors. The commonly used outcome measures are not designed to provide information on these domains. Follow-up of the cardiac arrest survivor needs to consider the cardiovascular burden as an important factor to prevent cognitive difficulties and future decline.

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Time to loss of brain function and activity during circulatory arrest

Cited by 57 publications

References 48 publications

Clinical pathophysiology of hypoxic ischemic brain injury after cardiac arrest: a “two-hit” model

Clinical pathophysiology of hypoxic ischemic brain injury after cardiac arrest: a “two-hit” model

Knowledge of basic life support among the students of Jazan University, Saudi Arabia: Is it adequate to save a life?

Neuroprognostication of Cardiac Arrest Patients: Outcomes of Importance

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