Cardiac Arrest

2016 ◽  
Author(s):  
Ji Y. Chong ◽  
Michael P. Lerario
Keyword(s):  
Cardiac Arrest ◽  
Brain Injury ◽  
Therapeutic Hypothermia ◽  
Neurological Examination ◽  
Functional Outcomes ◽  
Cardiopulmonary Arrest ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Mortality And Morbidity ◽  
Hypoxic Ischemic Brain Injury

Hypoxic–ischemic brain injury is common following cardiopulmonary arrest and is associated with high rates of mortality and morbidity. Therapeutic hypothermia has been helpful in increasing survival and functional outcomes in these patients. The neurological examination, neuroimaging studies, and ancillary serological and neurophysiological testing can be helpful in prognostication post-arrest.

scholarly journals Neuroprotective Role of Hypothermia in Hypoxic-ischemic Brain Injury: Combined Therapies using Estrogen

2019 ◽  
Vol 17 (9) ◽  
pp. 874-890 ◽  
Author(s):  
Nicolás Toro-Urrego ◽  
Diego Julián Vesga-Jiménez ◽  
María Inés Herrera ◽  
Juan Pablo Luaces ◽  
Francisco Capani
Keyword(s):  
Estrogen Receptor ◽  
Brain Injury ◽  
Therapeutic Hypothermia ◽  
Estrogenic Activity ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Estrogen Receptor Modulators ◽  
Hypoxic Ischemic Brain Injury ◽  
Underlying Mechanisms ◽  
Receptor Modulators

Hypoxic-ischemic brain injury is a complex network of factors, which is mainly characterized by a decrease in levels of oxygen concentration and blood flow, which lead to an inefficient supply of nutrients to the brain. Hypoxic-ischemic brain injury can be found in perinatal asphyxia and ischemic-stroke, which represent one of the main causes of mortality and morbidity in children and adults worldwide. Therefore, knowledge of underlying mechanisms triggering these insults may help establish neuroprotective treatments. Selective Estrogen Receptor Modulators and Selective Tissue Estrogenic Activity Regulators exert several neuroprotective effects, including a decrease of reactive oxygen species, maintenance of cell viability, mitochondrial survival, among others. However, these strategies represent a traditional approach of targeting a single factor of pathology without satisfactory results. Hence, combined therapies, such as the administration of therapeutic hypothermia with a complementary neuroprotective agent, constitute a promising alternative. In this sense, the present review summarizes the underlying mechanisms of hypoxic-ischemic brain injury and compiles several neuroprotective strategies, including Selective Estrogen Receptor Modulators and Selective Tissue Estrogenic Activity Regulators, which represent putative agents for combined therapies with therapeutic hypothermia.

Abstract 12: Cerebrovascular Pressure Reactivity Predicts Outcome in Diffuse Hypoxic-Ischemic Brain Injury

Circulation ◽  
2018 ◽  
Vol 138 (Suppl_2) ◽  
Author(s):  
Ramani Balu ◽  
Sanam Baghshomali ◽  
Benjamin S Abella ◽  
William A Kofke
Keyword(s):  
Cardiac Arrest ◽  
Brain Injury ◽  
Outcome Prediction ◽  
Reactivity Index ◽  
Ischemic Brain Injury ◽  
Icp Monitoring ◽  
Ischemic Brain ◽  
Pressure Reactivity ◽  
Hypoxic Ischemic Brain Injury ◽  
Cerebrovascular Pressure Reactivity

Introduction: Outcome prediction after diffuse hypoxic-ischemic brain injury (HIBI), which most commonly occurs after sudden cardiac arrest, remains fraught with uncertainty. Cerebral autoregulation (CA) normally limits fluctuations in cerebral blood flow through pressure induced changes in cerebral arteriolar diameter. CA is disrupted after brain injury, and the degree of autoregulatory failure correlates with the severity of brain injury. CA measurements may thus enable more accurate outcome prediction after HIBI. Hypothesis: We hypothesized that the degree of impairment in cerebrovascular pressure reactivity, one of the principle mechanisms of CA, correlates with the extent of HIBI and can predict outcome. Methods: Intracranial pressure (ICP) and mean arterial pressure (MAP) were continuously recorded for all subjects. The Pressure Reactivity Index (PRx) was calculated as a moving linear correlation coefficient between ICP and MAP for each 30 sec data epoch. PRx is positive when ICP increases in concert with MAP and implies impaired pressure reactivity. For each subject, both the mean PRx for the entire recording session as well as the proportion of PRx values > 0.2 (previously found to predict poor outcome in TBI) were calculated. Results: We included 22 consecutive patients with HIBI who underwent invasive ICP monitoring in this single center observational study between 02/2016-02/2018. Median age was 41 (range 20-77), 36% (8/22) survived to hospital discharge, and 18% (4/22) had return of consciousness. The median time of ICP monitoring was 101 hr (range 8-381 hr). HIBI was due to cardiac arrest in 19/22 patients and prolonged hypoxia in 3/22. Mean PRx was significantly higher in patients without return of consciousness (0.49 ± 0.05 vs. 0.036 ± 0.032, p = 0.001), as was the proportion of PRx values > 0.2 (0.73 ± 0.037 vs 0.34 ± 0.058, p < 0.001). All patients with return of consciousness had mean PRx < 0.2. Using this cutoff value, PRx had a 94% sensitivity and 100% specificity for predicting death or vegetative state. Conclusions: Continuous pressure reactivity measurements correlate with outcome after HIBI, and may be a useful adjunct for neuroprognostication. Future studies are needed to validate these findings in larger cohorts.

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