State of the art reportCerebral resuscitation after cardiac arrest: Research initiatives and future directions
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Cited by (141)
Clinical and microbiological features of drowning-associated pneumonia: a retrospective multicentre cohort study
2023, Clinical Microbiology and InfectionIntracranial pressure and autoregulation in trauma
2022, Cerebrospinal Fluid and Subarachnoid Space: Pathology and Disorders: Volume 2Predictors of survival and favorable neurological outcome in patients treated with targeted temperature management after cardiac arrest: A systematic review and meta-analysis
2018, Heart and LungCitation Excerpt :In our review, initial shockable rhythm was a predictor of outcome, which was in line with other studies.8,20 At the onset of cardiac arrest, initial non-shockable rhythm likely depletes oxygen earlier than shockable rhythm, which could lead to severe brain damage.35 For the above mentioned reasons, shockable rhythm may be a significant predictor of favorable outcome in patients treated with TTM.
Low spontaneous variability in cerebral blood flow velocity in non-survivors after cardiac arrest
2017, ResuscitationCitation Excerpt :An imbalance between local vasoconstrictors and vasodilators, characterized by high endothelin levels and initially low but gradually increasing cGMP levels is suggested to underlie the cerebral perfusion changes after cardiac arrest.30 Other factors that contribute to this reduced blood flow include a reduction in neuronal activity, vasospasm, edema, platelet and leukocyte adhesion and changes in viscosity.30–35 We hypothesize that these pathophysiological changes can contribute to the changes in MFVMCA variability after cardiac arrest and influence the state of dynamic autoregulation in these patients.
Middle cerebral artery flow, the critical closing pressure, and the optimal mean arterial pressure in comatose cardiac arrest survivors—An observational study
2017, ResuscitationCitation Excerpt :An imbalance between local vasoconstrictors and vasodilators, characterized by high endothelin levels, gradually decreasing nitrate concentrations, and gradually increasing cGMP levels is suggested to underlie the cerebral perfusion changes after cardiac arrest.3 Other factors that contribute to this reduced blood flow include a reduction in neuronal activity, vasospasm, edema, platelet and leukocyte adhesion and changes in viscosity.1,3,16–19 The incidence of intracranial hypertension after cardiac arrest is unknown, and has been studied in only a small number of highly selected patients.20–24
Research of the author's groups since the 1950s was supported by the US Army, the Pennsylvania Department of Health, the Asmund S Laerdal Foundation, and the National Institutes of Health.