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Questions and Answers
What happens to neuronal function when cerebral blood flow (CBF) decreases below normal levels?
What happens to neuronal function when cerebral blood flow (CBF) decreases below normal levels?
At what level of CBF does the brain show indications of potentially irreversible membrane failure?
At what level of CBF does the brain show indications of potentially irreversible membrane failure?
What is the term used for brain regions where neuronal dysfunction is temporarily reversible but neuronal death will occur if blood flow is not restored?
What is the term used for brain regions where neuronal dysfunction is temporarily reversible but neuronal death will occur if blood flow is not restored?
At what CBF level does the brain show isoelectric cortical EEG?
At what CBF level does the brain show isoelectric cortical EEG?
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What are the consequences of decreased CBF to approximately 10-15 mL/100 g/min?
What are the consequences of decreased CBF to approximately 10-15 mL/100 g/min?
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What level of CBF marks a time course of slow neuronal death over hours rather than minutes?
What level of CBF marks a time course of slow neuronal death over hours rather than minutes?
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What is the key difference between complete cerebral ischemia and incomplete cerebral ischemia?
What is the key difference between complete cerebral ischemia and incomplete cerebral ischemia?
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Why does incomplete cerebral ischemia show greater tolerance compared to complete global ischemia?
Why does incomplete cerebral ischemia show greater tolerance compared to complete global ischemia?
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During normothermic complete cerebral ischemia, what occurs within minutes that is catastrophic?
During normothermic complete cerebral ischemia, what occurs within minutes that is catastrophic?
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What factor contributes to the apparent tolerance for focal or incomplete ischemia?
What factor contributes to the apparent tolerance for focal or incomplete ischemia?
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What is the central event that occurs during cerebral ischemia?
What is the central event that occurs during cerebral ischemia?
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What ion gains entry into the cytosol ?
What ion gains entry into the cytosol ?
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Which enzyme system requires Ca2+ as a cofactor for activation?
Which enzyme system requires Ca2+ as a cofactor for activation?
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What initiates the activation of various cellular processes contributing to injury during excitotoxicity?
What initiates the activation of various cellular processes contributing to injury during excitotoxicity?
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Which neurotransmitter is released in massive quantities into the synaptic cleft during ischemia?
Which neurotransmitter is released in massive quantities into the synaptic cleft during ischemia?
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What type of injury is initiated by excessive glutamatergic activity?
What type of injury is initiated by excessive glutamatergic activity?
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What can lead to lipid peroxidation and membrane injury during the metabolism of arachidonic acid to prostaglandins and leukotrienes?
What can lead to lipid peroxidation and membrane injury during the metabolism of arachidonic acid to prostaglandins and leukotrienes?
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Which enzyme participates in DNA repair but can lead to energy failure when its activity is excessive due to DNA injury?
Which enzyme participates in DNA repair but can lead to energy failure when its activity is excessive due to DNA injury?
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In response to mitochondrial injury, what type of radicals can be generated along with superoxide free radicals?
In response to mitochondrial injury, what type of radicals can be generated along with superoxide free radicals?
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What effect does an increased preischemic serum glucose level have on the process of anaerobic glycolysis during ischemia?
What effect does an increased preischemic serum glucose level have on the process of anaerobic glycolysis during ischemia?
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What is the killer substance used by macrophages that can contribute to neuronal damage?
What is the killer substance used by macrophages that can contribute to neuronal damage?
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Which molecule, important for energy metabolism, becomes depleted as a result of excessive PARP activity during DNA repair?
Which molecule, important for energy metabolism, becomes depleted as a result of excessive PARP activity during DNA repair?
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What is a characteristic feature of necrotic neuronal death?
What is a characteristic feature of necrotic neuronal death?
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Which molecule is released into the cytoplasm from injured mitochondria ?
Which molecule is released into the cytoplasm from injured mitochondria ?
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What limits injury to surrounding neurons in apoptotic neuronal death?
What limits injury to surrounding neurons in apoptotic neuronal death?
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What is the key difference between necrotic neuronal death and apoptotic neuronal death?
What is the key difference between necrotic neuronal death and apoptotic neuronal death?
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During apoptosis, what is the role of activated caspase-3?
During apoptosis, what is the role of activated caspase-3?
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What initiates the formation of an apoptosome during apoptosis?
What initiates the formation of an apoptosome during apoptosis?
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What new understanding about postischemic neuronal injury has more recent data revealed?
What new understanding about postischemic neuronal injury has more recent data revealed?
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What contributes to the gradual expansion of cerebral infarction after focal ischemia?
What contributes to the gradual expansion of cerebral infarction after focal ischemia?
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Why does the occurrence of delayed neuronal death have important implications for studies on neuroprotective strategies?
Why does the occurrence of delayed neuronal death have important implications for studies on neuroprotective strategies?
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What is indicated by evidence of cerebral inflammation even 6 to 8 months after primary ischemia in experimental studies?
What is indicated by evidence of cerebral inflammation even 6 to 8 months after primary ischemia in experimental studies?
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What happens to neurons that survive the initial insult with more moderate ischemic insults?
What happens to neurons that survive the initial insult with more moderate ischemic insults?
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How does the severity of the ischemic insult affect delayed neuronal death?
How does the severity of the ischemic insult affect delayed neuronal death?
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Why is long-term evaluation of a therapeutic intervention important in the context of cerebral infarction?
Why is long-term evaluation of a therapeutic intervention important in the context of cerebral infarction?
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What is the mainstay in the reduction of brain injury in the setting of acute ischemic stroke?
What is the mainstay in the reduction of brain injury in the setting of acute ischemic stroke?
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What is recommended for patients with acute ischemic stroke when the time from symptom onset to treatment is less than 3 hours?
What is recommended for patients with acute ischemic stroke when the time from symptom onset to treatment is less than 3 hours?
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In selected patients, up to how many hours can the window for thrombolysis be extended from the onset of symptoms?
In selected patients, up to how many hours can the window for thrombolysis be extended from the onset of symptoms?
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What is a key contraindication to thrombolysis in patients with acute ischemic stroke?
What is a key contraindication to thrombolysis in patients with acute ischemic stroke?
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Which factor has considerably expanded the window for potential benefit from clot removal in patients with acute ischemic stroke?
Which factor has considerably expanded the window for potential benefit from clot removal in patients with acute ischemic stroke?
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What has limited the number of patients who may benefit from clot removal in the context of acute ischemic stroke?
What has limited the number of patients who may benefit from clot removal in the context of acute ischemic stroke?
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What characteristic defines tissue that is amenable to salvage in the context of thrombectomy for acute ischemic stroke?
What characteristic defines tissue that is amenable to salvage in the context of thrombectomy for acute ischemic stroke?
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What is the primary outcome observed in patients who met the enrollment criteria for the DAWN and DEFUSE 3 trials?
What is the primary outcome observed in patients who met the enrollment criteria for the DAWN and DEFUSE 3 trials?
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What is one of the important therapeutic objectives in patients who sustain a cardiac arrest?
What is one of the important therapeutic objectives in patients who sustain a cardiac arrest?
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What is an effective strategy in reducing mortality and morbidity in patients with altered mental status following cardiac arrest?
What is an effective strategy in reducing mortality and morbidity in patients with altered mental status following cardiac arrest?
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What was the outcome of induction of whole-body hypothermia in neonates with hypoxic-ischemic encephalopathy?
What was the outcome of induction of whole-body hypothermia in neonates with hypoxic-ischemic encephalopathy?
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How was passive rewarming achieved after inducing mild hypothermia in patients?
How was passive rewarming achieved after inducing mild hypothermia in patients?
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What does the text suggest about the incidence of complications in patients undergoing induced hypothermia?
What does the text suggest about the incidence of complications in patients undergoing induced hypothermia?
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What is one of the benefits observed in patients undergoing induced hypothermia post-cardiac arrest?
What is one of the benefits observed in patients undergoing induced hypothermia post-cardiac arrest?
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Why is maintaining adequate perfusion pressure after cardiac arrest considered important?
Why is maintaining adequate perfusion pressure after cardiac arrest considered important?
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What is a late phase complication that may occur after cardiac arrest?
What is a late phase complication that may occur after cardiac arrest?
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what is considered effective to control intracranial hypertension ?
what is considered effective to control intracranial hypertension ?
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which of the following is considered ineffective treatment after cardiac arrest ?
which of the following is considered ineffective treatment after cardiac arrest ?
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In a small cohort study, what effect did nimodipine show in patients after cardiac arrest?
In a small cohort study, what effect did nimodipine show in patients after cardiac arrest?
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What was the outcome of the multicenter lidoflazine cardiac arrest study regarding nimodipine administration?
What was the outcome of the multicenter lidoflazine cardiac arrest study regarding nimodipine administration?
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important therapeutic objectives after Complete Global Ischemia (Cardiac Arrest) ?
important therapeutic objectives after Complete Global Ischemia (Cardiac Arrest) ?
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Study Notes
- Pharmacologic agents to protect the brain from ischemic injury have not been identified.
- Thrombolysis is the main treatment for reducing brain injury in acute ischemic stroke.
- Thrombolysis with IV alteplase is recommended within 3 hours of symptom onset.
- Mechanical thrombectomy has expanded the window for clot removal in acute ischemic stroke.
- Trials showed improved outcomes in patients undergoing thrombectomy with substantial ischemic tissue.
- Endovascular treatment eligibility in acute ischemic stroke patients has increased due to recent trials.
- Anesthesiologist involvement in caring for these patients will significantly increase.
- The brain is highly vulnerable to energy failure during cerebral ischemia.
- Neuronal function deteriorates progressively with declining cerebral blood flow.
- Ischemic penumbra refers to brain tissue with reversible dysfunction but potential for irreversible damage.
- Energy failure during cerebral ischemia leads to membrane depolarization and excitotoxicity.
- Excessive glutamatergic activity initiates excitotoxicity and neuronal swelling.
- Glutamatergic receptors activation leads to calcium influx and cellular injury processes.
- Free radicals generated during cerebral ischemia contribute to oxidative injury and inflammation.
- Neuronal death in ischemia can occur through necrosis or apoptosis pathways.
- Apoptosis in neurons is initiated by the release of cytochrome c from injured mitochondria.
- Therapeutic goals in ischemic brain injury include maintaining normocapnia and normotension.
- Induced mild hypothermia has shown effectiveness in reducing mortality and morbidity after cardiac arrest.
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Description
Learn about the relevant considerations for complete global ischemia (cardiac arrest), including the importance of maintaining adequate perfusion pressure and the development of intracranial hypertension and cerebral edema post-resuscitation.
