chapter 11. quiz 4. Effects of Anesthetics on Cerebral Blood Flow

What happens to CBV during cerebral ischemia?

What occurs when autoregulation is impaired?

How does the cerebral circulation respond to a decreasing MAP?

What compensatory adjustments occur in normal subjects with initial CBV increases?

What can an increase in CBV lead to when intracranial compliance is reduced?

How do CBF and CBV typically vary when autoregulation is functioning normally?

In neuroanesthesia, why is control and manipulation of CBF important?

What is the approximate normal CBV in mL/100g of brain?

For an adult brain weighing approximately 1400g, how much can the total CBV change for a Paco2 range of 25 to 55 mm Hg?

Why are there few data on CBV compared to CBF, especially in humans?

which of the following statements are correct

50% increase in CBF can lead to

What effect does Ketamine have on cerebral metabolic rate (CMR) and cerebral blood flow (CBF) compared to most intravenous anesthetics?

How do intravenous anesthetics typically affect neurovascular coupling and cerebral blood flow (CBF)?

What is the net effect on cerebral blood flow (CBF) at the point of EEG suppression when barbiturates are administered?

What is the general effect of intravenous anesthetics on autoregulation during their administration?

What effects do intravenous anesthetics have on vascular tone?

What is the approximate reduction in cerebral blood flow (CBF) and cerebral metabolic rate (CMR) with large doses of thiopental causing complete EEG suppression?

What is the major effect of nontoxic doses of depressant anesthetics on cerebral metabolism, based on the observations?

In patients with severe head injury maintained in barbiturate coma for 72 hours, what happens to the blood concentration of thiamylal required to maintain EEG burst suppression over time?

During deep pentobarbital anesthesia, what is the effect on autoregulation and CO2 responsiveness?

What effect do further increases in barbiturate dose have on cerebral metabolic rate (CMR) beyond a certain point?

What effect does propofol have on regional cerebral blood flow (CBF) in healthy volunteers?

During propofol administration, what effect does hypocapnia have on cerebral blood flow (CBF)?

In what way are CO2 responsiveness and autoregulation affected in humans during propofol administration?

Why does the reduction in cerebral blood flow (CBF) during hypocapnia decrease with propofol administration?

How do propofol's effects on cerebral metabolism impact cerebral blood flow (CBF) and intracranial pressure (ICP)?

What is the approximate reduction in cerebral blood flow (CBF) with a dose of etomidate sufficient to produce EEG suppression?

How does the cerebral metabolic rate (CMR) suppression caused by etomidate differ from barbiturates?

In what scenario is etomidate ineffective in reducing intracranial pressure (ICP)?

What effect does etomidate have on cerebral perfusion pressure (CPP) in patients with intracranial tumors or head injuries?

What is the general trend of cerebral metabolic rate (CMR) suppression achievable with etomidate compared to isoflurane and barbiturates?

What effect did the administration of morphine as the sole drug have on global CBF and CMRO2 in humans?

What was the observed effect of administering morphine (1 mg/kg and 3 mg/kg) with 70% N2O on CBF and CMR?

What can histamine release caused by morphine lead to in terms of cerebral vasculature?

What was the impact of autoregulation between MAP values of 60 and 120 mm Hg in human volunteers anesthetized with a combination of morphine and N2O?

What was the general finding regarding net changes in awake control measurements of CBF and CMR with large doses of morphine?

What effect does fentanyl have on CBF and CMR in the normal quiescent brain?

How does high dose fentanyl (100 μg/kg) combined with diazepam affect CBF?

What is the effect of sedative doses of fentanyl (1.5 μg/kg) on CBF in various brain areas?

What remains unaffected by fentanyl according to the text?

What was observed in human subjects after the infusion of small doses of remifentanil?

Which area showed reductions in CBF when larger doses of remifentanil were administered?

What impact does the administration of 15 mg of diazepam have on cerebral blood flow (CBF) and cerebral metabolic rate (CMR) in patients with head injuries?

What effect did the administration of midazolam have on cerebral blood flow (CBF) in awake healthy human volunteers?

How does the extent of maximal reductions in cerebral blood flow (CBF) and cerebral metabolic rate (CMR) caused by benzodiazepines compare to narcotics and barbiturates?

What are the effects on cerebral blood flow (CBF) and cerebral metabolic rate (CMR) observed when diazepam are administered?

What effect did flumazenil have on cerebral blood flow (CBF) when administered to nonanesthetized human volunteers?

In patients with severe head injury and uncontrolled intracranial pressure (ICP), what side effect was observed when flumazenil was administered?

What unexpected phenomenon was observed regarding cerebral blood flow (CBF) and intracranial pressure (ICP) levels after flumazenil administration?

Why should flumazenil be cautiously used to reverse benzodiazepine sedation in patients with impaired intracranial compliance?

What is the likely effect of droperidol on cerebral blood flow (CBF) and cerebral metabolic rate (CMR) in humans?

What do occasional increases in intracranial pressure (ICP) observed with droperidol administration most likely reflect?

What effect is droperidol likely to have on cerebral metabolic rate (CMR) based on the provided information?

What effect does the (R)-ketamine enantiomer have on the cerebral metabolic rate (CMR) compared to the (S)-ketamine enantiomer?

How does ketamine affect global cerebral blood flow (CBF) at subanesthetic doses?

Which brain areas in humans show the greatest increase in cerebral metabolic rate (CMR) after ketamine administration?

What is the observed effect anesthetic doses of ketamine on global cerebral blood flow (CBF)?

How does autoregulation behave during ketamine anesthesia according to the majority of investigations?

What is the effect of large anesthetic doses of ketamine in patients with head injuries who are sedated with propofol?

Which statement best explains the effect of ketamine on intracranial pressure (ICP) in patients receiving adjunctive sedative drugs?

What is the likely impact of concurrent administration of sedative agents on the effects of ketamine on cerebral blood flow (CBF) and intracranial pressure (ICP)?

In what scenario might ketamine be best avoided as the sole anesthetic drug due to concerns about intracranial compliance?

What effect does lidocaine have on cerebral metabolic rate (CMR) and CBF in nonanesthetized human volunteers?

What effect did large doses of lidocaine have on the cerebral metabolic rate of oxygen (CMRO2) in dogs on cardiopulmonary bypass?

How did the reduction in intracranial pressure (ICP) compare between bolus doses of thiopental and lidocaine in patients undergoing craniotomies?

What is a reasonable adjunct for preventing or treating acute increases in intracranial pressure (ICP) based on the text?

What serum concentration range of lidocaine should be maintained to avoid seizures in awake humans?

What was the observed effect of large doses of lidocaine on seizures in anesthetized humans?

What changes in cerebral blood flow (CBF) and cerebral metabolic rate (CMR) were observed after the administration of a 5 mg/kg dose of lidocaine in nonanesthetized human volunteers?

What was the observed peak serum concentration range after a 2-mg/kg bolus of lidocaine?

which of the following drugs has the greatest reduction in CMR?

which of the following drugs has the greatest reduction in CBF?