chapter 11. quiz 2. Regulation of Cerebral Blood Flow

What is the lower limit of autoregulation (LLA) for cerebral blood flow in normal humans?

What is the upper limit of autoregulation (ULA) for cerebral blood flow in normal humans?

What is cerebral perfusion pressure (CPP) defined as?

How is autoregulation affected by rapid changes in arterial pressure?

How does the autoregulatory mechanism respond to an increase in mean arterial pressure (MAP) concerning cerebral blood flow (CBF)?

Which proposed mechanism of autoregulation involves a myogenic response of vascular smooth muscle to pressure changes?

Why is autoregulation of cerebral blood flow considered significant clinically?

What is the primary function of autoregulation of cerebral blood flow?

when the CBF become pressure-dependent (pressure-passive) and linearly varies with CPP.

According to the myogenic hypothesis, changes in CPP lead to direct changes in

What is the relationship between increased neuronal activity and local brain metabolism in terms of cerebral blood flow (CBF)?

Which factors are involved in the regulation of cerebral metabolic rate (CMR)?

What is the traditional view of neurovascular coupling?

Which by-products of metabolism are implicated in mediating neurovascular coupling?

What is the role of glutamate release due to increased synaptic activity in relation to cerebral blood flow?

How are regional cerebral blood flow and metabolism typically coupled?

What is the role of Glutamate in neurovascular coupling?

How does glutamate activation of metabotropic glutamate receptors (mGluR) in astrocytes affect cerebral blood flow?

What contributes to vascular dilation in the setting of reduced oxygen tension at the tissue level?

Which neurotransmitter released by nerves innervating cerebral vessels is NOT mentioned as potentially involved in neurovascular coupling?

How is the net result on vascular tone determined in neurovascular coupling?

What can influence CMR according to the text?

How do anesthetic drugs generally affect cerebral metabolic rate (CMR)?

What happens to the CMR when plasma concentrations of certain anesthetics like propofol increase?

Which component of cerebral metabolic rate (CMR) remains unaffected by anesthetic drugs?

What is the effect of increasing general anesthetics on CMRO2 when EEG suppression is completely achieved using any anesthetic agent?

In what scenario does the CMR increase extremely ?

What sets ketamine and nitrous oxide apart from other anesthetic drugs regarding their impact on CMR?

What is a distinguishing feature of the effects of barbiturates compared to isoflurane and sevoflurane on cerebral blood flow (CBF) and cerebral metabolic rate (CMR)?

At what approximate concentration of isoflurane associated with a burst-suppression pattern are cortical somatosensory evoked responses to median nerve stimulation difficult to elicit?

Why does a further decrease in cerebral metabolic rate (CMR) occur with temperature reduction beyond that at which EEG suppression first occurs?

What happens to cerebral blood flow (CBF) between 37°C and 42°C?

What effect does hyperthermia above 42°C have on cerebral oxygen consumption?

What is the primary difference between the effects of anesthetic drugs and hypothermia on cerebral metabolic rate (CMR)?

How do the EEG characteristics of burst-suppression states differ among anesthetic drugs?

What is the relevance of the EEG characteristics of burst-suppression states among anesthetic drugs?

What is the approximate decrease in cerebral metabolic rate (CMR) per degree Celsius of temperature reduction?

At what temperature range can hypothermia lead to complete suppression of the EEG?

What effect can hypothermia have on EEG when the temperature drops below 20-18°C?

How does a decrease in temperature impact cerebral metabolic rate (CMR)?

How does mild hypothermia affect the cerebral metabolic rate of oxygen (CMRO2) at 18°C compared to normothermic control values?

What explains the brain's tolerance for moderate periods of circulatory arrest at temperatures around 18°C and colder?

What is the primary effect of hypothermia on the basal component of the cerebral metabolic rate?

How does the cerebral metabolic rate respond as the temperature drops below the point where EEG suppression first occurs?

What is the relationship between cerebral metabolic rate and tolerance to circulatory arrest at colder temperatures?

How does cerebral blood flow (CBF) respond to hypocapnia when resting CBF is increased?

What happens to the cerebrovascular response to changes in Paco2 during severe hypotension?

How does moderate hypotension affect the response of cerebral blood flow (CBF) to hypercarbia?

What is the effect of modest hypotension on hypocapnia-induced vasoconstriction?

How do anesthetic drugs that increase resting CBF impact the response of the cerebral circulation to CO2?

What happens to the cerebrovascular response to changes in Paco2 under normal circumstances?

What happens to cerebral blood flow (CBF) when there is hypercarbia?

Which factor mediates the vasodilatory response to hypercapnia?

What effect does acute systemic metabolic acidosis have on cerebral blood flow (CBF)?

What happens to cerebrospinal fluid (CSF) pH and CBF levels after a sustained period of hyperventilation and Acute restoration of a normal Paco2 value ?

How does acute restoration of a normal Paco2 value affect cerebrospinal fluid (CSF) pH after a sustained period of hypoventilation ?

What is the theoretical risk associated with an acute restoration of a normal Paco2 value after hypercapnia?

What is the theoretical risk associated with an acute restoration of a normal Paco2 value after hypocapnia?

With hypercarbia, cerebral autoregulatory response is?

how much CBF changes for each 1 mm Hg change in Paco2 around normal Paco2 values?

when the CBF response to Paco2 is attenuated

How does the rostral ventrolateral medulla (RVLM) respond to hypoxia?

What is the effect of high Pao2 values on cerebral blood flow (CBF)?

What is the theoretical risk associated with hypercapnia followed by an acute restoration of a normal Paco2 value?

What effect does a reduction in Pao2 below 60 mm Hg have on cerebral blood flow (CBF)?

Which of the following variables leads to a more significant increase in cerebral blood flow (CBF) according to the text?

What mediates cerebral vasodilation during hypoxia, as mentioned in the text?

What role does deoxyhemoglobin play in hypoxia-induced increases in cerebral blood flow (CBF)?

What happens to cerebral oxygen delivery during hypoxia when arterial content is equivalently reduced by hypoxia or hemodilution?

How does opening of ATP-dependent K+ channels in vascular smooth muscle impact cerebral blood flow?

what is The relationship between oxyhemoglobin saturation, as evaluated by pulse oximetry, and CBF?

the greatest neurogenic influence appears to be exerted on ?

Which nuclei are likely to give rise to intraaxial pathways influencing cerebral blood flow?

What effect does hemorrhagic shock, characterized by high sympathetic tone, have on autoregulation of cerebral blood flow?

How does sympathetic denervation impact cerebral blood flow during hemorrhagic shock?

Activation of cerebral sympathetic innervation result in ?

What effect does anemia have on cerebral vascular resistance and cerebral blood flow (CBF)?

What is the impact of hypoxia compared to hemodilution on cerebral blood flow?

In patients with acute ischemic stroke, why is viscosity manipulation not beneficial in reducing cerebral injury?

How does a hematocrit of 30% to 34% impact oxygen delivery in patients with focal cerebral ischemia?

Why is viscosity not a target for manipulation in patients at risk due to cerebral ischemia?

In focal cerebral ischemia, why is reducing viscosity through hemodilution significant for increasing CBF?

What effect does the administration of epinephrine have on cerebral blood flow (CBF) under hypotensive epidural anesthesia?

reduction in cardiac output (CO) by approximately 30% results in a decrease in CBF by about:

What is the primary factor that influences cerebral blood flow (CBF) according to the provided text?

In which disease states does augmentation of cardiac output NOT increase cerebral blood flow (CBF) according to the text?

What is suggested by the relationship between cardiac output (CO) and cerebral blood flow (CBF) based on the available data?

Which factor is increasingly being recognized as an important determinant of cerebral blood flow (CBF)?

How do medications like β-antagonists and α2-agonists impact autoregulation according to the text?

How does congestive heart failure affect the capacity of autoregulatory mechanisms to maintain CBF in response to hypotension?

What role does the sympathetic nervous system play in the cerebrovascular response to hypotension?

How do hypercarbia and hypoxia affect autoregulation according to the text?

What is a major determinant of cerebral blood flow (CBF) according to the text?

What is the primary focus of anesthetics in modulating autoregulation according to the text?

What factor is deemed to render the static representation of cerebral autoregulation invalid?

In the context of autoregulatory curves, what is suggested to be more accurate than a single static curve?

What is recommended as a key part of anesthetic management concerning cerebral perfusion in individual patients?

How do medications like CCB, nitrates, ARB, ACEI impact autoregulation according to the text?