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chapter 11. quiz 2. Regulation of Cerebral Blood Flow

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

70 mm Hg

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

150 mm Hg

What is cerebral perfusion pressure (CPP) defined as?

MAP minus intracranial pressure (ICP)

How is autoregulation affected by rapid changes in arterial pressure?

It causes a transient alteration in CBF

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

It counteracts by narrowing vessel radius and increasing resistance.

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

Myogenic mechanism

Why is autoregulation of cerebral blood flow considered significant clinically?

It prevents excessive perfusion and hypoperfusion injuries.

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

To maintain a constant level of perfusion pressure

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

Above and below the autoregulatory plateau

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

tone of vascular smooth muscle

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

Increased neuronal activity results in increased local brain metabolism, leading to an increase in CBF.

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

A combination of metabolic, glial, neural, and vascular factors

What is the traditional view of neurovascular coupling?

It is based on a feed-forward mechanism where neuronal activity directly increases CBF.

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

K+, H+, lactate, adenosine, and ATP

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

Glutamate release enhances CBF by affecting vascular tone.

How are regional cerebral blood flow and metabolism typically coupled?

They are tightly coupled and involve a combination of various factors.

What is the role of Glutamate in neurovascular coupling?

Results in the synthesis and release of NO

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

Promotes prostaglandin and epoxyeicosatrienoic acids generation

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

Release of adenosine

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

Dopamine

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

By the relative contribution of multiple signaling pathways

What can influence CMR according to the text?

Functional state of the nervous system

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

Suppress CMR

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

CMR decreases proportionally

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

Housekeeping component for cellular integrity

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

CMRO2 remains similar

In what scenario does the CMR increase extremely ?

epileptic activity

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

They do not affect 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)?

with barbiturates, Uniform reduction in CBF and CMR throughout the brain

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

~1.5 MAC

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

Due to decreased energy utilization associated with both electrophysiological function and cellular integrity maintenance

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

Increases

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

Dramatic reduction

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

Hypothermia decrease both electrophysiological function and energy utilization associated with cellular integrity maintenance

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

They differ among anesthetic drugs

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

They may provide insights into differences in the neuroprotective potential of the drugs

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

6% to 7%

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

18°C-20°C

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

Complete suppression

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

Decreased CMR

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

It decreases to less than 10%

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

Decrease in CMRO2 below 10% of normothermic control values

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

Suppresses it

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

It decreases further

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

Lower metabolic rate leads to better tolerance

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

The reduction in CBF is more intense

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

No response is observed

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

The increase in CBF is reduced

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

Slightly affects vasoconstriction

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

They enhance the response to CO2

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

It increases with increasing Paco2 values

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

CBF increases significantly.

Which factor mediates the vasodilatory response to hypercapnia?

Nitric oxide (NO)

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

It has little immediate effect on 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 ?

CBF increases while CSF pH decreases.

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

It leads to CSF alkalosis.

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

Risk of cerebral ischemia.

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

increased CBF with a concomitant increase in ICP

With hypercarbia, cerebral autoregulatory response is?

response to hypertension is attenuated

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

1 to 2 mL/100 g/min

when the CBF response to Paco2 is attenuated

Paco2 of 75 to 80 mm Hg

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

By increasing cerebral blood flow (CBF)

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

CBF decreases modestly

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

Risk of ischemia

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

Rapidly increases CBF

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

Hypoxemic hypoxia

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

Both neurogenic effects and local humoral influences

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

Releasing NO and ATP

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

Cerebral oxygen delivery better maintained during hypoxemic hypoxia

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

Increases CBF

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

is inversely linear

the greatest neurogenic influence appears to be exerted on ?

larger cerebral arteries

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

Fastigial nucleus

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

Shifts the lower end of the autoregulatory curve to the right

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

Increases cerebral blood flow

Activation of cerebral sympathetic innervation result in ?

shifts the ULA to the right

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

Reduces resistance and increases CBF as a compensatory response to reduced oxygen delivery

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

Hypoxia significantly increases CBF compared to hemodilution

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

Reducing viscosity does not affect CBF in ischemic areas

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

It results in maximal oxygen delivery

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

Viscosity reduction does not enhance oxygen delivery

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

It further dilutes the blood, improving CBF in ischemic territories

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

Maintains CBF

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

10%

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

perfusion pressure

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

Traumatic head injury

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

The influence of CO on CBF varies depending on the clinical scenario

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

Cardiac output

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

By modulation of sympathetic nervous system activity

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

limit 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?

Decreases vasodilatory capacity of cerebral vessels

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

Attenuate autoregulation

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

MAP (perfusion pressure)

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

Suppression of autonomic neural activity

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

Multitude of factors affecting perfusion pressure

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

A family of autoregulatory curves

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

Maintenance of circulatory volume and cardiac output consideration

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

direct reduction of vasomotor tone

Learn about how the cerebral circulation regulates its resistance to maintain constant blood flow over a wide range of Mean Arterial Pressure (MAP) values. Explore the autoregulation limits, variations between subjects, and the concept of cerebral perfusion pressure.

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