Neuroanesthesia

Question 1

For a given blood pressure, the flow depends on the resistance of a vessel. An intact brain changes its vascular resistance to maintain adequate flow across a wide range of pressure. This is called … and produces constant blood flow, with MAP ranging between …

Answer 1

autoregulation

50 and 150 mm Hg

Question 2

Hypothermia decreases CMRo2; for every degree of centigrade drop in temperature,
there is a ..% decrease in the CMR

Answer 2

6% to 7

Question 3

The neurometabolic and neurovascular coupling is lost during hypothermia, making therapeutic hypothermia an risky means of controlling intracranial hypertension among patients with traumatic brain injury

T or F

Answer 3

F

The neurometabolic and neurovascular coupling is preserved during hypothermia, making therapeutic hypothermia an effective means of controlling intracranial hypertension among patients with traumatic brain injury

Question 4

PaO2 effect in the cerebral blood flow

Answer 4

The effect of Pao2 on cerebral vascular tone and CBF is not apparent until its levels decrease to 60 mm Hg, below which vasodilation can
increase the CBF

Question 5

Blood viscosity can also affect CBF. Low hematocrit (Hct) can decrease
the viscosity, providing an improved flow; however, it can also decrease blood oxygen content. A Hct of …% is suggested to produce the optimal O2 delivery

Answer 5

30% to 34

Question 6

Etomidate effects in the CNS

Answer 6

Etomidate does not have analgesic properties, and it can cause adrenal suppression. It results in rapid awakening after metabolism and redistribution. It decreases the CMRo2 and is a potent cerebral vasoconstrictor, decreasing the CBF and ICP. Etomidate can cause spike waveforms in the EEG, and because it can also cause myoclonus, the reaction may be mistaken for a seizure. Although it can activate seizure foci in patients with focal epilepsy, in high doses it can cause an isoelectric EEG; thus, it can also be used to terminate status epilepticus. Etomidate
has recently been used to help in the localization of seizure foci. It can augment amplitude during SSEP monitoring; it produces a marked increase in cortical amplitude and a mild increase in cortical latency, while its subcortical effects are variable

Question 7

Ketamine can slow the EEG waveforms and in high doses can cause burst suppression

T or F

Answer 7

T

Question 8

How does dexmedetomidine affect the cerebral blood flow?

Answer 8

Studies show the selective α2-agonist dexmedetomidine to be a cerebral vasoconstrictor. Because studies in animals showed no effect on CMRo2, there is a concern about brain hypoperfusion. However, in
humans a decrease in the CBF/CMR ratio has not been shown. A transient increase in blood pressure during the loading dose of dexmedetomidine followed by hypotension may be a concern in patients who should have strict blood pressure control following ICH or increased ICP.

Question 9

How is mitochondrial membrane integrity relevant for neuroprotection?

Answer 9

In general, necrosis is thought to occur in the acute phase in the core of cerebral infarct, whereas apoptosis is the predominant mechanism of neuronal death in the penumbra. This process involves the increase in
permeability of the mitochondrial membrane with increased influx of sodium and calcium into the mitochondria, resulting in depolarization.
The increased permeability of the mitochondrial membrane leads to the release of cytochrome c into the cytoplasm, which activates the caspase
enzyme system. The activation of caspases leads to programmed cell death or apoptosis