Neuro Pharmacology Flashcards

1
Q

Inhaled Anesthetics Impact

A

↓CMRO2 *except N2O
↑CBF d/t vasodilation
↑ICP

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2
Q

IV Anesthetics Impact

A

↓CMRO2
↓CBF
↓ICP

Opioids +/-

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3
Q

Local Anesthetics Impact

A

↓CMRO2
↓CBF
↓ICP

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4
Q

Ketamine Impact

A

+/- CMRO2
↑CBF
↑ICP

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5
Q

Nitrous Oxide

A

34x more soluble than Nitrogen in the blood

↑CMRO2, CBF, & ICP

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6
Q

α1 Agonists

A

Bolus transiently ↑CBF & cerebral SaO2 (2-5min)

CPP maintenance w/ α1 agonist vasopressors have minimal effect on the brain

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7
Q

α2 Agonists

A

↓CBF up to 25-30%

Results from reduced CMRO2

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8
Q

β Agonists

A

Small doses - minimal effect on CBF
Large doses ↑MAP (i.e. Epi > 0.05mcg/kg/min) + physiological stress = ↑CMRO2 & CBF up to 20%
β1 receptors mediate effects
Response exaggerated w/ blood-brain barrier defect

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9
Q

β Antagonist

A

Minimal or no effect on CMRO2 & CBF

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10
Q

ACEi & ARBs

A

Minimal or no effect on CMRO2 & CBF

Autoregulation maintained

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11
Q

Barbiturates

A

Dose-dependent ↓CBF & CMR until isoelectric EEG
Maximum CBF & cerebral metabolic reductions (nearly 50%) when flat EEG
↓ICP
ROBIN HOOD effect (reverse steal phenomenon)
- CBF redistributed to ischemic areas
↓CMR > CBF
Metabolic supply exceeds metabolic demand
Anticonvulsant except Methohexital

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12
Q

Benzodiazepines

A

Dose-dependent ↓CBF & CMR
↑reduction in CBF & CMR as compared to narcotics
↓reduction in CMR & CBF as compared to barbiturates, Propofol, or Etomidate
Moderate CBF reduction
1° Midazolam
Potential to prolong emergence
Anticonvulsant properties

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13
Q

Propofol

A

Dose-dependent ↓CBF & CMR
↓CBF exceeds metabolic rate
Short elimination half-life
Anticonvulsant
Commonly used as anesthesia maintenance in patients at risk to experience intracranial HTN
Most common neuro-anesthesia induction agent

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14
Q

Etomidate

A

↓CBF, CMR, & ICP
Myoclonus movements on induction
Not 1st choice anticonvulsant but sometimes used to treat seizures
Small doses potential to activate seizure foci in patients w/ epilepsy

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15
Q

Ketamine

A

Dilates cerebral vasculature & ↑CBF ↑ICP
Select activation limbic & reticular areas partially offset by somatosensory & auditory areas depression CMR does not change (controversial)

Less common in neuro-anesthesia d/t dissociative mechanism & difficult emergence
Advantages include stable hemodynamics in trauma

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16
Q

NMDA Antagonist

A

N-methyl-D-aspartate
Glutamate receptor
Functionally dissociates the thalamus from the limbic cortex

17
Q

Thalamus

A

Relays sensory impulses from the reticular activating system to the cerebral cortex

18
Q

Limbic Cortex

A

Involved the sensation awareness

19
Q

Ketamine PD

A

↑HR, BP, & CO
↑secretions
Nystagmus
Hallucinogenic effects mitigated by Midazolam

NMDA antagonism potentially protective against neuronal cell death in brain injury patient

20
Q

Opioids

A

Minimal effects on CBF, CMR, & ICP (unless ↑PaCO2)

Avoid Morphine d/t poor lipid solubility, slower onset, & long sedative effect duration

21
Q

Cerebral Blood Volume & Cerebral Blood Flow

A

Cerebral ischemia ↑CBV ↓CBF
MAP = CBF
Cerebral vasoconstriction limits CBV
Initial ↑CBV does NOT ↑ICP d/t compensatory adjustments (venous blood shifts to extracerebral vessels & CSF shifts to spinal compartment)

22
Q

What MAP does cerebral autoregulation maintain intact?

A

Normal blood pressure

MAP 70-150mmHg