Neuro Pharmacology Flashcards
Inhaled Anesthetics Impact
↓CMRO2 *except N2O
↑CBF d/t vasodilation
↑ICP
IV Anesthetics Impact
↓CMRO2
↓CBF
↓ICP
Opioids +/-
Local Anesthetics Impact
↓CMRO2
↓CBF
↓ICP
Ketamine Impact
+/- CMRO2
↑CBF
↑ICP
Nitrous Oxide
34x more soluble than Nitrogen in the blood
↑CMRO2, CBF, & ICP
α1 Agonists
Bolus transiently ↑CBF & cerebral SaO2 (2-5min)
CPP maintenance w/ α1 agonist vasopressors have minimal effect on the brain
α2 Agonists
↓CBF up to 25-30%
Results from reduced CMRO2
β Agonists
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
β Antagonist
Minimal or no effect on CMRO2 & CBF
ACEi & ARBs
Minimal or no effect on CMRO2 & CBF
Autoregulation maintained
Barbiturates
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
Benzodiazepines
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
Propofol
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
Etomidate
↓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
Ketamine
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
NMDA Antagonist
N-methyl-D-aspartate
Glutamate receptor
Functionally dissociates the thalamus from the limbic cortex
Thalamus
Relays sensory impulses from the reticular activating system to the cerebral cortex
Limbic Cortex
Involved the sensation awareness
Ketamine PD
↑HR, BP, & CO
↑secretions
Nystagmus
Hallucinogenic effects mitigated by Midazolam
NMDA antagonism potentially protective against neuronal cell death in brain injury patient
Opioids
Minimal effects on CBF, CMR, & ICP (unless ↑PaCO2)
Avoid Morphine d/t poor lipid solubility, slower onset, & long sedative effect duration
Cerebral Blood Volume & Cerebral Blood Flow
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)
What MAP does cerebral autoregulation maintain intact?
Normal blood pressure
MAP 70-150mmHg