Basic Neurophysiology Flashcards
Glutamate Receptors
NMDA
AMPA
Kainate
GABA-A Receptor Mechanis
Drugs acting on GABA-A
- opens chloride channels–>hyperpolarization
- BZs, barbs, prop, and etomidate
GABA-B Receptor Mechanism
2nd messenger system
Opioid Receptor Mechanism
Increased potassium and decreased calcium conductance resulting in hyperpolarization
Impact of volatiles on CBF
CBF increases as concentration of volatiles increase (so then ICP increases)
*iso>des>sevo
- direct cerebral arterial vasodilators (except N20)
- interrupt autoregulation (including N20)
CBF and CMR effect
- fentanyl
- ketamine
- volatile anesthetics
- prop/etomidate/barbs/BZs
- fentanyl: minimal reduction in CBF and CMR
- ketamine: increases CBV, variable effects on CMR
- volatiles: decrease CMR and increase CBF
- prop/etomidate/barbs/BZs: decrease CBF and CMR
*IV agents do not disrupt cerebral auto regulation or CO2 responsiveness
Drugs that decrease CSF production
Acetazolamide, furosemide, spironolactone, corticosteroids, isoflurane, vasoconstrictors
Class A nerves
large, myelinated peripheral nerves
A-delta: myelinated, low threshold for activation, and conduct fast
*nociception
A-alpha: motor and prorioception
A- beta and A-gamma: cutaneous touch, pressure and muscle spindles
Class C fibers
- non-myelinated or lightly myelinated nerves w/slow conduction velocities
- slow-pain and post-ganglionic autonomic system
Pain pathway and 1st, 2nd, and 3rd order neurons
- 1st order neuron: cell body in DRG w/fibers to the periphery, synapses on 2nd order neuron in dorsal horn of spinal cord
- 2nd order neuron: cell body in dorsal horn of spinal cord, sends transmission to contralateral hemisphere of spinal cord and sends signals up to STT and synapses in a variety of places (most important: thalamus, PAG, and reticular formation)
- 3rd order neuron: cell body in thalamus, signals to the sensory cortex
Hormonal response to pain
Increased:
- cortisol
- angiotensin II
- ADH
- catecholamines
- cytokines
- ACTH
- growth hormone
- glucagon
Role in pain:
- post-central gyrus
- anterior cingulate gyrus
- insular cortex
- Post-central gyrus: sensory
- Anterior cingulate gyrus: emotional response to pain
- Insular cortex: prioritizing pain and judging its degree
Postganglionic sympathetic fibers
Adrenergic (except sweat glands and some blood vessels)
Sympathetic nervous system pathway
Preganglionic fibers arising from the spinal grey matter in the thoracic and lumbar region exit the ventral rami (like motor neurons) and synapse after a short distance on a paired bilateral paravertebral sympathetic ganglion chain
Beta 2 effects
Bronchodilation
Smooth muscle relaxation
Insulin secretion
Glycogenolysis (lysis of glycogen in liver)
Creation and metabolism of norepinephrine
Tyrosine–>Dopa–>Dopamine–>Norepi–>Epi
Norepinephrine metabolism: MOA and COMT
Post-operative Cognitive Decline or Dysfunction (POCD)
Central cholinergic insufficiency
-other theory: anesthetic associated beta-amyloid phosphorylation, like that of Alzheimer’s
Risk Factors for POCD
- Age *by far most significant
- type and duration of surgery
- substance use
- low education
- physical infirmary
- hearing and visual impairments
- sleep deprivation
- high ASA status
- male gender
Benefits of mild intraoperatively hypothermia
- decreases neuronal oxygen demand while preserving energy sources (normal ATP and phosphocreatine levels)
- decreased CMR and CBF
*NO improvement in outcomes
CBF constant over what MAP range
60-160 mm Hg
CBF change per 1°C change in temperature
6% decrease in CBF with every 1°C decrease in temp
*50% decrease in CBF for every 10°C decrease in temp
Normal CSF production per hour and per day
21 ml/hr
500 ml/day
CSF flow
Lateral ventricles–>intraventricular foramina (of Monro)–>3rd ventricle–>cerebral aqueduct (of Sylvius)–>4th ventricle–>median aperture of 4th ventricle (foramen of Magendie) and lateral apertures of 4th ventricle (foramina of Luschka)–>cerebellomedullary cistern (cistern magna)–>subarachnoid space around brain and spinal cord
Total CSF volume
150 ml
Cranial volume mass composition
80% brain
15% blood
5% CSF
Normal ICP
<10 mm Hg
Which inhalation agent increases CBF the most?
Halothane
- up to 200% increase (20% for iso)
- hyperventilation can blunt this effect
Luxury Perfusion
Circulatory Steal Phenomenon
Luxury Perfusion: Combination of a decrease in neuronal metabolic demand w/an increase in CBF (metabolic supply) caused by volatile agents
Circulatory Steal Phenomenon: occurs in setting of focal ischemia- volatile agents can increase blood flow in normal areas of the brain, but not in ischemic areas, where arterioles are already maximally vasodilated. The end result may be a redistribution (“steal”) of blood flow away from ischemic to normal areas.
Robin Hood or Reverse Steal Phenomenon
- cerebral vasoconstriction in normal areas of brain, redistributing blood flow from normal to ischemic areas
- occurs with barbiturates because they cause vasoconstriction only in normal areas of brain tissue
Effect of barbiturates on CNS physiology
- decrease CMR, CBF, CBV (blood volume)
- increase CSF absorption
- all in all–>lower ICP
Ketamine and CNS effects
- only IV agent that dilates cerebral vasculature and increases CBF (50%), but no change in CMR
- increases in CBF, CBV, and CSF volume can potentially increase ICP in patients with decreased intracranial compliance
- may offer neuroprotective effects: NMDA blockade during periods of increased glutamate concentrations, as occurs during brain injury, may be protective against neuronal cell death (NMDA blockade reduces Ca2+ entry)
Effect of lidocaine
- decreases CMR, CBF, and ICP (but less than other agents) without significant hemodynamic effects
- may be neuroprotective
IV agents capable of producing burst suppression
- barbiturates, etomidate, and propofol
- NOT benzos, opioids, or ketamine
Anesthetic effect on evoked potentials
- IV agents generally have minimal effects
- Volatiles have marked effects
