CNS & PNS Flashcards
(50 cards)
The Edinger-Westphal nucleus consists of smaller preganglionic parasympathetics that travel in which cranial nerve?
CN III - oculomotor nerve
Mediates pupillary light reflex and accommodation
What sensations are transmitted by the afferent spinothalamic tract?
temperature
pain
touch
Name the main arteries from which the Circle of Willis arises.
ICAs –> MCAs
Vertebral arteries –> Basilar artery
ACA, anterior communicating, PCA, posterior communicating (connects anterior and posterior circulation)
What arteries do the ICA and VAs branch off of?
Right - brachiocephalic –> common carotid –> ICA, ECA
Left - aorta arch –> common carotid –> ICA, ECA
Subclavian –> vertebral arteries
What are the common sites of Vertebral artery dissection?
transverse foramen of C6
exiting at C2
Which artery is formed by the convergence of medial branches of the VAs just prior to the basilar junction?
Anterior spinal arteries
What is the final drainage location of the transverse sinus?
sigmoid –> internal jugular veins
What are the contents of the cavernous sinus?
CN III, IV, V1, V2, VI
ICA
Sympathetic plexus
What is a typical measure of total cerebral blood flow (CBF)?
750 mL/min
~15-20% of cardiac output
50 mL/100 g/min
List the main determinants of cerebral blood flow.
autoregulation
cerebral perfusion pressure
respiratory gas tensions
cerebral metabolic rate of oxygen consumption (CMRO2) coupling
temperature
viscosity
some autonomic influences.
When does autoregulation occur and what does it ensure?
(MAPs) of 70 and 150 mmHg
decrease in CPP or MAP –> vasodilatation
increase in CPP or MAP –> vasoconstriction
patients with chronic HTN –> autoregulatory curve is shifted to the right for the lower and upper limits
When is cerebral blood flow dependent on MAP or cerebral perfusion pressure?
At the extremes of MAP (<70 mmHg or >150 mmHg), where cerebral autoregulation is non-existent, or in situations where cerebral autoregulation has been compromised (e.g. traumatic brain injury, stroke), CBF is dependent on MAP or CPP.
How does cerebral blood flow change in response to changes in PaCO2?
CBF changes proportionately to changes in PaCO2 (1-2 mL/100g brain tissue/min/mmHg change in PaCO2)
thought to be due to CO2 diffusing across the blood brain barrier –> changes in the pH
How does cerebral blood flow change in response to changes in PaO2?
Unlike the vigorous reactivity to changes in PaCO2, CBF is only altered when there are EXTREME changes in PaO2.
minor change in CBF with hyperoxemia.
marked inc in CBF with hypoxemia (PaO2 <50mmHg)
How does cerebral blood flow change in response to changes in CMRO2?
blood flow increases or is greatest where CMRO2 is greatest
This safety mechanism provides protection against hypoxia or anoxia
By how much does cerebral blood flow change in response to a degree change in temperature?
CBF changes by 5-7% per degree Celsius change in temperature.
Both CMRO2 and CBF increase as temperature increases and vice versa
How do changes in viscosity affect cerebral blood flow?
Decreased viscosity (low Hct) –> increased CBF to preserve cerebral oxygen supply
In contrast, CBF decreases at extremes of increased viscosity, such as polycythemia
What happens to cerebral blood flow during periods of intense sympathetic drive?
parasympathetic (vasodilatory)
sympathetic (vasoconstricting)
noradrenergic fibers
intense or prolonged sympathetic drive –> vasoconstrict and restrict CBF
Under most circumstances, however, the other “drivers”(e.g., pCO2, CMRO2, PO2 at extremes) of CBF supersede sympathetic or parasympathetic effects.
What levels of cerebral blood flow are associated with an isoelectric EEG and irreversible brain damage (in ml/g/min)?
10-15 mL/100 g/min –> isoelectric EEG
<10 mL/100 g/min –> irreversible brain damage
What is the formula for cerebral perfusion pressure (CPP)?
CPP = MAP - ICP or CVP whichever is greater
Because ICP, CVP are usually <10mmHg, CPP is primarily determined by MAP
Normal CPP is ~80-100mmHg
What determines the ability of a substance to traverse the blood-brain barrier?
Size, charge, hydrophobicity and degree of protein binding determine ability to cross the BBB
Smaller, freestanding, more lipid-soluble molecules can cross the BBB >>> than larger, less lipid-soluble molecules with a higher degree of protein binding
What is the circulatory steal phenomenon or inverse steal?
In the normal brain, volatile anesthetics –> vasodilatation of cerebral vessels.
Arterioles are maximally dilated in areas of ischemia, = volatile anesthetics cannot further vasodilate these regions.
If volatile anesthetics are given in the setting of focal ischemia, blood flow may potentially be redistributed away from ischemic tissue to normal tissue and lead to further damage
Hypercarbia does the same thing
Name some factors that may alter cerebral autoregulation.
- chronic hypertension - shifted to the right
- hypercapnia –> vasodilaion
- hypocapnia –> vasoconstriction
- Anemia and hemodilution –> decrease the vascular tone –> increase CBF
- mild hypothermia impairs cerebral autoregulation
- mild hyperthermia enhances cerebral autoregulation
- Volatile anesthetics
How do volatile anesthetics influence cerebral blood flow auto-regulation?
significantly impair autoregulation
CBF is preserved to lower MAP
autoregulation in response to rising MAP is impaired
1 MAC or less, sevoflurane causes less impairment than other volatile anesthetics
