What arteries supply the blood flow to the normal brain?
Two carotid arteries (L/R) and two vertebral arteries (More posterior L/R)
What provides collateral circulation in the brain?
Circle of Willis
At what level of the spine do the carotid arteries bifurcate into the external and internal carotid arteries?
Describe the bifurcations of the internal carotid artery into the cerebral circulation.
Internal carotid artery give rise to 7 branches
It ultimately bifurcates into the anterior and middle cerebral arteries
Together, the anterior+middle cerebral arteries define the anterior cerebral circulation.
Which arteries supply the spinal cord and what parts of the spinal cord do they perfuse?
Anterior spinal arteries (2): anterior 2/3 of spinal cord
Artery of Adamkiewicz: thracolumbar cord (joins the anterior spinal artery in the lower thoracic)
Posterior spinal arteries (2): posterior 1/3 of spinal cord
Describe the flow of CSF.
Lateral ventricles --> interventricular foramina (of Monro) --> third ventricles --> cerebral aqueduct of Slyvius --> fourth ventricle --> spinal cord --> arachnoid granulations --> absorption via dural venous sinuses
How much CSF volume exists at anyone time? How much is produced in a 24 hour period?
150 mL at any one time
> 450 mL / day
What is the function of the CSF?
Cushions the brain
Maintains brain function by regulating pH and electrolytes
Carries away waste products and delivers nutrients
How does cerebral blood flow respond to changes in PaCO2?
As arterial CO2 increases from 25 mm Hg to 65 mm Hg, cerebral blood low increases in a linear fashion.
How can hyperventilation be used as a therapy in the context of a patient's neurology?
It can be used for short periods of time to relax the brain or decrease ICP.
How long does hyperventilation therapy last in decreasing ICP and why?
Hyperventilation will only decrease ICP for 4-6 hours.
After this time period, the body's compensates for it (metabolic compensation to hyperventilation) and ICP goes back up.
Early hyperventilation in traumatic brain injury is associated with poor/good outcomes. (Choose one)
Describe CBF relationship with changes in PaO2.
CBF response to changes in PaO2 is flat until PaO2 falls < 50 mm Hg (then it rises quickly)
CBF is maintained between CPP of __ to __ mm Hg.
What is the difference between communicating and obstructive hydrocephalus?
Communicating hydrocephalus: failure to absorb CSF (typically due to dysfunctional arachnoid granulations); evolves over years and characterized by barely perceptional changes
Acute hydrocephalus: direct obstruction or compression of a CSF passageway; rapid progression that may require external ventricular drainage
What are the effects of inhalational anesthetics on CBF and metabolism?
(Dose dependent effects)
0.5 MAC: CMR suppression > vasodilation (decreased CBF)
1.0 MAP: CMR suppression = vasodilation (CBF unchanged)
>1.0 MAC: vasodilation > CMR suppression (significantly increased CBF)
What is the effect of N2O on ICP and CBF?
it increases both.
What is the effect of most of our IV anesthetic agents on CBF amd CMR?
Mostly decreases or does nothing to either EXCEPT for ketamine which increases CMR significantly.
What information does EEG give us?
Depth of anesthesia
Indications for EEG include..
Burst suppression necessary for cerebral protection
EEG frequencies + names and their meanings.
Delta 0-3 Hz (deep anesthesia or coma)
Theta 4-7 Hz (transition to deep anesthesia)
Alpha 8-12 Hz (light anesthesia/relaxation)
Beta >12 Hz (awake)
What is burst suppression and what are the indications for it?
Burst supression: periods of normal brain activity interrupted by stretches of greatly reduced activity >10 seconds
Refractory high ICP
Cerebral vascular surgeries
What can we do to induce burst suppression?
Deep anesthesia with anesthetic agents (esp. propofol, barbs, benzos, isoflurane)
In BIS monitors what is the proposed optimal range to prevent intra op awareness?
In SSEP monitoring, what changes are considered clinically significant?
50% decrease in signal amplitude
10% increase in signal latency
What anestheic agents can depress SSEPs?
Which ones can enhance it?
Volatiles including N2O
Opioids (large boluses)
BUT can be enhanced by ketamine and Precedex
Which cranial nerve is monitored through BAEPs?
(brainstem auditory evoked potential)
What anesthetics effect MEPs?
Volatiles (more sensitive than SSEPs)
What is the Transcranial Doppler? What are its indications?
Noninvasive monitor that evalutes relative flow changes through the large basal arteries of the brain.
Suspected emboli (esp in TBI/traumatic brain injury)
Need for noninvasive ICP measurement
Indications for ICP monitoring...
All severe TBI/traumatic brain injuries (GCS < 9) with abnormal CT scans
Severe TBI in which pt is > 40 y/o, is posturing, or has SBP < 90
Ways to decrease ICP
30 degrees of head up (positioning)
Decrease CMR (anesthetics)
How can we provide cerebral protection?
Hypothermia (35-36C for mild ischemic risk; 33-35C for planned period of focal ischemia; <20C for prolonged cardiac arrest)
Volatiles (esp isoflurane)
Barbiturates (esp thiopental)