Neuro Red Memorize Material Flashcards
CBF normal
CBF-50ml/100 gm/ min (750 ml/min)
CBF % of CO
15-20% of cardiac output
CBF impaired values
CBF <20-25
cerebral impairment/slowing EEG
CBF < 15-20
isoelectric EEG
CBF <10
irreversible brain damage
Cerebral Autoregulation & CBF
The brain normally tolerates wide swings in blood pressures with little change in blood flow…like the heart /kidneys
Changes in flow result in vasodilatation & vasoconstriction to maintain flow
*In the normal brain
CBF remains with MAP 50 - 150
CBF & PaCO2 tensions
CBF is directly proportionate to PaCO2 between tensions of 20 - 80 mmHg
CBF changes per PaCO2 changes
Blood flow changes approximately 1-2 ml/100g/min per mm hg change in PaCO2
This effect is immediate & is thought to be secondary to changes in pH of CSF & cerebral tissue
critical oxygen tension & CBF
when O2 falls below 50 mmHg, rapid increase in CBF and arterial blood volume
Brain Tissue Oxygen Monitoring Systems
Critical Thresholds:
Goal: above 20-25 mmHg
Brain Oxygen <20 mmHg = cerebral ischemia
Brain Oxygen >50 mmHg = Luxury Perfusion
Local area of cerebral hyperemia or increased cerebral blood flow
Hyperemia may contribute to brain swelling & we can adjust therapies…
CPP and ICP
CPP normal = 70-100 mmHg
Since ICP is normally <10 mmHg, CPP is largely dependent on MAP
However, moderate to severe increases in ICP (** > 30 mmHg**) can significantly compromise CPP & CBF even in the presence of normal MAP
CPP low values and EEG
CPP < 50 mmHg - Slowing of EEG
CPP 25-40 mmHg - Flat EEG
CPP < 25 mmHg - Irreversible brain damage
CPP autoreg
CPP = the pressure gradient driving cerebral blood flow (CBF)
hence oxygen and metabolite delivery
The NORMAL brain autoregulates its blood flow to provide a constant flow regardless of blood pressure by altering the resistance of cerebral blood vessels
CPP and brain injury
These homeostatic mechanisms are often lost
CVR is usually increased
The brain becomes susceptible to changes in b/p!
Ischemic brain regions or those at risk of ischemia are critically dependent on adequate cerebral blood flow thus CPP
CPP is a…
Maintaining CPP is a cornerstone of modern brain injury therapy
CPP and mortality
Mortality increases approximately 20% for each 10mmHg loss of CPP
In those studies where CPP is maintained above 70mmHg:
The reduction in mortality is as much as 35% for those with severe head injury
CPP & MAP
CPP may be maintained by raising the MAP or by lowering the ICP.
In practice ICP is usually controlled to within normal limits (<20mmHg) and MAP is raised therapeutically
It is unknown whether ICP control is necessary providing CPP is maintained above the critical threshold
CBF values (again)
CBF 50 ml/100g/min - Normal
CBF <20-25 - Cerebral Impairment/Slowing of EEG
CBF < 20 - Isoelectric EEG/Irreversible brain damage
CPP abnormal values
CPP < 50 mmHg - Slowing of EEG
CPP <25-40 mmHg - Flat EEG
CPP < 25 mmHg - Irreversible
A - ICP
B – PaCO2
C – CPP
D – PaO2
Monro Kellie Hypothesis
INCREASE in the volume of any ONE requires a corresponding DECREASE in the other TWO components
Cushings Triad
- HTN
- Bradycardia
- Resp disturbances
CSF volume flow and photo
Lateral Ventricle
Foramina of Monro
Third Ventricle
Cerebral aqueduct of Sylvius
Fourth Ventricle
Foramen of Magendie
Foramen of Luschka
Cisterna Magna
SA Circulation
Absorbed in the arachnoid granulations over the cerebral hemispheres
CSF Dynamics - how much in body, produced amnt, where produced, and eliminated
100-160cc in the body
500cc produced q 24 hours
Production: Choroid plexus
**Elimination/Reabsorbed: ** Arachnoid villi
Effects of drugs: Enflurane/Lasix
Hyperventilation
In some patients, hyperventilation actually increased brain oxygen deficit.
Presumably was a result of vasoconstriction, which augmented ischemic states
Jugular venous hemoglobin oxygen saturation monitoring has become widely applied in the intensive care unit
***Remains impractical in most operative settings
Inverse Steal or Robin Hood Phenomenon
Back to hyperventilation:
Decreased PCO2 constricts normal vessels but not the ischemic areas (d/t vasomotor paralysis).
This is one reason we do hyperventilate patients with intracranial tumors and ICP
VA and Coupling
VA alter the normal coupling of CBF & CMR
The combination of a in neuronal metabolic demand with an increase in cerebral blood flow (metabolic supply) is termed luxury perfusion
May only be desirable during induced hypotension & it supports the use of a VA, particularly Iso, during this technique
VA and coupling - blood flow changes
In contrast to this potentially beneficial effect during global ischemia:
a detrimental circulatory steal phenomenon is possible with VA in the setting of focal ischemia
VA CBF in normal areas of the brain but not in ischemic are, where arterioles are already maximally dilated AKA: Vasomotor paralysis
cbf change per temp change
CBF changes 5-7% per C
cbf changes with hyperthermia
Hyperthermia - increases CBF & CMR
At 42 degrees C - O2 activity begins to decrease & may reflect cell dam
CBF changes with hypothermia
Hypothermia - decreases CBF & CMR
Decreases CMR by 6-7% per degree Celsius w/proportional decrease in CBF
At 20 degrees C - EEG = isoelectric
hypothermia and normo
There were** no significant differences between **the group assigned to intraoperative hypothermia & the group assigned to normothermia in the duration of stay in the intensive care unit, the total length of hospitalization, the rates of death at follow-up or the destination at discharge.
IHAST2 trial conc.
Conclusions: Intraoperative hypothermia did not improve the neurologic outcome after craniotomy among good-grade patients with aneurysmal subarachnoid hemorrhage.
Mannitol Dose
Initial: 0.25 - 1 g/kg over 30 min
Repeat: serum osmolality of 320mOsm/L
20% mannitol
Hyperchoremic metabolic acidosis
Need to determine the Anion gap
Anion gap = Major plasma cations - Major plasma anions
Anion Gap = NA - Cl + HCO3
Normal 140 - (104 + 24) =12 ( 9-15 meq/L)
Factors that may predict a higher postoperative morbidity rate:
patient-related factors
advanced age
comorbid states: DM/CAD/Altered LOC
Tumor factors
location / size / vascularity of tumor
neural involvement
prior surgery &/or radiotherapy
midline shift
Midline shift** > 5 mm and/or encroachment on CSF cisterns** suggest intracranial hypertension
Avoid preop pharmacologic sedation and ventilatory depression
inverse steal
Inverse Steal/Robin Hood Phenomenon- Vasoconstriction of normal vessels but not in ischemic areas (d/t vaso motor paralysis).
This is one reason we hyperventilate pts. w/ tumors and increased ICP.
luxury perfusion
Luxury perfusion- BAD-Perfusion in excess of metabolic needs. Vasodilatation to surrounding tissues. AKA
Circulatory/Cerebral Steal phenomenon-
localized ischemic areas are already maximally dilated . It you further dilate surrounding vessels, you “steal” blood flow to other areas of the brain away from the ischemic area…
N2O
Effects are generally mild & easily overcome by other agents or changes in CO2 tension…
Combined with other IV agents: N2O has minimal effects on CBF, metabolic rate, & ICP
Controversial…
Adding Nitrous Oxide to a VA, can further increase CBF
When given alone, mild cerebral vasodilatation with the potential to increase ICP
Ketamine
Generally increases CMRO2 & CBF
**If **PaCO2 maintained normal in presence of elevated ICP or cerebral trauma, then ketamine does not adversely alter CBF or ICP
Post crani emesis
Occurs in approximately 50% of patients
Appears to be largely prevented by ondansetron 4mg administered near the time of dural closure…
induction
STP, propofol, or etomidate
**Prompt induction **without ICP elevation
Muscle relaxant to facilitate endotracheal intubation & mechanical hyperventilation (BEWARE: coughing causes marked increases in ICP)
Succinylcholine does not significantly alter CBF or ICP in patients with neurological injury…
Mayfield Pin Placement BP increase
Goal: Not to have large hemodynamic swings in blood pressure.
with insertion & then after due to the fact you administered a longer acting agent and now there is “down time”…
No one way is “perfect”
Know that your SBP will predictably rise ~40mmhg
pin placement timing
Therefore need to lower b/p…
Do NOT let them start until you do this…
AND do NOT lower the b/p UNTIL they have pins in hand ready to go…
What does the evidence reveal & what do I do…
research and pin placement
“The effect of skull-pin insertion on cerebrospinal fluid pressure and cerebral perfusion pressure: influence of sufentanil and fentanyl”
Conclusion:
In anesthetized patients, an intravenous bolus of fentanyl(4.5 mcg/kg) or sufentanil (0.8mcg/kg) prior to skull-pin insertion results in stable values of CSFP, CPP, BP, and HR… The b/p was modified with phenylephrine / atropine were indicated
pin placement and meds
Minimum of 4 mcg/kg Fentanyl
Titrate Iso to NO more than 1.0 MAC
Propofol 1mg/kg, titrated to response
Esmolol/Ntg – Only if necessary
Lower SBP by ~40mmg
Consider Lidocaine*
PIN Placement
Lower Iso, Propofol, NTG effects gone…
B/P Normalizes
neuro positioning
Positioning…100% fio2
Ett/IV can dislodge
monitor vitals closely
can take longer than you think…
Position depends on tumor location
Supratentorial: supine
Infratentorial: prone or sitting (BEWARE: greatly increases risk of venous air embolism)
Reasons for Mannitol & Importance of “Perfect Timing”
Mannitol reduces brain bulk by creating an osmotic gradient across the “intact”blood brain barrier causing water to flux from the extracellular extravascular to intravascular compartments.
There also is evidence that mannitol improves deformability of red blood cells, thereby reducing viscosity promoting increased blood flow.
mannitol timing
Mannitol is best given PRIOR to the time of skin incision (typically 0.5 mg/kg) so the peak effect becomes available upon dural opening.
Additional mannitol may be of value if the brain is still “tight”.
what is common with mannitol if __ and __ are not repleted?
If F & E are not repleted with diuresis Hypokalemia ensues…VERY COMMON in neurosurgery…
5.Transient Hyponatremia & decrease in hgb concentration (acute hemodilution)
VERY COMMON
Refer to Handout related to Mannitol
Posterior Fossa Crani
VAE best non-invasive detection?
Precordial Doppler ultrasound near right upper sternal border is most sensitive non-invasive monitor (detects 0.25 ml)
VAE - invasive and most sensitive?
trans-esophageal echocardiography is most sensitive, but more invasive and cumbersome then doppler, “mill-wheel” murmur
VAE S&S
sudden decrease in ETCO2, increase in ETN2 , increase in PAP’s
hypoxemia, hypotension, dysrhythmias
where is the pituitary gland located?
These benign lesions originate from the cells of the pituitary gland, which is located in the **Sella turcica **- behind nose and ethmoid
most common secreting tumor
The most common type of secreting tumor is the prolactin tumor
pituitary tumor resection
DO NOT treat like other tumors (space occupying lesions)
Normovolemic, normotensive, normocapnic Do not shrink brain.
A full brain will push tumor down to surgeon-GOOD
circle of willis
cerebral aneurysm size and occurance
Cerebral aneurysms can by classified according to size in:
Small. If less than 12 mm in diameter** (78 %) **
Large. From 12 to 24 mm in diameter (20 %) **
GIANT. If more than 24 mm in diameter (2 %) **
cerebral vasospasm
occurs generally 3-4 days after bleed
**major cause of morbidity **
Cerebral Vasospasm symptoms
diagnosis
transcranial Doppler positive before symptoms:
worsening headache
hypertension
aneurysm coiling anesthesia plan
A-line PRE- INDUCTION
CVP as indicated
Triple H therapy may be used postop
Neurologic Monitoring
SSEP’s & BAER’s are useful for posterior circulation aneurysm
aneurysm coiling induction plan
REBLEEDING IS LETHAL
Careful B/P control
Weigh risk of full stomach vs adequate depth of anesthesia & relaxation
Titrate induction agent
Blunt response to intubation
Fentanyl
LTA
giant aneurysm considerations - size and hypothermia levels
GIANT = > 24mm
Hypothermic Circulatory Arrest
Mild Hypothermia: Core Temp down to 33C
Moderate Hypothermia: 32.5-33C
Deep Hypothermia: to 18C-Permits the brain to tolerate up to 1 hour of circulatory arrest
Profound hypothermia:<10C-Allows several hours of complete ischemia
Review article: “Anesthetic Management of Deep Hypothermic Circulatory Arrest for Cerebral Aneurysm Clipping” Anesthesiology: Volume 96(2) February 2002 pp 497-503
AVM’s
Arteriovenous malformations (AVMs) complex tangles of dilated, thin-walled blood vessels.
O2-ated blood is pumped by the heart to arteries to capillaries = nourished tissues
De-O2ated blood passes back via veins
AVM’s LACK the tiny capillaries
